(I [Greg] am republishing a lot of ‘legacy content’ from our PLOS Neuroanthropology weblog, which has been taken down, along with many of the other founding PLOS Blogs. Some of these, I am putting up because I teach with them. If you have any requests, don’t hesitate to email me at: greg (dot) downey @ mq (dot) edu (dot) au. I suspect many of the links in this piece will be broken, but I will endeavour to try to slowly rebuild this content. Daniel originally published 7 December 2012.)
I just dropped my two young children at elementary school. They were bright and smiling, one off to practice handbells for a Christmas concert, another to chat with friends before the first bell.
Neither noticed the police car newly parked beside the school. Neither had a penny for my thoughts, of what it must have been like for those parents in Newtown, dropping off beloved children and then not having them only a few minutes later.
Now at my computer, I think of the Connecticut State Police Spokesman Lt. J. Paul Vance, the man who has guided us through much of this tragedy. I remember his assurance on Friday that the police were doing everything to find out not only what happened, but why.
One narrative – that Adam Lanza was mentally ill – is already waiting in the wings, prepped as an explanation. Another – where guns are the culprit – has exploded already with full force. Lanza used a semi-automatic assault rifle with extended clips and shot his victims multiple times. He had hundreds of more rounds to continue his killing. Without that firepower, he couldn’t have killed so many so quickly before taking his own life when the police arrived.
The United States urgently needs more and better mental health care. Regulating guns like we regulate motor vehicles seems reasonable, given how many thousands die from gun shots and from car accidents every year. Neither, though, gets us much closer to why.
Mentally ill patients are not more violent than anyone else. Guns don’t shoot themselves.
We still need better answers. The horrendous violation that Lanza committed, against all social norms, against everything that is decent and good, stares back at us with such dark eyes.
On “Adam Lanza’s Mother”
Thinking the Unthinkable, where the mother of a violent 13 year old recounts her own struggles with her son, swamped social media over the weekend. A truly viral post.
I live with a son who is mentally ill. I love my son. But he terrifies me.
Long’s effective writing, evocative story, and sense of timing help explain how her post got circulated through so many Facebook pages. But she does one other thing that makes a huge difference. She speaks of how violence terrifies, and how little she can understand it. Yet there is her son, in the throes of fury and lashing out.
A few weeks ago, Michael pulled a knife and threatened to kill me and then himself after I asked him to return his overdue library books. His 7 and 9 year old siblings knew the safety plan—they ran to the car and locked the doors before I even asked them to. I managed to get the knife from Michael, then methodically collected all the sharp objects in the house into a single Tupperware container that now travels with me.
How to make sense of that? Pulling a knife over library books?!
Through her own experience, Long helps us catch a glimpse of the violence of being human, and to sense, at a distance, how quickly it can destroy life. For me, that is why the piece resonated. Newtown scares us deeply, the idea that someone can do such a thing. Yet Lanza did.
Soccer Mom Long also presages our societal response – fearful, distancing from the problem, controlling the pointy objects, and making it mental alone. And for me, that is deeply problematic. It fits violence into the wrong category, making it some natural object that we then try to control socially.
Don’t get me wrong. I think improvements in policing, gun control, and mental health care are all needed to help further reduce violence in our society. We need a multi-dimensional approach for a multi-dimensional problem.
But we also need better answers to the question Lt. Paul Vance posed for us, and so many have asked ourselves since Friday – Why?
Most of us hide our eyes from violence until some horrific event like the murders in Newtown force such things before our eyes. One of the braver things Obama did in his Friday press conference was to at least mention other massacres that haven’t caught the public’s attention so much – the murder spree in Chicago (over 400 this year) and the killing of six at a Sikh temple by a white supremacist.
One might cast a broader eye, and include the truly horrific number of murders in Mexico due to the drug war or the children killed by US drones abroad. Or to the past, and the killings of juveniles at the Dozier School in Florida. But black youth, religious minorities, foreigners, children of terrorists, and delinquents do not evoke the same sympathy. They do not force us to look longer. They should.
The movies are a enormous, constant, heavily influential part of an American culture that fetishizes violence and glamorizes, to the point of ten-year wars, a militarized, let-it-rain approach to conflict resolution… Culture shapes the expression of behavioral traits. The traits don’t rise inherent as an urge to play basketball or a plan to shoot up a Batman movie. A long conversation between the trait and the surrounding culture shape those expressions. Culture gives the impulse form and direction.
My wife, when she studied justified versus unjustified violence, found that justified violence – such as to save someone or even at times revenge – led people to approve more violence than violence that was deem unjustifiable. James Bond’s violence is legitimate, even thrilling.
We forget one thing about how culture works, something pointed out by Victor Turner and Claude Levi-Strauss many years ago – that symbols and meanings often work through dualities and oppositions. I still remember my street kid friend in Bogotá describing his life, that just like the morning sun comes over the city and the good people come out, so too the dark sun comes up at night and the dark people come out. And how they hated at times the people of the day, with their good lives and comfortable justifications and easy condemnations.
Our violent heroes don’t turn the other cheek. They go out and punish, often with multiple gun shots, those who are against them. Is it so hard to understand that our anti-heroes do the same?
Of Right Mind
Lanza killed little kids. Innocents most white and wide-eyed. I have called attention before to “running amok,” a cultural model and interpretation of violence, as one way to try to grasp how someone could engage in such horrid behavior. But one word that has stuck with me this time is “deranged.”
Someone in their right mind does not go out and kill kids. That is our sense of things, despite the regular news of parents who abuse and kill the children in their care. But they don’t then go and kill their neighbor’s kids.
Why “deranged”? I suppose because I find it hard to accept that someone like Adam Lanza was in their right mind. That even if there are cultural meanings he can draw upon, he still went and did it himself. And that I find comfort in thinking something inside his brain didn’t work the same way that things work inside my brain.
But I don’t mean mentally ill. Not at all. I mean violent. Violent in the most transgressive of ways. Violent in the most deliberate of ways.
If we’re going to think of violence as a sickness, then it is its own type of sickness, different in kind and in expression from the mental and physical ailments that also possess us. Violence is red in tooth and claw, seemingly primordial, until we recognize how socially regulated it is. We teach soldiers in violence, and then punish when they step outside the rules of engagement.
Violence relies on the tools at hand, on fists and knives and guns and planes, tools that we create and control. Violence has targets, often dehumanized, the japs or commies or crips on the other side, a fiction we can maintain until it is so roughly violated by something like Newtown. And violence works terror, that the overwhelming brutality of it will keep the other at bay and that we ourselves won’t be touched. But violence boils beyond the easy boundaries we try to place on it, and we are left once again in a land of no easy answers.
Teaching, tools, targets, and terror – that’s as close as I will get to a framework today. But I don’t want to end just yet. There remains the question of what to do.
President Obama has called for meaningful action. In government, meaningful action is often symbolic, done in speeches and codified into law. Gun control would at the very least signal that things have shifted, that we will not accept this type of violence, that we are willing to place limits on our freedom for the collective good of our children.
It is increasingly clear that the quick response time of police helped save lives in Newtown. We have gotten extremely good at rapid response. We are still very bad at how to deal with violence before or after that urgent moment.
We need to get better at dealing with young men and women prone to violence through our schools and in our neighborhoods. We need to engage in prison reform, and to rework our senseless jailing of so many non-violent offenders (often to great profit for the people who run prisons) and to direct many more resources to lowering alcohol and drug use rather than a continued engagement in a violent drug war. Much of the saved money from that “war” could then go to funding more community approaches to addressing violence. So, yes, reform before and after these violent acts.
Finally, I think of Jared Cano, the teenager who plotted to bomb a high school only a few miles from my home. Cano wanted to make it bigger than Columbine or Virginia Tech. Or now Newtown. He was turned in by a friend. That sort of everyday regulation is as important as anything else. It’s not all gun control, mental health resources, and rapid response. Sometimes it’s a different sort of bravery.
I’ll leave off with Cano’s words before he was sentenced to 15 years in prison.
I don’t want to be the bad guy. I want to be the good guy. The state ain’t gonna make an example. They’re gonna put me in prison. Let me make an example. I had a bad life. Let me change it around and do something good, not bad. Don’t make me the poster child for something evil. Let me be the poster child for something good. Let me do right. Give me a chance to do something right. To make my family proud. I don’t want all these people to think I’m crazy, trying to kill everybody. I want people to look at me as someone who was wrong and changed… and did something right.
[Added 2019. Greg.]
Jason Antrosio has suggested that we include a lot of the commentary because it was really good. So here are the most substantial comments that were made:
A comment by ‘Discuss White Privilege’ on 17 December, 2012:
Posting as DWP so as to keep continuity with comments I’ve made elsewhere that can be related to what I’d like to respond to here.
First, another great post, Daniel. Deeply thoughtful, as always.
Second, increasingly as I think about this tragedy, and certainly in response to my own reflection on the Sandy Hook shooting in comments I posted yesterday to Savage Minds, increasingly I feel dissatisfied with the term “mental illness” and the mental health/mental illness dichotomy. I don’t really think it serves us well, especially not in automatically associating ‘mental illness’ with violence in general, and mass killings (via gun violence) like the one Friday in Sandy Hook in particular.
Too many kinds of *social suffering* and embodied despair are collapsed into the category of ‘mental illness’, in ways that assume that one is either ‘mentally ill’ or not (i.e. ‘normal’, mentally healthy). It assumes that mental health/illness is discrete and not a spectrum (certainly gesturing towards Susan Bordo’s work on anorexia in Unbearable Weight here), in ways that prevent people from realizing that there is a spectrum of mental health, or lack thereof, and that many of the pathologized behaviors or perspectives/motivations that those labeled ‘mentally ill’ may engage in are also shared by those not labeled as mentally ill.
Moreover, I feel deeply troubled by the catch-all-ness of the term ‘mental illness’–encapsulating everything from mild depression to complete psychosis–because it really seem to obscure how different, and race-/culture-/structural-position-specific, the etiology of various conditions may be. This inattention to the specificity of cause helps to further stigmatize people, and to conflate forms of (social) suffering which may in fact be quite different and best understood in more separate categories of embodied suffering. Here I am certainly thinking about Jonathan Metzel’s work on race, implicit bias, and schizophrenia diagnosis (http://www.beacon.org/productdetails.cfm?PC=2087) and the persistent underdiagnosis of depression in black patients, who are instead diagnosed as having some violence-prone form of psychosis and/or impulse-control disorders due to racial stereotyping in diagnosis. I worry about how the current discussion of ‘mental illness’ in catch-all, dichotomized terms worsens such stigmatization and inaccurate diagnosis, especially in relation to larger conversations about who should be seen as a threat for potential violence because they have been labeled ‘mentally ill’.
Like you’ve written above, we need to rethink how we conceptualize and define violence if we are going to be able to better predict who is likely to be the next Adam Lanza. But I would also add that maybe we need to do away with the term ‘mental illness’ as well and find more specific categories for different kinds of embodied/social suffering which we use this term to describe. Such definitional specificity is itself a way to better narrow the range of people we should legitimately identify as deranged, violence-prone, and potential mass killers.
(I am republishing a lot of my ‘legacy content’ from our PLOS Neuroanthropology weblog, which has been taken down, along with many of the other founding PLOS Blogs. Some of these, I am putting up because I teach with them. If you have any requests, don’t hesitate to email me at: greg (dot) downey @ mq (dot) edu (dot) au. I suspect many of the links in this piece will be broken, but I will endeavour to try to slowly rebuild this content. Originally published 3 September 2010.)
The photos that accompanied news releases about quadrupedal people living in Turkey, members of a family that allegedly could not walk except on hands and feet, looked staged when I first saw them. Three women and one man scrambling across rocky ground, the women in brightly coloured clothing, the sky radiant blue behind them, their eyes forward and backsides high in the air – like children engaged in some sort of awkward race at a field day or sporting carnival.
For an anthropologist interested in human motor variation and adaptation, the family looked too good to be true. Subsequent reports and a string of papers confirmed that the families did exist, and they suffered from a condition that came to be called ‘Uner Tan Syndrome’ (sometimes ‘Unertan Syndrome’ or UTS). This story is not new, having already broken and exhausted itself on the waves of internet enthusiasm, but I’ve been wanting to write a sober reflection on the lessons I take from UTS for a while now, and my first major post on our new site seems like a good place.
Walking on all fours – we’ve all (or virtually all) done it – but most of us eventually become bipedal, even though the developmental pathways to striding around on two feet vary (see Adolph et al. 2010). The motor pattern is so dominant that bipedalism is considered a defining trait of our species, arising earlier in the paleoarchaeological record than many other distinctive hallmarks of humanity. When I teach my introductory human evolution course, students, like generations of evolutionary theorists, are always surprised by the skeletons of ‘Lucy,’ and now ‘Ardi,’ with ape-like brains and increasingly human-like lower bodies (if they’re not surprised, they pretend to be, probably to humour me).
I’ve previously written about my fascination with human flexibility in movement, including extraordinary forms of mobility (in a piece on the ‘Monkey King,’ an amazing Indian building climber), so Üner Tan, Emeritus Professor from Cukurova University in Turkey and member of the Turkish Academy of Sciences, has been generously sending me pre-print articles and other materials on Uner Tan Syndrome. This piece is made possible by his openness and dogged persistence in spreading the word about this remarkable condition.
Tan first described the syndrome in 2005, based initially on five members of the Ulas family from a small village near Iskenderun, Turkey (seen in those initial photos). He later found families in Adana and small villages near Gaziantep and Canakkale for a total of 14 cases (18 cases in total, but four of which may not have the fully fledged condition from other families) (see Tan 2005; 2006a, b, c; 2010).
From the initial reports, when the number of cases was quite small, Nicholas Humphrey and John R. Skoyles from the London School of Economics and Roger Keynes University of Cambridge, in an LSE discussion paper, opined, ‘even if it is indeed a one-off pathological condition, we think there may be anthropological lessons to be learned from it’ (2005: 11). I couldn’t agree more: although rare (though not ‘one-off’), cases of human quadrupedalism are a fascinating window in on the dynamic developmental processes that so reliably – but not inevitably – produce bipedalism in humans.
Symptoms of Uner Tan Syndrome
In the initial cases of Uner Tan Syndrome, the distinctive and defining symptom of quadrupedalism was accompanied by a number of other cognitive and neurological problems, including especially cerebellar irregularities such as ataxia in the trunk, or the inability to coordinate muscle movement, and intellectual deficits such as delayed or absent speech and ‘conscious experience’ problems.
Humphrey, Skoyles and Keynes (2005: 8 ) reported on a number of the cases and found:
signs of cerebellar dysfunction including: intention tremor, dysdiadochokinesis (inability to execute rapidly alternating movements particularly of the limbs), dysmetria (lack of coordination of movement typified by under- or over-shooting the intended position), and nystagmus (involuntary rhythmic eye movement, with the eyes moving quickly in one direction, and then slowly in the other). However, the cerebellar signs are relatively mild, and they are no more pronounced in the quadrupeds than in the one affected brother who walks bipedally.
MRI and PET scans of a number of the families found inferior cerebellar hypoplasia, an underdevelopment in the cerebellum, particularly the vermis, the narrow area between the two brain hemispheres; mild atrophy in the cerebellar cortex and slightly simplified cerebral gyri, or an overly smooth surface; and a reduced corpus callosum, the white matter structure that connects the hemispheres, in three of the families, but not in the fourth (see Tan et al. 2008). Different subjects seemed to have slightly different anatomical abnormalities, but the consistent neurological abnormalities afflicted primarily the cerebrum and overall gyrification, the parallel ridges, of the cerebellar cortex (see, for example, Ozcelik et al. 2008: 4234).
In spite of their other motor deficits, however, their balance (while quadrupedal, that is) was quite stable and the individuals involved were also capable of fine motor coordination. Some of the women affected, for example, did fine needlework. The fact that they were not more severely affected is important because, as Humphrey, Skoyles and Keynes (2005: 9) point out:
The capacity for walking upright is highly resilient in human beings. In fact humans typically remain bipedal in the face of much greater obstacles to balance and coordination than those experienced by the subjects we have described here. Individuals with bilateral labyrinthine dysfunction, and loss of lower limb proprioceptive sensation are nonetheless typically bipedal. Bipedality can even occur in the complete absence of the cerebellum. There is a recent report of a young man with congenital agenesis of the cerebellum who nevertheless learned to walk and ride a bicycle.
Why can’t they walk?
Because of the pattern of Uner Tan Syndrome within families and its association with consanguineous marriage, or marriage between cousins, most researchers initially suspected that an autosomal recessive gene mutation might be involved.
Sure enough, in 2008 in an article in the Proceedings of the National Academy of Science, Tayfun Ozcelik and colleagues (2008a) reported that the quadrupedal families had a cluster of related genetic abnormalities, mostly to chromosomes 9p24 and 17p, although one affected family did not have abnormalities to either of these chromosomes (for a review, see Tan 2010). In two of the four Turkish families, the abnormality occurred with the VLDLR gene on 9p24, which encodes the very low-density lipoprotein receptor, also implicated in another genetic disorder, Disequilibrium Syndrome (DES-H), where balance and movement problems are also compromised. Although DES-H sufferers have severe walking difficulties, however, no reported cases walk quadrupedally.
Cross-checking against unaffected family members and other members of the community confirmed the likelihood that a mutation to VLDLR might be the culprit, although a cautionary note is that one family member who had the genetic abnormality could walk normally.
VLDLR is involved in the reelin pathway, a glycoprotein regulated mechanisms that moderates neuronal positioning, alignment and migration in the cerebellum; reelin binds to the VLDLR gene and helps get neuroblasts in the right place and configuration for the cerebellum (for a more detailed discussion, see Türkmen et al. 2008). Mice with impaired reelin genes (RELN) or VLDLR abnormalities wind up with abnormal cerebellae, although VLDLR abnormalities can be asymptomatic in mice, only revealed on autopsy (or presumably, if they stuck the little mice in little mice-sized MRIs and got them to sit still) (see Trommsdorff et al. 1999).
However, Ozcelik and colleagues suggested after a thorough gene mapping study that Uner Tan Syndrome was genetically heterogeneous, even in the limited sample of the four Turkish families (2008a: 4234). I’ll come back to that at length in the next post because I think calling every example of habitual and facultative quadrupedalism an example of a single ‘Uner Tan Syndrome’ is misleading, but misleading in a direction that forces us to question whether Uner Tan and others cases of quadrupedalism are actually demonstrating something much broader than a gene causing a disorder, the extreme cases of VLDLR genetic abnormality being only part of the picture.
Tan and colleagues’ (2008) earlier PET and MRI-based study of the original two families likewise showed divergent results: the UTS sufferers in one family had central vestibular deficits, leading to noticeable abnormalities in the brain scans (cerebellar and vermial atrophy and reduced metabolic activity), whereas the second family had peripheral vestibular deficits and ‘quasi-normal’ scans. The team acknowledged that ‘the quadrupedal gait may have different origins, such as developmental delay in the transition from quadrupedality into bipedality during babyhood’ (ibid.: 335). In simple terms, different mechanisms appeared to be producing the extremely unusual results in the families, the development of bipedality stymied by a range of possible obstacles. The diversity was striking because the condition was so rare; if different abnormalities could produce it, why was habitual human quadrupedalism so rare?
Cerebellum problems and gait ataxia
Abnormalities in the cerebellum often lead to gait ataxia or a kind of disordered, ‘drunken’ form of walking. As Morton and Bastian (2007) discuss, damage to the cerebellum likely leads to a number of effects including difficulties in modulating rhythmic movement, even though the movements could be generated by the brainstem and spinal chord. Disruption of this higher order movement orchestration function might explain the instability of walking with cerobellar hypoplasia because, although individuals can produce leg movements, they would have a harder time coordinating the relations between those leg movements. Walking successfully isn’t just doing leg movements but getting the rhythmic oscillations of the limbs synchronized so that one off-step does not disrupt the smooth transfer of weight or trigger a cascade of increasingly awkward or unbalanced movements that might eventually cause the walker to topple over.
In short video clips that Prof. Tan has sent me, a young boy with UTS can be seen standing up and trying to move his feet, but he starts to wobble, apparently due to an inability to control the steps, and quickly falls down. Admittedly, the falling looks well rehearsed, a kind of slumping straight down, as if he isn’t trying to stay up, but that’s likely an effect of his previous experience trying to walk bipedally. In contrast, when walking on hands and feet in another clip, he’s not wobbly at all, but moves smoothly and confidently, quickly getting about a small house.
In addition to coordination problems, damage to some portions of the cerebellum can lead to difficulties maintaining balance in a host of postures, including sitting and standing, as well as walking. The Uner Tan Syndrome cases, however, seem to have problems primarily with walking, and could stand, albeit in awkward positions in some cases. Although vertical posture control conceivably might be compromised to some degree with UTS, the impairment is not so great as to inhibit standing, perhaps because the posture does not exceed the capacities of the impaired cerebellum (patients with cerebellum lesions, however, do often have problems standing upright).
Finally, Morton and Bastian (2007, p. 83) suggest that the cerebellum facilitates adapting movements to perturbations, preserving smooth functioning in shifting situations. Although separating this from the first function in the descriptions of the individuals with Uner Tan Syndrome is difficult, especially working from the published papers alone and a few videotapes, this might also help explain the specific quadrupedal movement. Several of the papers on UTS describe that the subjects could stand but quickly reverted to a four-limbed stance when they tried to step forward. We don’t know if, given ideal situations, the UTS patients might be able to walk, only losing balance when they can’t compensate for variations in conditions. Just judging from the little tape I’ve seen, I think the problem is more profound than this, but it’s hard to tell as learned inability – a lifetime of being unable to walk bipedally – might deter any serious attempt in the older children.
Damage to the cerebellum usually produces distinctive patterns of motor problems; stroke-related insult or gunshot wound to the upper part, for example, can produce problems with gait and balance whereas similar injuries to the lower cerebellum might affect movements of the hands and arms. Fine motor control tends to be affected more by lateral damage; whole body by medial injury.
The Uner Tan Syndrome patients, however, seem to control their bodies, except for their torsos, reasonable well with some issues about aiming movements, tremors, and the like. And yet they lose their ability to walk upright, a remarkably resilient capacity, while developing marked, even extraordinary compensatory facility in quadrupedal movements.
That is, if we focus only on their deficits, we miss the fact that they also have this exceptional ability, one that normal, bipedal humans would be hard-pressed to imitate. Try moving about in a ‘bear walk’ for a while (I have, as the next post will explain), and you’ll quickly realize that, if this is the ‘default’ body position when you can’t balance, most of us have lost the ‘default’ through disuse.
Is Uner Tan Syndrome genetic?
Confronted with the evidence that the genetic abnormalities among the Turkish cases were heterogeneous, and that in one case, an abnormality could not be found, and with a sibling who had the mutation but was able to walk normally, some researchers have concluded that the condition is not solely genetic in origin.
In a working paper (2005) and in a response (2008) to Ozcelik and colleagues’ (2008) piece in PNAS, Humphrey, Skoyles and Keynes offer a more complex etiology for quadrupedalism, one that takes into account the social situation in which a person with equilibrium difficulties finds him- or herself. Humphrey’s team suggests that the ataxia alone would not produce the condition: ‘additional factors must have been at work, operating in the childhood environment, that combined with the ataxia to produce the unprecedented outcome’ (Humphrey et al. 2005: 9).
Humphrey and colleagues (2008: 10) suggest that a convergence of elements more likely explains Uner Tan Syndrome, pointing to a study of children’s movements that highlighted how the ‘bear-crawl’ might form a rare but surprisingly stable intermediate stage that could supersede or entirely replace ‘knee-crawling’:
The bear-crawl has several advantages over more typical knee-crawling, and it can temporarily prove to be an especially good way of getting around. Indeed Ales Hrdlicka, who seventy five years ago wrote a definitive (though now largely forgotten) treatise on this kind of crawling, Children Who Run on All Fours, remarked that “The most common effect of the all- fours method of progression appears to be more or less of a delay in walking erect. . . These children are quite satisfied with their easy and rapid on-all-fours, and were they left to their own devices and not influenced by other examples, they might possibly keep on, on hands and feet, for a longer time if not indefinitely.”
In other words, ‘bear-crawling’ works, so when children discover it (approximately 5% of the time in American children), the development of walking can be delayed because the incentives to abandon quadrupedal movement when doing it on the knees — slowness, difficulty, lack of mobility — are not as great in the ‘bear-crawlers.’ They get better at moving without having to get bipedal.
Humphrey, Skoyles and Keynes (ibid.) go on to suggest a scenario where that ‘bear-crawling’ might continue, potentially into adulthood:
suppose now that an infant who was a bear-crawler were also to have a congenital brain condition which made balancing on two legs unusually difficult. Suppose moreover that such an infant were, in Hrdlicka’s words, to be less than usual “influenced by other examples” (or, more to the point, more than usual influenced by similar examples within its own family), and furthermore that the infant were to be more than usual “left to its own devices” by its caretakers. The stage might well be set for a version of the bear-crawl gait to be carried on into later life, becoming modified and improved until it did in fact become an effective substitute for bipedalism.
As collaborating evidence, although hardly proof, the authors offer that, 1) the mother reported all of her nineteen children were ‘bear-crawlers,’ even those that became bipedal; 2) once one child permanently adopted quadrupedal movement, subsequent children would have had a mature model; 3) the father regarded the children as ‘gifts from God’ with which he could demonstrate love; and 4) a local doctor said that the family passively accepted the condition and did not attempt physiotherapy. Both the third and fourth point would be a point of contention with other researchers.
Türkmen and colleagues (2008: 1073) reach a similar, albeit less elaborate, conclusion after considering the comparison between the Uner Tan Syndrome cases with Disequilibrium Syndrome: although the genetic mutation causing cerebellar hypoplasia and subsequent ataxia is necessary, it is not sufficient to explain human quadrupedalism.
Confronted by Humphrey and his colleagues in a published letter, Ozcelik and his research team (2008b) intensify the argument for a genetic origin for Uner Tan Syndrome. From the final paragraph of their letter, the reason for the intensity of their response is clear: the researchers are aware that some popular accounts of the Turkish families suggest that the parents’ religious beliefs, their understanding of their children’s condition as divinely ordained, contributed to the condition (the authors cite this piece by Anjana Ahuja in The Times Online). Acknowledging developmental dynamics might contribute to a ‘blame the victims’ family (or religion)’ diagnosis. In contrast, Ozcelik and colleagues (2008a: 4236) wrote in the earlier article, and confirm in their letter (2008b), that several of the families actively sought medical and remedial help, including one unaffected sibling who became a physician, and one family discouraged quadrupedal walking without success. (Ironically, Tan 2010: 81, contradicts this assertion.)
Is quadrupedal walking an atavism?
Throughout the discussion of Uner Tan Sydrome, many of the researchers suggest that the quadrupedal walking pattern might be an atavism, a resurgence of a trait from a more distant ancestor that had otherwise disappeared, like a human caudal appendage (a tail) or hind limbs on a dolphin or whale (e.g., Tan et al. 2008; on atavisms, see Hall 1984; specifically on tails, see Bar-Moar et al. 1980). For example, Humphrey and colleagues (2005: 11) ask:
Given that all five individuals developed the same adult gait, as if following the same developmental programme, there are grounds for asking: where could the “memory” for such a programme have come from? Does it in fact represent an atavistic trait, that has been exposed – possibly for the first time in recent human history – by the remarkable conjunction of circumstances?
Brian Hall (1984) defines atavisms as ‘reappearance of a lost character (morphology or behaviour) typical of remote ancestors and not seen in the parents or recent ancestors of the organisms displaying the atavistic character.’ Ironically, although they disagree on the cause of the syndrome, many of the writers seem to agree that quadrupedalism is an evolutionary ‘rediscovery’ or atavism, an assertion which I find pretty difficult to demonstrate.
Prof. Tan (2006c; 2008), himself, has argued that UTS may be a rare case of ‘reverse evolution’ or ‘devolution,’ an argument that has been strongly resisted by other researchers (see, for example, Herz et al. 2008). Most would argue that the concept of ‘devolution’ or ‘reverse evolution’ is simply not coherent, assuming that evolution is normally, necessarily ‘progressive,’ an understanding anathema to some of the most basic evolutionary principles about irreversibility and non-teleology (that evolution isn’t directed ‘progress,’ just variation, survival and change in relation to shifting selectie environments).
In fact, the argument that human ancestors might have once walked on the ground like chimpanzees (knuckle-walking) or walked quadrupedally on the ground at all prior to becoming terrestrial bipeds has been losing ground in recent years as evolutionary theorists increasingly argue that terrestrial bipedalism may have emerged directly from arboreal ways of moving. That is, instead of first descending to the ground and walking like our chimpanzee or gorilla cousins, instead, our ancestors may have developed other forms of aboreal bipedalism and quadrupedalism that they transferred to the ground (see Thorpe et al. 2007; Stanford 2006).
The recent reports about the hand and wrist structure of ‘Ardi,’ the remains of an Ardipithecus ramidus, seem to support the arboreal bipedalism hypothesis and to suggest that palmigrade quadrupedalism may have, in fact, been an ancestral form of locomotion. Ardi’s skeleton demonstrated some of the hallmarks of bipedalism with no trace of the reinforced knuckle and wrist structure that tends to accompany knuckle-walking. Among the long-awaited analyses of Ardi that appeared last year in Science, Owen Lovejoy and colleagues (2009) specifically discussed the forelimb and hand, detailing how this species of hominid might have moved about (for a summary). The long and short is that Ardipithecus likely moved quadrupedally in trees (carefully walking atop branches) and bipedally on the ground, although this is subject to dispute.
If Ardipithecus was an arboreal quadruped and a terrestrial biped, the argument that terrestrial quadrupedalism is an atavism starts to look a little less convincing. Either we’d have to assume that the pattern of ground movement is a very, very old atavism, predating the move of primate ancestors into an arboreal niche (and thus probably predating the rise of true primates somewhere around 50-80 mya) or disregard the mechanical differences between moving in trees and moving on the ground, including the importance of grasping branches while moving (which Ardipithecus would have been able to do with both hands and feet).
I’m less convinced of the argument that quadrupedalism is an ‘atavism’ because I don’t think quadrupedalism is so difficult to explain that we need to assume a left-over ‘program’ in the brain stem for quadrupedalism getting reactivated. As I’ll discuss in the second post, I think quadrupedalism is ‘closer to the surface’ in humans than we tend to recognize, so becoming habitually quadrupedal is not such a great leap back in devolutionary terms, and that dynamic models of how locomotion emerges better explains, not just human quadrupeds, but also some pretty exotic bipeds that I want to add to the discussion.
Even the fact that the various sufferers of Uner Tan Syndrome develop diverse gaits undermines the argument, in my opinion, that the motor pattern results from a motor ‘program,’ atavistic or otherwise. The initial five subjects from the family in Iskenderun, for example, had two distinct forms of moving, the one male walking with his legs much closer together, whereas his sisters splayed their rear legs. Later quadrupedal walkers studied by Prof. Uner Tan, which I’ll discuss in the next post, relied on bent legs, fundamentally changing the biomechanics of the movement, shifting the position of the pelvis, the angles of the joints, the position of the head, and a host of other crucial variables.
Things get more interesting…
(Well, at least in my opinion.) Were this the state of the situation, I’d probably be interested, but I wouldn’t be posting it as my first substantive column on our new PLoS blog. Consanguineous marriage, genetic abnormality, terrestrial quadrupedism, suggestions that human quadrupedalism might be an evolutionary atavism… heady stuff.
But Dr. Tan keeps finding more and more cases of children and adults who walk on all four, emailing me articles of ‘new cases’ of UTS, and many are clearly not cases of fully blown Uner Tan Syndrome. Some have normal cognitive functions, only convert to quadrupedalism when they’re in a hurry, become quadrupedal later in life, or obviously move in unusual ways due to paralysis from childhood polio.These cases stretch the definition of UTS to the breaking point, but they fill out our account of human quadrupedalism.
I must confess, I’ve never met Uner Tan, and his emails to me are brief, so I have very little sense of what he’s like, but he’s clearly had his interest piqued by these families that he initially documented, so he’s got at least a mild fascination with people who move this way. For that, I’m sympathetic because I’ve got it, too. But the implications of these additional quadrupeds suggests to me that we need to move in a different direction to understand human diversity in ways of moving, away from thinking solely in terms of genetic abnormality and evolutionary atavism….
But to read about that, I’m afraid you’re going to have to turn to Part 2, because this post is getting too long. Come back tomorrow for Part 2: ‘2 legs good, 4 legs better’: Uner Tan Syndrome, part 2.
For more information:
Hrdlicka, A. 1931. Children who run on all fours, and other animal-like behaviors in the human child.New York: McGraw-Hill.
Lovejoy CO, Suwa G, Simpson SW, Matternes JH, & White TD (2009). The great divides: Ardipithecus ramidus reveals the postcrania of our last common ancestors with African apes. Science (New York, N.Y.), 326 (5949), 100-6 PMID: 19810199
Susanne M. Morton,, & Amy J. Bastian (2007). Mechanisms of cerebellar gait ataxia The Cerebellum, 6(1), 79-86 DOI: 10.1080/14734220601187741
Tayfun Ozcelik, Nurten Akarsu, Elif Uz, Safak Caglayan, Suleyman Gulsuner, Onur Emre Onat, Meliha Tan, & Uner Tan (2008). Mutations in the very low-density lipoprotein receptor VLDLR cause cerebellar hypoplasia and quadrupedal locomotion in humans. Proceedings of the National Academy of Sciences, 105 (11), 4232-4236 DOI: 10.1073/pnas.0710010105
Ozcelik, Tayfun,, Nurten Akarsu,, Elif Uz,, Safak Caglayan,, Suleyman Gulsuner,, Onur Emre Onat,, Meliha Tan,, & Uner Tan (2008). Reply to Herz et al. and Humphrey et al.: Genetic heterogeneity of cerebellar hypoplasia with quadrupedal locomotion. Proceedings of the National Academy of Sciences, 105 (23) DOI: 10.1073 pnas.0804078105
Stanford CB (2006). Arboreal bipedalism in wild chimpanzees: implications for the evolution of hominid posture and locomotion. American journal of physical anthropology, 129 (2), 225-31 PMID: 16288480
Tan, Meliha, Sibel Karaca, and Uner Tan. (2010). A New Case of Uner Tan Syndrome—with Late Childhood Quadrupedalism. Movement Disorders, 25 (5), 652-653 DOI: 10.1002/mds.22951
Tan, U. (2005). Unertan Syndrome: Quadrupedality, primitive language, and severe mental retardation; a new theory on the evolution of human mind. NeuroQuantology, 4, 250–255. (Abstract and downloadable pdf)
Tan, U. (2006a). A new syndrome with quadrupedal gait, primitive speech, and severe mental retardation as a live model for human evolution. International Journal of Neuroscience, 116, 361–369. (Abstract and downloadable pdf)
Tan, U. (2006b). Evidence for “Unertan Syndrome” and the evolution of the human mind. International Journal of Neuroscience, 116, 763–774. (Abstract and downloadable pdf)
Tan, U. (2006c). Evidence for “Uner Tan Syndrome” as a human model for reverse evolution. International Journal of Neuroscience, 116, 1539–1547. (Abstract and downloadable pdf)
Tan, Uner (2007). A Wrist-Walker Exhibiting No “Uner Tan Sydnrome”: A Theory for Possible Mechanisms of Human Devolution Toward the Atavistic Walking Patterns. International Journal of Neuroscience , 117 (1), 147-156 DOI: 10.1080/00207450600936866
Tan, Uner. 2008. Discovery of Unertan syndrome and reverse evolution: as an “Aha!” experience. NeuroQuantology 6, 80-3. (abstract)
Tan, Uner. 2010. Uner Tan Syndrome: History, Clinical Evaluations, Genetics, and the Dynamics of Human Quadrupedalism. The Open Neurology Journal 4, 78-89. (abstract)
Uner Tan, Sadrettin Penccedile, Mustafa Yilmaz, Ayhan Oumlzkur, Sibel Karaca, Meliha Tan, & Mehmet Karatascedil (2008). “Unertan Syndrome” in two Turkish Families in Relation to Devolution and Emergence of Homo Erectus: Neurological Examination, MRI, and pet Scans International Journal of Neuroscience, 118, 313-336 DOI: 10.1080/00207450701667766
Tan, Uner, & Meliha Tan (2009). Unertan Syndrome: A New Variant of Unertan Syndrome: Running on All Fours in Two Upright-Walking Children International Journal of Neuroscience, 119 (7), 909-918 DOI: 10.1080/00207450902828050
Thelen, E., & Smith, L. B. (1998). Dynamic systems theories. In W. Darnon and R. M. Lerner (Eds.), Handbook of Child Psychology: Vol. 1. Theoretical Models of Human Development, 5th ed. New York: John Wiley & Sons, 563–634.
Thelen, E.,, & Ulrich, B. D. (1991). Hidden skills: A dynamic systems analysis of treadmill stepping during the first year Monographs of the Society for Research in Child Development, 56 (1), 1-98 DOI: 10.2307/1166099
Thorpe, S. K. S.,, R. L. Holder,, & R. H. Crompton (2007). Origin of Human Bipedalism As an Adaptation for Locomotion on Flexible Branches Science, 316 (5829) DOI: 10.1126/science.1140799
Trommsdorff M, Gotthardt M, Hiesberger T, Shelton J, Stockinger W, Nimpf J, Hammer RE, Richardson JA, & Herz J (1999). Reeler/Disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2. Cell, 97 (6), 689-701 PMID: 10380922
S Türkmen,, K Hoffmann,, Osman Demirhan,, Defne Aruoba,, N Humphrey,, & S Mundlos (2008). Cerebellar hypoplasia, with quadrupedal locomotion, caused by mutations in the very low-density lipoprotein receptor gene European Journal of Human Genetics, 16, 1070-1074 DOI: 10.1038/ejhg.2008.73
(I am republishing a lot of my ‘legacy content’ from our PLOS Neuroanthropology weblog, which has been taken down, along with many of the other founding PLOS Blogs. Some of these, I am putting up because I teach with them. If you have any requests, don’t hesitate to email me at: greg (dot) downey @ mq (dot) edu (dot) au. I suspect many of the links in this piece will be broken, but I will endeavour to try to slowly rebuild this content.)
At the beginning of the film clip, Bajau fisherman Sulbin sits on the side of a boat on the coast of Borneo, gulping air, handling his speargun. And then, he drops into the water. The footage suddenly changes and becomes arresting: silent, dreamy, slow, and so blue. Sulbin strokes deliberately and descends until he strides along the bottom of the ocean, holding his breath, and hunts for fish through handmade goggles. [I’ve had to get a new version of the video clip, 2019.]
Finally, after a couple of minutes, he spears a fish and heads for the surface. The narrator tells us that Sulbin could stay down twice as long and dive deeper if necessary. Most viewers, unfamiliar with free diving, exceptional if they can hold their breath longer than thirty seconds, are quite likely to be shaking their heads by the end of the clip, wondering at the ability of the human body to adapt to life in water. Life as an amphibious human can appear so alien that it’s stranger than science fiction, but painfully beautiful to watch.
I stumbled across the video clip in part because of my academic interest in free diving. Earlier this month, I was supposed to attend a free diving workshop in New Zealand with one of the sport’s world record holder, Will Trubridge (or see the story on the Times Online). The workshop fell through at almost the same time I was diagnosed with multiple hernias, so my first free diving experience likely wouldn’t have worked out – I’m still hoping to do it as part of my ethnographic research on extraordinary human performance in the near future.
But the clip of Sulbin on the BBC series, Human Planet episode, Oceans, has inspired me to write a little bit about Homo aquaticus (kidding), adaptation, culture, and what this sort of remarkable human adaptation might imply for the idea of ‘human nature.’
Sulbin’s ability is remarkable, but like so many exceptional human skills, it relies not on innate difference from other individuals, but on the steady cultivation of peculiar changes in the body and in how it is experienced. What I hope to suggest is that amphibious humans point to the most basic fact of human nature: that we seem particularly adept at finding ways to adapt ourselves – biologically, psychologically, behaviourally, technologically – to a host of niches that then rebound back upon us and shape how we develop. We are a peculiar self-made species.
This piece is probably best seen as one in a series I’ve been crafting on how human adaptation to situations that we place ourselves in map out the envelope of our bodies’ malleability. Human skills and adaptation show us how our brains and nervous systems can be trained to do amazing things. Frequent readers will know that I think much of the discussion of ‘human nature,’ carried out by — to put it nicely — exceptionally sedentary theorists, severely underestimates what our bodies are capable of doing.
Too often, in discussions of human adaptation, we allow a flabby distinction between three basic types of adaptation: genetic, phenotypic (or physiological), and cultural (or technology). What I’ve been playing with, and will return to at the end of this piece, is the inseparability of these, especially the last two: physiology and culture. The Bajau fisherman Sulbin shows us how biology and culture are inseparable because what he does ends up shaping his body, but only because he grew up around people who knew how to manage becoming human in this distinctive amphibious way and because his adaptations play upon how his nervous system works, including some intriguing quirks.
If you’re mad keen to learn more about human adaptation and my ongoing obsession, you might check out samples of my work on human quadrupedalism (part two), barefoot running, barefoot climbing, and even overhand throwing (the piece is specifically on ‘throwing like a girl’). I’ll be posting more in the months to come, so if you’re interested in what the human body can be made to do, pay us a return visit periodically.
‘Sea gypsies’ in Southeast Asia
Sulbin is a member of a number of groups who live wholly or partially as oceanic nomads or sea foragers in South-East Asia. As the BBC website explains:
Few peoples have a deeper connection with the sea than the Bajau Laut of South-East Asia. Sometimes known as “sea gypsies”, they live in house boats or stilt houses built on top of coral reefs and when they do spend the occasional night on solid ground they often report feeling ‘landsick’.
Malaysia’s best Bajau free-divers can dive to depths of over 20 metres and stay there for several minutes on a single breath as they go in search of fish. And as if that weren’t enough, studies on some “sea gypsy” children from Thailand and Burma show that they have unusually good underwater-vision because their eyes have adapted to the liquid environment.
The Bajau Laut’s livelihood is traditionally totally dependent on the resources of the sea so spear-fishing is vitally important to them, but different cultures have very different ways of catching fish. (BBC website).
I won’t go into the ethnographic material on the Bajau and other groups called ‘sea gypsies’ (such as the Moken, who live along the coasts of Thailand, Burma and increasingly into Malaysia). If you’re interested, I’ve placed some links to more material on the Moken and other groups at the end of this article. Some of the groups experienced a recent spike in interest when they apparently avoided serious casualties in the Boxing Day Tsunami of 2004 because they ‘saw signs in the waves’ of the trouble to come.
This post is really about adapting to diving, and that happens a lot more broadly than just in ‘sea gypsy’ populations. Although SCUBA and other techniques are replacing breath-hold diving, traditional divers cultivated incredible abilities in the production of sponges in Greece, and pearls in places like Polynesia and the Persian Gulf. The practice is still widespread among recreational divers, competitive divers, and even in some industries, such as among seafood harvesters in Japan and Korea, where an estimated 20,000 professional divers still worked with minimal equipment as late as the 1990s (see Park et al. 1990, cited in Ferretti 2001).
Learning to ‘hold’ your breath
Human ‘adaptation’ to water is both conscious and unconscious, as so many things about human behaviour. Even the most basic adaptive reflexes have to be shaped and elaborated, although they can often be learned in implicit, indirect ways or found in basic form very early. For example, one of the most reliable reactions to a startling new sensation is to gasp, a potentially deadly maladaptive approach to dealing with being dunked in the water. Fortunately, when water hits the pharynx or larynx, glottal spasms clamp the throat shut with a glottal spasm in part of what is referred to as the ‘diving reflex’.
If we’re going to enjoy the whole underwater swimming experience, however, we’ve got to be taught to stop the airway voluntarily and close the glottis muscularly, or to exhale. It’s more pleasant than just plunging into the water and trusting that the ‘diving reflex’ will save you from winding up with a couple of lungs full of the stuff by triggering a glottal spasm. In other words, the reflex has to be cultivated into a skill.
The online web resource eHow suggests, in How to Teach a Baby to Hold Breath Underwater, that you first condition an infant by essentially an associative learning process where dipping a washcloth in water is followed shortly by dripping water over his or her face. The writer advocates following this up at a pool with a learned association between ‘1… 2… 3…’ and subsequently being splashed in the face, later substituted by short immersion. The diving reflex can cue the early learning, but the goal is to build a more robust voluntary behaviour and to do it in a way that doesn’t so traumatize the kid that he or she never wants to go back to swimming lessons.
When I taught swimming lessons last century (it seems like that long ago), this sort of learned association was also the way that we taught infants, but we also, if we had a particularly difficult case of a gulper, tried to teach the infant to hold its breath by blowing into its face. Either way, though, the early stages of teaching breath holding, at least in my experience, almost always involve a few rough first attempts, with coughing and crying almost inevitable. With the slightly older kids, you could teach them to exhale as they went under (‘blow bubbles’), but some coughing and inhaled water, again, was likely inevitable at some point.
My point is that holding your breath is not something that humans do naturally, although breath control is actually really important for speaking and other human abilities. Breath holding in water may be an easy reaction to instill, but it relies upon someone teaching you or some sort of training, building on top of a more primitive, widely held reflex. Since my father is a non-swimmer, I know firsthand that there’s nothing ‘natural’ about being able to survive in water.
In fact, the Alliance for Safe Children (an Asian NGO) points out that, in some parts of the world, drowning is one of the leading causes of child mortality, contributing approximately fifty deaths each dayin Bangladesh (in contrast, that’s Australia’s typical annual total). According to the WHO, drowning is the third most common cause of unintentional injury death worldwide (WHO ‘Drowning,’ fact sheet #347).
The ‘breakpoint’: involuntary breathing
Your body wants you to breathe as the oxygen you took in with your last breath gradually converts to carbon dioxide. A powerful involuntary mechanism overrides most intentional attempts by humans to hold their breath, as M. J. Parkes (2006) outlines, long before you are actually in any distress. Try to hold your breath until you pass out, and most people will simply not be able to manage it (I’m not actually recommending this experiment).
As we hold our breath, above or below the water, the body slowly converts the oxygen our bodies store in our lungs and blood into carbon dioxide. Levels of oxygen decrease (to hypoxia), and carbon dioxide increases (to hypercapnia). Left long enough, the lack of oxygen will eventually cause brain death from cerebral hypoxia and heart attack, but most of us get nowhere close to dangerous levels when we hold our breath. As Parkes writes (2006: 2-3):
although the simplest clue to the breakpoint mechanism should emerge from identifying any manoeuvre enabling breath-holding to unconsciousness, scientific reports of breath-holding to unconsciousness are rare and inconsistent, despite popular mythology. Schneider (1930) stated that ‘it is practically impossible for a man at sea level to voluntarily hold his breath until he becomes unconscious’, and subsequent scientific literature supports this in adults. [Anecdotal descriptions of losing consciousness describe subjects breath-holding at low barometric pressures, with low oxygen mixtures or with severe voluntary hyperventilation…]
In fact, Fitz-Clarke (ibid: 57) reports that ‘almost all extreme breath-hold divers have experienced loss of consciousness upon emersion in their career’ likely as a result of the carbon dioxide build-up, especially with depressurization on the ascent from deep free dives. In addition, partial, temporary loss of motor control (called ‘sambas’ by the divers) were relatively common in the competition Fitz-Clarke observed.
(The practice of diving, especially the pursuit of records, is still dangerous, so much so that in 1991, the World Conference of Underwater Activities stopped recognizing absolute records for depth and started to more tightly restrict competitive free diving. The drive to go deeper and deeper, using more and more elaborated assistance, was putting lives at risk. In contrast, in the competition Fitz-Clarke observed, safety standards were very high, as they are in sanctioned free-diving events, with assistance divers in the water with competitors and all participants carefully observed.)
The ‘breakpoint’ mechanism, when you feel an almost overwhelming impulse to breath, turns out to be a convergence of a number of reflexes that are quite difficult to study. One key component, however, is chemoreceptors that detect the levels of gas in the blood, especially carbon dioxide surplus. We know chemoreceptors play a role because boosting oxygen levels and decreasing absorbed carbon dioxide in the bloodstream — for example, by gulping air as Sulbin appears to be doing — can extend the amount of time that you hold your breath, although many physicians will caution against it.
But research into breath holding has found that there’s no fixed threshold, either of oxygen or carbon dioxide, that will lead to involuntary breathing, so researchers like Parkes (2006) have argued that chemorecption alone cannot explain the break point. Neurological research has shown that the central nervous system begins to try to restart respiration, including through the diaphragm, before the impetus to breathe becomes almost irresistible to an untrained individual.
Parkes argues that the central respiratory rhythm, an autonomic rhythm like the cardiac rhythm, persists during a breath hold, even though voluntary breath holding suppresses it active expression. This means that breath-holders are not so much stopping their breathing voluntarily as they are holding their chests open and resisting the respiratory rhythm. Parkes (2006: 8-9) points to a range of evidence which suggests that the respiratory rhythm intensifies during the breath hold, even causing more widespread respiratory-anticipating reactions like ‘trachial tugging’ in the lead up to the break point.
Similarly, in a competitive static apnea event, in which divers hold their breaths in stationary positions, Fitz-Clarke (2006: 59) found that most divers experienced involuntary contractions of the diaphragm several minutes into the event. Successful competitors were able to continue to hold their breath even though the nervous system sought to reinitiate breathing.
In other words, as the voice-over says with the video of Sulbin, exceptionally long breath holding requires that a person learn to resist powerful involuntary reflexes, especially spasms in the diaphragm as it attempts to contract in order to re-initiate breathing. When you breath hold, you are not so much ‘running out of air’ as you are fighting powerful impulses to breath when you don’t really need the oxygen yet. Breath holding like Sulbin is doing is the active over-coming of automatic processes by conscious suppression; it’s ignoring pain and involuntary muscle actions because you know you don’t need to do what they’re screaming at you to do.
Without these impulses, how long could you hold your breath? Many people may have heard that three to five minutes without oxygen will cause irreparable brain damage, so they might assume that about four to five minutes would be the maximum that a person could hold his or her breath. They would be wrong.
Breath holding is less dangerous to the brain then cardiac arrest, because during a breath hold, the brain is still connected to oxygen stores in the lungs and the body quickly starts making adjustments to stretch this oxygen store last as long as possible (Fitz-Clarke 2006: 60). In fact, in static apnea (stationary breath holding) competitive breath holders can last five to nine minutes as the body puts into place a range of survival responses and competitors learn to make the most of the oxygen they’ve got.
Making your last breath last
So how can you make your breath last as long as possible if you’re going to have to fight your body to do it. Not all people have the same ‘breakpoint,’ of course, and even the same subjects can demonstrate a wide range of breath-hold times, increased by distraction and by repeated trials (Parkes 2006: 2). But a range of techniques can stretch out your oxygen supply.
First, if you know what to do before entering the water, you can start out ahead. Although physicians warn not to hyperventilate or gulp air prior to diving, Fitz-Clarke (2006: 56-57) found in a study of a competitive free diving event that
almost all athletes employed “lung packing” in the water prior to submersion. This is an inspiratory technique for hyperinflating the lungs using the pharyngeal and glottic muscles in a repetitive manoeuvre resembling gulping or swallowing
‘Lung packing’ or hyper-inflating the lungs to some degree (not to dizziness) before diving is discouraged for a number of reasons, but it can put more air into the lungs to start with, boost the blood oxygen level in the blood slightly, and – most importantly and dangerously – suppress the level of carbon dioxide in the body. With less carbon dioxide, you’re breathing reflex is going to be delayed, but this may also be the reason that free diving participants pass out with some frequency; they run low on oxygen before carbon dioxide levels get high enough to prompt breathing.
The simplest way to make your breath last is to do as little as possible and to stay calm. The record for stationary breath-holding is much longer than the record for any dynamic activity. In addition, the calmer you can stay, the more you will suppress your heart rate, decreasing the speed at which your body runs through its oxygen supply.
If you’ve got to move, move slowly and as efficiently as possible, like Sulbin as he lazily swims toward the bottom. The more you thrash and the harder you work, the faster you’ll convert your oxygen to carbon dioxide. Free divers seek to improve their performance by finding the most hydrodynamic postures and eliminating every redundant movement. As Ferretti (2001: 256) writes: ‘As a consequence, the improvement in the dive record [depth] took place without significant changes in the duration of the dives, which remained steady at around 3.5 min.’
The good news is, your body is going to help you. Thanks to evolution, you’ve been born with a mammalian dive reflex that might keep you alive, or help you to stay under water way longer than you might expect.
Dive reflexes, human and mammalian
The remarkable human ability to adapt to free-diving arises, in part, from the body triggering specific nervous system responses, including a reaction to deprivation from oxygen that can be seen in walruses and other aquatic mammals. Megan Lane explains on the BBC website, quoting freediving instructor Emma Farrell, the author of One Breath, A Reflection on Freediving:
The mammalian dive reflex – seen in aquatic animals such as dolphins and otters, and in humans to a lesser extent – helps, says Farrell.
“It’s a series of automatic adjustments we make when submerged in cold water. It reduces the heart rate and metabolism to slow the rate you use oxygen.”
In fact, the human dive reflex seems to be triggered especially by apnea (the abrupt stop of oxygen intake) and by cold (see Speck and Bruce 1978). You can make use of the dive reflex, if you ever need to relax, by temporarily putting your face into cold water; your heart rate should drop, which can be a really godsend if you have to do something that’s ramping up your excitability.
The dive response is generally said to be composed of three changes:
bradycardia, or a slowing of the overall heart rate;
peripheral vasoconstriction, or the shutting of capillaries on the body’s extremities; and
shunting of blood into the torso, especially the chest, which helps to resist increased pressure.
In most people, the drop in heart rate from the dive reflex is not as great as in other mammals; while most humans decrease by about 10-25%, some mammals can drop to as little as 10% of their normal heart rate (Speck and Bruce 1978).
The human dive reflex, however, can increase with training (Schagatay et al. 2000). A trained diver’s heart rate can drop profoundly during a dive. Some studies have found veteran divers with pulse rates as low as 20-24 beats per minute, especially at the deepest parts of their dives (see Ferretti 2001: 263).
Veteran breath-hold divers, such as pearl divers and marine harvesters, can even demonstrate a more profound cardiac adaptation to diving that can be found in some of the most dedicated competitive free divers, which is not found in other mammals. Scholander and colleagues (Scholander et al. 1962: 189) found that Australian pearl divers demonstrated cardiac arrhythmias, perhaps a defense against asphyxia developed at birth they theorized. As these divers went deep, the interval between heartbeats sometimes became irregular; in one case, a diver at 30 m depth had one interval of 7.2 seconds. Extrapolated, this would be the equivalent of a pulse of eight beats per minute!
Scholander and colleagues argue that this arrhythmia is phylogenetically ancient; fish taken from water exhibit similar cardiac responses. The dysrhythmic response, however, together with an increase in blood pressure, make the human dive reflex a bit dissimilar from the mammalian dive reflex found in species like seals and otters.
Vasoconstrition on the periphery of the body and the centralization of blood flow likely increases the efficiency of the body for the duration of the dive (see Ferretti 2001: 262-263). The less the blood is carrying oxygen out to the peripheral muscles and skin, the more energy (and oxygen) is available to the central organs.
The peripheral body parts end up relying more on anaerobic energy production, leading to a build up of lactic acid. So even if you’re swimming along dreamily looking to spear a fish, the muscles in your hands and outer extremities will start switching over to the metabolic process you would use during anaerobic exercise, leading to the possibility of cramps and the same kinds of pains you would feel with lactic acid buildup.
Accommodating the pressure
One of the dangers of diving is, of course, the increased pressure. Every 10 m of depth raises the pressure on the body by one atmosphere, compressing gas to half its previous volume within the body while the body’s tissue largely remains the same volume.
Boyles’ Law holds that gas expands and contracts depending on the pressure, so the descent into high-pressure depths can compress gasses that might later expand dangerously if the body decompresses too quickly. Since every 10 m halves the volume of a gas, a 30 m dive (to four atmospheres of pressure) would temporarily compress eight liters of air (a ballpark figure for good lung capacity) down to a single liter of volume.
The earliest research on breath-hold diving assumed that the maximum depth of any diving was determined by the residual volume of the lungs. Theorists assumed that, once the pressure crushed the volume of the air in the lungs below the minimum size of the lungs, the lungs would implode. But as dive records grew deeper and deeper, especially past Bob Croft’s 73m record in 1968, researchers began to suspect that the body was alleviating the danger of the pressure to the thorax through some sort of adaptation.
As Ferretti (2001: 256) reviews, theorists realized that one way the body might respond to the pressure of the dive was to ‘blood shift’ or to shunt blood from the extremeties into the abdomen. Imagine the arms and legs are like toothpaste tubes and, under pressure, the blood squeezes into the thorax, which helps to keep the chest from collapsing even though the remaining air in the lungs shrinks and shrinks following Doyle’s law.
Subsequent research has found that, in addition to increased blood volume in the chest cavity, the body also responds with an arching of the diaphragmatic dome upwards (so that the abdomen compresses more than the chest), an engorgement of pulmonary blood vessels (those in the lungs), and an increase in the diameter of the heart (Ferretti 2001: 256-257). In some ways, all of these are not so much ‘adaptations’ as they are simply how the body responds mechanically and hydraulically to the increasing pressure. Fortunately for free divers, their lungs are not in the fingertips or toes, or the increasing pressure would be a much greater problem for anyone trying to dive.
Most people who watch Hollywood thriller also know vaguely about the dangers of ‘the bends,’ when depressurizing overly quick from very deep dives leads compressed gas to bubble up in the joints, causing severe pain. ‘The bends’ are not so specifically a danger brought about by compression, but rather by the decompression as one ascends from a dive.
In fact, the complications are even more numerous, as decompression can lead to pulmonary barotrauma (burst lung) or tears in the lung tissue that can result in emphysema and air emboli, which can block arteries. Overly rapid decompression can lead to air bubbles forming within the brain or spinal cord (causing paralysis or sensory impairment) and in other bodily systems.
Some Bajau and other ‘sea gypsies’ do die of decompression side effects; repeated dives to 10 to 20 m depths actually carry a high risk of decompression sickness, according to the Human Planet website. The danger is increased by rudimentary ‘diving equipment’ that allows divers to stay down longer at slightly deeper depths. For example, compression divers in the Philippines encountered by the Human Planet team were using garden hoses hooked to air compressors to pump down air and extend their time to work underwater.
But even at shallow depths, the pressurization-depressurization of the body can be dangerous. Already at 10 to 20 m, the compression of the air in the sinuses and then re-expansion can cause damage, especially if the diver can’t successfully equalize the pressure between sinus cavities and ears, for example. It’s hard to even imagine how the body can withstand the compression and then depressurization on competitive free dives; the world record for a sled-assisted plunge is more than 200 m.
21 atmospheres of pressure on the air in the lungs and sinuses, and then all released on the way back up!
Physical change from pressure: adaptation?
The situation of how human bodies can ‘adapt’ to the pressure of free diving is a more complicated and ambivalent case of human adaptation then just the dive response, however. ‘Adapting’ to depths can include multiple ways to deal with pressure change; for SCUBA divers, the solution is to develop guidelines for safe diving, use equipment that accurately measures one’s depth, and protocols for decompression, including charts that show safe ascension rates.
Since diving is an everyday activity, the Bajau deliberately rupture their eardrums at an early age. “You bleed from your ears and nose, and you have to spend a week lying down because of the dizziness,” says Imran Lahassan, of the community of Torosiaje in North Sulawesi, Indonesia. “After that you can dive without pain.” Unsurprisingly, most older Bajau are hard of hearing. When diving, they wear hand-carved wooden goggles with glass lenses, hunting with spear guns fashioned from boat timber, tyre rubber and scrap metal.
In his review of the literature on breath-hold diving, Ferretti (2001: 255) tells a story of a similar adaptation in a European diver:
A remarkable performance was accomplished in 1913 by a Greek fisherman ashore the island of Skarpanthos, in the Aegean Sea: this man was able to rescue the anchor of an Italian ship, which was grounded at a depth of 70 m, by means of three consecutive breath-hold dives with a 15-kg counterweight on his belt. The ship physician reported that this diver suffered of emphysema and had no eardrums (please refer to the medical report in Appendix 1). The fisherman understated his achievement and claimed that he was used diving to 110 m… [I’ve put the whole medical report below if you’re as fascinated by this as me.]
I keep putting ‘adaptation’ in scare quotes because carrying around ruptured eardrums may not seem like some folks’ idea of ‘adaptation,’ which may imply a less ambivalent form of biological compensation.
The case of ruptured eardrums from diving also highlights the interlacing of phenotypic and cultural adaptation. The Bajau undergo a phenotypic change (an ‘adaptation’) because they train themselves to go to these depths; without the social support and knowledge, they probably wouldn’t be diving so deep in the first place. Then, when the pain and scary symptoms set in, fellow Bajau like Imran Lahassan tell them how to deal with the damage; lie down, wait, you’ll be fine,… well, a bit hard of hearing.
Of course, ruptured eardrums are damage to the body, like emphysema, but they are also an adaptation, in the sense that they make the body better suited for diving. From the outside, we may look at the trade-off and say, ‘that’s crazy,’ but we face our own health-related trade-offs as our bodies adapt to the artificial environments we create for ourselves. A Greek fisherman capable of recovering an anchor 70 m below the surface might look at the trade-offs of sedentary life and say, ‘that’s crazy! Look at the price their bodies pay for what they do!’
I’ve written about similar adaptations in a book chapter that’s forthcoming for next year, when capoeira practitioners encourage each other to forge on in training through pain until the body adapts, in the case I discuss in the chapter, to putting your head on the ground. These sorts of biological changes highlight the inseparability of culture and biology, that our bodies are shaped by collective knowledge just as so much of the shared wisdom in practical communities is precisely about how the body functions, its limits, and what sort of adaptive trade-offs are even possible (as well as support structures to encourage and facilitate these changes).
Building a better diver’s body
Over time and repeated dives, the divers’ bodies adapt to diving. Bavis and colleagues (2007), drawing on research on human adaptation to hypoxia (low oxygen levels, especially at altitude) and on animal models, suggest that the human respiratory system may have ‘plasticity’ at a number of different levels, from autonomic behavioural adaptations (breathing differently), to structural changes that affect lung volume, and even to biochemical shifts, such as changes to red blood cells. As they put it, adaptation can occur through ‘modifications to the gas exchanger, respiratory pigments, respiratory muscles, and the neural control systems responsible for ventilating the gas exchanger’ (ibid.: 532).
For one thing, in veteran divers, the dive reflex becomes exaggerated: bradycardia increases so that heart rates become abnormally low, and the divers’ responses to hypercapnia (high carbon dioxide levels) become blunted. Ferretti (2001: 259) reviews findings that trained free divers are able to absorb almost twice as much carbon dioxide into the blood before needing to breathe. According to Ferretti and Costa (2003: 208-209), similar ventilatory responses have been found in synchronized swimmers, underwater hockey players, submarine escape tower trainers, and Royal Navy divers. Since the increase in carbon dioxide levels is the primary stimulant to breathe, the ability to tolerate higher levels of CO2 in the blood (hypercapnia) would allow divers to avoid gasping in conditions that would be hard to resist for normal individuals:
the condition of hypercapnia that was maintained during most of the dive, which could even lead to a reversal of pulmonary carbon dioxide transfer, would compel the diver to resist the drive to breathe elicited by the stimulation of central and peripheral chemoreceptors. This opposition would be facilitated by the observed blunted ventilatory response to carbon dioxide. Carbon dioxide sensitivity could be a primary determinant of the breath-hold duration, at least in professional divers. It is noteworthy that also diving mammals, which are frequently exposed to high arterial PO2 and PCO2 values…, are characterised by blunted ventilatory responses to carbon dioxide compared with non-diving mammals of similar size. (Ferretti 2001: 260)
To my knowledge, no studies have been done on the ‘sea gypsies’ of cardio-vascular adaptations or ventilatory response to hypercapnia. All research on human hypoxia adaptation of which I’m aware focuses on high altitude populations, where the pressure to adapt would be constant and thus — possibly — more pronounced than in breath-hold diving populations, who only dive when they are foraging or working.
But — and this is the caveat — the actual accomplishments of breath-hold divers like Sulbin, Greek fishermen, pearl diving Polynesians, and the Ama of Korea are pretty startling, with the ability to stay under water and remain active for long periods of time, so the phenotypic adaptations involved may be quite dramatic.
Sometimes intermittent adaptive pressure, especially severe and gradually increasing pressure, can have greater effect than constant but less severe environmental effects. Remember, I’m talking about phenotypic adaptation, not genetic selection over multiple generations.
The BBC website, for example, mentions the possibility of the spleen contracting to squeeze out more haemoglobin, an effect seen in some research on the Ama:
During breath-holding, oxygen stores reduce and the body starts diverting blood from hands and feet to the vital organs.
Our bodies have a way to compensate. Underwater pressure constricts the spleen, squeezing out extra haemoglobin, the protein in red corpuscles that carry oxygen around the body.
“Not enough research has been done to know if it wears off when you’re not diving,” says Farrell. “But I know people who do a lot of deep training – as Sulbin does – whose blood is like that of people living at high altitude.” In high altitudes, there is less oxygen and so the amount of haemoglobin in blood increases.
This increasing efficiency and trainability (Schagatay et al. 2000) is what makes me a little uncomfortable with referring to the changes as part of a ‘dive reflex,’ in part because I’m not entirely sure that the term ‘reflex’ is universally parsed in the same way. Clearly, bradycardia and peripheral vasoconstriction are common responses; heck, you can even argue that vasoconstriction is not so much an adaptation as a direct consequence of the mechanical and hydraulic ways that pressure affects the body (in other words, it might be hard to call vasoconstriction an ‘adaptation’ given some definitions of the word – you could call it a ‘consequence’).
A fully blown human ‘dive reflex,’ with profound bradycardia, vasoconstriction, cardiac dysrhythmia, (possibly) splenic contraction, even eardrum rupture, because the complex really requires priming from multiple dives, is rather a phenotypic adaptation, with all the messy complexity that I have suggested is implied in the term. That is, the dive adaptation builds upon innate reflexes, but it also requires cultural niche construction and social support and results in physiological change.
In other words, my problem with ‘reflex’ as a description of what happens to the body during an oxygen-depriving is not merely semantic. I think it misrepresents the role of consciousness and experience in the physiological response to a very basic sensation: if you’re not ready and accustomed to hypoxia and pressure, immersion is not going to produce the fully blown ‘reflex,’ in part because your interpretation of the event (‘crap, I need to breathe’) may not allow you to grapple with your body’s involuntary reflexes (such as spasms in the diaphragm). I daresay it’s quite possible that some conscious interpretations of what is happening (‘crap, I am DROWNING!’) may even completely unravel even the basic ‘dive reflex,’ for example causing the heart rate to spike in spite of the tendency toward bradycardia.
The commentator on the video clip says that Sulbin’s heart rate can drop to 30 beats per minute, and competitive free-divers can achieve even lower rates. But they do so, in part, by seizing willful control of the autonomic system through proxy variables, specifically emotional states. They don’t just benefit from the ‘dive reflex’; they drive a consciousness-to-emotion-down-to-autonomic chain to get more out of the dive reflex than just the 10-25% reduction in heart rate that most of us would get (if we don’t panic, in which case we might not even get that).
Will Trubridge, for example, like many competitive free divers, uses meditative and mind-body techniques borrowed from yoga. Sulbin uses his pre-dive routine, including a smoke to ‘relax his chest’ and air gulping. That is, the ‘reflex’ can be elaborated into a well-schooled top-down technique for self-management that ends up exerting control over autonomic systems like the cardio-pulmonary system.
As I write this, I realize that I’ve got a couple more things to add about this video that I can’t really fit into my central argument, so I’m just going to put them here. Although I’m fascinated by diving and could go on, I just want to quickly highlight a couple of the ways that life and water can lead to human adaptation to a more amphibious existence:
One of the strangest things about the footage of Sulbin is his apparent negative buoyancy: he walks along the bottom and doesn’t just bob up to the surface. When most people hold their breath, they are positively buoyant; the air inside the torso offsets the slightly greater-than-water density of bodily tissue so that most people will bob to the surface when they hole their breath.
As you hold your breath, the total air in the lungs does gradually decrease, so you become slightly less buoyant near the end of a breath-hold. But for most people, the only way to really sink is to exhale a bit to get to negative buoyancy.
Being extremely lean can make the body sufficiently dense that a person is negatively buoyant, even when holding a full breath. Being lean also helps you to stay under water longer because, if your lung volume remains constant, decreasing your overall weight means more oxygen for every kilo of oxygen-burning bodyweight. So if you want to hold your breath a long time, it helps to diet.
2. Body temperature
Spending a lot of time in water can play havoc with the human body’s ability to maintain a constant temperature. The thermal conductivity of water is twenty-five times greater than air (Reilly and Waterhouse 2005: 74), so being dipped in water below body temperature can quickly lead to hypothermia. Without insulated gear, however, Korean divers can spend hours in the water at 10 degrees Celsius in January, conditions under which hypothermia should have been likely. Hong and Rahn (1967) found, however, that divers did not have thicker layers of subcutaneous fat. In fact, during the coldest seasons, an elevation in their basal metabolic level—an incredibly rare seasonal variation in human metabolism—left them unable to eat enough to keep from slowly losing weight. They turned up the internal furnace.
In addition, the divers’ vascular systems appeared to adapt, restricting heat loss from blood vessels near the skin by constricting them (ironically, to below the level of obese individuals). Their skin became cool to the touch; if the furnace was up, they were also closing off less important rooms in the house. In addition, the shiver response was suppressed because it speeds up the body’s radiation of heat. Ferretti and Costa (2003: 208) note that adaptation to cold has also been found in Australian aborigines who sleep nearly naked in the cold; in trained Arctic scuba divers, even when they wore wetsuits (it’s still bloody cold); and in Canadian fishermen who repeatedly immerse their hands in water at 9-10 degrees. The adoption of wetsuits by the Ama, however, has led to a decrease in their bodily adaptation to cold-water resistance.
3. Underwater vision
In research that’s far too interesting for me to just discuss in passing, Anna Gislén and collaborators (2003) found that children among the Moken, one of the indigenous groups called ‘sea gypsies,’ developed the ability to see nearly twice as well as European children under water. Because water has a higher density than air, light passing from water into the eye does not refract as much, so our pupils do not redirect it sufficiently to focus the image on the retina (instead, the light converges beyond the back of the eye, where the accurate image cannot be perceived). Moreover, since our pupils respond to the decreasing light that strikes the eye as we dive deeper by dilating, the lens flattens and exacerbates the distortion still further.
Gislén found that Moken children’s pupils responded in the opposite way when diving, constricting (which the eye would normally do in bright light) so that the lens caused the image to converge on the retina. Gislén and a team was able to train European kids to do the same thing upon her return (Gislén et al. 2006). Again, an ‘automatic’ system or reflex could be re-directed through training, whether or not the individuals involved were explicitly aware of what their nervous system was learning to do.
Like I said, way too interesting for a little note, but this will have to suffice for now…
Ferretti (2001: 267-268) provides an English translation of the medical report done on the Greek fisherman who successfully dove 70 m for the lost anchor, and I feel I must reproduce it in its entirety:
Haggi Statti Giorgios, born in Simi, sponge diver, 35-year-old, married, four children, all alive and healthy. He is 1.70 m tall and weighs 65 kg. His resting thoracic perimeter is 0.92 m, being 0.98 m after a maximal inspiration, and 0.90 m after a maximal expiration. Dark-skinned, slim, he has an ordinary muscle mass. Although an examination of the thorax reveals a remarkable lung emphysema, the upper part of the thorax has not yet reached a large size, even if it is somewhat convex and rigid. The heart tones are far, but regular. The pulse rate is 80-90, and the respiratory rate is 20-22. Nothing abnormal in the nervous system, nor in the eyes. He has impaired auditory function because of the complete lack of the eardrum in one ear, and only the remnants of one in the other. He sfufered from no illness, except for a trachoma, healed after surgery. He reports only pain in his back, which he tolerates resignedly. When asked to hold his breath in the ordinary ambient, he first refused, claiming that the test had no value because he could resist much more under water. Then he accepted, and it resulted that his capacity under these conditions is only 40 s. Yet in the rescue operations he dived to depths varying from 40 to 60 m, and even to 80 m, staying under water for 1.30-3.35 min. He claims that he has reached 110 m, and that he can stay at 30 m for up to 7 min. Statti emerged from all dives in good shape and vigour, as demonstrated by the way he jumped into the boat and released the water that had entered his nose and ears. When questioned on the phenomena he feels during the dives, he says he perceives none. Probably accustomed since childhood, he does not perceive them. He only says he feels all pressure on his shoulders. Nothing on his eyes. He also claims that at 80 m, despite the weakening of light, one can see enough to work, if the water is clear.
On a similar note, one of the accounts of Sulbin on the BBC website reports that his abilities do not come from his clean living. According to their website: “Anyone who thinks this is an example of what a non-smoker’s lungs can do will be disappointed,” says Hugh-Jones. “Sulbin smokes like a chimney. He says it relaxes his chest.”
Like I said: ‘adaptation’ is a pretty neutral word for what can be a far more complicated reality.
Bavis, R., Powell, F., Bradford, A., Hsia, C., Peltonen, J., Soliz, J., Zeis, B., Fergusson, E., Fu, Z., Gassmann, M., Kim, C., Maurer, J., McGuire, M., Miller, B., O’Halloran, K., Paul, R., Reid, S., Rusko, H., Tikkanen, H., & Wilkinson, K. (2007). Respiratory plasticity in response to changes in oxygen supply and demand Integrative and Comparative Biology, 47 (4), 532-551 DOI: 10.1093/icb/icm070
Ferretti, G. (2001). Extreme human breath-hold diving European Journal of Applied Physiology, 84 (4), 254-271 DOI: 10.1007/s004210000377
Fitz-Clarke JR (2006). Adverse events in competitive breath-hold diving. Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc, 33 (1), 55-62 PMID: 16602257
Ferretti G, & Costa M (2003). Diversity in and adaptation to breath-hold diving in humans. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 136 (1), 205-13 PMID: 14527641
Gislén A, Dacke M, Kröger RH, Abrahamsson M, Nilsson DE, & Warrant EJ (2003). Superior underwater vision in a human population of sea gypsies. Current biology : CB, 13 (10), 833-6 PMID: 12747831
Gislén A, Warrant EJ, Dacke M, & Kröger RH (2006). Visual training improves underwater vision in children. Vision research, 46 (20), 3443-50 PMID: 16806388
Hong, Suk Ki, and Hermann Rahn. 1967. “The Diving Women of Korea and Japan.” Scientific American 216 (5): 34-43.
Park YS, Shiraki K, Hong SK (1990) Energetics of breath-hold diving in Korean and Japanese professional divers. In: Lin YC, Shida KK eds. Man in the sea. Best, San Pedro, Calif., pp 75-87.
Reilly, Thomas, and Jim Waterhouse. 2005. Sport, Exercise and Environmental Physiology. Edinburgh: Elsevier.
Schagatay E, van Kampen M, Emanuelsson S, & Holm B (2000). Effects of physical and apnea training on apneic time and the diving response in humans. European journal of applied physiology, 82 (3), 161-9 PMID: 10929209
SCHOLANDER PF, HAMMEL HT, LEMESSURIER H, HEMMINGSEN E, & GAREY W (1962). Circulatory adjustment in pearl divers. Journal of applied physiology, 17, 184-90 PMID: 13909130
Speck, D. F. and D. S. Bruce. (1978) Effects of varying thermal and apneic conditions on the human dive reflex. Undersea Biomedical Research 5(1): 9-14.
If you follow Neuroanthropology, either here or on Facebook, you may have noticed something new. We’ve had a bit of a facelift to this site and added a page: Anth 207 Neuroanth 101. This new venture is an effort to generate open educational resources for people interested in psychological anthropology: students, teachers, researchers, the curious…
We’ll be adding more videos slowly, as well as suggested readings, other related resources, reflection questions, and notes. The goal is to start building an open resource for those who want to start learning about neuroanthropology.
UPDATE: After a quick consultation with partner-in-online Daniel Lende, we’ve decided to go whole hog with the new look, new feel, and all-neuroanthropology message. I’ve done a quick rename to ‘Neuroanthropology 101’ with the goal of making it clear what we’re doing, and hopefully making a space to which other neuroanthropologists will want to contribute.
It started on this blog. In 2007, Greg and I co-founded Neuroanthropology. Five years later our book is out! “The Encultured Brain” will be published by MIT Press this Friday, August 24th, 2012. You can already order itat Amazon!
The brain and the nervous system are our most cultural organs. Our nervous system is especially immature at birth, our brain disproportionately small in relation to its adult size and open to cultural sculpting at multiple levels. Recognizing this, the new field of neuroanthropology places the brain at the center of discussions about human nature and culture.
Anthropology offers brain science more robust accounts of enculturation to explain observable difference in brain function; neuroscience offers anthropology evidence of neuroplasticity’s role in social and cultural dynamics. This book provides a foundational text for neuroanthropology, offering basic concepts and case studies at the intersection of brain and culture.
“The Encultured Brain” is really two books in one – the approach Greg and I have built to neuroanthropology, and other researchers using neuroanthropology in their own work. So at under $40 on Amazon, it’s a great deal!
#1: Our comprehensive take on neuroanthropology – an introduction to the field and the book, an in-depth statement on what neuroanthropology is, the evolutionary background to this approach, an outline for future research, and our own expert examples on balance and addiction.
#2: Nine case studies by other researchers, covering memory, PTSD, primates, skill acquisition, humor, autism, male vitality, smoking, and depression. These additional chapters really push “The Encultured Brain” into a new space, for they show how scholars are already using neuroanthropology to address an array of research problems.
Neuroanthropology now comes in two forms on Facebook!
The Blog – With Extra Content
If you want to follow everything that we’re doing on the Neuroanthropology PLOS blog, and you also want short, fun posts that Greg and I have specifically written for Facebook, then head over to the Neuroanthropology Blog Facebook Page. I just stuck the great photo featured here up on Facebook – just a sample!
Neuroanthropology Interest Group
An active interest group – with lots of shared links and discussion – is growing quickly on Facebook. Here you can share and discover news stories and journal articles, and engage with like-minded people who want to explore the intersection of neuroscience and anthropology.
Inside the Mind of a Pedophile
-Absolutely incredible comments on this post, as readers continue to debate pedophilia, the people who have done it, and the children and families who have suffered from it
It’s hard to believe that we’ve had 1,000,000 onsite visits in three years, plus all the other people who’ve read this site through Google reader or other rss feeds. When we started, we never expected to have such success with this site. So thank you!
And now we’re doing the same great stuff over on Neuroanthropology on PLoS. Here are five of our top posts since September 1st:
Anthropology, Science, and Public Understanding
-The American Anthropological Association dropped the word “science” from the mission statement included in the association’s long-term plan, and the media and blogosphere erupted. Here’s the post that kicked off Neuroanthropology’s extensive coverage of the controversy
The Culture of Poverty Debate
-The controversial Culture of Poverty idea has made a comeback. Here’s coverage of the good and bad about the media reports and research on the renewed look at the links between culture and poverty