Breast cancer and other unknowns -- between a (probalistic) rock and a (probabilistic) hard place

The New York Times Magazine cover story on Sunday was disturbing.  With "Our Feel-Good War on Breast Cancer," Peggy Orenstein, herself a woman with a history of breast cancer, confronts the frustrating lack of progress in understanding what causes this disease that has or will touch so many of us, the best ways to detect it, how to treat it, which messages to convey to at-risk women (which is, of course, essentially all of them) and how best to do it.

It has been four decades since the former first lady Betty Ford went public with her breast-cancer diagnosis, shattering the stigma of the disease. It has been three decades since the founding of Komen [the best-funded breast cancer foundation in the US]. Two decades since the introduction of the pink ribbon. Yet all that well-meaning awareness has ultimately made women less conscious of the facts: obscuring the limits of screening, conflating risk with disease, compromising our decisions about health care, celebrating “cancer survivors” who may have never required treating. And ultimately, it has come at the expense of those whose lives are most at risk.

A central ongoing debate is over mammography and whether it saves lives. It's clear that it doesn't detect all tumors, and that it does detect tumors that would disappear with no intervention, and tumors that will never metastasize, and may itself be a risk factor, and yet it's the primary tool for health education and prevention that the breast cancer advocacy groups have, and which they fiercely defend. Despite statistical evidence that it may not save lives and could be causing a lot of harm.

What is 'risk' and how do we know?
People who pay attention are told that this procedure, or that treatment, has certain 'risk' associated with it, or some 'probability' of success. These are difficult words for ordinary people and even for professionals. And the problem is by no means confined to complicated biomedical situations. There is the emotionally subjective aspect of risk, as in "oooh, that's risky", in which emotions override considerations of numbers, often very misleadingly. And there is the scientifically subjective aspect of risk, as in "significant at the 0.05 level." (0.05 is just an arbitrary cutoff for 'signficance' -- another loaded and widely misperceived word).

But even if we overlook these aspects of subjectivity, there is another that is at least as important. A risk is a value between 0 (can't happen) and 1 (certain to happen). How is that determined? It's estimated from some sample of data, in which some number, say m, of observations were made, and some number, n, of them experienced the outcome for which the risk is estimated as n/m. But that is retrospective, meaning it only relates to what happened to those we studied, and there are all sorts of problems in making the data 'representative' of what we want to estimate. Did we measure all the proper variables that might affect the risk. Did we measure the exposures and outcomes accurately enough? Did we sample enough people, and were they 'random' relative to the causes and effects we want to understand?

Even if all went well, there is the inescapable fact that what we want for making decisions, such as clinical decisions on treatment, are clear-cut answers, and we can't get them because they don't exist. Every patient is different, there are multiple kinds of breast cancers, as most other cancers, and multiple ways to get the disease, so predicting an individual's risk of disease is impossible to do with very much precision. Even women with BRCA1 or 2 mutations that are strongly associated with risk aren't at 100% risk, and at some times in history, have been at much less risk than others.

And risks cutting in all directions
It is not just the risk of cancer we have to consider. It is the risk of cancer that might be due to having a mammogram. It is the risk (or probability) that the test will accurately detect a cancer. It's the risk that the cancer being detected would otherwise have progressed to become a health danger (rather than regressing and just going away unnoticed). There is the emotional risk of having a diagnosis.

Then there is the risk of any sort of treatment: biopsies, surgeries of this or that type, radiation treatment, chemotherapy. And risks associated with aspects of life that might yet induce a cancer if you don't already have one, or induce another if you do. And risks are often in these cases not just some simple probability, but the probability of living 1, 5, or 10 years, or of no recurrence.

Every one of these is a probability of sorts that has to be estimated. Since risk factors, such as lifestyles that might be associated with disease, are always changing, and we don't even know what most of those factors are, and since any treatment must be followed up on a large enough number of people to know how well (in probability terms!) it works, women are caught between many probabilistic rocks and probabilistic hard places.

It's exquisitely painful to have to deal with so many competing uncertainties in so very personal an area, when everyone is doing his or her best to evaluate options and knowledge for the shared goal of avoiding or treating disease. Our society is very poorly trained to deal with probabilities in any serious quantitative way; we're more used to high and low values that we can think of as won't-happen or will-happen. And the subtleties play on the scientists and physicians, too. No matter how sincere you are, you want your patients to do what you think is best, as unemotionally as possible, based on your personal assessment of this host of competing probabilities. And you are also embedded in this subjectivity, because you want your view to be correct, and you are always vulnerable to shading the evidence to suit your preferences.

There is plenty of advocacy, dissembling, careerism, vanities, and all that in those dealing with these issues, both patients and perhaps especially researchers and clinicians. New findings that challenge the currently accepted verdict of probabilities are emotionally adopted or resisted.

One might say that much of this includes improper or uninformed behavior. But the problem is that our knowledge, and probabilistic 'knowledge' in particular, is shaky and difficult to handle and would be if we were all saints with IQs of 200.

Trying to balance incomplete information, probabilistic estimates imperfectly arrived at, emotional reactions, and the poor understanding of probabilities plagues even the most honorable and objective of us. And it's generally even worse.  Probabilities and risks in cases like this are averages based on analysis of groups -- patients treated this way or that, screening populations, and so on.  But the risks you need to know about are for you, though is far from clear that everyone in one of these risk groups has the same risk.

It is not even clear that there is advice one can give: since the many relevant probabilities are all imperfectly known, to imperfectly known extents, the most we can do perhaps is acknowledge the realities, that the kind of evidence we must weigh is just the way science works these days.  When, whether, or how we might conceive of the problems differently, to get closer to actual individuals rather than groups, when everybody is different, is an open question--but one of widespread relevance.

Unfortunately, at this time in history of course, even in so painfully urgent and important areas as diseases like cancer, life is a roll of the dice -- and we don't even know what kind of dice we're rolling.

Yes, species are adaptable, but there are limits

For a species, habitats are successful in the long term when they sustain seasonal balancing between food sources and prey.  Flowers that insects feed on have to be in bloom when the insects that feed on and pollinate them have hatched and are looking for food, insects that a given species of bird feed on have to have hatched when that bird has arrived back from its winter or summer migrations, and so on.  So, climate change has the potential to disrupt complex habitats if migration times change, flowering times change, the timing of thaws and hibernations change, food species can't survive the changes, etc., all of which are occurring at the present time. It is likely that some of this has always been taking place, but generally at not nearly the rapid pace we see today.

So a paper in last week's Science is of interest.  In "Population Growth in a Wild Bird Is Buffered Against Phenological Mismatch," Reed et al. describe the effect of recent climate change on the cycling of a European songbird, the great tit, and its food sources.  In theory, gradual environmental change is less of a threat than rapid change because directional selection would favor organisms with extreme trait values that allow them to best adapt to the change, and because that change would be gradual enough that useful variation would be present and the selective intensity would not simply make the species extinct.

When this is the case, the average organism would do less well in the new environment than a subset of organisms with more extreme but adaptive trait values.  If environmental change is rapid, however, there may not be enough genetic variation in a population to allow it to adapt and keep pace with the changes.  And so the population is expected to experience reduced fitness, or a 'demographic cost' as the speed of change increases. If too severe, extinction is the ultimate price.

The Reed et al. study was a test of whether disruptions in the phenology, or seasonal timing, of predator and prey interactions affected the demography of the predator population.  If food is no longer available in abundance at the right time due to climate changes, is there a measurable effect of natural selection on traits that affect phenology in, in this instance, the tit?

We studied great tits (Parus major) in the Netherlands in relation to the phenology of their caterpillar food supply. This part of Western Europe has experienced substantial spring warming in recent decades related to global climate change. Great tits rely on caterpillars to feed their chicks and strive to match their breeding time with the pronounced seasonal peak in caterpillar biomass, which enhances offspring survival. Previous studies illustrated how climate change has produced a steadily increasing mismatch between great tit and caterpillar phenology in our study area, because the caterpillar food peak has advanced in response to rising spring temperatures at more than twice the rate of great tit laying dates. When temperatures during the period after great tits have laid their eggs (late spring) are high, the mismatch is larger (by 2.96 ± 0.43 days per 1°C increase, F1,36 = 47.40, P < 0.001), because caterpillars develop faster under warmer conditions and hence the food peak is early relative to the great tit nestling phase. The greater this mismatch, the stronger is directional selection for earlier laying dates (linear regression slope = –0.007 ± 0.003, F1,36 = 5.066, P = 0.031).

That is, the hypothesis is that great tits that lay their eggs early enough to take advantage of the peak supply of caterpillars to feed this chicks will produce more surviving offspring than those who continue to lay eggs at the later date.  And, this would be an 'extreme' trait, so presumably the great tit population would decline in years when the peak caterpillar supply was later than usual.  And, keep in mind that if we are considering this as an evolutionary effect, the variation must have a genetic basis.

But, the researchers don't find this.  Nor do they find an association between population growth and directional selection; phenological mismatch in this instance doesn't affect fitness (the genetically based reproductive success).  They controlled for the effects of variation in winter food supply (beech nuts), but found that it had no effect on fitness either.

Population growth as a function of (A) annual population mismatch
and (B) annual standardized selection gradient.  Source: Thomas et al.,
Science 26 April 2013 Vol. 340 no. 6131 pp. 488-491

Why is fitness not affected by this predator/prey timing mismatch?  The authors suggest two reasons.  One, the timing of egg laying is never optimal for all females relative to the peak supply of caterpillars because the peak supply window is always narrower than the variation in timing of egg laying.  So, fitness is never optimal for the entire population.

And second, reduced survival of hatchlings due to scare food supply is offset by improved survival of fledglings because there's less competition due to lower population size.  The survival of young birds is highly correlated with population density.

Again, we would note that even if there were  a difference in fitness, it would have no evolutionary relevance unless it were due to specific genetic variation.  This is easy to forget, even if an effect were found. 

In our book, The Mermaid's Tale, after which we named this blog, we suggested a set of general fundamental principles of life that 150 years of observation since Darwin have made apparent.  (We've blogged about these principles before, including here.)  We referred to one such principle as 'facultativeness', or the ability to adapt, which we have suggested must have been one of the earliest traits to evolve given that it is so ubiquitous.  Another word we've used to describe this is 'slop', or imprecision -- as opposed to the exquisitely finely-tuned adaptation that many people think of when they think of the effects of natural selection.

Timing of egg laying in the great tit, however it is determined, is clearly imprecise, and there's still variation in the trait.  And, importantly, that imprecision is tolerated.  It has not been drummed out of the population by natural selection, balancing or not.  And that's a good thing for great tits, given that their food supply varies.

It might be tempting to interpret these results as meaning that climate change isn't going to be a problem because organisms will just adapt.  And yes, organisms are adaptable -- within limits. Including the great tit.  But many species have already gone extinct, and many more will do so.  The Reed paper documents the response to a 3 degree temperature change.  As with the proverbial frog in a pot of water set to boil, there's no reason to think these results are generalizable to the greater changes to come.

If evolution has led to, or tolerated, facultativeness, there is still the question as to how it is maintained.  We don't suggest that there is a gene 'for' such a trait.  Instead, genetic mechanisms have evolved the ability to react to environmental conditions, rather than requiring very precise environments.  The result is that organisms can survive and reproduce in a range of circumstances.  This should not be a surprise to anyone, but may seem so if your view of evolution is that natural selection fine-tunes every species for  highly specific, restricted circumstances.  There's a word for species that were so programmed:  extinct.

Intestinal microbes and heart disease -- we are what we eat

And now another in our irregular series on the role of anything-but-genes in chronic disease.  We've posted about the possible role of inflammation in many late onset or chronic heart disease, diet and lifestyle in heart disease, inflammation in asthma, cleanliness in asthma, inflammation in macular degeneration, and so on.  Diseases, it must be noted, for which hundreds of millions of dollars have been spent on the search for risk factor genes.  The excuse for this, used by geneticists to garner many huge grants, and with little other rationale for obviously environmental problems, was that they'd find important (major) segments of the population that were genetically susceptible to these environments.  We need not here belabor the thinness (from the beginning) of that rationale, because there are more important things to think about.

Steak; Wikimedia

For decades, primarily thanks to findings from the Framingham Study, it has been accepted wisdom that red meat is a risk factor for heart disease.  Why?  Because eating red meat was thought to raise cholesterol, which leads to hardening of the arteries, and then cardiovascular disease.  That led the pork and chicken industries to promote their implied-safer products (e.g., "the other red meat!").  Eggs, too, were implicated for a while because the yolks are high in cholesterol, though they were taken off the danger list some time ago (unfortunately, too late for some of us, who have developed a reflex egg-aversion, but given the cycling of risk factors, maybe that egg-aversion is a good thing).

Recent meta-analyses were not able to confirm the association between saturated fat and cholesterol and cardiovascular disease, a rather stunning finding that suggested that there may be other, perhaps correlated, environmental factors involved.  Two recent stories by Gina Kolata in the New York Times present just such alternative risk factors.

Kolata's story on April 7 suggested that indeed it's not the saturated fat or the cholesterol in meat that's to blame but the response of microbes in the gut to a constituent of the meat, carnitine in particular.  In a paper published in Nature Medicine, researchers at the Cleveland Clinic propose that when we eat meat the microbes in our gut convert carnitine into trimethylamine (TMA), which the liver then converts into TMAO, trimethylamine N-oxide, thought to be the real culprit in cardiovascular disease (CVD) because it causes atherosclerosis, hardening of the arteries.

The researchers compared the response of meat eaters and vegans to ingesting carnitine, and found that vegans didn't produce TMAO. Studies have shown that microbial composition of the gut does indeed vary with diet, among other things (geography, pregnancy, etc.) and meat eating presumably feeds a subset of microbes that vegans don't host.  Theirs don't make TMAO.    

Hard boiled eggs; Wikimedia

Kolata's story in yesterday's Times reports that a constituent of eggs might also be converted into TMAO by microbes in the gut.  In a paper published in the New England Journal of Medicine on Wednesday, the same researchers propose that when we digest the phosphatidylcholine, or lecithin, in eggs, one of the constituents is choline.  Intestinal microbes convert choline into TMA which, again, the liver converts into TMAO.  Other major sources of lecithin include liver, beef and pork.

Damn!  Do we have to stop the meat and eggs again?

Researchers confirmed the middleman (or middle-microbe) effect of intestinal flora by having their subjects take an antibiotic that wiped out the gut bacteria before they ate hard-boiled eggs.  With the microbes gone, TMAO levels in the blood didn't rise.  Only when the microbes were back to normal levels did TMAO rise. 

So, yes, foods high in fat and cholesterol may be associated with risk of heart disease.  But it's not because of the fat and cholesterol per se, but because these substances are present in foods that also have the constituents that gut microbes convert into what seems to be a true risk factor for atherosclerosis, TMAO. Not to mention that gut microbes are heavily determined by what we eat, as well.

We've 'known' for decades that red meat was a heart disease risk factor, and it was clearly because of fat and cholesterol.  This became lore.  The beef industry provided beef with less fat, the pork industry sold us on 'the other red meat', the poultry industry crowed, especially when eggs went back on the list of foods okay to eat.  

Vegan food pyramid; Wikimedia

And there was clearly a genetic component to heart disease risk, and/or to obesity, because CVD seems to run in families, and obesity is a risk factor, and this made many genetics labs crow.  Except that it was confusing when people with no family history of heart disease or thin people had heart attacks.

Despite the billion dollar industry that investigating, preventing and treating heart disease has become, it remains the leading cause of death in the US and other countries.  Number one.  Clearly we're doing something wrong -- including throwing a lot of money away on genetic studies that we knew really were going nowhere fast.  The intestinal microbe connection might turn out to be a huge advance in our understanding of heart disease, and it might well be that simple dietary changes and pharmaceutical approaches to cultivating 'good' microbes in our gut will prevent heart disease in many people -- leading the pharmaceutical industry to be the big crowers this time around. Of course, we can expect the genetic industry to say that some people are susceptible to the bugs' in their guts, but others (once we do the GWAS, whole genome sequencing, and 'personalized genomic medicine') will be cleared to go for the Egg McBreakfasts (with bacon).

But, this isn't likely to be the next health-research miracle, even if it gets promoted as one.  We would caution that this explanation will account for only some heart disease, even if the findings, which would be quite valuable to know, hold up.  Just as with every other complex disease, there are multiple pathways to this trait.  Why, for example, is smoking such a clear major risk factor?  Heart disease will remain a heterogeneous trait, difficult to predict, and not always possible to prevent.  But still, it's always refreshing when some innovative researcher breaks free of group think and provides new ideas on perplexing subjects.

The greatest irony, or should we say the last laugh, goes to the bugs who continue to outwit us and take us to our graves.

Bitter taste receptors in the most unexpected places

Another in our very irregular series on unexpected biological function.  We've written before about spermatogenesis genes found in the brain, and vision-related opsins found in unseeing sea urchin spines.  Today it's bitter taste receptors in the airways -- and testis, and brain, and immune cells, and gastrointestinal tract.  And they may soon be harnessed for the treatment of asthma.  

More than 300 million people have asthma worldwide, a disease that is estimated to cause 1 in 250 deaths.  Prevalence has spiked in the last three decades, and it's still not clear why, though the hygiene hypothesis, the idea that we're too clean, which provokes our immune system to overreact, has gained traction.

There is a lot of variation in the disease -- some people have asthma with allergies, some with exercise, some with respiratory infections, people react differently to existing therapies, some are able to keep their disease well-controlled and others not, and so on.  Of course many genetic studies of asthma have been done, but to date no definitive genes with large effect have been identified. 

Like most complex diseases, it's likely that 'asthma' encompasses a variety of diseases, with a variety of causal circumstances, and again as with other diseases, this complicates the search for causes, both genetic and environmental, as well as treatments.  "Those of us who treat asthma know that it's very different in each person.  It's almost as if each person is an n of one," physician and asthma researcher Fernando Martinez told The Lancet in 2006, when the journal did a special issue on the disease.  In the same issue, the editors called for an end to the use of the word asthma entirely. 

This is all in line with the idea of personalized medicine, genomic or otherwise.  Treatment tailored to every individual.  But is it possible that all cases of asthma may have one thing in common that a single treatment could correct?

Asthma is characterized by wheeze, which happens when smooth muscle cells in the airways contract, causing narrowing of the airways and subsequent difficulty breathing.  Current therapies include bronchodilators, β₂ adrenergic receptor agonists, that act on β₂ adrenergic receptors to relax smooth muscle and cause airways to dilate.  They don't work for everyone, however, and can have adverse side effects. 

A paper recently published in PLoS Biology reports that smooth muscle in airways has bitter taste receptors, G-protein-coupled receptors, that trigger a cellular response.

Bitter taste receptors (TAS2Rs), a G-protein-coupled receptor family long thought to be solely expressed in taste buds on the tongue, have recently been detected in airways. Bitter substances can activate TAS2Rs in airway smooth muscle to cause greater bronchodilation than β2 adrenergic receptor agonists, the most commonly used bronchodilators. However, the mechanisms underlying this bronchodilation remain elusive. Here we show that, in resting primary airway smooth muscle cells, bitter tastants activate a TAS2R-dependent signaling pathway that results in an increase in intracellular calcium levels, albeit to a level much lower than that produced by bronchoconstrictors. In bronchoconstricted cells, however, bitter tastants reverse the bronchoconstrictor-induced increase in calcium levels, which leads to the relaxation of smooth muscle cells.

So, the search is on for bitter tastants that would be good candidates for a new and more effective class of bronchodilator.  By addressing a response that is characteristic of all asthma, constriction of the airway, this approach could be a much needed one-size-fits-all kind of drug, with fewer side effects than the current class of bronchodilators.

But why are bitter receptors in these unexpected places?  Olfactory receptors have also been found expressed in some tissues other than the nasal passageways, to the extent that someone once suggested that, in their diversity and uniqueness, they could be used body-wide as a kind of tissue-specific molecular 'area code'.  This doesn't seem likely, as there hasn't been much in that line of evidence for several years.

But these stories do show the diversity of gene functions and uses.  Do bitter taste receptors in the airways mean anything?  Have they got there by chance alone, with no historic nor adaptive function?  Could their presence there be a simple developmental side effect of their needing to be properly expressed in the tongue, which develops in nearby tissues in the embryo?  If so, why are they in the testis, and immune cells, suggesting they have multiple and diverse functions?

We've written many times about roadblocks to understanding. What we think we know too often blinds us to what we don't know.

Open access, peer-reviewed Human Evolution resources

Updated with new content: October 30, 2013

I'm pleased announce a new open access, peer-reviewed resource for students and educators interested in human evolution and biological anthropology in general.

We've launched three rooms in the brand new Biological Anthropology series
1. Scientific Underpinnings
2. Living Primates
3. Human Fossil Record... which includes the following articles:

• Overview of hominin evolution - Herman Pontzer
• A primer on Paleolithic technology - Joe Ferraro
• The earliest hominins: Sahelanthropus, Orrorin, Ardipithecus - Denise Su
• The robust australopiths - Paul Constantino
• Homo erectus - A bigger, smarter, faster hominin lineage - Adam Van Arsdale
• Archaic Homo sapiens - Christopher Bae
• Neanderthal behavior - Gilliane Monnier
• The transition to modern behavior - Sarah Wurz
• Homo floresiensis: Making sense of the small-bodied hominins from Flores - Karen Baab
• Testing models of modern human origins with archaeology and anatomy - Christian Tryon and Shara Bailey
• Evidence for meat-eating by early humans - Briana Pobiner
• Reconstructing hominin life history - Tanya Smith and Zeray Alemseged
• Paleoecology and paleoenvironment: A case study of Plio-Pleistocene mammals from Laetoli - Kris Kovarovic 
• Milankovitch cycles, paleoclimatic change, and hominin evolution  - Chris Campisano

See also

• Dating rocks and fossils using geologic methods - Dan Peppe

I'm pointing you specifically to the Human Fossil Record resources within the Biological Anthropology topic because I am the editor for those (with by far most of the work done by the authors and the reviewers), but I hope you stumble on the useful resources located in the other two BioAnth rooms and also under "Genetics" and "Ecology" as well.

To fill in some of the (present) gaps in our room at Scitable, or to complement it, you might want to check out these articles in the special Paleoanthropology issue in EEO that are now available to all with an Internet connection!  http://link.springer.com/journal/12052/3/3/page/1

And you can also, thanks to open access, download all of the (yes, all, not just the latest) Australopithecus sediba papers:
http://www.sciencemag.org/content/340/6129/163.full

[update July 20]... and all these papers on the evolution of early Homo:
http://blog.wennergren.org/2012/12/current-anthropology-special-issue-human-biology-and-the-origins-of-homo/

I just couldn't wait any longer to announce this resource in spite of the kinks: (1) many of these articles were written in 2011 but due to delays on the production end weren't posted until recently;  (2) seven more articles for the Human Fossil Record room are complete and have been for a while but are still undergoing production; (3)  some of the articles are not listed in the correct (or any) room or topic though they clearly exist and are retrievable via Google, which prompted me to list them here all together; (4) many of the articles were written with others in mind and have parenthetical dead links to others that are not yet posted.

I will update this list as more articles become available. As I learn more I'll let you know if this resource will continue to grow, with existing articles being updated over time, or not.

Here's to finding these articles to be useful in your courses or for your personal edification! Thanks for your patience as the kinks get worked out and the gaps in knowledge get filled in. And thanks to the authors and the reviewers!

A lesson on lessening, from economics

By now we've all heard that an Excel spreadsheet error nearly brought down the world economy.  It has been reported by New York Magazine, for example, and the BBC, The Economist, among many other places.  It's a sobering story, a cautionary tale not only about economics but also about science and belief. It's an unwelcome caution, but one we should heed.

Confronting trying economic times, the question became whether governments should spend their way out of the crisis or cut spending to manage the crisis -- should they go the way of Hayek and embrace austerity or Keynes, and increase their spending.  Austerity was the way many countries chose to go -- too many, according to Keynesians, of course -- buoyed by a study done by Harvard economics professors, Carmen Reinhart and  Ken Rogoff, former chief economist of the International Monetary Fund, who delivered their results in a talk called 'Growth in a Time of Debt' at an economics meeting in 2010 (subsequently published here).  They reported that economic growth slows dramatically when a country's debt is more than 90 percent of it's gross domestic product.  Indeed, that there is a "non-linear response" to debt. 

That seemed clear enough, and strong justification for austerity.  In fact, there was a widespread near-panic about the catastrophe that would ensue if budgets were not cut drastically, and quickly, and of course the debate is ongoing as Greece, Spain, and other European countries struggle to right their economies.

But a graduate student at UMASS/Amherst, Thomas Herndon, tried to replicate the Reinhart/Rogoff study, and could not.  He repeatedly wrote to Reinhart and Rogoff to ask for their data, and to his surprise eventually they sent him the original spreadsheet in which they'd made their calculations.  That's when Herndon found that they'd mistakenly neglected to include five major nations in their figures and had selectively included data sets in their calculations in a way that seemed, to Herndon, to yield results that were, at best, disputable, and called their conclusions into question.  Herndon and colleagues wrote up their findings in a paper published on April 15, that has gotten huge play.

Here's the abstract from that paper:

Herndon, Ash and Pollin replicate Reinhart and Rogoff [RR] and find that coding errors, selective exclusion of available data, and unconventional weighting of summary statistics lead to serious errors that inaccurately represent the relationship between public debt and GDP growth among 20 advanced economies in the post-war period. They find that when properly calculated, the average real GDP growth rate for countries carrying a public-debt-to-GDP ratio of over 90 percent is actually 2.2 percent, not -0:1 percent as published in Reinhart and Rogo ff. That is, contrary to RR, average GDP growth at public debt/GDP ratios over 90 percent is not dramatically different than when debt/GDP ratios are lower.

The authors also show how the relationship between public debt and GDP growth varies significantly by time period and country. Overall, the evidence we review contradicts Reinhart and Rogoff 's claim to have identified an important stylized fact, that public debt loads greater than 90 percent of GDP consistently reduce GDP growth.

They conclude the paper saying, "Specfically, RR's findings have served as an intellectual bulwark in support of austerity politics. The fact that RR's findings are wrong should therefore lead us to reassess the austerity agenda itself in both Europe and the United States."

From Herndon et al.

Reinhart and Rogoff have responded (e.g., the Monday 22 episode of BBC Radio 4's More or Less and at length here) thanking Herndon et al. for finding the error, but reiterating their conclusion that high debt and slowed growth go hand-in-hand.  "We do not...believe this regrettable slip affects in any significant way the central message of the paper or that in our subsequent work."  Though we must say that, to our eye, the figure above from the Herndon et al. paper suggests the correlation is weak, at best.

The Economist has published a comparison of the original and the revised figures.  You decide whether you think the differences are significant or not.  Note that for the 'Above 90' value, which is the issue at hand, the RR report showed a negative mean value, whereas the corrected value is strongly positive.  So the average growth rate for countries with debt above 90% should have been 2.2 rather than -0.1.  Whatever your interpretation of the critique and what it means about austerity measures around the globe, we'd bet that it has a lot to do with how you felt about austerity measures before the Herndon paper came out.  And correlates strongly with how you voted.
 

Published April 17, The Economist

This is clearly another nail in the coffin of the self-flattering myth that science is about objectively doing one's best to falsify his/her hypotheses. No one's going to change their mind.  Not politicians.  Not even scientists.

An analogy: The 9/12 Syndrome
On 9/11, the US was infamously attacked in what is still often described as the worst way in our history (well, that's if you don't count the Revolutionary War, the Civil War, or the genocidal wars we waged on the Native Americans).  We were attacked by rabid fundamentalists who somehow thought that killing people flying on business or vacation was a way to correct some political wrongs they imagined that we were doing.

Americans shared their shock and horror at these attacks.  But how was this tragedy explained?  On 9/12, the day after the attacks, the punditry crept out of the woodwork and.....not a single person's ideas were changed!  If you were a gun-toting right-winger, you said "See, I told you we needed to be getting tough with the rest of the world!"  But if you a dove-releasing left-winger, you said "See, I told you we should not have been being the world's bully!"

The events were used, after the fact, to reinforce polar opposite opinions by those who had been waging political battles to advance their views. The reason is that people simply have a hard time seeing somebody's view other than their own and that of their friends.  We in science are human (despite our occasional claims to superiority) and are vulnerable to exactly the same kind of complacency.  Bragging, not apoligizing, is rather too much our way of life.

In the case of recent economics, hugely negative effects have resulted, because politicians bought into convenient ideas, in part citing this influential 'research' in their support.  The word's in quotes because it's treated by the public, politicians, and scientists as if it were the same as 'gospel.  But who knows how many thousands--or millions--of people lost homes or jobs, were driven into crime, disease, divorce or dispair and the like, or even died because of lost access to affordable medical care, because government policy did not come to their rescue--because of a polarized commitment to some preconception?

The lesson is to lessen our claims, not just to adopt things uncritically if they fit our preconceptions.  It's the hardest kind of lesson to learn, in a society that does not reward modesty.  Still, we should do it.

Mighty mites...or mighty misleading?

The April 11 broadcast of BBC 4's Material World included a discussion of the rapid evolution of mites.  A paper published online on April 8 in Ecology Letters described an experiment in which researchers at the University of Leeds brought soil mites into the lab, put them into 18 test tubes at high population densities, removed 40% of the adults from 6 tubes, 40% of the juveniles from a further 6 test tubes, and didn't harvest any from the remaining tubes.

As described by Futurity.org,

Researchers found significant genetically transmitted changes in laboratory populations of soil mites in just 15 generations, leading to a doubling of the age at which the mites reached adulthood and large changes in population size.

The results have important implications in areas such as disease and pest control, conservation and fisheries management because they demonstrate that evolution can be a game-changer even in the short-term.

Said a post-doctoral collaborator on the project, “The age of maturity of the mites in the tubes doubled over about 15 generations, because they were competing in a different way than they would in the wild. Removing the adults caused them to remain as juveniles even longer because the genetics were responding to the high chance that they were going to die as soon as they matured. When they did eventually mature, they were so enormous they could lay all of their eggs very quickly.”

"Our study proves that the evolution effect--
the change in the underlying biology in
response to the environment--can happen
 at the same time as the ecological
response.  Ecology and evolution are
intertwined," says Tim Benton.
(Credit: University of Leeds, via Futurity.org)

Now, the experiment and its results sound interesting.  If the investigators did their genetics right, they showed that a number of genes, 7 of which they said they'd identified, contribute to the life-history change.  So these results might provide worthwhile results in terms of understanding the control of metamorphosis or growth etc. in this species, and probably therefore beyond it.

However, in our view this story totally misrepresented what it had found, in a way that reflects the current mesmerization of science as well as the public, in terms of making huge unwarranted claims and invoking genetic determinism way beyond reason.  Why do we say this?

The author of the study who was interviewed seemed to claim, and the interviewer accepted without question, that his results cast doubt on the central Darwinian tenet that evolution is a very very slow, gradual process.  This is dramatically wrong in at least three respects.

First, this was not natural selection, imposed blindly by the natural ecology of any species, but instead was imposed intentionally from the outside in a way thoroughly controlled by the investigator and made very intense.  It is, in fact, artificial rather than natural selection. Darwin used artificial selection as his model for natural selection, claiming that the same process that farmers and dog or pigeon breeders used to achieve desired states was what occurred in nature, if at a generally invisibly slow pace.

The mite experiment is different from agricultural, orchid, tulip, pigeon race-horse, or pigeon breeding in that the investigators, unlike breeders, apparently didn't specify in advance what trait they were selecting for.  They let the natural genetic variation in their mites determine the responses to the crowding and unnatural dietary conditions.  But the selection was comparably intense (in one experiment, only half the introduced mites survived to reproduce), and intentionally and consistently imposed.

Second, slow gradualism is by all reasonable evidence a typical but not the only way that selection can occur in nature.  Drought, infection and so on can certainly cause rapid evolution in nature.  It just seems to be relatively unusual.  And major changes that Darwin was referring to were those that led to the production of new, complex adaptive traits--like bats flying despite having non-flying mammalian ancestors.  Mite life-span calibration differences are not like that in that there is no reason to think fundamental reorganization was required, or some novel trait.  We have vast amounts of data far more consistent with gradualism as the general pattern than with highly speeded-up adaptation, but even for the latter we have long had theoretical understand of when and how that can occur.  If life is about anything, it's about exceptions rather than rigid rules.

Third, only the most ideological Darwinist these days refuses to recognize that much of evolution occurs without any substantial, much less systematic natural selection.  Genes and the traits to which the contribute can evolve 'neutrally', changing over time just by chance.  So a modern Darwinian has to recognize that the degree of natural selection, and the tightness of adaptation are fluid, variable, and often far less deterministic than Darwin himself seemed generally to believe.   After all, he had vastly less data on time, paleontology, comparative biology, or genetics than we do today.  Anyone who sticks too closely to Darwin's own ideas (and it was the investigator himself who contrasted his results to Darwin), is like someone sticking to the Bible to explain the world:  Darwin was a brilliant world-changing scientist, but he made mistakes and the 150 years since his main work have greatly modified much of what he said. 

Scientists and the journalists who report their work seem simply unable to restrain their exaggeration.  There are many reasons for this, and we're all only human.  But it should be resisted because misrepresentation, intentional or otherwise, or misapplication of theory or even the concept of theory can be very misleading.  We should strive to do better ourselves, and to restrain our own natural tendencies to gild our work and ideas.  It's hard to do, but important.

Aiding and abetting murder--criminals with impunity!

Aiding and abetting a crime is itself a criminal offense.  If you help stake out a bank or drive the getaway car, you can go to jail for it.  And you should.

Murder is a very serious crime, and aiding and abetting murder (or mass murder) is a serious criminal offense.  Or so we thought.

Unfortunately, for many Americans, aiding and abetting murder is perfectly fine and beyond the reach of the law.  Or, more accurately, the law has been intentionally kept at beyond arm's reach for such felons--and strangely, kept so by the felons themselves!

The US Congress has intentionally aided and abetted thousands of murders and other killings by refusing, once again, to limit the rights of citizens (it should be called citizens' wrongs) to bear arms of the most nasty sorts.

Now our noble congressmen always argue that they are just protecting the noble right of citizens to secretly own weapons, so they can do things like hunt polecats out on the range or fend off the Marines when they storm your neighborhood in some sort of coup.  They claim--the congressmen, not the Marines--that they don't kill anybody.  And the NRA is as pure as ivory soap.

But we live in the age of science, not out on the range.  The arguments are a pile of range cattle droppings, because one can't claim innocence any longer.  Everyone knows very well that thousands will be shredded at the hands of trigger-pullers that the Honorable(?) congressmen are directly enabling.  Their refusal to act, or rather their intentional enabling acts, should be viewed by the law as no different from other sorts of aiding and abetting, punishable by the full force of the law.

(We must here admit to a bit of curiosity as to what a polecat slain with a burst of a hundred rounds of hollow-tips looks like.  That curiosity is probably too morbid to admit to openly, but in any case all we could find on the web was this 'Before' shot of a polecat begging a National Rapine Association (NRA) member for mercy.  The request was denied, of course, but the  'After' shot was rated X and can't be shown on a family blog.)

Gunslingers are brave, one would think.  But the brave act is the right act, not the one that gives lower priority to children's flesh than to being re-elected to the job (because it provides nice group meals and complete health care and retirement benefits that even most NRA members don't qualify for).  These gutless wonders of bravery, to whom we mistakenly give security passes to go into the Capital, have been properly taken to task by Gabrielle Giffords, but her moving words should lead us to move.  They're gutless because they want campaign money, even if they know that a huge majority of the voters want to see fewer machine guns in schools and homes.  But you can't really expect looney's to try to restrain other looneys.  So, it's time to clean the Capital of what sullies it, to our national shame; too bad there's not an election for a couple of years (the gutless wonders hope you'll forget their craven acts by then, and maybe that cynicism is correct, though we hope not).

If you want to say something to these wonderful enablers, who drive the guntoters' getaways, you won't find them at the scenes of the crimes they abet.  No.  But you can find them, on Sunday, in church, thinking they're showing what good people they are. 

Aspens

Aspens

All day and night, save winter, every weather,
Above the inn, the smithy and the shop,
The aspens at the cross-roads talk together
Of rain, until their last leaves fall from the top.

Out of the blacksmith's cavern comes the ringing
Of hammer, shoe and anvil; out of the inn
The clink, the hum, the roar, the random singing -
The sounds that for these fifty years have been.

The whisper of the aspens is not drowned,
And over lightless pane and footless road,
Empty as sky, with every other sound
No ceasing, calls their ghosts from their abode,

A silent smithy, a silent inn, nor fails
In the bare moonlight or the thick-furred gloom,
In the tempest or the night of nightingales,
To turn the cross-roads to a ghostly room.

And it would be the same were no house near.
Over all sorts of weather, men, and times,
Aspens must shake their leaves and men may hear
But need not listen, more than to my rhymes.

Whatever wind blows, while they and I have leaves
We cannot other than an aspen be
That ceaselessly, unreasonably grieves,
Or so men think who like a different tree.

Edward Thomas

It is national Poem in Your Pocket Day.  We offer this poem to all our readers, but with special thought for Ed Hessler, longtime reader of this blog, who has kindly sent us many beautiful verses over the years.

Galileo was a blogger, starry-eyed at that

Holly wrote a fine post a few weeks ago about why she blogs.  Her point?  Science blogging is a major way science is communicated now.  There are many many great science blogs out there, and the number is growing all the time.  So many academics are blogging that promotion and tenure committees and college deans are just going to have to consider it when they evaluate their faculty.  Talk about impact factor.  Sure, we can quibble about how impact should be quantified, but that's a problem that can be solved. Meanwhile, good blogging will enhance the visibility of the blogger's department and school, will increase and even make the blogger's reputation, will be a vehicle with which the blogger sharpens her thinking about the topic of the day, and most importantly, will communicate science in an immediate, effective, interactive way to anyone and everyone with access to a computer.

Blogging carries information, but with a much more immediate sense of the excitement, and the controversies, that scientific discoveries involve.  It communicates across a broad swath of society, and public engagement is important for many reasons.

But: blogging is not new!
It's well-known that Galileo was a rebel, the "Father of Modern Science", a believer in observation and experimentation, astronomer, champion of Copernicus, irritant to the Catholic church, but it's less well-known that he was a blogger.  A fine BBC 4 radio program, Great Lives, tells the story.

Galileo seems to have come by his iconoclasm naturally.  His father, Vincenzo Gallilei (1520-1591), was a late Renaissance musician, a lutenist, composer and theorist who challenged the contemporary view of music.  He wrote an important dialogue discussing alternative views of music theory, and was one of the leading voices of the musical revolution that led into the Baroque period.

It is said that the father was instrumental in the making of the son, the observational scientist, because he himself applied method to how he investigated music.  He was also a man who valued thinking about and questioning accepted theory, as well as communicating ideas, and perhaps this, too, was a major influence on his son.  But Galileo was rebellious, too.  His father wanted him to study medicine, but he was more interested in math and physics.

Galileo is reputed to have been a great teacher, a man with charisma "at the top of his game in explaining and communicating to people" (to quote physicist Dr David Berman, Galileo expert on the program).  He loved being popular, talking to important people and impressing them -- "it was a political thing for him".  It's significant that he wrote in common Italian, regional dialects even, because he was writing for people who might be interested in learning but didn't have access to rarefied Latin tomes.

Berman tells the story of Galileo being asked, "Don't people need shepherds?" His reply was something along the lines of, "People only need shepherds if you're in a jungle and you can't see the way.  If you can just illuminate the way, and everything is clear, people can see for themselves."

But, according to Berman, he didn't want to just explain.  He also wanted to change the way in which people viewed the world.  And to do this he began to dismantle the way science had been done for 2000 years, since the time of Aristotle, including the idea of absolutes such as that the moon was a perfect round sphere.  He believed in observation, in experiments that could begin to approximate the truth.

So, he made lenses for telescopes, and instruments that allowed him to make observations with which he challenged the standard view of the cosmos.  In his first book, The Starry Messenger (or Sidereus Nuncia), published in vernacular in 1610, and a quick sensational best-seller across Europe, he said, and showed with drawings, that his new tool revealed that the moon had mountains, and wasn't a perfect round sphere as had been thought for many centuries, and he wasn't afraid to say so.  "It is a very beautiful thing, and most gratifying to the sight, to behold the body of the moon, distant from us by almost 60 early radii, as if it were no farther away than two such measures..." and "Perhaps other things, still more remarkable, will in time be discovered...with the aid of such an instrument." And, later, "We shall prove the earth to be a wandering body surpassing the moon in splendor, and not the sink of all dull refuse of the universe; this we shall support by an infinitude of arguments drawn from nature."  Today's popular science writers and journalists can't top that!

What Galileo reported with such elegance was a shock, but among other things, confirmed his idea that truth had to be built from observation, not belief.  And the public had to accept the realities of reality!

It was Galileo's questioning of not just the hoary Aristotelian world-view but the nature of the universe itself that got him into trouble with the Church.  However, he was politically astute and managed not to be burnt at the stake, even at the cost of house arrest for the final years of his life.  But, the word got out.  His book, and another in dialogue form that was widely readable, promoting, among other things, the idea that the Earth revolved around the Sun. He did another, later volume also in dialogue form, about basic physics, where he studied gravity, physical forces, and even relativity before Einstein. 

Galileo knew that the way to influence people's thinking was exactly this -- accessible dialogues in classical Platonic form, that were very accessible to the lay reader, and had rather ignorant foils (e.g., a character named Simplicio) whose arguments (often those of the accepted view) were easy to dismiss in Galileo's clever way.  Here is an illustration for his 'Dialogue Concerning the Two Chief World Systems' in which he challenged the earth-centered view the universe:

These works were quite successful and, although it took a while for the Church to realize it, the ideas were catching on.  When the Church did recognize this and tried him, it wasn't for heresy per se, but for going against the papal order not to teach (though there was some doubt as to whether the order had ever been given).  The genie had been blogged right out of the bottle!

By the time he died, Galileo's books were widely known and he had been communicating, even when in house arrest imposed by the Church, with well-known scientists throughout Europe.  His ideas were not only widely known, but well-accepted.  This was so even by some of the leading Church scholars, whether or not they could publicly say so.  He was a great communicator.  He would have had great glee at the stir he caused, the attention it received, and his deep reach into society....just like today's best bloggers.

The smell of sex (in flies)!

Wikimedia Commons: B. Nuhanen

There are so many theories and evolutionary Just-So stories about how sex 'is', and how humans evolved 'for' this or that behavior or sensory involvement and so on, that one can hardly keep track, much less keep calm about so much of the nonsense being purveyed.

Of course, humans don't use pheromones or odors as intensely as most other animals do--or, at least, we have fewer functional odor or  pheromone receptor genes.  However, despite the visual cues, the kissing the red lips (see our earlier post on this delicious subject), there are those who also still claim that odors are important in who we choose to mate with (or who may choose us).  Even genes in the MHC (or HLA) immune) system are credited with this role.  Recall the sweaty T-shirt and female dormitory studies?  This has to do, if true, with issues related to competition between the fetus and the mother while the fetus is in utero, or various things of that sort, according to those who feel it is important (mating to enhance HLA genetic diversity is supposed to have fitness-enhancing value).

Well, there is a new paper, with the appealing title The smell of love in Drosophila, in the journal Frontiers in Physiology. The humble fruit fly has been studied to death (usually, literally!) so that a great deal is known about its genome, development, and behavior.  Mating is of course an important part of the tiny folks' lives, so it is natural to look at how or whether they use olfactory cues, or even depend on them.  Presumably, they don't 'think' about mating as we do, and don't go on dinner or movie dates, so how do they find members of the opposite sex and choose to do what comes naturally?

Ziegler et al, in this paper, examine members of the flies' large repertoire of olfactory receptor genes, and find one called OR67d that detects a compound, CVA, that is an emitted pheromone that the male transfers to the female during copulation (does this affect their prior choice?  We don't  know).  The authors say this transfer then makes the female less attractive for other males after she's mated and presumably gives the first guy's sperm a fighting chance to father the next generation of flies.

Another gene, OR47b, is reported to be activated by fly odors and hence to enhance courtship that depends on taste pheromones (products of different genes).  IR84a is one of these that detects compounds called PAA and PA.  But these are not pheromones that the flies produce!  Instead, they are found in fly foods (maybe a dinner date isn't such a bad idea if you want, well....).  PAA is an aphrodisiac for males (if the females could only intentionally lace their favorite fly's meal).

This has little to do directly with human sex and mating, perhaps.  But what it shows is that even in the purportedly simple fruit fly, sex, a most central aspect of evolutionary fitness, is a complex trait--and involves an important aspect of the environment: it's not all in the genes.

Of course, there are likely to be all sorts of indirect or unknown things of this sort that affect humans.  Naturally, the perfume industry works very hard to find them.

The evolution of peculiar human traits. Sigh

In one short window of Twitter feed on a Sunday morning, people are tweeting and retweeting links to a  a story in the Guardian called "Why do humans cry?", a blog post called "Why do I sigh?".  And, on our ride back to Pennsylvania from Tennessee after the physical anthropology meetings on Saturday, the BBC played a piece on why humans kiss.  The question of why we do X usually has two meanings -- what biological function does X serve, and why did it evolve, though, surprisingly, only the first question is addressed re. the sigh (but we can fix that).  And 'why' always means the natural selection explanation, as is routinely assumed to be necessary and appropriate.

Why do humans cry?  Darwin couldn't think of a biological purpose, but scientists today can, writes Mark Honigsbaum in the Guardian.

In recent decades, scientists have offered several accounts of how the capacity for tears may have given early hominids an adaptive advantage. These range from the aquatic ape theory, according to which tears were an adaptation to saltwater living, to the notion that by blurring our vision tears may serve as a "white flag" to potential aggressors – a signal that the crier is incapable of harm. Then there are the straightforward biological theories, such as the claim that tears evolved to keep the eye moist and free of harmful bacteria.

But perhaps the theory enjoying the widest currency at the moment is the notion that tears are a form of social signalling that evolved from mammalian distress calls – a clear visual signal in other words that someone is in pain or danger and needs help.

Now a new book, Why Only Humans Weep, by Ad Vingerhoets, explains that adult humans are the only mature mammals who continue to signal distress, by crying, even if it might also signal their presence to a predator.  He further suggests that the human's relatively large visual cortex evolved to perceive the nuances of emotion we show on our faces.  "In addition, crying is an emotional expression that signals appeasement and supplication in adults – something that he argues would have been advantageous in early human communities as a means of promoting greater mutual trust and social connectedness."  We also cry tears of happiness and joy, and empathy.

Gustav Klimt; The Kiss (Wikimedia Commons)

Why do we kiss?  This is answered by the BBC's "The Why Factor".  The biological reason is that it's pleasurable, and appeals to all five senses.  And it evolved because our primate relatives signal sexual receptivity with bright red, swollen genitalia, but when our ancestors began to walk upright, their sexual receptivity signal switched   to their full, pink lips, which have a 'come hither quality about them'.  This is called "the genital echo" (the reddened genital signal moved upwards, and this also explains why human breasts evolved to be larger than the mammary glands of our non-human primate relatives -- they look like sexually appealing buttocks).  This could be when lipstick evolved as well, but it's hard to say since it doesn't preserve well in the fossil record.



Why do we sigh?  One researcher who addressed this question received the IgNobel Prize for his efforts.  KH Teigen in 2011, though, in fairness (and sounding a touch defensive) he told one blogger he was doing the work to make the point to his students that there were subjects that haven't yet been studied by psychologists.

The answer is that sighing helps your breathing when you're stressed, is an expression of annoyance, and it's a "mental reset button".  How do we know?  Teigen and colleagues at the University of Oslo used a questionnaire to elicit the feelings people associate with sighing, feelings about others sighing vs themselves sighing (we do it when we're frustrated but others when they are sad).  And they gave participants two puzzles, one easy and the other one impossible, and asked people to try to solve them, but to quit whenever they wanted to.  They counted sighs as people worked on the puzzles.  Seventy seven percent of people sighed, most 4 times.

Researchers at the University of Leuven (Vlemincx et al.) also studied sighing, and have just published a new review on the subject.

The causes and consequences of sighing are reviewed and integrated in the proposed model in which sighing is hypothesized to function as a resetter in the regulation of both breathing and emotions, because it restores a balance in respiratory variability fractions and causes relief.

So, researchers have answered the question of what biological function sighing might serve, but we're astonished that they haven't addressed the evolutionary question which would be, essentially, what is it about sighing that caused our early ancestors who sighed best to have more children?  Since no one else seems to have answered this, we may as well.

If it's true that when we see someone sigh, we think that person is sad, then clearly it evolved for much the same reason crying evolved.  (Except that it involves the auditory part of our brain, not the visual, which is a bit of a problem.  Why isn't our auditory cortex more highly evolved?)  So, as we evolved living in small bands, we were empathetic and when someone close to us was sad, we would have wanted to help.  And, well, it's a short path from helping someone feel happier to mating with them -- sometimes it's one and the same act -- so this may well explain the origins of sighing.

Oh, except that cats sigh, dogs sigh, hell, maybe even lizards sigh.  So, we need an explanation that predates our earliest hominin ancestors.  Well, dogs are empathetic, so maybe our explanation still holds water.

Prairie dogs kissing (Wikimedia)

And as for kissing, although it has a magical, neurological, 5-sense etc. evolutionary origin, as explained by the interviewees on The Why Factor, and is therefore also part of our unique Darwinian heritage, well, yes, it's true that it's not universal and has only spread worldwide in more recent times.

Nothing like water tight explanations of everything in Nature!  It seems anybody, journalist or professor (anthropologist or not) is qualified to write books or be interviewed internationally, with essentially nobody questioning either the explanations offered, or the offerer's credentials, or whether anybody has such credentials when it comes to some of these evolutionary 'explanations'.

Sure, it's possible that crying, sighing and bussing were naturally selected.  That is, that those who cried, sighed and kissed best had the most children, and therefore that the traits became fixed in the human population.  But this is something that can't be tested, nor can the reason these traits evolved be ascertained.  But that doesn't stop people from speculating.

And it's possible that these traits have a significant biological function.  But these can't be ascertained with certainty, either.  And, they have to be shown to serve the same purpose cross-culturally, which Darwin certainly tried to do with his speculations about emotions, but which is very difficult.

Speculation is fun, not new, and it pays the bills, so why bother to complain about it, except for the myth that science is about knowledge, and science programs are about education. Supposedly.

Anthropology meeting: lots of good people, but not much action

We're at the American Association of Physical Anthropologists (AAPA) annual meeting, this year being held in Knoxville, TN.  The University of Tennessee has long had a very good faculty in biological anthropology, changing over the years but retaining status as substantial contributor to the field.

The attendance seems substantial, but the program itself seems rather short on hefty content.  There are several symposia to honor the careers of noteworthy biological anthropologists, from UT's history and beyond, and there are some good overview papers and various interesting poster presentations.

But, unlike many physical anthropology meetings of the past, there are few if any announcements of major findings.  No big splash fossil or genetic findings, no new primate species discovered in the wildes of Nowhere.  Instead, the program at least judging by titles, consists of a plethora of papers on very restrictive topics.  In the past, major new findings in paleontology or primatology or in human genetics and osteology would be presented here.

Unless we learn of more broadly applying presentations to be given, our impression is that a great increase in the number of faculty in this subject and the pressure to present new findings in rapid-fire fashion has largely sliced and diced work into rather minimalist, very focused but narrow presentations.  Most of these topics could be presented in an online format, and it is not clear that the wheeling and dealing is worth the cost of the travel and so on to have such a meeting.

Our own area, genetics, seems rather thinly represented given the big media news that genetic findings (or claims of them) make every week.  Over the years, mainline human genetics seems to have drifted away from the AAPA members or their use of these meetings.  More human geneticists are operating out of medical schools, often with a rather shallow understanding of evolution (but more money), and both geneticists and paleontologists have chosen to present their results on the hyper-media stage than at specialist meetings such as these.  In part, but only in part,  the depth of knowledge and use of technology that properly trained anthropologists can muster has a hard time competing with the resources of the medical school NIH-funding world, where teaching is often considered a kind of 4-letter word.  In part, anthropology has indulged too much in over-simplified evolutionary notions and has avoided the high level of technology and molecular and computing skills needed in this field, rather than being the more knowledgeable watch-dogs of the Just-So stories and promises coming out of NIH.

And yet....
Still, the meeting has not been a failure for us by any means.  We've already met many very good scientists and friends, and had a very fine dinner and conversation with our great MT co-conspirator Holly Dunsworth, the elegant and thoughtful contributor of so many wonderful posts on our blog.  And we've talked with Holly and others about ways we might encourage universities to revise their faculty evaluation criteria to take appropriate account for tthe active and successful use of social media (moving towards what we've called Broadreach University, the second Gutenberg-like transformation of intellectual communication).  One wonders if in-person meetings of the kind we're attending will be changed to something different, or if the old style (posters, podium presentations, plenary talks) will have legs into the future.

Holly is involved in many creative projects for the dissemination of knowledge about genetics and evolution (and more), both for public education and to improve teaching, along with her own research on evolutionary topics.

If we hear interesting presentations in the next couple of days here, we'll write about them.

What counts as 'research'? Should this?

As we have discussed a few times here, notably on our post 'Gutenberg II.  Broadreach University', times are changing for universities and the measures of academic achievement should change as well.  In this regard, academic life is supposed to contribute to the 'teaching, research, and service' (TRS) triumvirate, and that's how academics are evaluated.

If classical on-paper publishing with classical by mail peer review, and classical classroom teaching and in-person talk deliveries have been the measures of quality, and all that is changing, what should the criteria be now?  Should social media--like this blog--be considered legitimate venues for TRS?

Blogs, tweeting, online publication and commenting engage the public at all levels, not just academic 'peers'.  They thus provide service (and free, too!). They can teach the public, at all levels, not just in the classroom.   They report new data results (online journals) but also synthesis and explanation (blogs and social media as well as various online pubs).  Many legitimate 'research' activities in many academic fields, especially but not only the social sciences, arts, and humanities are just of this sort.

Blogs et al. are not bound and printed, and come out piecemeal rather than in big or occasional chunks.  They are not the same as formal research experimental results, but that is just one aspect of academic research.  But they can have the same kind of thoughtful synthesis, data presentation, and analysis.   They can probe new ideas, revive or present facts or even data.  Indeed, synthesis and making sense of data are perhaps as important, if not more important, than generating new data themselves--though of course science would quickly starve without new data.

It's real work and it's peer-reviewed
As we can attest, blogging in a serious way (as we, and many others, try to do), and even commenting and other social-network interactions, are a lot of work--we often spend hours on a single post, or work one up over several days or weeks.  Blogs are less systematic, often less thorough, than a major paper or book.  But the tendency in academics is already to parcel up one's research into 'least publishable units', as a way of gaming one's CV and so on.  Social media just speed that up, but make it more immediate and allow responses, and peer review is more broad and quicker.  Posts stay available and are searchable--we get comments every week on posts that are weeks or months or, occasionally, years old.

Blogs by academics or their equivalent are done seriously and, hopefully, very carefully because we know that if we goof we'll hear about it and, unlike typical peer review, the commentary will be globally public.  Good blogs, and we hope this is one of them, are viewed round the world.  Not, usually, by an army such as follow popular culture blogs, but by a mix of people with serious interests and qualifications.  We hope to stimulate thought and to be stimulated by responses.  So we write just as much with who may see what we write in mind as we do when we write a standard academic paper or book.

Evaluating which blogs and commentaries are valuable and which are just nasty riffs, superficial, or by trolls is a challenge, but the many commenatries on similar problems with peer review (including ones we have done here) show that the social media change the details but not the issues.

If the move is to free, worldwide, instantaneous communication of knowledge, knowledge of all sorts, not just hard-science experimental results, and of free online data bases of those results, then we need to embrace it, legitimize it, and revel in the freedom it provides.

As we've noted before, maybe the real shakers of innovation will be freed from the shackles of traditional, highly framed degree programs, and will scan for the knowledge they need to do what they want to do.  That, after all, was the traditional goal of giving people an 'education'.