SLA Biomedical & Life Sciences Division Blog

Elephants

Elephants constitute the largest living land animals today and their ancestors have held that status going back to the mammoths and mastodons (Rohland et al 2010). There are actually three species of extant elephants. One is found in India (Elephas maximus indicus) and two live in Africa. The two African species feature one that primarily lives in dense jungle/woodlands mostly in equatorial and west Africa  (Loxodonta Africa cyclotis) and one that sprawls across the savannahs of eastern and southern Africa (Loxodonta Africana Africana). There is a small zone of hybridization in central Africa, although this is not as common in the wild as it is in zoos.

Elephants in Asia

Elephants now number a few hundred thousand in Asia, where perhaps as many as a million used to roam. They are more common in India than any other state although Bangladesh and all the Southeast Asian countries have significant populations.

A particular feature of the lives of some elephants in Asia, as opposed to Africa, is that at one time a  significant proportion of them were used in hauling operations in remote areas (generally in the lumber industry) and some still are. (They have largely been supplanted by trucks, tractors, and specialized mechanized equipment).

A much smaller percentage today are housed in temple quarters owing, in part, to their connection with Hindu religious traditions, and for use in ceremonies and festival parades. (This is not to say they live a cosseted life, owing to factors that will be discussed shortly).  The majority that remain in India and Sri Lanka, at least, live in forest preserves, where some attempts are made to conserve them (Badola et al 2010, Baskaran, Udhayan & Desai 2010, Govindaraj 2010, Gubbi 2011).

While both Asian and forest elephants in Africa routinely prefer leaves and twigs from trees and bushes, they can switch to grasses opportunistically. One of the favorites of Asian elephants  (and forest elephants in Africa) are tree fruit, which are a major cash crop, which puts them in conflict with farmers, although ironically in Sri Lanka at least, farmers are, in consequence,  turning to citrus production, in part because elephants there do not prefer it. However, by far the  the largest cash crop in all Asia, rice, is often raided by elephant bands at harvest time (Chelliah et al 2010, Jotikapukkana,  Berg, &  Pattanavibool 2010, Santiappillai & Reed 2010, Santiapillai et al 2010). Deaths to both elephants and humans are not infrequent  in trying to scare off the elephants and preserve the harvest (Doyle et al 2010).

Elephants in Africa

While a tiny percentage of African elephants can be found in  zoos and circuses, they are overwhelmingly wild, undomesticated animals, whose  present population numbers are  in the hundreds of thousands,  down from the millions as recently as the early twentieth century.

The forest type are significantly more threatened (Bechem & Luhunu 2010, Bouche et al 2010, Lindsell, Klop & Siaka 2011, Lindsell, Klop, &  Siaka 2011, Rood, Ganie  & Nijman 2010 ) than the savannah species.

While there are some truly gigantic game parks (large relative to European and even most North American equivalents), a significant number of African elephants of both types are still living close to the park borders  or in unrestricted areas where deadly clashes with ivory poachers (Martin & Martin 2010, Messer 2010) and  natives hunter-gatherer tribespeople and indigenous farmers are a sorry fact of life (Graham et al 2010, Monney,  Dakwa, & Wiafe 2010, Ouattara, Soulemane, Nandjui & Tondoh 2010). Elephants are scarcely alone in their fatal encounters with humans and their crops. To the surprise of many who think them solely placid water plant eaters, hippos also frequently raid crops and attack and kill humans who try to fend them off (Kendall 2011).

The Diet & Water Needs of Elephants Actively Determine the Landscape

Because they are so large, elephants (particularly African Savannah elephants) are seen as much as shapers of their surroundings rather than as being shaped by their surroundings.  They do this largely through the long term effects of  their dietary  habits and water-seeking (Buitenwerf, Swemmer & Peel 2011, de Knegt et al 2011, O’Connor 2010).

Probably no other animal in the wild has its diet and travel ways  so thoroughly analyzed through the seemingly continuous analysis of their poop: largely because the droppings are  enormous and  easily located  with  fresh new specimens available to researchers at least once daily from individual elephants  so changes in thier diet can be  monitored (Codron et al 2011).  

When African savannah elephants enter a field which contains a mixture of trees, shrubs, and grasses, they may choose any one of them for forage to obtain the 400 lbs. or so of vegetation that they typically ingest every day. However the choice most likely to be adverse to the local ecosystems occurs when they forage on  the youngest trees or the mid-level shrubs.

Why would they do this? At certain times of the year (mostly during dry spells) ordinarily grass-loving  savannah elephants are likely to find  greater nutritional density in the browse from trees and bushes than from the available grasses.  The impact of savannah elephant browsing in terms of lost shade and diminished topsoil retention  can be immediate , and recovery can take quite a while, particularly if an area has already been logged commercially (Bonnell, Reyna-Hurtado, & Chapman 2011).

However, during the rainy season almost all savannah elephants switch back almost exclusively to tall lush (and presumably more nutrient-dense)  grasses, sparing the damage to trees and mid-level shrubs (Codron et al 2011).

Interestingly a number of trees and mid-level shrubs have evolved mutualisms with insects, which do not appreciably harm the trees,  whereby the insects will instead bite/harass the elephants who attempt to browse on them (Goheen & Palmer 2010).

This savannah elephant tree and mid-level brush browsing would seem to be entirely detrimental to the landscape save for perhaps three offsetting behaviors.

First, elephant dung is a tremendous source of food to burrowing insects, such as termites and dung beetles,  whose ferocious level of industry further mixes  the animal waste into the substrate (60% of which is actually relatively undigested  and serves as an excellent mulch) actually enriching the soil (Aarrestad et al 2011, Banks et al 2010, Levick 2010) and supporting  more green growth.

Second, savannah elephants are also among the first to return to areas of the veldt that have been burned via lightning storms, as they can better tolerate the coarse remnants digestively, and their subsequent droppings actually speed the recovery of the local ecosystem in terms of small grazers returning to well fertilized tender growth (Sensenig, Demment & Laca 2010).

 

Third, elephants are actually rather good at finding underground water and will use their tusks to dig up what become temporary water holes that a wide variety of other animals can subsequently share (Augustine 2010,  Franz  et al 2011). These water holes may become more permanent when the rains come, changing the landscape for the better on the largely arid savannahs. This behavior is perhaps even more altruistic than might be expected since it is almost exclusively only during water hunting forays and "well digging"  that the distracted elephants experience the otherwise rarely  successful attacks of lions on their drought-weakened young (Joubert 2006, Loveridge et al 2006). 

However, elephant overpopulation may not be entirely offset by the good the herds  do, and even abundant rainfall may not provide enough vegetation to sustain densely crowded elephant  populations (Hayward &  Zawadzka 2010).

Elephant Sensory Capacity, Intelligence & Sociability

Elephants have enormous and exceptionally well developed brains (Fowler &  Mikota2006, Hakeem et al. 2009, Hart & Pinter-Woman 2008, Shoshani, Kupsky & Marchant 2006). They possess self-awareness, recognize themselves in mirrors (Plotnik, de Waal, & Reiss 2006, Plotnik et al 2010), and demonstrate innate intelligence at least on a par with primates and are possibly as bright as dolphins (Byrne, Bates &  Moss 2009).

They have excellent hearing and communicate with a wide variety of vocalizations that seem to convey not only specific information but also mood states (Nair et al 2009, Soltis, Blowers, & Savage 2011).

While they have a keen sense of smell (Santiapillai &  Read 2010) they have terrible eyesight (Baproda et al 2010, Pettigrew et al 2010).

They are highly social and live for the most part in matriarchal groups and practice a great deal of caring for one another’s offspring  (Bates 2008, Bradshaw &  Schore 2007, De Waal 1998, De Waal 2006,  Lee 1987).

They appear to show sadness at the death of important individuals from their group, especially matriarchs (Douglas-Hamilton et al 2006).

There is much that we still do not understand about an elephant’s interior life  (Irie &  Hasegawa 2009) but we do know that it seems built for cooperativity with its own kind (Schulte 2000) and that elephants actually suffer in captivity when kept alone and isolated from other elephants (Nolen 2011).

Perhaps the most intriguing insight into elephant intelligence and willingness to cooperate is documented by Plotnik et al (2011). In an experiment conducted with the cooperation of mahouts (handlers who maintain a special lifelong welfare oversight and training  relationship with a particular elephant ) conducted in a Thai elephant refuge center, a  series of elephants were trained to pull a rope, for which they were rewarded with corn in a bowl.

The table on which the corn was placed was later rigged with a special rope with two ends, both ends of which had to be pulled in order for the table to slide within reach, and for the bowl then to be emptied of its corn.

No elephant acting on his or her own could pull the rope and make the table slide forward. Instead, the rope merely pulled out from the table.

If, in a pair of elephants one of them pulled at the rope but the other did not, the table would not slide forward, and no reward was forthcoming either.

Eventually, the elephants determined that they would somehow have to do this rope-pulling task together without any prompting from their mahouts, and did so.

Their techniques varied. Some pulled from their side using their trunk and their mouth. Others used only their trunk.

One particularly clever female managed to have her male elephant partner do all the real work, for she simply trapped the rope on her side under her foot, making her partner have to pull twice as hard on his end  to get the table to slide forward.

Elephants who saw no rope around the table eventually did not bother going forward to manage in some other way to obtain the corn. They sensed (correctly as it turned out) that without the rope there was no use wasting their time.  

However, the elephants developed a sense of patience. Some elephants who knew that another elephant might be nearby would advance  to the  usual location of the rope on  his or her side alone, and wait for another elephant to show up on the other side.

 If none showed up, the dsappointed elephant  moved away. But they had an unusually long period in which they were content to stay in hope: 45 seconds. This is much longer  than chimps and a variety of other animals tested along similar lines.

Interestingly, their intent to seek cooperative opportunities was not extinguished if no one showed up. They would try again later, and as test showed, they often succeeded.

What is the future of the elephant?

Despite the fact that encroaching human population and elephant habitat loss are very real threats, there is a significant shift among many citizens in countries where elephants are native. They have come to see that elephant conservation and resultant eco-tourism may well be a better way to make a living than subsistence farming or ivory poaching (Fischer, Muchapondwa & Sterner 2011), and in addition, that such preserves as are being set up allow  for as much space as possible about which elephants might forage and roam, especially including protection of incoming sources of water (Jotikapukkana,  Berg,  & Pattanavibool 2010), and that temple and zoo animals be allowed to live in groups where they could develop a social life or elephant culture (Vanitha, Thiyagesan, & Baskaran 2011).

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Tuberculosis, TB, is on the Rise Again

If there was a celebrity cause of death of the last millennium, it was probably tuberculosis. According to an unsigned, but rather exhaustive inventory,  matter-of-factly entitled "List of tuberculosis victims" http://en.wikipedia.org/wiki/List_of_tuberculosis_victims, which I fact-checked for  two dozen or so names,  it does seem likely that all of the following died of TB or its complications: John Calvin, Cardinal & Regent of France Richelieu,  Saint Theresa and Saint Bernadette Soubirous of Lourdes, all of the Bronte sisters, Elizabeth Barrett Browning, John Keats, Eugene O’Neill, William Somerset Maugham, D.H. Lawrence, George Orwell, Alexander Pope, Washington Irving, Moliere, Sir Walter Scott, Laurence Sterne, Henry David Thoreau, Robert Louis Stevenson, Jean-Jacques Rousseau, Frederic Chopin, Igor Stravinsky, Anton Chekhov, Maxim Gorky, Simon Bolivar, President James Monroe, Eleanor Roosevelt, Alexander Graham Bell, Louis Braille,  Immanuel Kant, Florence Nightingale, Baruch Spinoza, Ho Chin Mihn & W.C. Fields. But TB is scarcely a “dead disease. ”  Every year over 9,000,000 new cases are reported and 2,000,000 die from it. (Das & Horton 2010, Lonnroth et al. 2010). This is in contrast to the numbers who died during the recent, much more highly publicized H1N1 misnamed “swine flu and/or bird flu” epidemic: 14,286, according to the European Centers for Disease Control & Prevention.

 

Who Gets TB Today?

 

While anyone can conceivably get TB today,  the following are among the most likely victims today. Poor urban dwellers (Cantwell et al 1998) with a history of alcoholism (see, for example Mathew et al 2010) and smoking (see for example  Silva et al 2010)……although neither poverty nor alcohol nor tobacco use cause TB of themselves). Recent immigrants to developed Western countries from underdeveloped countries in Africa, the Middle East & Central Asia, or South East Asia (see for example Buu et al 2010, Menzies et al 2010), where TB is much more common. Certain isolated indigenous peoples, including some Native American Indian tribes (Breault & Hoffman 1997) .  Dairy herdsmen and slaughterhouse workers, veterinarians,  doctors, nurses, dentists (see for example Cadmus et al 2010) workers and the very people who fight TB the most: Public Health workers (Hanscheid & Grobusch 2010, Jong Lee et al 2010,  Ling & Menzies 2010). And just about anyone with HIV, particularly in Sub-Saharan Africa. TB hits children (Marais & Schaff 2010)  and the elderly (Mori & Leung 2010) much harder than adults.

 

From What, Where or Whom Do They Get TB?

 

Well over 90% of TB is transmitted from person-to-person. In other words if you have been exposed to people who are in their active stage of  TB, people whose  levels of Mycobacteria tuberculosis bacteria are such that they are abundant in their sputum which is sprayed about mostly through coughing and sneezing, long enough or in the right close circumstances, you can contract TB. Single digit percentages of TB are contracted from animals or animal products: most commonly through consuming unpasteurized dairy products and occasionally red meat. The causative agent is Mycobacterium bovis (so-called bovine or zoonotic TB).  (Chickens can get their own form of TB, but transmission of that type to humans is not common, although chickens can give it to cows, where it causes Johne’s Disease).  

 

However, TB is an equal opportunity disease: people can get it from their relatives, their cows, dairy products, and even from wildlife, and can give it right back to the sources they got it from or their uninfected  herd or pack mates (Rock et al 2009)! Humans can infect cattle, whose excreta infects wildlife (in the US mostly deer, in the UK mostly badgers, in Africa wild buffalos and wildebeest, and anything that eat the wildlife or the cattle,   so that wolves, lynxes, lions can get it and give it back too through saliva and excreta.) Humans can transmit the bovine form just as well as they can the more common M. tuberculosis form to other humans or to animals, and animals can give humans either type as well. Indeed, the best theory of TB origins have it arising from mutations of very tough soil-born versions which became capable of infecting  livestock which in turn infected herdsmen.  North Africa, Europe and Asia seemed to have developed both human and bovine types before the disease spread to Australia or the Americas. Indeed, traces of TB have been found in wooly mammoth and ancient musk oxen and bison  frozen remains and bones on both sides of the Bering Strait, with a trail running down through the west coast of the US (Rothschild & Martin 2006).

 

Given that TB seems so infectious, why don’t more people have it?

 

The short answer in the western world of North America and most of Europe, is that more people used to have it, but three developments halted its more rapid spread, and knocked down its numbers dramatically.  First, TB patients were very often quarantined in sanatoriums, cutting down on further person-to-person transmission, although health care workers at those facilities even now have elevated chances.  Second, dairy products overwhelmingly  became sold to the public only after pasteurization – a heating process which kills the bacteria. Cows that tested positive for TB in their milk were often put down or successfully treated with antibiotics until the infection cleared and even the antibiotics that cured them also cleared from appearance in the milk. Third, a number of drugs were developed that knocked down or completely eliminated the Mycobacteria in both humans and livestock. A fourth factor is now clear: some people and animals have an unusual genetic propensity for resisting the disease, while others have heightened genetic susceptibility (Allen et al 2010).

 

Can’t people be easily diagnosed, take their medicines, and get cured?

 

The diagnosis of TB is usual done by a tuberculin skin text (the PPD) and/or chest x-rays. While the PPD is still usually quite reliable, it does give out a small number of false negatives and false positives. One reason for the false positive, is that foreign-born patients may have received doses of BCG vaccine, which triggers this result. These vaccines are commonly used in an attempt to prevent TB in Europe, Africa and parts of Asia, but owing to limited effectiveness, are  rarely used in the US.  Chest x-rays however, seem to be even less useful on close examination than were previously thought (Eisenberg & Pollock 2010), although they are still frequently required as a condition of employment, of  attending college, or joining the military, a practice going back to the times of WWII. More sophisticated tests are constantly being developed, but most are  more expensive and less widely distributed than  their predecessors (see for example Chen et al 2010, Graham 2010,  Idh et al 2010).

 

The real problem with medications is two-fold: Many patients are non-compliant because the course of drug treatment can be months long, and they start feeling better sooner than the mycobacteria are totally eliminated. Patients with the quiescent “latent” form of TB often have no symptoms at all, and only know that they have TB owing to a PPD test, and resent having being forced to take medications, particularly after they are reassured that they are unlikely to be able to give anyone else TB while the disease is in its latent stage……the problem is that a number of other medical crises can precipitate the development of active TB disease, and that they become quite infectious to others and very sick themselves.   While many governments subsidize the cost of these medications, they are  not always free. Furthermore, in western societies, many immigrants of uncertain legality are leery about complying with  government agencies for fear that they will be deported (see for example Kulane, Ahlberg & Berggren 2010).

 

Perhaps an even larger problem is the development of resistance to standard drugs of choice like Isoniazid (INH) and Rifampin (RIF) and a few other analogues that have served us well for several generations. Multiple Drug Resistance (MDR -----resistant to two standard drug types ) and Extensive Drug Resistance (XDR ----- resistant to all four standard drug types) are becoming a problem for hundreds of thousands (Dheda et al 2010, Hasan et al 2010,  Metcalfe et al 2010). Most of these patients will either become stabilized for short periods of time on ever more exotic combinations of drugs taken on a trial basis,  with the hope that their disease reverts to latency. But many more will die.

 

What can be done now?

 

• Immigrants from countries where TB is endemic need to be screened using more sophisticated tests such as the QuantiFERON®-TB Gold (QFT-G), QuantiFERON®-TB Gold In-Tube test (QFT-GIT); and T-Spot®.TB test. They are only moderately more expensive and show good results (Idh et al 2010). These test must be  administered with scrupulous oversight and integrity of recordkeeping in settings that include modern instrumentation (Nkengasong et al 2010). Patients who test positive should be thoroughly treated before being allowed to immigrate. The developed world to which these unfortunate people wish to move must underwrite the higher cost of better diagnosis and treatment as being in its own enlightened self-interest.

 

• As suggested by practical trials in places like Taiwan (Tsai et al 2010), paying patients financial incentives for compliance with long term drug treatments for latent TB may be more effective and cheaper than police pursuit or treating full-blown TB cases that emerge from untreated latent TB.

 

• Drug research into new anti-TB agents must continue apace. (see for example Patel, Khani & Rajani 2010).

 

• Research into treatments for AIDS is in many cases also preventive or concurrent for  dealing with TB, so that advances in one almost always aid the other (Pathak, Wentzel-Larsen & Asju 2010, VanZyl-Smit et al 2010.

 

• Continued vigilance concerning  Mycobacterium bovis in farm animals, farm products and wildlife, is a relatively low-cost means of holding down  to about 60,000 deaths annually this form of TB. Providing the means for  immunizing and treating animals and/or absolute guarantees of compensation for putting down  infected animals are at this time the best that can be done, and barring a foolish abandonment of pasteurization and a generalized return to raw milk products, likely to succeed (see for example Wee et all 2010) and perhaps even reduce those numbers. For an exhaustive overview of this story see the forthcoming Hardin, Crandall & Stankus (2010).

 

• Fundamental research into the cooption of the host  immune system and the drug resistance bacterial genetics of Mycobacteria will likely give us the best long term outcome, while we fight on public health and pharmacological fronts for now (Behar, Devangai & Remold 2010).

 

Tony Stankus FSLA [email protected] Life Sciences Librarian, Science Coordinator & Professor

University of Arkansas Libraries MULN 223 E

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Allan, K. M., E. Murphy, and J. G. Ayres. 2010. Assessment of respiratory health surveillance for laboratory animal workers. Occupational Medicine (Oxford, England) 60 (6) (09): 458-63.

 

Allen, A. R., G. Minozzi, E. J. Glass, R. A. Skuce, S. W. J. McDowell, J. A. Woolliams, and S. C. Bishop. 2010. Bovine tuberculosis: The genetic basis of host susceptibility. Proceedings of the Royal Society of London .Biological Sciences 277 (1695) (09/22): 2737-45.

 

Andersen, B. M., G. Syversen, H. Thoresen, M. Rasch, K. Hochlin, B. Seljordslia, I. Snevold, and E. Berg. 2010. Failure of dry mist of hydrogen peroxide 5% to kill Mycobacterium tuberculosis. The Journal of Hospital Infection 76 (1) (09): 80-3.

 

Becerra, Mercedes C., Sasha C. Appleton, Molly F. Franke, Katiuska Chalco, Jaime Bayona, Megan B. Murray, and Carole D. Mitnick. 2010. Recurrence after treatment for pulmonary multidrug-resistant tuberculosis. Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America 51 (6) (09/15): 709-11.

 

Behar, Samuel M., Maziar Divangahi, and Heinz G. Remold. 2010. Evasion of innate immunity by Mycobacterium tuberculosis: Is death an exit strategy? Nature Reviews.Microbiology 8 (9) (09): 668-74.

 

Breault, J L, and M G Hoffman. 1997. A strategy for reducing tuberculosis among Oglala Sioux Native Americans. American Journal Of Preventive Medicine 13 (3): 182-188.

 

Buu, Tran N., Dick van Soolingen, Mai N. T. Huyen, Nguyen N. T. Lan, Hoang T. Quy, Edine W. Tiemersma, Martien W. Borgdorff, and Frank G. J. Cobelens. 2010. Tuberculosis acquired outside of households, rural Vietnam. Emerging Infectious Diseases 16 (9) (09): 1466-8.

 

Cadmus, Simeon I., Victoria N. Okoje, Babafemi O. Taiwo, and Dick van Soolingen. 2010. Exposure of dentists to Mycobacterium tuberculosis, Ibadan, Nigeria. Emerging Infectious Diseases 16 (9) (09): 1479-81.

 

Cantwell, M F, M T McKenna, E McCray, and I M Onorato. 1998. Tuberculosis and race/ethnicity in the United States: Impact of socioeconomic status. American Journal Of Respiratory And Critical Care Medicine 157 ( 4 Pt 1) : 1016-1020.

 

Chen, Ru, Yingzuo Bi, Guohai Yang, Zhiling Liu, Zhihui Liu, Bijian Zeng, and Tiezhu Tong. 2010. Development of a fluorescent microsphere-based multiplex assay for simultaneous rapid detection of mycobacterium tuberculosis complex and differentiation of M. tuberculosis and M. bovis in clinical samples. Diagnostic Molecular Pathology: The American Journal of Surgical Pathology, Part B 19 (3) (09): 172-9.

 

Das, P., and R. Horton.  2010.  Tuberculosis-time to accelerate progress.  The Lancet 375 (9728):  1755-1756.

de Klerk, Lin-Mari, Anita L. Michel, Roy G. Bengis, Nicolaas P. J. Kriek, and Jacques Godfroid. 2010. BCG vaccination failed to protect yearling African buffaloes (Syncerus caffer) against experimental intratonsilar challenge with Mycobacterium bovis. Veterinary Immunology and Immunopathology 137 (1-2) (09/15): 84-92.

 

De Schutter, Iris, Kinda Schepers, Mahavir Singh, Françoise Mascart, and Anne Malfroot. 2010. Latent tuberculosis in a newborn: Diagnostic challenges. European Journal of Pediatrics 169 (9) (09): 1155-8.

 

Dheda, Keertan, Robin M. Warren, Alimuddin Zumla, and Martin P. Grobusch. 2010. Extensively drug-resistant tuberculosis: Epidemiology and management challenges. Infectious Disease Clinics of North America 24 (3) (09): 705-25.

 

Eisenberg, Ronald L., and Nira R. Pollock. 2010. Low yield of chest radiography in a large tuberculosis screening program. Radiology 256 (3) (09): 998-1004.

Graham, Stephen Michael. 2010. Research into tuberculosis diagnosis in children. The Lancet Infectious Diseases 10 (9) (09): 581-2.

 

Hänscheid, Thomas, and Martin Peter Grobusch. 2010. Biosafety and tuberculosis laboratories in Africa. The Lancet Infectious Diseases 10 (9) (09): 582-3.

 

Hardin, Amy, Philip Crandall & Tony Stankus. 2010. The zoonotic tuberculosis syndemic:  A literature review & analysis of the scientific journals covering a multidisciplinary field that includes clinical medicine, animal science, wildlife management, bacterial evolution & food safety. Science & Technology Libraries, 29 (4): in press.

 

Hasan, Rumina, Kauser Jabeen, Asho Ali, Yasraba Rafiq, Rabia Laiq, Babar Malik, Mahnaz Tanveer, et al. 2010. Extensively drug-resistant tuberculosis, Pakistan. Emerging Infectious Diseases 16 (9) (09): 1473-5.

 

Idh, Jonna, Ebba Abate, Anna Westman, Daniel Elias, Helena Janols, Aschalew Gelaw, Assefa Getachew, et al. 2010. Kinetics of the QuantiFERON((R))-TB gold in-tube test during treatment of patients with sputum smear-positive tuberculosis in relation to initial TST result and severity of disease. Scandinavian Journal of Infectious Diseases 42 (9) (09): 650-7.

 

Jong Lee, Kyung, Young Ae Kang, Young Mi Kim, Sang-Nae Cho, Jin Wook Moon, Moo Suk Park, Se Kyu Kim, Joon Chang, and Young Sam Kim. 2010. Screening for latent tuberculosis infection in South Korean healthcare workers using a tuberculin skin test and whole blood interferon-gamma assay. Scandinavian Journal of Infectious Diseases 42 (9) (09): 672-8.

 

Kolattukudy, P. E., N. D. Fernandes, A. K. Azad, A. M. Fitzmaurice, and T. D. Sirakova.  1997.  Biochemistry and molecular genetics of cell wall lipid biosynthesis in mycobacteria.  Molecular Microbiology 24 (2):  263-270.

 

Kulane, Asli, Beth M. Ahlberg, and Ingela Berggren. 2010. "It is more than the issue of taking tablets": The interplay between migration policies and TB control in Sweden. Health Policy (Amsterdam, Netherlands) 97 (1) (09): 26-31.

 

Ling, Daphne, and Dick Menzies. 2010. Occupation-related respiratory infections revisited. Infectious Disease Clinics of North America 24 (3) (09): 655-80.

 

Lönnroth, K., K. G. Castro, J. M. Chakaya, L. S. Chauhan, K. Floyd, P. Glaziou, and M. C. Raviglione.  2010.  Tuberculosis control and elimination 2010-2050:  Cure, care, and social development.  The Lancet 357 (9728):  1814-1829.

 

Maragou, Chrysoula, Nadia Theologie-Lygidakis, Panayotis Ioannidis, Antonia Stenou, Sophia Kanavaki, Ioannis Iatrou, and Maria N. Tsolia. 2010. Primary tooth abscess caused by Mycobacterium bovis in an immunocompetent child. European Journal of Pediatrics 169 (9) (09): 1143-5.

 

 

Mathew, Trini A, Alan L Shields, Aizhan Imasheva, Sonya S Shin, Sergey P Mishustin, Gennady G Peremitin, Aivar K Strelis, Galina V Yanova, Shelly F Greenfield, and Jennifer J Furin. 2009. Knowledge, attitudes, and practices of physicians in Tomsk Oblast tuberculosis services regarding alcohol use among tuberculosis patients in Tomsk, Russia. Culture, Medicine And Psychiatry 33 (4): 523-537.

 

Marais, Ben J., and H. S. Schaaf. 2010. Childhood tuberculosis: An emerging and previously neglected problem. Infectious Disease Clinics of North America 24 (3) (09): 727-49.

 

Menzies, Heather J., Carla A. Winston, Timothy H. Holtz, Kevin P. Cain, and William Mac Kenzie R. 2010. Epidemiology of tuberculosis among US- and foreign-born children and adolescents in the United States, 1994-2007. American Journal of Public Health 100 (9) (09): 1724-9.

 

Metcalfe, John Z., Elizabeth Y. Kim, Grace Lin S.Y., Adithya Cattamanchi, Peter Oh, Jennifer Flood, Philip C. Hopewell, and Midori Kato-Maeda. 2010. Determinants of multidrug-resistant tuberculosis clusters, California, USA, 2004-2007. Emerging Infectious Diseases 16 (9) (09): 1403-9.

 

Mori, Toru, and Chi Chiu Leung. 2010. Tuberculosis in the global aging population. Infectious Disease Clinics of North America 24 (3) (09): 751-68.

 

Nkengasong, John N., Peter Nsubuga, Okey Nwanyanwu, Guy Gershy-Damet, Giorgio Roscigno, Marc Bulterys, Barry Schoub, Kevin M. DeCock, and Deborah Birx. 2010. Laboratory systems and services are critical in global health: Time to end the neglect? American Journal of Clinical Pathology 134 (3) (09): 368-73.

 

 

Patel, Navin B., Imran H. Khan, and Smita D. Rajani. 2010. Pharmacological evaluation and characterizations of newly synthesized 1,2,4-triazoles. European Journal of Medicinal Chemistry 45 (9) (09): 4293-9.

 

Pathak, Sharad, Tore Wentzel-Larsen, and Birgitta Asjö. 2010. Effects of in vitro HIV-1 infection on mycobacterial growth in peripheral blood monocyte-derived macrophages. Infection and Immunity 78 (9) (09): 4022-32.

 

Reuter, Morgan A., Nicole D. Pecora, Clifford V. Harding, David H. Canaday, and David McDonald. 2010. Mycobacterium tuberculosis promotes HIV trans-infection and suppresses major histocompatibility complex class II antigen processing by dendritic cells. Journal of Virology 84 (17) (09): 8549-60.

 

Rock, M., B. J. Buntain, J. M. Hatfield, and B. Hallgrimsson.  2009.  Animal-human connections, "one health," and the syndemic approach to prevention.  Social Science and Medicine 68 (6):  991-995.

 

Rothschild, B. M., and L. D. Martin.  2006.  Did ice-age bovids spread tuberculosis?  Naturwissenschaften 93 (11):  565-569

 

Silin, Muriel, Fabienne Laraque, Sonal S. Munsiff, Aldo Crossa, and Tiffany G. Harris. 2010. The impact of monitoring tuberculosis reporting delays in New York City. Journal of Public Health Management and Practice: JPHMP 16 (5) (2010): E09-17.

 

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Tsai, Wen-Chen, Pei-Tseng Kung, Mahmud Khan, Claudia Campbell, Wen-Ta Yang, Tsuey-Fong Lee, and Ya-Hsin Li. 2010. Effects of pay-for-performance system on tuberculosis default cases control and treatment in Taiwan. The Journal Of Infection 61 (3) (09): 235-43.

 

van Zyl-Smit, Richard,N., Laurence Brunet, Madhukar Pai, and Wing-Wai Yew. 2010. The convergence of the global smoking, COPD, tuberculosis, HIV, and respiratory infection epidemics. Infectious Disease Clinics of North America 24 (3) (09): 693-703.

 

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The Renaissance in Neanderthal Studies: Publication of the Neandertal Genome Sequence Is Yet Another Addition to Our Growing Scientific Knowledge

The publication of a draft sequence of the genomic sequence of Neandertal  in the May 7, 2010 issue of Science sets a new high-water mark in paleoanthropology coups  for that journal, even after their breakout last year with the publication of the details of the skeleton of Ardipithecus ramidus in its October 3, 2009, issue, pp.60-106.

What Is The Genome’s Most Striking Finding?

People of European and Asian ancestry share between 1%-4% of their DNA with Neandertals, but people of purely African ancestry apparently do not (Green, Krause, Briggs et al. 2010). It had been the predominant view prior to this that Neandertals and early modern humans did not mate. But if they did, it would have been expected that Africans as well as Eurasians would have Neandertal DNA.

Does This Mean That All Mankind Did Not Come Out Of Africa?

Not necessarily. It most likely means that that at some point, at least two groups of forerunners of modern man, who may well have come out of Africa,    traveled to and settled within points in Europe and Asia.  It appeared that at some point, for a period lasting several thousand years at the least, Africans stop migrating  to Europe and Asia often enough to have mated with these now isolated   Northern forerunners.

It may well have been that Africans were deterred by their better judgment,  since Europe and Asia were undergoing repeated Ice Ages during this period, and the living conditions in Africa were likely superior.

In any case, there is no doubt that both Africans and the Northern migrants continued to evolve separately, despite isolation from one another.

One of these two isolated Eurasian groups  consisted of the Neandertals, and the other Eurasian group was,  for lack of a better understood term,   the most widely recognized group of early modern humans, which we might call the  Cro-Magnons.  (Although Early Modern Human is the more encompassing and scientifically preferred term today).

 The cited DNA analysis from the journal Science now shows beyond a reasonable doubt that Neandertals and Early Modern Humans did mate -----at least in the Middle East between Europe and Asia -----and have some viable offspring at some point and exchanged genetic material that remains in our modern DNA today. 

The studies showing no Neandertal DNA in Africans used the DNA of the  Shan and Yoruba tribes in Africa, groups which had never left the African continent, and not the DNA of other groups , particularly  African-Americans, who have largely intermarried with Europeans and to some extent, Asians, and whose progeny therefore are the result of later intermarriages which may well  show some Neandertal DNA as well.

Had Anyone Predicted This?

Forhan, Martiel and Blum (2008) cited below were one of the more recent groups that showed how it could be so, but a minority had been in favor of the idea all along. Arguably the best known of these is Erik Trinkhaus  of Washington University in St. Louis, who has long argued from anatomical studies.  

Why Did It Take So Long to Come to This Seemingly Decisive Determination?

While there was always some suspicion that Neandertals and Early Modern Humans had mated based on anatomical blends of the two types seen in some fossil finds that were suggestive of “hybrids, ”  it was thought that a DNA analysis would provide the gold standard test. But this gold standard test was frustrated earlier by a number of confounding variables.

1. Could they find a sample or samples that were unambiguously Neandertal to everyone’s satisfaction. (They eventually did, in a cave that was by unanimous consensus,  a purely Neandertal site that had not later been occupied by Early Modern Humans.)

2. Would they be able to screen out the two major contaminating sources of non-Neandertal DNA: microbes like bacteria, viruses and molds on or in the specimen, and then modern human DNA that somehow got into or onto  the samples? (Yes, even most critics contend that extraordinary steps were taken….although even some of this team’s initial findings suggested that it was extremely problematic.)

3. Was there enough computing power and clever enough computer algorithms to do the sequence screening, sorting, and matching necessary for the task? (Yes, read the story by Pennisi cited below: Computer Kid Makes Good” for an excellent account of the group's bioinformatics leader. For technical details see Burbano, Hodges & Green et al 2010 cited below)

Is Widespread Acceptance of this Finding A Sure Thing?

In an excellent essay by John DeVose (2009) he notes, based on a study of several other paradigm shifts in the field,  that on average, it takes a generation of paleonanthropologists  (about 20 years of new Ph.D.s coming into the field and adding their weight to one side or another) to come to a new consensus, so we really have about that long before the next generation of researchers fully buy into this Neandertal genetic proposition, or not, before we can say it’s a  done deal.

What Else Do We Know About Neandertals?

Superior Tool Makers

Neandertals were far better tool makers than was previously thought (See Moncel, Chacon, Coudenneau & Fernandes 2009) , and not only made better finished blades than many Modern Early Humans, but procured better raw materials from farther distances than expected (Bar-Yosef & Van Peer 2009).  But like early modern humans, and modern humans today, it was obvious that most Neandertal tools were made for, and used by,  right-handed individuals (See Uomini 2009).

But Not Good Clothing Designers

While it seems likely that Neandertals wore hides and furs as capes, it seems unlikely that they the sewed seams necessary to make close-fitting garments, owing to the scarcity  of bone needles common among Early Modern Humans (See Sorenson 2009). (Neandertals did use awls, which would allow for fasteners of drape-like garments.)

They  Nonetheless Accessorized

Pigments and seashell fragments typical of making bodily ornaments and body paints or make up have been found in Neandertal settings in Spain (See Zilhao et al 2010).

 

Great hunters

Analysis of cave animal remnants and  isoptopic studies of Neandertal bone all concur: Neandertals were fearless and apparently socially well organized pack hunters of rather fiercesome predators: cave bears, and dire wolves  and giant wild bulls (aurochs) and  wooly mammoths and mastodons. It appears that they competed with giant hyenas for reindeer and deer. (See Richards, Taylor, Steele et al 2008, and Richards & Trinkhaus 2009 cited below).

And Maybe Fishermen

It appears that at least those Neandertals in Spain, and perhaps near Gibraltar, caught and ate fish , and harvested shellfish. They may also have hunted, killed and eaten seals if not whales (See Stringer, Finlayson, Barton et al 2008, and also Nowell & Horstwood 2009,  but see also Klein & Steele 2008 which reflects a more conservative judgments).

And Even Bronco-Riders  (& Maybe Cannibals)

Berger & Trinkhaus (1995) noted that Neandertal bobnes show an awful lot of healed fractures from which the Neandertals clearly lived to hunt another day. It has been suggested that Neandertals  literally jumped upon or wrestled with their big game thereby incurring these  fractures through violent struggle. (Today’s rodeo riders show remarkably similar patterns of broken and healed fractures on x-ray studies).  Other Neanderthal  bone remains show cut marks made by stone tools, suggestive of warfare and cannibalism, but there is also evidence that Neandertals buried their dead with herbs and flowers as well as with tools to be used in the after-life, suggesting that they had a reverential attitude towards the bodies of the dead…..although this does not necessarily preclude eating your in-laws or enemies for revenge.

They Used Fire for Cooking But Not for Forest Clearing for Agriculture

Comparison of Neanderthal and Early Modern Human sites shows that they seemed equal in their use of fire, and at least European populations of both hominids did not appear to use fire to clear out woodland for farming, as had been seen in some of the oldest Asian populations. Neandertals did, however, dry  and/or smoke their meat ------ think of Neandertals as the founders of beef jerky. (Sorenson 2009).  

They Lived in Heated Apartments

Some excavations showed that Neandertals lived in caves or constructed rock shelters with a compartmentalized pattern of sleeping spaces and heat sources so that there was a sequence of a fireplace every nine feet or so near each sleeping spot (Vallverdu, Vaquero, Caceres et al 2010).

There is a Good Deal of Debate on If & How Well Neandertals Spoke

There are two diametrically opposed views here: Krause, Laluenza-Fox, Orlando et al 9 2007) say that a key gene connected to the ability to speak distinctly  FOXP2 was present in both Neandertal and Early Modern Humans  while Coop, Bullaughey Luca & Przeworski ( 2008)  say that such a result seemed more likely owing to contamination of the fossil DNA with modern human traces.

But They May Not Have Been Great Musical Instrumentalists

Despite good tool-making skills and with some support for the fact that they could speak (and presumably sing) well enough, only Early Modern Man seems to have a record of making musical instruments (Conrad, Malina & Muenzel 2009).  

What Did Neandertals Look Like?

Short & Stocky

In terms of modern humans: They were shorter, squatter, stored more fat around their bellies, and had  shorter, thicker  arms and legs, had thick short necks and rather big heads (See DeLeon, Ponce, Golovanova et al 2008, and Weaver 2009).

Pale Skinned  & Red Headed

In other words, they looked exactly like me, except that while I have the fair skin genetic analysis has determined was common among Neandertals, I do not have the red hair most often predicted (See Healy 2008). 

With Modern (not Broad Flat) Noses Sticking Out

Both Neandertals and early modern humans began to have more prominent noses over time, largely because our brains needed more space within the skulls (Mladina, Skitarelic & Vukovic 2009).  Nonethless, there were enough differences so that a trained paleonantropologist  can pretty much quickly tell a Neandertal from an early modern human by their nasal cavity within the skull ( Schwartz, Tattersall & Teschler-Nicola 2008).

 

With Really Big Teeth In Front & Back

Neandertals had bigger, and faster growing teeth (Smith, Harvati, Olejniczak et al 2009) ,  but thinner enamel (Olejniczak, Smith, Feeney et al 2008). This may not have been a disadvantage given that thicker enamel is more necessary if one has a diet higher in grains and nuts which need more through grinding does meat (See Rivals, Moncel & Patou-Mathis 2009).

 

Not All Neandertals Lived in the Same Regions: They had Distinct Ethnicities

Neandertals had three well-established populations which which can be differentiated based on remains: the Western European, the Southern European and the Middle Eastern (see Fabre, Condemi & DeGioanni 2009). There is evidence  over travels and intermarriage among them however. Given that they migrated at least partly with interregional marriage as an outcome, it should not be so unlikely that they mated with nearby Early Modern Humans.

Why Did Neanderthals Die Out?

The consensus opinion is that they simply were outnumbered by Early Modern Humans who were better at marshalling resources that added to one’s chances of surviving, particularly plant-source foods and possibly early agriculture. This reduced dependence on a hunting-only diet may have meant that Early Modern Humans could survive periodic scarcities of wild game better, and in doing so increase their numbers relative to Neandertal populations within the same regions within which both groups competed for resources (See Banks, D’Errico, Francesco et al 2008). There is a more recent, but not widely supported  hypotheses that they may have died of the equivalent of “Mad Cow Disease” through their overdependence on animal diets, which may well have included inadvertently eating animals with transmissible encephalopathogies (See Riel-Salvatore 2008 & Underdown 2008).

Tony Stankus, FSLA [email protected] Professor, Life Sciences Librarian & Coordinator of Science Librarians

University of Arkansas Libraries MULN 223 E

365 North McIlroy Avenue

Fayetteville AR 72701-4002

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Did Communal Defense Against Historic Epidemics in East Asia Lead to Conformist Cultures Where Genes That Predispose Toward Depression & Anxiety in Western Individuals Actually Became Advantageous for East Asians?

One of the most intriguing recent papers seeking to document the notion that genes and cultures co-evolve comes from Chiao & Blizinsky (2010) of  Northwestern University.

Tracking A Gene that Predictably Leads to Increased Depression & Anxiety In Western Societies

One of their starting points is arguably the most studied mental health gene, the serotonin transporter functional polymorphism , 5-HTTLPR,  (Canli & Lesch, 2007; Caspi et al, 2003; Lesch et al, 1996; Pezawas et al., 2005; Risch et al, 2009; Sen, Burmeister & Ghosh, 2004;  Taylor et al, 2006; Uher & McGuffin, 2008).

Conventional wisdom derived from the abundant scientific and clinical literature  has long held that persons have the short form of 5-HTTLPR, have a distinctly higher chance of developing mood disorders, particularly major depression and anxiety, particularly if triggered by stressful life events. Those with the long form of 5-HTTLPR seem to enjoy a measure of protection, despite adversities in their life histories (Fox, Ridgewell & Ashwin, 2009).

The World Wide Reported Frequency of Depression & Anxiety Disorders

Chiao & Blizinsky note however, that the statistical prevalence of diagnoses for depression and anxiety disorders varies across nations and cultures. For example, certain Asian nations, most notably Taiwan, South Korea, and especially the People’s Republic of China,  report markedly lower rates, while the US , UK, and Australia report among the highest rates.(Weissman et al, 1996)

Does this mean that people are deliriously happy in the Peoples Republic and consistently sad in the US? The answer to this is clearly No, but there must be something to account for this   consistently reported  difference.

Does this mean that there are many more psychiatrists in the US, UK and Australia  who will diagnose mood disorders and write SSRI prescriptions? The answer to this is yes, although Chiao & Blizinsky factor this out. (They do report that there may be more cultural stigma in seeking treatment for depression and anxiety in East Asian countries, but also note that countries like Mexico and Brazil also have a lower rate of diagnosis and treatment of mood disorders,  despite the fact Brazilians and Mexicans are not notably ethnically or politically  related to these East Asian groups, have greater access to psychiatrists, and not any particularly well documented social disapproval of seeking some form of help for situationally induced emotional distress.)  

Chiao & Blizinsky also account for  variations in Gross Domestic Product, per-capita earnings, and a number of other factors that would be expected to sway incidence  of depression and anxiety. In terms of wealth measurements, the US, UK and Australia do quite well (even in this economic recession we would still do relatively well against most other nations), and certainly would not be predisposed to a higher frequency of mood disorders in need of  SSRIs if this was driven primarily by chronic economic want.

Furthermore, there  is quite a disparity in per-capita wealth between the Asian people of the Peoples Republic of China on one hand and Asians in South Korea and Taiwan on the other, with the latter two significantly wealthier by most measures. Yet, the low rate reported for diagnosis and treatment of mood disorders is essentially the same across all three counties.

The World Wide Distribution of the Short Form of 5-HTTLPR Favoring  Depression/Anxiety

Chiao & Blizinsky then hypothesized that  this disparity in depression and anxiety must be a case where  more Americans, Brits, and Aussies, must have the short form of the 5-HTTLPR.

But almost exactly the opposite is the case. East Asian nations with very low reported  rates of depression and anxiety have among the very highest frequencies of the short form of 5-HTTLPR within their population.

Ordinarily, this would cause the overthrow of the well established linkage of the short form of 5-HTTLPR with increased propensity for adverse mood disorders, but not even Chiao and Blizinsky   believe that to be necessary.

Why Then Don’t  East Asians with  Short Form 5-HTTLPR Develop Depression & Anxiety As Often?

Chiao & Blizinsky argue that at least historically, if not currently, cultures evolved in Asia with the  kind of structure that buffered  the genetic propensity for mental reactions in people who would ordinarily become notably   depressed and anxious over adverse “triggering”   life events and circumstances.

They note that what   bound these Asian cultures together in the past was a strong emphasis on economic order and social harmony. At least historically, if not currently,  deprivation was a common experience, and losses were shared  across the population. 

The idea of casting out depressed or anxious people with the notion that it would greatly improve communal circumstances, seemed  alien concepts for such a long period of time in historic East Asia  that people with the short form of 5-HTTLPR were able to reproduce and perpetuate this gene to an extraordinary degree, because it did not come with social or economic consequences that caused them to die out in East Asia (Gintis, 2004).

But critically, “blaming behaviors”  for failure in these cultures tended not to fall on individuals who had become depressed or anxious, but rather on a lack of well-coordinated collective effort or on the mandate of Heaven.  Indeed, individuals in East Asian cultures in the past have historically “construed” their sense of self-worth largely in relation to what they could help their village or extended clan accomplish rather than what they could accomplish on their own. And, if nothing was accomplished, then it was a matter beyond the control of the village or the clan, and particularly, not their fault as an individual .

In East Asia, a culture of communal fatalism, in these regards seemed the most sensible, because the range of an individual’s choice of occupations,  and the degree to which one’s economic or social lot could be improved, were much more narrowly circumscribed than in western cultures.

Any individuals in historic East Asian cultures  who consistently expressed outspoken optimism  and tried to persuade the community to hope for substantially better returns by creatively making fundamental changes in the social or economic order  were likely taken as being mental ill in these societies in historic times.

In fact, people lacking in optimism and personal initiative -----people who would be regarded as depressed and anxious people in western societies -----might very well have fit right in with a fatalistic culture.

If Historic Asian Cultures Did  Not Evolutionarily Discriminate Against Those with the Short Form of 5-HTTLPR, Did  This Form Offer Evolutionary Advantages Within Those Cultures?

It has been proposed that one way that the brains of individuals with the short form of 5-HTTLPR malfunction is with heightened sensitivity of their amygdalas (Hariri et al, 2002; Munafo, Brown & Hariri, 2008; Pezawas et al, 2005 ).

The amygdala is that portion of the brain that adds emotional emphasis that not only concentrates one’s thoughts on important tasks and memories in an effort to prioritize them,  but is absolutely essential for danger avoidance.

One measure in which depressed and anxious persons, particularly those with the short form of 5-HTTLPR excel in an adverse sort of way, is their ability to operate in a self-protective fashion via a state of hypervigilance  in terms of their amygdala function. (Osinsinsky et al, 2008). Their amygdalas  seems to “fire” sooner, “fire” more often, and  “fire”  to a greater degree. Their amygdalas seem to signal danger everywhere (Beevers et al, 2007).

In western cultures, this hypervigilance is  seen as making the affected person appear  afraid of everything, and would be expected to contribute to his or her  sense of hopelessness. In particular, it would  make the person disinclined to try out things that would help them break out of their adverse mood.

In western cultures, such individuals might be seen by others, and eventually see themselves,  as self-defeating  pessimists or even cowards. The social or economic disadvantages they have, or the failures they experience,  might well be attributed to flaws in  their character, such as lack of initiative or courage.

In evolutionary terms in western cultures, such individuals are not likely to thrive and reproduce in large enough numbers to pass on their genes to a large proportion of subsequent generations, because hypervigilant behaviors that stifle  self-improvement and economic advancement are socially unattractive, and  put them at a disadvantage against optimistic, creative individuals who are valued more highly in western societies.

In other words, in western societies, these would be the very people who would be strongly advised “to get help” including consulting psychiatrists who would diagnose and treat their depression and anxiety so as to improve their function in society. This  “be treated or be ashamed of oneself, ” culture , of course, might well explain the higher reported rates of diagnosis in western cultures for those syndromes, despite the reduced rate of the short form of the 5-HTTLPR gene.

But Chiao & Blizinsky note that a highly active amygdala, spurred by inheritance of  the short form of 5-HTTLPR,   confers advantages in historically highly conformist groups. It served as an early warning system to register signs of disapproval, particularly in the facial expressions of members of their in-group.

This might well explain that while people across cultures recognize the general emotional nature of facial expressions (anger, happiness, disgust, sadness, etc. ), they differ greatly in their sensitivity to the depth of the emotions,   and nuances within expressions, when dealing with people from outside their culture.

This may be particularly true of westerners encountering Asian cultures.

In other words, a westerner who is completely fluent in Mandarin might well address an audience in Beijing, and even understand that the  tersely  worded polite  verbal feedback is insincere. That foreign speaker could  even sense that the listeners were in fact angry, but  cannot gauge as well as  Chinese members of the same audience, just how angry the members of the audience are, or whether or not the faces in the audience were expressing a mix of emotions.  

Gauging when  a person is right to be afraid is particularly important to reproductive success in authoritarian regimes that historically held sway in East Asia. An inability in those cultures in those times,  to determine that one was in trouble was  likely to get a person incarcerated or worse, definitely limiting their chances to pass on any genes.

Where Does the Notion of Protection Against Infectious Diseases Come Into This Story of the Variance in Effect of a Gene Between Differing Cultures & Nations?

Randy Thornhill at the University of New Mexico has assembled a team of evolutionary biologists and evolutionary psychologists who have developed a model for the evolution of cultures based on how epidemics of microbes and parasites adversely influenced them, and on the measures those cultures took to defend themselves. In their analysis (See  Fincher et al, 2008) those societies that were repeatedly hit by infestations responded by collectivist, protectionist measures, where the free will and “out-of-line” behavior of nonconformist members was seen as a danger to the entire group.  Xenophobia that encouraged quarantine and authoritarianism to enforce hygiene (as much as was understood in those era, at any rate) worked to limit the impact of these infectious disease disasters, and by extension according to Chiao  & Blizinsky,  individuals whose genetic makeup inclined them to conform and closely identify with groupthink, were vastly more likely to live long enough to be able to pass on those genes, than we freethinking western-types, it would appear.  

It is not hard to see  now that the same short form of 5- HTTLPR genes  can make for a differing way of viewing one’s success and sense of worth. The short form can actually promote the construal of oneself  as an obedient  contributor to the health and wealth of the commune  in Eastern cultures, while in Western ones  it leads people to see themselves as, at best, failed   initiators of actions that determine one’s individual achievement and status, and thereby determine their self-worth.

Tony Stankus, FSLA, [email protected] Life Sciences Librarian, Science Coordinator, & Professor

University of Arkansas Libraries MULN 233 E

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Voice: 479-575-4031

Fax: 479-575-4592

 

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:

Switching Gender: A Surprising Finding About the Lack of Permanency of Gender-Specific Structure & Functioning of Cells Within Adult Sex Organs Once a Genetic Switch That Promotes a Distinctly Female Identity is Turned Off

Recent papers in the prestigious journal Cell (see Sinclair & Smith, 2009; Uhlenhaut et al., 2009) have uncovered a startling phenomenon: The clear differentiation of  most mammalian sexual organ cells into either distinctly male (testicles) or female (ovaries) organs might not be determined once and for all during embryonic development.

It has become a doctrine of faith that except in extremely rare cases of intersex (now preferentially termed as Disorders of Sex Development),  having XX chromosomes led the developing embryo turned fetus  turned newborn baby along a path that led to her having functional ovaries and ova and not testes and sperm. 

This differentiation in the fate of the unspecialized “go-either-way” gonad  was thought to be a self-reinforcing phenomenon. XX chromosomes produced proteins that accelerated early either-one-way-or-the other-way  development towards an irreversibly female mix of circulating hormones, that in turn influenced the formation of distinctly female  sexual  organs  and in most cases, seem to influence the development of  sex differences in the brain in terms of structure and  gender self-identity.  Once the gonads became distinctly female they would be secreting a hormonal mix that was so predominantly  estrogen based that the “pre-ovaries”  not only became mature ovaries, but stayed that way,  and particularly with the onset of puberty, produced  even greater amounts of estrogens which further feminized appearance and function throughout adulthood.

The reverse was also thought to be true: XY chromosomes drove the production of androgens which essentially masculinized the either-or gonads towards maleness. Once the gonads became testicles they would doubtlessly produce male traits that would become even stronger after puberty.

BLAMING MOM FOR CASES OF AMBIGUOUS GENDER

There were a number of  rare exceptions to the rule. Most concerned XY male children with anatomically ambiguous genitalia, and occasionally the reverse: XX females with male-like genitals.   

It was thought that the prenatal level of circulating sex hormones might have an influence  on the  developing embryo   that   blurred distinctions in terms of the absolutely either-or anatomy, physiology and gender identity.  

While gender identity is thought to be far more complex that just having certain chromosomes  and being born with either male or female anatomy,   one of the first strategies in persons born with discordant gender identity , is in fact, hormone manipulation that aims towards the desired gender.

In a sense,  if the  maternal-fetal hormonal environment “made a mistake” then one of the first steps was to reverse it by   tilting the circulating hormone levels. Males who wish to have their bodies match their female identity would be given female hormones, and vice-versa.

At some point in time, the ovaries, testicles, and external sex organs would be removed or surgically repurposed, even as the transgender hormones had to be continued because it was seen as dogma that the gonads could not switch which hormones they were making.

THE PROBLEM OF MENOPAUSE FOR THE CONSENSUS THEORY OF THE IRREVERSIBILITY  OF GONAD DEVELOPMENT & FUNCTION

One other major problem with the theory that gonads were irreversible in gender structure and function is the masculinazation  of post-menopausal females. It was generally thought that the ovaries simply aged out of being efficient producers of female hormones, and the tiny amount of male hormones remaining simply began to circulate and influence the body more towards some masculine traits like hirsutism in particular. But there was no thought that the ovaries could actually become testicles, although in extreme cases of masculinization of secondary sex characteristics, it sometimes appeared that way.

THE INTERPLAY OF SRY, Sox 9, & FOXL2

IN SERTOLI, LEYDIG, GRANULOSA & THECA CELLS

While mice used in the lab are not, of course, human, their sexual anatomy, especially the development of the gonads towards one sex or the other  is highly comparable.

The team of of Uhlenhaut et al.  looked at the intermediate biochemical compounds and pathways that, within both mice and humans,   regulate  two general categories of sexual organ cells  specific to their gender.  These regulated cells are the Sertoli and  Leydig cells for the testicles and the granulosa and theca cells for the development and function of ovaries and ova.

The team   started with a focus on gene-produced complexes known in molecular biology shorthand as  SRY and Sox9.

SRY is basically an initiator of  sexual specialization. Without its action, there is neither female nor male sex cell development. The key is maintaining a certain balance.

When  SRY is uninhibited,  it appears to favor maleness by stimulating Sox9.  SRY’s action is modulated in females before birth by a trio of  other gene-produced complexes acting in concert:  beta-catenin, WNT4, and RSPO1. They  keep down the production of Sox9, leading to femaleness.  

After birth, another complex, known by in molecular biology shorthand as FOXL2, picks up where the trio left off in downregulating Sox9.

HOW A CANCER CHEMOTHERAPY AGENT ALLOWED FOR A SELECTIVE SHUTDOWN OF FOXL2

The team hypothesized that FOXL2 interacts with the classic female hormone estrogen and its receptors in a synergistic way.  More importantly, they  hoped that if they could find an agent that would silence the pro-female FOXL2 complex, they might witness the cessation of at least some female hormone production at the cellular level.  They looked to a drug famous for silencing estrogen receptors in cases of estrogen-driven cancers, particularly breast cancer: Tamoxifen.

The injected  tamoxifen had the desired effect.  Ovaries began to shut down estrogen production, and in particular, they appeared to do so by interfering with FOXL2, just as predicted.

What was unpredicted was that once FOXL2 was blocked, these mature  ovaries cells began to change sex. The female theca cells within them began to morph into male  Leydig cells. The female granulosa cells inside were becoming  male Sertoli cells.  In other words, well past the age of embryos, where maternal environments are thought able to influence gender anatomy, function and identity,  these important sex-specific cells were transgendering long after such a thing was thought possible.

It turns out that without FOXL2, it is conceivable that even mature adult ovaries can essentially become and perhaps act like testicles, and that FOXL2 has to fight off Sox9 throughout the lifespan of the ovary in order for it  to stay an ovary.  

WHY THIS MATTERS

This matters because it gives us an insight how we might better handle   persons with gender identity discordance. It might one day be possible to switch the nature of their gonads by selectively turning off a critical pathway, so that the post-birth ovary can indeed become a testicle and start producing male hormones on its own, as opposed to supplying male hormones and surgically removing ovaries, or vice-versa perhaps for males wishing to become females.  Some surgery and some injected hormone manipulation might still be necessary, but some of it could likely be avoided or minimized.

Perhaps even more importantly to women undergoing menopause, particularly those undergoing unwanted early menopause, insights from this research might find ways to unblock FOXL2, so that it could continue to counterbalance Sox9, and allow ovaries to continue to act like ovaries, and particularly allow for both those younger women who had unusually premature menopause and for  older professional women who had delayed childbirth, now to have children, or offset unwanted effects of female hormone loss without ingested or injected hormones.

Tony Stankus, FSLA [email protected] Life Sciences Librarian, Science Coordinator & Professor

University of Arkansas Libraries MULN-223E

Fayetteville, AR 72701

Voice 479-575-4031

Fax: 479-575-4592.

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Ida & Ardi: Comparing The Scientific Debuts Of Darwinius Masillae And Ardipithecus Ramidus, The Fossil Remains Of Two Putative Multimillion Year Old Ancestors Of Modern Man

The Newest Oldest

Announcements to the media and lay public of the “newest oldest” fossil ancestors of mankind happen every few decades.

Often a news conference is often involved, usually featuring what looks like an Indiana Jones impersonator (minus the bull whip) ------   someone who is actually a sunburned field scientist “forced” uncomfortably and uncharacteristically to wear a tweed sport coat for the occasion (often sans tie), but also often with a weather-beaten soft hat, itself constituting a kind of field researcher chic.  

These media events  are usually arranged  after one serious, significant paper,  or more often, a series of serious,  significant papers in top journals of general science such as Science, Nature, the Proceedings of the National Academy of Sciences, or in the top more specialized journals of paleoanthropology, such as the American Journal of Physical Anthropology or its formidable competitor, the Journal of Human Evolution, has appeared, and some time for its discussion has passed.

This sequence of scientists having their say first in arenas that matter a great deal to them than they do to the general public, such as the aforementioned journals, is for a very good reason.

The manuscripts that make it into those journals often have to face grueling rounds of peer-review qualifying critiques first, and then, and only then, is it customary for reporters have a go at the news.

A key feature of such a paper is that it takes  fully into account previously published research that disagrees with the new findings, which the new paper has cited and discussed as completely as possible, and through which, the authors of the new paper demonstrates fully, that those earlier findings are wrong and they then provide the  reasons for this new assessment.

This sequencing of holding off on public announcements, and having full disclosure of contradictory arguments that have been published in the reputable scientific literature is intended largely to avoid at the least,  any overreaching of the scientific evidence  by its discoverers, and, at the worst,  to make cases of fraud extremely difficult, if not impossible,  to foist on either the community of scientists or on the general public, in most cases.

Furthermore, this sequence keeps science and to some degree, scientists, from being distrusted, or made laughing stocks, because subsequent investigations by news reporters, will not be able to uncover any trickery or hyperbole, that suggests that there was a conspiracy of scientists, to simply make the story up for the sake of publicity for a particular institution, or for the enrichment of the individual scientist’s funding.

This would not be because scientists or their sponsors are particularly good at covering all traces of fraud or exaggeration.

It’s because there aren’t any to speak of in the first place.

This is not to say that some of the most reputable universities, natural history museums,  and research foundations, do not seize, as often as possible, on favorable, substantially verified,  and scientifically thorough  news, whose first appearance was in a science journal of some renown,  in a manner  that encourages stronger political and financial support for research done by their researchers.

Ida

Ida is the pet name for the fossil remains of a primate scientifically classified as Darwinius massilae. It got its scientific name from the founder of modern evolutionary theory, Charles Darwin,  and from the district within Germany in which it was found: Grube Messel, “the Messel Pit” a place near Frankfurt.  The pet name Ida matches that of the  daughter of Jorn Hurum, one of the underlying scientific paper’s coauthors.

The paper was not published in one of the established elite journals, but on May 19^th, 2009, rather in an open access, free-to-all-readers, electronic  journal, PLoS ONE,  that is making a bid to join those other  journals at the top, and perhaps even to displace them.

In doing so, PLoS ONE  was taking a risk it saw as worthwhile, because the back story of this paper  seemed so compelling. Likewise, the authors of the paper were taking a risk in not going to one of the better known elite journals, but had the advantage of very speedy publication, a strength emphasized by that journal, which is, to its credit, also peer-reviewed as a measure of quality control.

There are several undeniable scientific firsts and truths about Ida, and the paper reporting her findings:

·     It is the oldest fossil primate found to date, reliably dated at over four  million years old.

·     That the scientists who eventually acquired the two halves of the fossil, clearly identified from the start, than an earlier collector had tried to forge marks that would show half the fossil to be of itself, a complete outline, whereas, the other half, which was eventually purchased by the Natural History Museum of the University of Oslo, was in fact, its almost totally complete, and unfalsified partner.

·     It is stunningly well preserved, and almost completely intact, with not only the hard skeleton, but also the outlines of several of the major organs, and perhaps even of its stomach contents.

·     The specimen is of a female.

·     The skeleton had an unusually complete set of erupting teeth, that squarely placed it as an adolescent of the species, probably about 9 months to one year old.

·     It can be reasonably determined to have been weaned and feedings independently at the time of its death. The diet was most likely fruit and leaves.

·     Based on comparisons with primitive primates that are still living, Ida would have had the potential life span of 20 years.

·     Ida was a locomotory generalist. She was not specialized for climbing, but could do so. She was not built for a life of constant leaping, but could leap is she wanted to do so.

·     Her skull and particularly her eye sockets are more like primitive primates who have nocturnal lives.

All of the above statements seem scientifically well supported by the fossil data. If there were no further pronouncements, Ida would likely have stood, uncontested, as one of the top two finds in paleoanthropology over the last five years.

But instead, Ida was introduced on the following day, May 20^th ,2009, to the public at a gala news conference at the American Museum of Natural History in New York City, about the same time a television documentary on the find narrated by Sir Richard Attenborough, was to appear.

And, a  book for the lay public was surprisingly  also ready for distribution (see Tudge & Young, 2009, cited below), a circumstance that would have been virtually impossible without the leaking of the information to the book’s authors by members of the research team.

There even was t-shirt line available whose front said: “The Link: This changes everything.”

New York City mayor Michael Bloomberg, somehow managed to be the host for this major media  event, in which he termed the fossil find “the missing link connecting humans and apes.”

Ordinarily, a scientific claim made even by a highly educated lay person  like the mayor  would have been quickly forgotten by the scientific press and public, because  they understand, at least in the long run,  that being a  politician and media mogul who runs even a large city does not qualify Mayor Bloomberg as a paleoanthropologcal expert.

Even the claim made at the press conference by Sir Richard Attenborough: “The link until now was missing. Well, it is no longer missing. ” could be forgiven as being the opinion of a distinguished narrator of nature and history films, as opposed to being that of a distinguished scientist.

But  ultimately,  it was what the scientists at the news conference had to say that has had the most staying power.

One of the authors, Jorn Hurum, father of the daughter Ida, proclaimed that “It will probably be pictured in all the textbooks for the next 100 years.”

Jens Franzen, another author on the team, reportedly said: “When our results are published, it will be just like an asteroid hitting the earth. She is the eighth wonder of the world.”  

The scientists present said that they were deliberately pumping up the excitement of this paleontological find, because this kind of self-promotion is done with great effect by rock bands and star athletes all the time, and should be tried out by scientists as well.

None of this went down very well with the rest of the scientific community.

There were two notable disconnects:

First, unlike their public pronouncements, there was no direct claim that Ida was clearly the missing link, but rather that she was a lemur-like animal, and that descent from  lemur-like animals was  one possible route to the coevolution of monkeys, apes, and man that deserved more serious consideration.

Second, despite 27 pages of double-columned text and illustrations, and 81 references, the paper did not appear seriously to engage the consensus opinion that  the lemur line has given us lemurs, and not monkeys, apes, or humans, and in fact, it has only given us a small number of contemporary lemurs and their kin.

On the day of this posting,  a paper in Nature (see Seiffert et al., 2009, cited below) suggests that Ida is a representative of a dead end species that is at best a very remote relative, and a relative only in the sense that she is a primate, more than any kind of direct or common ancestor.

In other words, it’s like my saying that I’m a relative of Michael Bloomberg, just because we are both humans. (Well, it is true that we are also both Republicans, but he’s still the only one of us who is a billionaire.)

Ardi

Ardipithecus ramidus is also a find of some 4+ millions year old, and was also female.

She, and many fossil scraps of her contemporaries were found in the Awash River basin, a part of the Afar district in Ethiopia, ironically about 50 miles from where the famous Lucy, a relative youngster at only 3 million or so years,  was found.

There was in fact, a documentary film being made in conjunction with the find, but in contrast to the relatively  rushed and rather quick to judgment “The Link”, “Discovering Ardi” has been ten years in the making.

And while there were simultaneous news conferences in  the US and Ethiopia, about the most excited utterance to have been reported in the media world-wide came from one of the many coauthors, C. Owen Lovejoy from Kent State University:  “It (meaning Ardi, the archeological site and/or  the museum) is just a treasure-trove of surprises”.  

In contrast to the  race to publish, that seemed to be the case with Ida, the large scientific team that ultimately included more than 40 predominantly western university-based authors and scores of Ethiopians, both scientifically trained, as well as careful layperson fossil hunters and security guards (known as Obama Police, at their own insistence) was pressured to release results by a scientific community that had grown impatient of waiting over 15 years to have them written up.

The master of ceremonies of the release of the real science, so to speak,  was not Mayor Michael Bloomberg, but rather the distinguished and perhaps more avuncular-appearing  Bruce Alberts, Ph.D., a past president of three major scientific societies, a member of the National Academy of Sciences, and Editor-in-Chief of the journal Science. His single page introduction to a special section in the October 2^nd, 2009 issue of Science, that was devoted to Ardi, was modest and served primarily to provide context for the 11 coprehensive anlyses, totaling almost 100 pages, including many diagrams and illustrations,  and buttressed by hundreds of citations.

·     Not unlike Ida, Ardi was small.

·     Ardi appeared to have a somewhat larger brain, and more evolved feet. She could walk easily  on ground or  along the length of the horizontal branches of he trees, and and she could climb to get into those trees.

·     Ardi did not, however,  have strong arms, suitable for swinging through the trees or for knuckle-walking (these appear to have evolved later in monkeys and apes.)

·     Ardi’s dentitition also suggested a largely fruit and leaves diet.

·     Ardi’s habitat, which was much more extensively analyzed, was woodland rather than wetland or dry plains.

·     Ardi’s neighbors  included various kinds of antelope-like creatures that also favored woodland habitats, and which browsed rather than grazed.

·     Ardi has a better claim to have been a common ancestor to humans, monkeys, and apes, but abundant as is, the evidence, it is not pressed relentlessly  or with much showmanship. Ironically in terms of those who think like publicists, this has caused it to be received far more seriously by the scientific community.

Of course, there is still a bit of unusual flair. In a style that is very unlike that of most articles in Science,  head shot photographs  of some of the authors are included. I counted at least ten Indiana Jones hats!

Tony Stankus, FSLA [email protected] Life Sciences Librarian, Science Coordinator, and Professor

University of Arkansas Libraries MULN 233 E

365 North McIroy Avenue

Fayetteville AR 72701-4002

Voice: 479-575-4031

Fax: 479-575-4592

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The Amygdala’s Role In Learning, Memory, Social Intelligence, Criminal Behavior, Mood Disorders And Especially The Retention of Traumatic Memories In Adult PTSD

The amygdala comprises two almond-sized-and-shaped portions of the mid-brain, that are becoming more and more common targets for study. The numbers of  research reports involving the amygdala  has been skyrocketing with each passing year. As of the date of this blog, September 9, 2009, PubMed reports 21,633 papers in which the amygdala is mentioned, 1933 of them being major review articles. 

And while there are two units (left and right sides of the brain) to the amygdala, it is more often discussed as if it were one organ, so the singular term “amygdala”, and the common usage plural “amygdalas,”  not the Latin plural “amygdalae” is used here and throughout most of the medical literature.

The amygdala is connected with the prefrontal cortex, an area involved with our highest intellectual properties,  and receives sensory inputs from it all the time. But the amygdale is not a part of the conscious brain.  It does not think through images or situations in a sophisticated way. Instead it is part of the limbic system, an evolutionarily highly conserved area that was well developed in animals before man, and is part of an active  vigilance-for-survival  mechanism.

The amygdale  is like  a guard dog that never sleeps.  It instantly senses danger and calculates magnitude of risk in microseconds. It then passes the message on to the hippocampus, which then routes the message to memory and action centers which help initiate responses and activate coping mechanisms. 

 Simultaneously ,  the amygdale causes cause a flood of cortisol, a notable stress hormone, throughout the body. Indeed the “gut sense” that one is in danger is quite literally through the action of the amygdale in prompting “fight-or-flight” hormone surges.

Descartes’ Rational Mind vs. Body Dualism Exploded by Damasio and LeDoux’ s Emotional Brain and Amygdala

Nonetheless, it has become increasingly clear that the amygdale is not just a fear machine.

The study of the function of the amygdale has helped resolve one of the great debates in neuroscience over the last 250 years: Whether the Body (in this case, the amygdala and the brain)  governed the Mind (in this case, the sense of consciousness, self-awareness, thought processing, learning and memory), or whether these were two truly distinct operations.

This debate has largely been framed through a challenge to the thinking of Rene Descartes, 1596-1650,  a French philosopher and scientist, who posited that   man had a rational mind, intellect or soul whose functioning was largely independent of the body and its body parts and which did not have to obey the laws of physics. He gave the mind  and thought processes a higher place, saying “I think, therefore, I am.”

In other words, explanations of the operation of the mind, soul or intellect ----including problems of consciousness, thought, learning and memory----cannot, according to Descartes,  be reduced to the laws governing biology, chemistry & physic, which clearly have dominion over the body and its parts. 

Therefore,  according to Descartes, the study of thought processes   and learning were  properly outside the field of medicine, and  suitable only for philosophy courses.

Descartes did allow for the pineal gland to be the possible location of the soul or intellect, but basically saw clear jurisdictional lines  separating the body and most of its organs from all things that are the product of the “rational” mind: thoughts, memories, and especially the acquisition of new knowledge.

However, it  is now increasingly well-argued in works by two of  the last century’s greatest neuroscientists,  Antonio Damasio (University of Iowa),  author of Descartes’  Error: Emotion, Reason and the Human Brain (1995), and of The Feeling of What Happens: Body and Emotion in the Making of Consciousness (2000)and Joseph LeDoux (NYU), author of The Emotional Brain: The Mysterious Underpinnings of Emotional Life (1996) and of The Synaptic Self: How Our   Brains Become Who We Are,  that  an actively functioning emotional-alarm-circuit  amygdala (clearly a body part) allows for new information  to be better incorporated into memory (clearly a intellectual process that Descartes saw as “rational” and not Body-Part-Independent) and subsequently into action.

Indeed our sense of reality and what we pay attention to (in a sense our own construction of the  conscious world in which we see ourselves living ) are in many ways amygdala-dependent .

Or in the view  of Damsio and LeDoux, “ We feel, as well as think, therefore, we are who we are in the world as we perceive it”

The amygdala may very well do this by helping the brain identify salient points of new inputs (whether they have red or green flags indicating either danger or reward) and to prioritize them by the use of the “magnitude dial” of the amygdale (important enough to pay close attention, or not so important or threatening and therefore, something to ignore).

Ultimately, as Damasio and LeDoux would argue, we tend better to learn and remember those things that have particular, added  emotional emphases in our lives, and we have to work harder at recall to retrieve information that has no special meaning.

In other words, we remember that on July 3^rd, our mother died, but we cannot recall what we had for breakfast on November 15^th,  because that was not an unusually emotionally charged occurrence.

Incoming information about a death in the family is processed by the amygdale as a fearful new fact, which gives it additional weight in its routing, storage, and availability for retrieval within the brain.  Whether you had oatmeal or eggs is likely not.

A well-functioning amygdale also appears to help us interpret the emotional state of others through accurately processing the emotions they display through their facial expressions.  This conveys an evolutionarily important advantage, because seeing the signs of either collective panic (danger) or group jubilation (opportunity)  in the demeanor of others enables you better to  take action sooner.

You need not personally see the coming tidal wave to realize that you must run to higher ground. Likewise, you can determine if your parent or teacher is happy with you, or angry, before they ever say a word.

  Shrunken or Damaged Amygdala

It is perhaps no surprise that persons with ADHD  who have trouble focusing have been revealed in some studies to have a diminished amygdalas, reducing their ability to see what is important and to pay attention to it.

Likewise, persons with Aspberger’s Syndrome and more severe Autistic Spectrum Disorders, have diminished amygdalas,  suggesting that their inability to zero in on people’s faces or activities, keeps them unaware of the emotional states of others. They have a reduced ability to formulate a Theory of Mind that is important to learning  throughout the lifespan.

In other words, they cannot pay attention to what is being demonstrated by others and imitate it as part of learning or social integration, because they view all incoming information as having equal threat or reward potential, and therefore being of no particular worth of paying attention to one thing or person over another thing or person.

At the worst,  some autistics  see all incoming information as being consistently threatening, and will disengage from the outside world, because such a constant threat level is unsustainable owing to the inner turmoil it generates.

A similar pattern of behavior, where suspiciousness and a sense of being attacked, is found in some patients with Alzheimers, when the beta-amyloid plaques that are characteristic of the disease, interfere with the operation of the amygdala.

A legal hot-button issue is that some brain imaging studies have found that criminal sociopaths have diminished amygdalas. (see the work by Yaling Yang, an expert on the brain abnormalities of psychopaths and pathological liars, and her co-workers, at UCLA, below). Shrunken or malfunctioning amygdales  are associated with a lesser ability to determine the emotional states of other persons, so that presumably, the criminal had little or no ability to realize the depth of pain and suffering he or she was inflicting. This is argued by some criminal defense attorneys as allowing for a medical or psychiatric disability that eliminates or reduces culpability for their crimes.

 However, usage of such defenses also opens up the possibility that if the diminished amygdalas are the cause of the criminal behavior, then perhaps the criminal should be confined to an asylum for the criminally insane until the amygdalas “get back to normal,” an anatomical  recovery that may take longer than the usual prison sentence, assuming it ever happens.

Persistent, Dysfunctional Fearful Memories and PTSD

Obviously one of the major clinical concerns where the amygdala may play a role is in patients with persistent anxiety and depression. A wide variety of brain function and imaging studies do in fact, implicate amygdala dysfunction or hyperactivity activity  in  the linkages of the amygdale to the hippocampus or the prefrontal cortex. 

Therapies that have achieved the most success seem to have help to break, at least temporarily, the association of some reasonably neutral stimuli (for example,  a loud noise) with a particularly traumatic memory (for example, a bomb going off).  In other words, they disrupt, at least temporarily, the negative  Pavlovian cycle of  stimulus and automatic response.

But a developmental brain study breakthrough in the journal Science by Gogolla et al. cited in detail below, shows why this may actually be easier in children than in adults.

It turns out that at about four weeks of age (which translates into some years within early human childhood)  in lab rats  that had been exposed to Pavlovian fearful conditioned stimuli, the memory of that fearful stimuli, and the associations that came with it, seemed permanent, and could be brought again and again  to the surface with only modest levels of adverse stimuli, even after several months (many years in human aging). They couldn’t forget.

However, before that age , these painful associations and the memory of the fear became extinct.

The difference appears to be a protective protein coat that encapsulates certain areas of the amygdala beginning at four weeks. 

The coat appears to eliminate, or at least greatly reduce the loss of fearful memories, generated by training with negative Pavlovian stimulus and responses, perhaps as an adult survival aid. In other words, adults who remembered what was dangerous had an evolutionary advantage over those who kept forgetting.

However, the same team of scientists that discovered this memory-entrapping protein coat for the amygdala, also came up with a line of  rats  that were genetically deficient in producing that protein and developing that amygdale coat.

 These rats lost their fearful memories and anxiety routinely past the four weeks critical point, despite having been exposed to a similar negative Pavlovian stimulus and response training.  In other words, no coat means  no recall of fearful memories or triggering of “Pavlovian panic” in the rats.

Whether or not this could somehow be adapted to humans with PTSD is uncertain, and the wisdom of effectively erasing a large portion of,  if not all,  adverse memories and fear responses would surely be a matter of great ongoing medical and psychiatric debate.

Tony Stankus, FSLA, [email protected] Professor, Life Sciences Librarian & Science Coordinator

Univesity of Arkansas Libraries MULN 223 E

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Belly Fat, Inflammation, Type II Diabetes, Anti-inflammatory Drugs and Anti-Oxidants: Studying Metabolic Syndrome, Possible Cures, & Discovering the Very Subtle Ways They Might Work at the Molecular & Cellular Level All at the Same Time

The pathway of medical and pharmaceutical research is often portrayed as straightforward : First, characterize a disease thoroughly,  and when that’s finished,  find a drug by some sort of trial and error process with rats and then humans. 

But in fact, at any given time, researchers are simultaneously characterizing the many manifestations of a disease and its interrelations with other diseases, trying out putative folk remedies and natural products that have  a fair amount of positive, anecdotal evidence, as well as doing research at the molecular and cellular level to determine what biochemical processes underlie or control some step of the disease process.

The doctors who treat the whole patient  continue to  do a kind of clinical epidemiology which tends to reveal new trends and apparent associations, which gives them something new to say  to the drug researchers, even as the work of molecular and cellular biologists gives them something to report  to the drug discovery people and the clinicians at any given time.

Research in understanding and hopefully curing disease  is better pictured as occurring at traffic intersections than at rest stops on a one-way highway.

A Case Study of Making Clinical Associations Between Well Known Diseases: Metabolic Syndrome

The  routine usage in diagnosis of the broadly encompassing term Metabolic Syndrome  is only about 40 years old, although the various diseases associated with it were very well known many decades before that.

Basically, a patient presents with an inordinate amount of belly fat, a sedentary lifestyle, and often, early signs of adult-onset diabetes. There is a strong association of this syndrome with heart disease, stroke, fatty liver, and various cancers, although it was probably rare for any one physician to have a patient show up with all of these diseases all at once.

For clinical internal  medicine, the first step was make the links that all these separate illnesses seemed tied together in a statistical sense. The  determination that Metabolic Syndrome was a useful diagnostic concept was far more driven as much by cumulative clinical chart reviews, than by well-worked-out “a priori”  theories of what the underlying cause was.  

What prolonged experience in the clinical realm suggested was that patients who had a lot of visceral fat tended to get adult onset diabetes. But it was also true that patients with abundant visceral fat also tended to have coronary artery disease and also get strokes. And patients with visceral fat also seemed to come down with certain cancers. Many of them also had livers as if they were alcoholics, even if they did not actually drink alcohol.

Even after this realization of a strong link was made, the treatments and clinical advice for the separate component diseases that were a part of this cluster tended to be very distinct, and not always transferrable from one disease to another. One did not give radiation treatment for diabetes. Insulin shots did not seem beneficial in cancer. The warning signs of stroke were very different from those of liver failure.

But even after the realization that these diseases were clearly linked, there was no stop in trying to find separate cures for each and every one of them. They all had their own separate research and treatment charities, advocacy groups, and even NIH institute buildings, and even if no one came up with the mythical all-in-one cure, they all regularly came up with some new information to share at that traffic jam intersection of differing researchers.

What Did Work to Ease the Very Different Manifestations of Metabolic Syndrome?

One of the first realizations of a clinical strategy that worked, at least for many, if not all patients with one of the cluster of diseases, was to encourage them to lose weight, and in particular, to exercise more, with the underlying goal of reducing that belly fat. This was bostered by the fact, that there was substantial evidence that for many patients, the fatter they got, the worse their metabolic syndrome and its consequent component diseases seemd to come into play.

But this simple  weight loss/exercise prescription was hard for patients to follow, and did not seem to have an underlying basis in science. It just seemed to be an association between two occurrences: weight loss and/or exercise and betterment of symptoms, not a unambiguous display that weight loss or exercise somehow caused improvement of symptoms by some definite mechanism.

A couple of other statistical associations also came on the scene.

First, as is the case with most seemingly promising cause-and-effect explanations, some patients did lose weight and got better, while others did not. Some patients who never lost weight, never got the syndrome, even if they  were quite fat around the stomach. And, of course, some people who were never fat got one or more of the component diseases anyway. 

What helped make sense of these seeming failures of fool-proof cause-and-effect predictions for outcomes, was yet another series of observations.

First, for  some patients (viscerally obese or not) these diseases ran in families, with perhaps the fattest family members having the worst of it, but even some slender ones were affected as well.

This suggested that there was a genetic component. This of course, put the nucleic acids and proteins  research community, the molecular biologists,  to work to sort out what genes might be involved, and then, what proteins might be encoded by specific segments of DNA. Their working theory was that if you could somehow shut off or counter those genes, you’d have a good shot at a cure.

Second, some people seemed to have in their geographic location, and on inspection, usually in their diet much more so than the particular the rhythms of their daily lives, some protection against developing the component diseases of metabolic syndrome, in many cases despite having  what should be the predisposing girth.

This put ethnopharmacologists and nutritionists on the trail. What was it about those French people who drank a lot of red wine (despite a diet high in butter, and both saturated and unsaturated fats) that made them better off? And what about those  tea drinkers (sometimes black or green tea and sometimes herbal blends)?  And eating blueberries seemed to help in some way for some people. Was the apparent reduction in having the consequences of  having a belly fat body caused by these additions to their diet, or was it just a coincidence?

 This research community then began to try to isolate just what specific chemicals might be in that wine, those teas, or in the blueberries, that seemed to confer that protection.

And it was not long before promising substances like the antioxidants called polyphenols  (which are found in tea and in a number of fruits and vegetables) and resveratrol and procyanidin(s) (found in red wine) were tested for their possible association with reductions in the incidence and severity of metabolic-complex-related diseases.

They were found in some cases to work well with rats but not so well with humans, or in some cases, to work well with humans, but more so, for some humans, but not others. 

These paradoxes did not stop pharmacological research, but they did cause pharmacologists to question  if there was a common underlying mechanism that made these compounds effective for some people or lab animals that had certain genetic markers and protein-producing patterns, but not for people with other markers or patterns. It was time for a chat with the molecular biologists.

A Clinical Reconceptualization: Belly Fat Behaves Like an Endocrine Organ

It took less than a decade after the grand idea that all these disparate diseases might well be part of a common syndrome, for a key idea to emerge: just as the pancreas that produces insulin is an endocrine organ, and when it functions poorly diabetes results, it was entirely possible that the accumulated belly fat became an endocrine organ of its own, secreting some combination of chemicals or blood factors that caused insulin resistance, which in turn caused the strongly associated adult diabetes, which in turn was strongly associated with heart disease, and strokes, if not necessarily certain cancers.

But endocrine organs can secrete more than one substance that affects the body in a single way. They can secrete more than one variant or conformer of a hormone, or secrete a hormone that  can have more than one possible effect, depending where it docks within the body. This is particularly likely when a kind of heterogeneous , almost accidental organ made up of belly fat and random tissue  is involved.

This led to a hunt for other substances that could be caused by the errant belly fat endocrine organ, and a number of them turned up. Belly fat was associated with high levels of Cardiac Reactive Protein (associated with heart attacks), Tumor Necrosis Factor (associated with cell death), and certain kinds of  white blood cells which produced elevated  levels of lab proteins associated with a number of the differing component diseases within the metabolic syndrome.

The clinicians then had to talk with the biochemical and drug communities to help figure out what some of the commonalities were among these disparate but abnormal levels of substances and numbers of cells.

Inflammation as a Working Unifying Concept

What became clear was that many of these substances were the result of inflammation in the body. In some cases, some initial presence  of these substances caused even more damage over time, which caused the production and release of even more inflammatory responses, in a kind of vicious cycle that had to broken for the patient to get better.

The clinical  approach became more focused for diagnosis and the measurement of the success of any proposed medical treatment on  how well  the medicine or the procedure was working to reduce the signs of inflammation. As a corollary clinicians asked pharmacologists (and vice-versa) would some anti-inflammatory drugs used for other causes, work in metabolic syndrome related diseases?

Pharmacologists  turned around and asked their molecular biology friends what appeared to be the connections between the genes of people who showed high levels of inflammation and those that had had one or more of the component diseases of the metabolic syndrome. Furthermore, they wanted to know what were the genetics of those people who seemed to respond to given drugs or had a protective effect from some antioxidants like the polyphenols. The ideal goal at this molecular level was to see if drugs could be made for people who did not enjoy that protective effect, but that worked as well.

Some State Of The Art Papers Today

Right now we are seeing the ongoing exchange of ideas across disciplines and levels of biological organization. No one group has all the answers, but this does not keep the clinicians from compiling data on the commonalties signs, symptoms and diseases among their  patients , nor  restrain the pharmacologists from finding out what is the  key  compound and its most active site, when sorting out  some heterogeneous natural product that has hundreds of components,  nor does  it undercut the love of molecular biologists to explain diseases at the cellular level.

Rather, they all take whatever they’ve heard lately  at that traffic intersection of  different specialties, and see if it makes sense for their working explanations of what is going on with patients with metabolic syndrome, and its related diseases like adult-onset diabetes, and see if they can get a better diagnostic test, treatment, or preventive medical practice out of it.

Tony Stankus, FSLA, [email protected], Professor, Life Sciences Librarian & Science Coordinator

University of Arkansas Libraries MULN  223 E

365 North McIlroy Avenue

Fayetteville, AR 72701-4002

Voice: 479-401-0021

Fax: 479-575-4592

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A Clash of Explanations: How Evolutionary Psychology & Human Behavioral Ecology Differ on Rape & Other Transgressions: Sharon Begley’s Newsweek column “ Why Do We Rape, Kill and Sleep Around?”

Two academic fields that share the topic of explaining how human behavior has evolved over time and place are increasingly finding themselves at odds.

These contending fields are Evolutionary Psychology and Human Behavioral Ecology.

Sharon Begley, in a Newsweek column to appear in the 2009,  June 29^th,  issue, entitled “ Why Do We Rape, Kill and Sleep Around?” (www.newsweek.com/id/202789/output/print)  brings to the fore a debate on this topic that should be of increasing interest to BioMedical Librarians, particularly those who serve programs in forensic psychiatry and biological anthropology.

Evolutionary Psychology: Eons-Old Genes Compel Necessary (If To Ours Sensibilities,  Distasteful) Behaviors That Improve The Survival Of The Fittest Among Mankind

Evolutionary Psychology, at its core, suggests that humans inherit deeply imbedded, strongly driving,  and often rather specific traits and urges that confer on their holders an evolutionary advantage.

The Evolutionary Psychology  argument goes something like this (and this explanation does contain an element of circular logic).

 A human behavior that has historically played out,  over and over again for tens of thousands of years, whether good or bad in terms of current morality, persists because it has to have been advantageous for the doers of the deeds that result, in the sense they survive long enough to  pass down the gene(s) that compelled them to act out that way in the first place.

Such genes are  thought to be genuinely adaptive or purposeful, not merely random, decorative or optional, according to evolutionary psychology, because their very persistence is proof that they have earned their place  in the assortment of behavioral genes that must be passed on from generation to generation for the species to survive.

This theory presupposes a kind of parsimonious behavioral gene safety deposit box with a limited capacity, in the sense that organisms, including, man presumably do  not save or carry around behavioral genes that serve no purpose.

Reduced to is simplest terms, evolutionary psychology  argues that the only real measure of evolutionary success for an organism, including for a man, is whether or not his particular genes are perpetuated. If not, the organism, and the man, is merely an evolutionary dead end. This mindset is perhaps best embodied   in portions of the best-selling book by Richard Dawkins, The Selfish Gene. (cited below.)  And to a great degree, Human Behavioral Ecology, is incline to degree.

Human Behavioral Ecology: Genes Favor Brains that Are Flexible in Dealing with Changing Conditions Over Eons

Behavioral Ecology posits that at any point in the history of life, an organism, including a man, adapts to his constantly changing environment and its resources, including the presence of other humans, by trying out an assortment of behaviors, and to the degree that he learns quickly enough through these  trial-and-error situations, what works and what does not, he eventually optimizes his chances of surviving, and thereby of passing down his genes.

According to Human Behavioral Ecology,  the behavioral genes that matter most are those that enable man to learn to assess situations quickly enough to survive long enough to mate and pass on genes to surviving children who themselves “learn to learn.”

According to Human Behavioral Ecology, the ability to recognize when a hard-wired behavior is no longer adaptive, is itself, an evolutionarily favored adaptation, and perhaps a superior one.

In a sense, a seemingly fixed, hard-wired, brain-driven behavior, the kind to which Evolutionary Psychology often points, even if it has survived for ten thousand years for some adaptive reason in the past, is, according to Human Behavioral Ecology,  likely to be wiped out, if it results in behaviors that are so rigid as to no longer serve a purpose, or behaviors that costs more to put into play than they will likely yield in survival benefits.

Hard-Wired Brain Modules for Purposeful Menace?

These propositions would be entirely academic if they involved only debates over issues such as whether or not our brains have specifically evolved areas or dedicated synaptic pathways for language or writing, for facial recognition of clan mates and detection of the emotional states of others, for the avoidance of poisonous snakes or carnivores, or for the use of tools and the ability to make fire.

The problem comes when forceful sexual behavior, or group domination through intimidation, war-making and   theft of resources is debated by these two groups.

Typically the evolutionary psychologist argue that behavioral uses and abuses along these lines are essentially hard-wired into the brain, and in some cases, they may still serve an adaptive function that will perpetuate greater numbers of people who are thus hard-wired.

Even if this behavior is no longer adaptive, the evolutionary psychologist argues, the person with the genes that drive this behavior often cannot hold it in check, because his brain, is, after all, hard-wired to do it.

This is where Begley’s column comes in.

While discussing a variety of related issues, authors, and sources, she  particularly takes to task more recent popularizations and/or over heatedly titled academic books dealing with evolutionary psychology. She focuses especially on  Randy Thornhill, Craig Palmer and  their book, A Natural History of Rape: Biological Bases of Sexual Coercion (cited below). 

In an attack that is essentially one-sided, she picks out an explosive  proposition concerning rape that she  suggests is emblematic of the wrong-thinking of evolutionary psychologists, and counters it heavily with studies and interviews from the opposing side.

It should be noted that not all of the critics of this theory or of evolutionary psychology in general, that she and others cite, are scientists of the same high caliber of many of the pro-EP movement. Critics on Begley’s side  do include notable scholars from other fields: Philosophers,  cultural anthropologists, sex crime prosecutors and feminists in general. But the column gives the impression that the evolutionary psychologists are currently without an effective response to their critics, on this and on related issues.

Is Genetically-Driven Rape A Good Way to Increase the Chances All Your Genes Will Be Passed on to Succeeding Generations?

The most damning assertion Begley attacks is that held by some prominent evolutionary psychologists that rape by males of women is an evolutionarily effective way to increase their progeny, particularly progeny who will behave just like rapists do.

The theory of these particular evolutionary psychologists goes that the more women the rapist impregnates, the more likely the rapist will have children, particularly sons, who have this same strong desire to dominate the sexual activity and reproductive lives of as many women as possible, giving the rapist as many offspring as possible.

This theory is based on some anthropological evidence among primitive tribes, and even on studies of relatively modern human cultures ,  in which rape is frequently used by the most dominant males, who thereby presumably succeed in have the most offspring, and therefore  in passing on their genes.

Begley particularly counters this argument via a study (cited below) done by  Smith, Borgerhoff-Mulder & Hill (respectively of the University of Washington, UC-Davis and the University of New Mexico at the time, but now at Arizona State University)   in which those authors  argue that even under the Stone Age hunter-gatherer-warrior Ur-scenario on which some rape-as-hard-wired-adaptation evolutionary psychologists predicate their theory, rape is unlikely to be a sure path on the road to passing on one’s genes.

 

Why Rape in Primitive Societies Is Less Likely to Succeed Evolutionarily Than It Would First Appear

·        Not all women raped are likely to be ovulating and fertile at the time or rape, and opportunity costs for mating with willing women fertile women are incurred. (Moreover, in some societies preadolescent girls and post-menopausal women, neither of whom can have children are often violently raped, suggesting that having progeny is not the motivation for rape  in at least some cases.)

·        Many women who are raped will have spontaneous or induced abortions. A momentary coercive  fertilization on the part of the rapist can be short-circuited by biology or the woman’s own intervention, even in some very primitive societies

·        Women are not necessarily inclined to care for the offspring of rape. They may just kill them outright or enslave them to serve her “legitimate” children, reducing the survivability of the rapist’s genes for the next generation, and in the latter case, actually promoting the survival and prosperity of  children who  are not the result of rape.  

·        Women who already have a consensual sexual relationship, particularly one based on emotional bonds with a rapist,  may, from a response based on open or covert jealousy, undercut the health or well-being of the rapist. In many primitive societies the vast majority of food is actually brought in by women who are gatherers as opposed to by men who are hunters. Jealous women may reduce or stop supplying the rapist with gathered food or other creature comforts out of disapproval, reducing his reproductive fitness and likelihood of passing down his genes.

·        In many primitive societies, as in most modern societies (excepting those where so-called “honor killings”  focus rage on the victimized woman), retaliation against the rapist is likely to materialize in the rapist  being specifically targeted for death by the offended parties. This retaliation may even extend to other members of the rapist’s family and clan. Under this scenario, the cost of making a child by rape may be overwhelmed by having the rapist and all the rapist’s other children killed in a counterstrike.

·        Other family members or members of the rapist’s clan may decide that the trouble caused by a rapist is not worth the purported gains, and take action against him on their own, to forestall retaliatory strikes, and to minimize local sexual tensions and rivalries within the clan.

·        While the process of rape is undoubtedly traumatizing for its victims, those victims can in some cases, subsequently learn preemptively to defend themselves or to strike back lethally at this or other rapists unexpectedly. Once an overwhelmed victim, does not means always an overwhelmed victim. Furthermore, women can organize collective self-defense or commit to revenging after-the-fact for crimes committed against any one of their number.

 

Tony Stankus, [email protected] FSLA, Professor, Life Sciences Librarian, Coordinator of Science Collections

University of Arkansas Libraries MULN 223 E

365 North McIlroy Avenue

Fayetteville, AR 72701-4002

Voice: 479-409-0021

Fax: 479-575-6656

 

Buss, D.M. (2000). The Dangerous Passion: Why Jealousy is as Necessary as Love and Sex. New York, The Free Press.

 

Buss, D.M. & Malamuth, N. (1996). Sex, Power, Conflict: Evolutionary & Feminist Perspectives. Oxford University Press.

 

Dawkins, R. (2006). The Selfish Gene, 30^th Anniversary Edition. Oxford University Press.

 

Duntley, J. & Shackelford, T.K. (2008). Evolutionary Forensic Psychology: Darwinian Foundations of Crime and Law. Oxford University Press.

 

Kokko, H. (2001). Human rape: Adaptive or not? (2001). Trends in Ecology & Evolution, 16, (9), 488-489.

 

Lalumiere, M.L., Harris, G.T., Quinsey, V.L., Rice, M.E. (2005). The Causes of Rape: Understanding Individual Differences in Male Propensity for Sexual Aggression. Washington. DC.: American Psychological Association.

 

McKibbin, W.F., Schackelford, T.K.,Goetz, A.T.,m & Starrat, V.G. (2008). Why do men rape? An evolutionary psychology perspective. Review of General Psychology, 12, 86-97.

 

Smith, E.A., Borgerhoff Mulder, M. & Hill, K. (2001). Controversies in the evolutionary social sciences: A guide for the perplexed. Trends in Ecology & Evolution, 16, (3), 128-136.

 

Smith, E.A., Borgerhoff Mulder, M, & Hill, K. (2001). Human rape: Adaptive or not?’ A Response from Smith, Borgerhoff Mulder & Hill.  Trends in Ecology & Evolution, 16, (9), 489.

 

Thornhill, R & Palmer, C. (2000). A Natural History of Rape: Biological Bases of Sexual Coercion. Cambridge, MA: MIT Press.

 

Travis, C.B., Editor, (2003). Evolution, Gender & Rape. Cambridge, MA: MIT Press.

 

Autistic Toddlers and Young Children: Are their Deficits in Interpreting the Ordinary Human Emotions of Others Tied In with Underlying Deficits in Paying Preferential Attention to Ordinary Human Motion in General?

A recent paper (March  26, 2009) in the very prestigious journal , Nature (Klin et al. 2009, cited below),  gives us an example of the high interest maintained by the neuroscience , developmental psychology, and special education communities in new research developments in autism.

This particular paper is intriguing because it compares the performance of normal toddlers of about 2 years of age, with developmentally delayed toddlers without autism at the same age, and with autistic 2 year olds, on certain visual tasks.

There may still be a substantial remnant  of people in the helping professions who, perhaps depending on older literature,  tend to lump together the symptomatology of very young autistic and developmentally delayed children  as if they always or often shared the same deficits, and these conditions were hard to tell apart at this stage of their young lives. 

This paper was, in part, about setting the symptoms and disorders apart.

The Advantage of Preferential Gaze for Normal Motion in  Social Learning   in Toddlers 

Klin et al. explore a fairly striking anomaly, and while others may be inclined to disagree  (see Parron et al. 2008, cited below), their work suggests that toddlers with autism   do not follow the normal motion of living things preferentially, the way normal toddlers do.

What does this mean? 

Recognition and focus on   normal, expected  biological motion is one of the ways that most  infants and certainly all normal children by toddler age, survive.

They learn to recognize a mother or father or sibling in part because the first salient thing they notice is that people are characterized by some degree of motion and certain types of movement, and that some of the movements are particular to family members in dealing with them, while other movements are characteristic of strangers.

This is an evolutionarily important survival skill because it is also related to the detection of danger from living things that are moving at them in unexpected ways. For example,   a feral dog coming to attack them, or a  horse rearing up to kick them.

Danger awareness is also reinforced by observing the motion of parents or siblings to other moving subjects.

Seeing  sibling or parental motions in response to moving threats or opportunities   on a repeated basis is one help to toddlers in learning, but only if the toddler is likely to turn its focus on the  sequence of action that is pertinent to the threat or opportunity.

In other words, the toddler has to learn to engage in joint visual attention.

Learning appropriate movements and responses from the observation of the movement and response of others is related to,  or sometimes used synonymously,  with  phrases like “Joint Perception & Action Processes, “ or the more colorful  “Motor Priming & Contagion.”

Autistic toddlers can certainly see biological motion ----- there are no predictable optically (eyeball anatomy) based visual impairments that are particularly characteristic of autistic toddlers---- but   many autistic toddlers do not attribute anything special to either normal or abnormal motion.  

But lack of sensitivity to the alarm or exhilaration motions of others short-circuits joint perception and action processing or motor contagion, which eventually leads to a lack of “Social Contagion” the  empathetic adoption of mood and actions of people in a group.

It is important to understand that not all autistic children are born equally impaired, and this, along with the kinds of behavioral therapy  and family support they get, often explains why some become high functioning, while others cannot progress greatly.  

There are widely varying degrees of deficits and different types of coping strategies  among autistic individuals,  to such a degree that   most autistic individuals are now commonly diagnostically categorized  as being at some point on a continuum  of Autistic Spectrum Disorders,  ASDs, that ranges from the mild end of Asperger’s  Syndrome to  much more profound pervasive developmental disorders.

But for the purposes of this brief survey, and in terms of the paper by Klin et al, 2009, we will use the term autistic without further distinctions, in part because at age two, the degree of lifetime impairment may not be easily determined.

Moving Connect-the-Dots or Point-Light Displays

In the Klin et al. 2009 study,  autistic toddlers did  not appear to have developed an age-appropriate gazing that is preferentially oriented to recognize and pay closer attention to ordinary  biological motion as opposed to abnormal, and somewhat nonsensical motion,  under normal circumstances. 

But they also found  that autistic toddlers might tend to pay special attention more frequently when the viewing of ordinary  biological motion is somehow reinforced by   another sensory modality.

How were these findings accomplished?

In the Klin study, toddlers were shown what might be called moving Connect-the-Dots figures.  These were actually videos of moving people with only certain large bright dots visible on the screen ------the bright dots for example might be placed at the major joints of the body and on the head,  limbs and feet.

The “dots” re-enacted child’s games like peek-aboo, pat-a-cake  and  showed  motions like legs and arms moving and  hands clapping.

The  experimental “shows”  of motion involved split screens and a matching sound track that followed one of two  motion sequences being simultaneously shown on the split screen.

One half of the screen would be playing the moving dots in normal motion. This was the screen where it was expected that normal children would focus their attention preferentially  because the motion of these dots were natural,  representing  biologically predictable movements, that could be readily perceived as games.

It was not clear whether or not the developmentally delayed or autistic toddlers would do the same.

The other half of the split screen display displayed the same  sequence of action but with the moving dots displaying that action upside down.

It was clearly expected that the normal toddlers   would avoid gazing at this half of the screen, because its motion  was jarring and did not make sense to them.

It was not clear what were the responses of the developmentally delayed and autistics toddlers would be.

In all cases, it was expected that a preferential focus on the dots going through normal motions  would be would be reinforced to some degree  by the fact that the soundtrack, in all but one of the videos of motions, featured only human voices whose narration matched the normal actions depicted on the screen, but did not match not the upside down ones.

But something unexpected turned up.  

While the autistic toddlers were essentially random in which screen they watched, favoring one as much as the other,  the developmentally delayed and normal toddlers each showed much more focus and gaze time on the normal , right-side-up movement and sequence of action.

In fact, the response of both of normal and developmentally delayed toddler groups was so alike that it was impossible to determine from performance on this test which toddlers  were normal and which were developmentally delayed.

It was however, exceptionally easy to determine which kids were autistic because of this lack of preferential gaze in favor the normal sequence of action.

 In fact, this type of screening looks to be a pretty good differential diagnostic tool for autistic toddlers at two years old, especially for sorting them apart from the developmentally delayed at this early age.

The larger implication of this lack of preferential gaze is that it  predisposes  the autistic toddler to missing out on a whole cascade of motion associated cues that would help them make sense of the world and particularly of human actions and emotions  in the world much better.

But there is more to this study.

Serendipitously,   during the recording of one of the action sequences,  the synchronized sound track  actually picked up more than just the human voice narration.  The sound track had also picked up and subsequently played back the   loud clapping sounds  that matched the clapping motions on the screen.

When the autistic toddlers heard the clapping simultaneously with the visual moving connect-the-dots or PLDs  of the person clapping, the autistic toddlers paid notably more attention to the half of the split screen that displayed normal motion.

The autistic toddlers  did not do as well as normal or the developmentally delayed toddlers , but they certainly did better in attending to the side of the split screen that portrayed normal motions  when sound was added as a stimulus at the same time, raising what the researchers referred to as the Audio-Visual Synchrony value of the video show as a whole.

Therapeutically, this suggests that behavioral training with autistic toddlers and children might go better to the degree that it is reinforced with simultaneous additional sensory cues, although other research shows that too many cues, even if intended as reinforcing,   may flood the autistic child with “too much information” to focus and interpret.

Mouth Watching, Lip Reading & Being Unfazed by Upside Down

It is clear that autistic toddlers and infants can detect motion as opposed to lack of motion, and may in focus on some particular moving feature of a person, when interacting with them.

For example, some studies show that many autistic children focus intently on the movement of the mouth when someone is speaking to them.

They appear to be like lip-readers, trying to make sense of what is said by  comparing what they see in terms of the mouth’s current motions, with their past experience of what those mouth motions seemed to indicate by way of words or outcomes.

Likewise some autistic children have the ability to recognize people despite the image of those people   being inverted,  with a success rate far beyond normal children, who like this author, get confused when something familiar in its top-down orientation is  presented turned upside down.

This appears to be the result of the autistic child focusing only on some key feature that is salient to them, to the exclusion of everything else.

In a sense, the ability of some autistic children to be able to match one pattern with another,  works  like the FBI’s finger-print matching computer.  They resolutely focus on certain features that are fixed in relation to one another, and ignore everything else.

Autistic kids have also been shown in many cases to have better ability to identify pictures when the background is distorted, confusingly camouflaged,  or the focus or resolution of the picture may not be optimal.

But these special focusing  abilities come at a considerable cost, because, particularly in normal human interactions, the expression of the whole face in terms of the eyes, the nature of the smile or grimace, the accompanying hand gestures and the adjustments to the posture of a person convey as much or even more information about the emotional context of a situation than do just the words or the lip movement alone.

This is a phenomenon that has been exhaustively studies for well over 100 years, including works by Darwin, where he shows that nonverbal dues indicate emotional states and signal action intent,  in not only man but in many animals, and as shown in numerous studies by Ekman and others, is universal across human cultures around the world.

Normal, and even developmentally delayed children, seem to be able to take several facial, gestural, and postural cues into account simultaneously, and make a reliable guess as to the mood or underlying message of the person being viewed, ironically even if they cannot identify the person in a subsequent lineup of pictures as well as do some autistic subjects.

In a related phenomena, when other normal viewers would get frightened or upset enough to lose confidence in their ability to make the identification, the autistic viewer has not registered the  emotional stressor for either the person being viewed or even of themselves, because they do not process context,  and can excel in the identification task.

Autistic children,  it seems, are sometimes excellent leaf identifiers, but, sadly, not good at  conceptualizing the whole forest of the expressions and emotional states of others.

Or, as some put it, many autistic children have a reduced ability to develop a Theory of (the) Mind (of others.), or an understanding of their mental state.

It is not that autistic toddlers are “obtuse” but rather, that   their gaze and focus may be either too “acute” on a fixed circumscribed set of features,  or as seen in this study of toddler autistics, so fundamentally  indifferent to  the motions ----- normal or abnormal, subtle or more striking,------ that it  holds them back in the normal progression of learning  better to encode context and nuances at the same time as they learn to make  identifications  later in life, at least when they are  without the right kinds and amounts of reinforcing sensory synchrony at an early age.

Tony Stankus [email protected] Life Sciences Librarian & Professor

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