I’m not going to mention any names. All I’ll say is this: A person I know visited a major research center last year and saw a demonstration of organ removal and some other experimental stuff. A person also visiting asked the famous high-level researcher doing this work if blood was ever blue. What he said was not recorded in detail, but it was very much like this statement I found on the Internet:

… human blood is red as soon as it is oxygenated. Blue blood flows through veins back to the heart and lungs…..
[source: Some Guy on Yahoo Answers]

My friend was disturbed by this, as s/he had been teaching high school students for years that blood is not blue. Her understanding of the situation was that people thought blood was blue because standard anatomical drawings and models depict arteries as red and veins as blue, and because if you look at your veins they are blue. Obviously veins are not clear, but if you don’t think that out you might assume that you were seeing blue blood.

So another year goes by and the same thing happens again. Another visit to the operating theatre, another person asks about blue blood, another confirmation that blood is blue.

Now, I’ve seen both veins and arterial blood either seeping or gushing (respectively) out of various organisms, including humans and various other mammals, on a number of occasions. My grandmother used to spurt out blood now and then because of a condition she had. As I study hunting, I’ve observed lots of thrashing around blood spurting and seeping mammals. I’ve cut myself and I’ve donated blood. And so on.

I’ve never seen blue blood. I’ve seen darker red and lighter red blood. But never blue.

Now, going back to Yahoo Answers, which I am NOT recommending as a source for actual information, but which is a good source for what regular people sometimes think, we have the following three quotes:

Melissa says: When blood gets oxygen it turns red but in your veins it is blue just look at them.

Avondro says: Myth, it’s always red. It goes a darker red, purple-like (Some call it blue) when starved of Oxygen.

SS Agent Dick Wakka says: Somewhat true. Blood is very bright red when it is in the pulmonary vein in the lungs, when it is highly oxygenated. During it’s journey back to the heart after circulating through the body, it is a little blue when it is deoxygenated, but more of a maroon-blue mix. … This is the truth.

Agent Dick gives as a citation a “medical student.” Well, I’ve got a citation of a leading blood researcher at a major research institution that says blood is blue.

I think there are two things going on here, one having to do with physics and the other with culture.

The physical issue is about color. Is “purple” a kind of red, or is it a kind of blue? Beyond that, is blood that is “dark red” or “purple” really purple? Or is it dark red. See my point?

The cultural issue is that more surgeons and folks like that, for much of recent history, are males, and males are bad at color, on average. I’m not talking about color blindness, but rather, color indifference.

So here is what I think: If a person who says to themselves “Blood is blue in our veins” thinks either of the following:

… That blood is blue, like this:

… Or, that blood is “blue” in that you look at your veins and see blue, thus you are seeing your blue blood….

… Or, that you look at an anatomical chart and see the veins drawn in as blue, therefore the blood inside them is blue…

… then that person is laboring under a misconception.

If a person thinks that this “blue blood” is purple, then they may also be laboring under a misconception. The HTML Internet Purple looks like this:

(I know, it looks dark blue to me as well.)

And the Pantone purple looks like this:

(I’ve never seen blood that looks like this)

Pantone Dark Red looks like this:

… but not very much like the darker shades of blood that I’ve seen.

I think dark blood looks a little like this:

This color is 24% red, 2% green, 2% blue, but at a saturation of 92 with a color value of 24 and a hue of 0 degrees. Whatever that means.

(By the way if your computer’s video display is not set to a high value for number of colors shown, all of the above may look like only one or two colors. And, since all video screens are different, I might be seeing something different than you are…)

Anyway, the color that I personally think resembles blood in its darker state is not purple. It is red with a lot of darkness added to it. Or a lack of lightness, or whatever. But it is red.

Human, mammal, and many other organism’s blood is red. But finding out if this is “true” is like squeezing blood from a stone.

If you would like a PDF version of this post, for use in class, here it is.

Photo Credit: postbear via Compfight cc

That is probably true sometimes. But we have sequenced the entire human genome, so shouldn’t we know about all the genes? Well, yes and no. We may have a list of genes found in a sample of humans, but “The Human Genome” can consist of a single individual (though it does not) and miss variation between individuals, i.e., it may not be a record of all of the possible alleles (variants) of each gene. Also, beyond the scope of this discussion but worth mentioning, a “gene” is not a simple concept. Whether or not a gene is expressed, where, when, and exactly what product it produces is not entirely encoded in the gene itself, but rather, elsewhere in the genome, or not encoded at all, but rather, dependent on external, non-genetic factors. So that complicates things too. So, if there is a trait that you think must be genetic, but years of research have failed to find it, the existence of a human genome and the prior acquisition of a lot of genetic data does not necessarily mean that the genetic information that determines the trait in question is not there. You can continue to believe that the genetic code for the trait will eventually be found

Except when you can’t.

There are two separate ways in which people sort out which traits are assumed to be genetic from those that are assumed to be not genetic. Both are heuristic, one is valid, and one is not. Let’s start with the one that is valid.

Suppose, as before, there is a trait that is seemingly inherited in families in such a way that a genetic trait would be, in the time tested manner that with respect this trait “offspring resemble their parents” as Darwin noted. The next question you can ask is this: Is it biologically sensible that this trait is inherited genetically, or is there a better, obvious, non-genetic mode of inheritance? If the trait is a physical feature such as eye color, then we have a sensible biological explanation for the trait having to do with developmental process we know something about and a set of metabolic pathways that produce various molecules such as pigments. The idea that this trait is genetic is biologically sensible, so even if you can’t find any, or all, of the genetic determinants of this trait, you can figure they are out there somewhere. Suppose, though, that the trait is a behavioral one that we see people in real life learning. For example, what language a person speaks generally follows the same kind of inheritance pattern many clearly genetic traits follow. With respect to spoken language, most of the time, offspring resemble their parents. But, rather than there being a sensible biological explanation for this trait, there is a sensible cultural explanation for this trait, so we don’t even look for the genetic variants for “French” vs. “Mandarin” vs. “English.” We simply assume this is not genetic.

The second method, the incorrect one, is to work with an article of faith. Broadly speaking, and I oversimplify greatly here, there are two primary articles of faith that often inform people’s thinking, shaping their assumptions, about genetics. Both usually have to do with behavioral traits in humans, but this can apply to physical traits as well. One article of faith asserts that humans are born as a blank slate, and all of their behavioral characteristics, such as their personality, intelligence by one measure or another, and so on, are added by experience. The other is the inheritance assumption, that some or much of an individual’s personality, intelligence, etc is determined by genes. There is not necessarily a consistent logic behind either of these assumptions, though various schools of thinking will include, often, a logical framework. However, this method of coming to a conclusion about the genetics or lack thereof behind various traits relies on one important element regarding genetic systems: Ignorance. If you are a blank slatist, then the absence of a clear pathway from genes to behavior means that your hypothesis can’t be falsified. If you are a genetic determinist, then the lack of such a pathway can be attributed to ongoing ignorance about the genes. The former might then be expected to live in fear that a gene will be found for their favorite learned behavior, and the latter might be expected to to live in a state of hubris, firmly knowing and asserting a truth that is not yet known but someday will be.

My impression is that over time there are fewer and fewer pure genetic determinists out there, and few and fewer blank slatists. I think the reasons for that shift have little to do with increasing knowledge, and more to do with changes in how one plays the academic game of argument, but that is discussion for another time. There is a danger in that shift, though. In the absence of any useful research results, if blank slatists start to admit that there could be some sort of genetics behind behavior, and determinists start to admit that experience and learning can also play a role, then we are converging on an increasingly simplified view of what is really a very complicated process. We should be gaining more complex, nuanced, and better informed views of how behavior arises, not simpler ones. Probably.

Over the last few decades, there have been a few important changes in how we should view human behavior over generational time and variation in those behaviors within and across categories (gender, ethnicity, geography, etc.). In short, certain behavioral traits have shown, synchronically (lacking the perspective of change over time) patterns that look genetic. For example, some families seem to be extra smart. Some have suggested that some “races” are smarter than others (at another time we can discuss why there really are no races, but let’s use “race” here as a potentially valid sampling strategy, which it can be even if the underlying races are fictions). We also see assertions of behavioral differences between the primary sexes (male vs female).

These observations are really statements about variance. Two groups are different, but vary within. There is overlap in the trait (i.e., IQ) but the means vary. We can statistically test the validity of the asserted differences in means by examining the variance in each sample and seeing if the mean of one sample fall within the predicted range of the central tendency of the others. In other words, asserting that there is a statistical difference between two groups is a process that involves understanding the variance of the underlying population(s) and samples. So, the questions can all be reframed in this manner:

Is the variation we see in trait X across certain groups best explained by underlying corresponding variation in the genetic system, or by the variation found in some other cause?

People fight vigorously over the underlying cause of IQ differences between groups. Some say it is primarily genetic, some say it is primarily not genetic, but rather, related somehow to what has become known as “lived experience.” Over the last couple of decades, there have been many attempts to explain observed variation in IQ using socioeconomic status, diet, education, issues having to do with test making or testing procedures. All of these factors have been shown to explain differences between groups to a modest to large degree in several studies. In other words, if you want to explain variation in IQ using non-genetic explanations, you can have some real success.

The genetic explanation of variation in IQ has had success in one main area which is irrelevant. This is the fact that genetically determined developmental differences between people that affect function that are generally classified as disorders predict large IQ differences. But this set of effects is not related to the question being asked.

The strongest evidence for a genetic underpinning of IQ is probably the large scale racial model solidified years ago by J. Philippe Rushton. He demonstrated that there is a grouping of brain sizes by race, with Asians having the largest brains, Caucasians the second larges, and Blacks the smallest (these race terms are his). He then showed that these brain sizes correlated with IQ difference. The modern psychometric literature assumes a racial difference in IQs, and asserts that this difference is real, but does to by citing sources that then site sources that ultimately cite Rushton. Rushtons all the way down, as it were.

The problem with this is that Rushton’s analysis was bogus. The brain sizes were taken from such sources at hat sizes for army conscripts classified by race, with the hat sizes used to estimate brain size. The Black (African) brain got smaller because Rushton subtracted a factor from that estimate of brain size, using an archaic thick skulled African fossil to assume that Africans have very very thick skulls. Correspondingly, the Asians were assumed to have thin skulls, and thus, got larger brains. The IQ data is similarly adulterated. In one part of the study, Rushton needed an “African” (native) IQ value, so he used the results of a test administered by racist anthropologists commissioned by the Apartheid government of South Africa to prove the inferiority of Blacks. And so on. The bottom turtle in this edifice is a fake.

The range of variation across “racial” groups (or other groups) in modern IQ data is very small compared to the change in IQ measured or estimated over decades of time through the 20th century within a single large and diverse population (Americans). If IQ is genetically determined and a stable feature of behavior, then there has been more evolution of these genes over less than 100 years of time in the US than we see across any two groups of modern humans. That is impossible. Again, IQ does not behave nicely as a genetic trait.

The discovery of a gene or set of genes that would underly IQ has not happened. In some recent studies, IQ is assumed to be very complex and the result of many different genes, and there is some statistical evidence for this. But, there is a big problem there too. Any trait can be linked to a set of genetic variants if the set of genes is large enough. That is a statistical effect and it is not really a link. More like a party trick, or a con game. (In fact this method is a con you may have heard of. I send 10,000 people an email predicting that a certain stock will go up, another 10,000 people an email predicting it will go down. One or the other happens. I then send 5,000 of the people who got the “correct” prediction another prediction, and 5,000 of them the opposite prediction. Now, 2,500 people have gotten two correct predictions from me. I keep doing that until I’ve got several dozen people convinced I am a stock market genius, and I take their money.)

Generally speaking, many behavioral traits have been explained, in part and sometimes in large part, by factors that are not genetic, while at the same time, the hunt for the presumed underlying genes have come up empty. There was great optimism up through the 1990s that genetic underpinning of human behavior … genetic variation corresponding to behavioral variation … would be found. But even as early as 1993 this was being questioned. Here is a sidebar, reproduced in full, from a Scientific American article by John Horgan summarizing the work up to that time:

Behavioral Genetics: A lack of progress report (1993)

CRIME: Family, twin and adoption studies have suggested a heritability of 0 to more than 50 percent for predisposition to crime. … In the 1960s researchers reported an association between an extra Y chromosome and vio-lent crime in males. Follow-up studies found that association to be spurious. MANIC DEPRESSION: Twin and family studies indicate heritability of 60 to 80 percent for susceptibility to manic depression. In 1987 two groups reported locating different genes linked to manic depression, one in Amish families and the other in Israeli families. Both reports have been retracted. SCHIZOPHRENIA: Twin studies show heritability of 40 to 90 percent. In 1988 a group reported finding a gene linked to schizophrenia in British and Icelandic families. Other studies documented no linkage, and the initial claim has now been retracted. ALCOHOLISM: Twin and adoption studies suggest heritability ranging from 0 to 60 percent. In 1990 a group claimed to link a gene—one that produces a receptor for the neurotransmitter dopamine—with alcoholism. A recent re-view of the evidence concluded it does not support a link. INTELLIGENCE: Twin and adoption studies show a heritability of performance on intelligence tests of 20 to 80 percent. One group recently unveiled preliminary evidence for genetic markers for high intelligence (an IQ of 130 or higher). The study is unpublished. HOMOSEXUALITY: In 1991 a researcher cited anatomic differences be-tween the brains of heterosexual and homosexual males. Two recent twinstudies have found a heritability of roughly 50 percent for predisposition to male or female homosexuality. These reports have been disputed. Another group claims to have preliminary evidence fo genes linked to male homosexualty. The data have not been published.

This is from a study by Jay Joseph on the “Classical Twin Method in the Social and Behavioral Sciences”

The classical twin method assesses differences in behavioral trait resemblance between reared-together monozygotic and same-sex dizygotic twin pairs. Twin method proponents argue that the greater behavioral trait resemblance of the former supports an important role for genetic factors in causing the trait. Many critics, on the other hand, argue that non-genetic factors plausibly explain these results…. In 2012, a team of researchers in political science using behavioral genetic methods performed a study based on twin data in an attempt to test the critics’ position, and concluded in favor of the validity of the twin method and its underlying monozygotic–dizygotic “equal environment assumption.” The author argues that this conclusion is not supported, because the investigators (1) framed their study in a way that guaranteed validation of the twin method, (2) put forward untenable redefinitions of the equal environment assumption, (3) used inadequate methods to assess twin environmental similarity and political ideology, (4) reached several conclusions that argue against the twin method’s validity, (5) overlooked previous evidence showing that monozygotic twin pairs experience strong levels of identify confusion and attachment, (6) mistakenly counted environmental effects on twins’ behavioral resemblance as genetic effects, and (7) conflated the potential yet differing roles of biological and genetic influences on twin resemblance. The author concludes that the study failed to support the equal environment assumption, and that genetic interpretations of twin method data in political science and the behavioral science fields should be rejected outright.

With respect to psychiatric disorders, from the same author:

The psychiatric genetics ?eld is currently undergoing a crisis due to the decades-long failure to uncover the genes believed to cause the major psychiatric disorders. Since 2009, leading researchers have explained these negative results on the basis of the ‘‘missing heritability’’ argument, which holds that more effective research methods must be developed to uncover presumed missing genes. According to the author, problems with the missing heritability argument include genetic determinist beliefs, a reliance on twin research, the use of heritability estimates, and the failure to seriously consider the possibility that presumed genes do not exist. The author concludes that decades of negative results support a ?nding that genes for the major psychiatric disorders do not appear to exist, and that research attention should be directed away from attempts to uncover ‘‘missing heritability’’ and toward environmental factors and a reassessment of previous genetic interpretations of psychiatric family, twin, and adoption studies.

And from researcher Tim Crow:

A substantial body of research literature, identified by nine out of ten papers on genetics in the recent ISI research front on schizophrenia, claims to have established associations between aspects of the disease and sequence variation in specific candidate genes. These candidatures have proven unreplicated in large sibling pair linkage surveys and a targeted association study. Even if the case for an association be regarded as a lucky guess (assuming one gene in 30 000 was guessed right) the large linkage and association studies provide no evidence of sequence variation relating to psychosis at any of these gene loci. Thus this body of work must be regarded as an indicator of the extent to which the ‘eye of faith’ is able to discern meaning in complex data when none is present.

I could go on. There have been further criticisms of the twin studies, for example. The most interesting, potentially, of these studies was on twins reared apart, more or less separated at birth. Commonalities among such individuals would be strong evidence for a genetic underpinning, because these individuals were raised in completely different environments so there would be no chance of a learned or cultural component other than a general background effect of having been raised n the same planet, or in the same country. Right? Well, no. Twins separated at birth were mostly twins that were not all that separated. After all, where do researchers actually find twins truly and distantly separated at birth, especially in the days when people seeking birth parents had hardly become a thing yet? Many of these twins, probably the vast majority, were separated only in the sense that they were raised by different members of the same family, or separately by divorced parents. Many were raised in the same neighborhood or often, the same house. My brother and I are not twins, but we were “raised apart” by the criteria of the twin studies because my family was distributed among the rooms of a two family residence, so technically he and I had bedrooms at different addresses.

In sum, it is easier to find sociological, cultural, or environmental explanations for variation in human abilities, intelligence, or personality traits. The seeming inheritance by family of some of these traits may well be a combination of something genetic and something experiential or cultural, but when looking for the actual underlying causes, genetics has repeatedly come up wanting while environmental explanations do a good job of addressing a fairly large part of the variation we see. Models of race based differences are so poorly done, and are often highly politically motivated, that they should never be trusted. That scientific ship sailed a long time ago.

Maybe the blank slate theory isn’t so bad after all. It does not imply that just anything can happen when making a human being out of a sperm and an egg. After all, it is a blank slate and not a blank whatever. But it is probably not true that some people’s lived experiences are written on slate, while others on white boards, and still others on smart boards, even if there are some people who I’m sure assume that they were.

Selected references:

Horgan, John. 1992. Eugenics Revisited. Scientific American. June.
Joseph, J. (2011). The Crumbling Pillars of Behavioral Genetics. GeneWatch, 24 (6),4–7. Web page
Joseph, J. (2012). The “Missing Heritability” of Psychiatric Disorders: Elusive Genes or Non-Existent Genes? Applied Developmental Science, 16(2), 65–83. doi:10.1080/10888691.2012.667343
Joseph, J. (2013). The Use of the Classical Twin Method in the Social and Behavioral Sciences : The Fallacy Continues, 34(1), 1–40.
Lewontin, R. Human Diversity. 2000, Scientific American Library.
Marks, J. (2008) Race: Past, Present, and Future. In: Revisiting Race in a Genomic Age, edited by B. Koenig, S. Lee, and S. Richardson. New Brunswick, NJ: Rutgers University Press, pp. 21–38. PDF
Marks, J. (2008) Race across the physical-cultural divide in American anthropology. In: A New History of Anthropology, edited by H. Kuklick. New York: Blackwell, pp. 242–258. PDF
Tizard, B. (1974). IQ and Race. Nature, 247, (5349), 316.

Other posts of interest:

• How to get rid of spiders in your house
• Why is your poop green?
• How many cells are there in the human body?
• Is there really a plot hole in Harry Potter Goblet of Fire?
• How long is a human generation?
• Is blog ever really blue?
• How to not get caught plagiarizing
• The origin of the domestic chicken
• What are the three necessary and sufficient conditions of Natural Selection?
• How do I get rid of foot fungus?
• Which is better, Tap Water or Bottled Water?
• Has Global Warming stopped?

Also of interest: In Search of Sungudogo: A novel of adventure and mystery, which is also an alternative history of the Skeptics Movement.

Resorting to jigsaw puzzles?

Like science?

Then you are in luck! Try the new Dr. Livingston’s Anatomy Jigsaw Puzzles, based on art created by Mesa Schumacher, a Certified Medical Illustrator from Johns Hopkins University.

Dr. Livingston’s Human Anatomy Jigsaw Puzzles come in three volumes so far, a head, a thorax, and an abdomen. The maximum dimensions of each puzzle would make this a 1000 piecer for sure, but since they are not rectangles they run closer to 500-600 pieces. They are also not terribly hard. Some of the puzzle perimeters have a double edge: the actual edge of the puzzle, and the edge of the illustration (ie., skull) running close and in parallel, so that 12% or so of the puzzle practically does itself. Also, you can’t really be a good anatomical drawing and ahve the kind of vagueness that a harder puzzle tends to have. But that’s OK because you will want to do all of them in a short time anyway.

I believe there are plans to make a total of seven puzzles, but at the moment there are only the three mentioned above available.

From the abstract:

Over a decade ago, the Atacama humanoid skeleton (Ata) was discovered in the Atacama region of Chile. The Ata specimen carried a strange phenotype—6-in stature, fewer than expected ribs, elongated cranium, and accelerated bone age—leading to speculation that this was a preserved nonhuman primate, human fetus harboring genetic mutations, or even an extraterrestrial. We previously reported that it was human by DNA analysis with an estimated bone age of about 6–8 yr at the time of demise. To determine the possible genetic drivers of the observed morphology, DNA from the specimen was subjected to whole-genome sequencing using the Illumina HiSeq platform with an average 11.5× coverage of 101-bp, paired-end reads. In total, 3,356,569 single nucleotide variations (SNVs) were found as compared to the human reference genome, 518,365 insertions and deletions (indels), and 1047 structural variations (SVs) were detected. Here, we present the detailed whole-genome analysis showing that Ata is a female of human origin, likely of Chilean descent, and its genome harbors mutations in genes (COL1A1, COL2A1, KMT2D, FLNB, ATR, TRIP11, PCNT) previously linked with diseases of small stature, rib anomalies, cranial malformations, premature joint fusion, and osteochondrodysplasia (also known as skeletal dysplasia). Together, these findings provide a molecular characterization of Ata’s peculiar phenotype, which likely results from multiple known and novel putative gene mutations affecting bone development and ossification.

Figure 1 from the paper:

You will read here and there on the internet that this individual’s body was likely deposited within the last 50 years.

However, that “fact” is itself a deletion style mutation. Somewhere along the line a zero was deleted from the number “500” in the original report. While this mutation is not as interesting as the mutations that led to the odd development of this unfortunate person, it is fully ironic.

The original paper is open source, and available HERE, which is why I’m not spending a lot of time in this post explaining the details. You can read it yourself!

Also, there’s a movie from 2013.

A study just published in the Proceedings of the National Academy of Sciences explores the question of pee-pee size and female preference in humans. The study involved making a set of 3D models of human males of various relative body sizes, and fitting them out with various size flaccid pee-pees. These were shown to a sample of Australian women to get their reactions.

The assumption of this study is that at some time in the past humans did not wear clothing, so that information about pee-pee size in men would be available to women who could observe flaccid pee-pees and then choose sexual partners. That assumption is limited, perhaps flawed, in at least three ways:

1) We have no idea when men started to cover their pee-pees on a regular basis. Ethnographically, there are very few cultures where men walk around with exposed pee-pees, though there are several cultures in which men attempt to highlight and perhaps exaggerate the sizes of their when mommy and daddy want to show each other how much they love each other equipment using various techniques. Since foraging people around the world, who stand in as models for the human “paleolithic,” often cover both male and female “down there” areas, it stands to reason that the practice of covering up is old, even if it has not always been practiced. Archaeological evidence of early Rainbow (African and Asian Rainbow stiffy/ergaster) strongly suggest that our ancestors, well before they became Rainbow sapiens, lived in a fairly wide range of habitats suggesting but not proving that clothing was developed as far back as just under 2 million years ago. If there was a period of universal exposure of the entire body, it may well have been much earlier than the evolution of anything looking like modern human culture and mating systems.

2) It is highly unlikely that human or pre/proto-human females would determine mating preference on the sole or primary basis of the details of the experience of copulation, assuming that some degree of paternal investment in offspring or the female herself was important. A better model of human you know what suggests that females would look for a wide range of features, mostly behavioral, in long term male partners, and these longer term relationships would have more of an effect on selection (for a particular size pee-pee) than a single variable.

3) There is not strong reason to believe that if females were interested in pee-pee size as a factor in copulation that they would use flaccid pee-pees to make assessments. The correlation between stiffy pee-pee size and flaccid pee-pee size is poor. In addition to this, in a social group in which no one wears clothing, other sources of information about stiffy pee-pees would certainly be available. Pee-pees would be stiffy at random times now and then, and in a social system where females make short term decisions about copulation, there would certainly be long term availability of information via the usual linguistic channels, after the evolution of language or proto-language, which would presumably be early(ish) in human evolution.

However, given these caveats, it may be reasonable to carry out the experiment reported in this paper because, well, why not?

The researchers note that human flaccid (visible) pee-pee size is notably larger than that of our relatives, the great apes. This suggests that visual evaluation of pee-pees was a selective force in human evolution. From the abstract of the paper:

Compelling evidence from many animal taxa indicates that male genitalia are often under postcopulatory s#xual selection for characteristics that increase a male’s relative fertilization success. There could, however, also be direct precopulatory female mate choice based on male pee-pee traits. Before clothing, the nonretractable human pee-pee would have been conspicuous to potential mates. This observation has generated suggestions that human pee-pee size partly evolved because of female choice. Here we show, based upon female assessment of digitally projected life-size, computer-generated images, that pee-pee size interacts with body shape and height to determine male sexual attractiveness. Positive linear selection was detected for pee-pee size, but the marginal increase in attractiveness eventually declined with greater pee-pee size (i.e., quadratic selection). pee-pee size had a stronger effect on attractiveness in taller men than in shorter men. There was a similar increase in the positive effect of pee-pee size on attractiveness with a more masculine body shape (i.e., greater shoulder-to-hip ratio). Surprisingly, larger pee-pee size and greater height had almost equivalent positive effects on male attractiveness. Our results support the hypothesis that female mate choice could have driven the evolution of larger pee-pees in humans. More broadly, our results show that pre-mommy-and-daddy-showing-each-other-how-much-they-love-each-other selection can play a role in the evolution of down there traits.

What have we learned from this study? Perhaps, mainly, something about the reaction a certain subset of Australian women have to male pee-pee size. However, we can also guess that human you know what, including details such as this, are a product of our rather complex and difficult to parse culture. I am uncomfortable linking these results to either the behavior of paleolithic humans or to a model of sexual selection, given that human s#xuality today is so diverse and clearly constructed from exposure to enculturation and lived experience. Is this scientific evidence that when people say things like “size does not matter” or “it’s how you use it that counts,” they are kidding? Perhaps. In Australia. But probably not.

To me, a more interesting study would look at biological and cultural variations in the relationship between flaccid pee-pee size and stiffy pee-pee size, and how information about these things would be made available in different normative cultural settings. For instance, I would predict that if pee-pee size matters in relation to either female mate choice or male-male competition, this relationship would be strong (and flaccid pee-pees generally larger) in societies where men don’t cover up, but uncorrelated (with little selection on flaccid pee-pee size) in societies where men do cover up.

See also this at The Stochastic Scientist.

Mautz, B., Wong, B., Peters, R., & Jennions, M. (2013). Pee-pee size interacts with body shape and height to influence male attractiveness Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1219361110

Some of the symptoms of the autistic condition Asperger Syndrome, such as a need for routine and resistance to change, could be linked to levels of the stress hormone cortisol, suggests new research led by the universities of Bristol and Bath.

Normally, people have a surge of this hormone shortly after waking, with levels gradually decreasing throughout the day. It is thought this surge makes the brain alert, preparing the body for the day and helping the person to be aware of changes happening around them.

However, a study by Dr David Jessop from the University of Bristol and Drs Mark Brosnan and Julie Turner-Cobb from the Department of Psychology at the University of Bath, has found that children with Asperger Syndrome (AS) do not experience this surge.

Press release