SLA Biomedical & Life Sciences Division Blog

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, tstankus@uark.edu 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.

 

Lowering Triglycerides: Dieting, Exercise, Niacin, Statins, Fibrates, Nuts & Fish

Low-density cholesterol (LDL or “bad cholesterol”) and high-density cholesterol (HDL or “good  cholesterol”) seem to get most of the coverage in popular level medical news reporting, but a third factor in most blood tests of lipids involves triglyceride  levels, and they deserve more attention. 

There Aren’t Good vs. Bad Types Of Triglycerides. Just Good vs. Bad Levels

A healthy level of triglycerides is actually very necessary for the energy cycle to continue in the body. Triglycerides are a highly energy efficient form of circulating fuel, and yet are also their own kind of gas can, in that they  can also store unused  calories in the forms of fats for later use by parking themselves in fat cells  spaced between and among  muscle and visceral cells. 

Triglycerides can be made in the body via a variety of pathways. They most often seem to be synthesized from dietary carbohydrates (commonly in the liver), but can be  imported more directly from the digestive breakdown of certain dietary fats.

Unfortunately, no matter whether home-grown or imported, excess circulating  triglycerides can be metabolically transformed into larger and larger, harder-and-harder-to-break-down fatty deposits.

These are often found in blood vessels and termed atherosclerotic  plaques. Dislodging these plaques, however, can be dangerous because they can travel through the blood stream and eventually block coronary or carotid arteries, leading to heart attacks and strokes, respectively.

In essence, the body’s other cells go from having   a small tank of gas you could put into your trunk,   to  living in a highly congested neighborhood where most of the neighbors are gas stations.

In adults, triglyceride levels above 150 mg/dL are suspect, and levels above 200 mg/dL are now universally recognized as unhealthy. In addition to the cardiovascular consequences, they are  strongly predisposing to  the twin troubles of  metabolic syndrome and  adult onset diabetes.  

Having too high a level of triglycerides is variously termed in the medical literature. Sometimes it is called   hypertryglyceridemia, or more generally, dyslipidemia, and many articles lump studies of  triglycerides with those of cholesterol levels using the umbrella term for the whole group, lipoproteins.

 

What disposes us to have too high triglyceride levels?

Historically, a number of factors  seem to be associated in adult patients to overly high levels of triglycerides.

The most common in adults is obesity.   

Next is  diabetes.

 A third   is excessively low levels of thyroid hormones.

A  fourth is  kidney failure, particularly  for patients on dialysis. 

Somewhat rarer are pancreatitis and inherited diseases of triglyceride synthesis and metabolism.

Smokers, frequent drinkers of alcoholic beverages,  people with high-blood pressure  ------ and particularly those with high levels of low-density cholesterol are also much more likely to have high triglyceride levels.

Curiously, some vegetarian or near vegetarian diets high in rice and starches, have been implicated as well.

In recent years, four additional developments have also heightened awareness of high levels of triglycerides.

First, among adults, there is a now substantial population of HIV positive patients, who as a concomitant of the disease process or its antiretroviral medicines, are now living long enough to develop seriously high triglyceride levels with the risk of acute coronary artery disease. Literally hundreds of thousands of these patients will now likely die of heart disease before AIDS gets them.

Second, with an increased number of baby-boomers coming to an age where having prostate cancer is common, there is increasing worry that removal of the prostate and/or treatment with androgen blockers or feminizing hormones will have adverse effects on triglycerides.

Third, a debate has opened up as to whether or not high triglyceride levels should be attacked sooner than adulthood in the millions of kids who are already frankly obese (and particularly if they are already diabetic), and who, untreated, are perhaps likely to simply graduate into the adult complications of high levels of triglycerides.

Fourth, the hope for pharmaceutical  leptins  to control or modify triglycerides any time soon  has largely waned.

General Strategies for Reducing Triglyceride Levels

The question then becomes, how best to bring down triglyceride levels?

While many of us are loathe to hear it once again, regular exercise of at least one half hour and arguably a whole  hour, several times a week,  has a  good record of lowering triglycerides.

Weight  loss, often as little as a 10% drop, yet another often claimed panacea for all of life’s adult ills, actually also proves to be  highly effective in dropping triglycerides.

And boring as it is to hear, diet and exercise together work even better.

Conventional Pharmaceutical Treatment of High Triglyceride Levels

By  far, the most common drug interventions in the U.S. to lower triglycerides involve the use of prescription strength niacin and one or more of the statins.  (See, for example,  Bays, 2008, cited below).

This combination has had fairly good results although certain forms of niacin may have cumulative liver toxicity in the long run, and liver function tests are recommended every six months.

Alternatively, particularly in Canada, and especially when dealing with diabetic patients, fibrate drugs are used. (See, for example, Barter & Ryle, 2006, Steiner, 2007,  or Goldenberg, et al., 2009, cited below). 

Commercial Nutritional Supplement Approaches to Lowering Triglycerides

Far less  commonly recommended, and with substantially fewer articles in the literature to support taking them  include larger doses of Vitamin D,  increased intake of glucomannan and other sources of soluble fiber,  and certain soy concentrates.

Dietary Ingredient Approaches to Triglyceride Level Reduction: Nuts and Fish

 While a fairly wide variety of good dietary practices and food choices (eat more fruits and vegetables, prefer whole grains to refined ones, eat less red meat, etc.) are all recommended for the reduction of triglyceride levels, the two most common food items that are especially  advisable are various nuts and fatty fish.

The literature in favor of certain tree nuts (particularly walnuts,  hazelnuts, and pistachios) as agents for lowering triglycerides has been quite favorable.

 Hopes for miracles from increased almond consumption have not yet been demonstrated in a very large scale clinical trial or via  a rigorous meta-analysis , although  many small studies are positive. 

Cashews, macadamias, and even the usually despised Brazil  nuts  have their triglyceride-lowering supporters, although their studies basically show that eating them is not necessarily bad for blood lipid levels in healthy people,  as opposed to their being uniformly reliable agents for triglyceride reduction.

It should be noted that in almost all these studies, funding was provided by nut producers,  or the owners of companies whose products contain nuts.

 Nonetheless, those studies were all conducted by independent   labs at schools of nutrition or medicine, and appeared in refereed journals with a longstanding reputation for scientific   integrity.

Fish whose tissues have high lipid levels, and are known to be good sources for omega-3 fatty acids, such as sardines, herring, mackerel, and salmon are also routinely recommended, as are over-the-counter supplements containing omega-3s.

But perhaps most promising along these lines is a new prescription strength omega-3 preparation, Lovaza. (see Dall & Bays, 2009, cited below), perhaps combining it with a statin. (see Davidson et al. 2007, and Barter & Ginsberg, 2008, cited below).

Tony Stankus, FSLA  tstankus@uark.edu

Professor, Life Sciences Librarian & Science Coordinator

University of Arkansas Libraries MULN 223 E

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Voice: 479-575-4031

Fax: 479-575-4592

 

Almario, R.U., Vonghavaravat, V., Wong, R., Kasim-Karakas, S.E. (2001). Effects of walnut consumption on plasma fatty acids and lipoproteins in combined hyperlipidemia. American Journal of Clinical Nutrition, 74, 72-79.

Bader, M. S., & Kelly, D. V. (2008). Diagnosis and management of common chronic metabolic complications in HIV-infected patients. Postgraduate Medicine, 120(4), 17-27.

Barter, P., & Ginsberg, H. N. (2008). Effectiveness of combined statin plus omega-3 fatty acid therapy for mixed dyslipidemia. The American Journal of Cardiology, 102(8), 1040-1045.

Barter, P.J. & Ryle, K.A. (2006). Cardioprotective properties of fibrates: Which fibrate? Which patients? What mechanism? Circulation, 113 (12), 1553-1555.

Bays, H. (2008). Safety of niacin and simvastatin combination therapy. The American Journal of Cardiology, 101(8A), 3B-8B.

Becker, D. J., Gordon, R. Y., Morris, P. B., Yorko, J., Gordon, Y. J., Li, M., et al. (2008). Simvastatin vs.  therapeutic lifestyle changes and supplements: Randomized primary prevention trial. Mayo Clinic Proceedings.Mayo Clinic, 83(7), 758-764.

Bergouignan, A., Trudel, G., Simon, C., Chopard, A., Schoeller, D. A., Momken, I., et al. (2009). Physical inactivity differentially alters dietary oleate and palmitate trafficking. Diabetes, 58(2), 367-376.

Brunzell, J. D., Davidson, M., Furberg, C. D., Goldberg, R. B., Howard, B. V., Stein, J. H., et al. (2008). Lipoprotein management in patients with cardiometabolic risk: Consensus conference report from the American Diabetes Association and the American College of Cardiology Foundation. Journal of the American College of Cardiology, 51(15), 1512-1524.

Curb, J.D., Wergowske, G., Dobbs, J.C., Abbott, R.D., & Huang, B. (2000). Serum lipid effects of a high mono-saturated fat diet based on macadamia nuts. Archives of Internal Medicine, 160 (8), 1154-1158.

Dall, T. L., & Bays, H. (2009). Addressing lipid treatment targets beyond cholesterol: A role for prescription omega-3 fatty acid therapy. Southern Medical Journal, 102(4), 390-396.

Davidson, M.H., Stein, E.A., Bays, H.E., Maki, K.C., Doyle, R.T., Ballantyne, C.M. et al. (2007) Efficacy and tolerability of adding prescription omega-3 fatty acids 4g/d  to simvastatin 40mg/d in hypertriglyceridemic patients: An 8-week randomized, double-blind, placebo-controlled study.  Clinical Therapeutics, 29(7), 1354-1367.

Frassetto, L.A., Schloetter, M., Mietus-Synder, M., Morris, R.C., Jr. & Sebastian, A. (2009). Metabolic and physiologic improvements from consuming a Paleolithic, hunter-gatherer type diet.  European Journal of Clinical Nutrition, epub ahead of print. doi:10.1038/ejcn.2009.4.

Fruchart, J. C., Sacks, F., Hermans, M. P., Assmann, G., Brown, W. V., Ceska, R., et al. (2008). The residual risk reduction initiative: A call to action to reduce residual vascular risk in patients with dyslipidemia. The American Journal of Cardiology, 102 (10 Suppl), 1K-34K.

Gebauer, S.K.,  West, S.G., Kay, C.D., Alaupovic, P., Bagshaw, D. & Kris-Etherton, P.M.  (2008). Effects of pistachios on cardiovascular disease risk factors and potential mechanisms of action: A dose-response study. American Journal of Clinical Nutrition, 88(3), 651-659.

Goldenberg, I., Benderly, M., Sidi, R., Boyko, V., Tenenbaum, A., Tanne, D., et al. (2009). Relation of clinical benefit of raising high-density lipoprotein cholesterol to serum levels of low-density lipoprotein cholesterol in patients with coronary heart disease (from the Bezafibrate Infarction prevention trial). The American Journal of Cardiology, 103(1), 41-45.

Harper, C. R., & Jacobson, T. A. (2008). Managing dyslipidemia in chronic kidney disease. Journal of the American College of Cardiology, 51(25), 2375-2384.

Jenkins, D.J.A., Kendall, C.W.C., Marchie, A., R. Josse, T.H.  Nguyen, Faulkner,  D.A. et al. Almonds reduce biomarkers of lipid peroxidation in older hyperlipidemic subjects. Journal of Nutrition, 138 (5), 908-913.

Kamanna, V. S., & Kashyap, M. L. (2008). Mechanism of action of niacin. The American Journal of Cardiology, 101(8A), 20B-26B.

Karalis, D. G. (2009). Intensive lowering of low-density lipoprotein cholesterol levels for primary prevention of coronary artery disease. Mayo Clinic Proceedings.Mayo Clinic, 84(4), 345-352.

Knopp, R. H., Paramsothy, P., Atkinson, B., & Dowdy, A. (2008). Comprehensive lipid management versus aggressive low-density lipoprotein lowering to reduce cardiovascular risk. The American Journal of Cardiology, 101(8A), 48B-57B.

Maahs, D. M., Wadwa, R. P., Bishop, F., Daniels, S. R., Rewers, M., & Klingensmith, G. J. (2008). Dyslipidemia in youth with diabetes: To treat or not to treat? The Journal of Pediatrics, 153(4), 458-465.

Malaguarnera, M., Vacante, M., Avitabile, T., Malaguarnera, M., Cammalleri, L., & Motta, M. (2009). L-carnitine supplementation reduces oxidized LDL cholesterol in patients with diabetes. The American Journal of Clinical Nutrition, 89(1), 71-76.

Mercanligil, S.M., Arsian, P., Alasalvar, C., Okut, E., Akgul, E. Pinar, A. et al. (2007). Effects of hazelnut-enriched diet on plasma cholesterol and lipoprotein profiles in hyercholestrolemic adult men. European Journal of Clinical Nutrition, 61, (2): 212-220.

Morgan, W.A. & Clayshulte, B.J. (2000). Pecans lower low-density cholesterol in people with normal lipid levels. Journal of the American Dietetic Association, 100, (3): 312-318.

O’Keefe, J.H., Gheewala, N.M. & O’Keefe, J.O. (2008). Dietary strategies for improving glucose, lipids, inflammation, and cardiovascular health. Journal of the American College of Cardiology, 51, (3): 249-255.

Phung, O. J., Makanji, S. S., White, C. M., & Coleman, C. I. (2009). Almonds have a neutral effect on serum lipid profiles: A meta-analysis of randomized trials. Journal of the American Dietetic Association, 109(5), 865-873.

Rajaram, S., Haddad, E.H., Mejia, A. & Sabate, J. (2009). Walnuts and fatty fish influence different serum lipid fractions in normal to mildly hyperlipidemic individuals: A randomized controlled study. American Journal of Clinical Nutrition, 89 (5), supplement pages 1657s-1663s.

Ravikumar, B., Gerrard, J., Dalla Man, C., Firbank, M. J., Lane, A., English, P. T., et al. (2008). Pioglitazone decreases fasting and postprandial endogenous glucose production in proportion to decrease in hepatic triglyceride content. Diabetes, 57(9), 2288-2295.

Rimmer, J. H., Rauworth, A. E., Wang, E. C., Nicola, T. L., & Hill, B. (2009). A preliminary study to examine the effects of aerobic and therapeutic (nonaerobic) exercise on cardiorespiratory fitness and coronary risk reduction in stroke survivors. Archives of Physical Medicine and Rehabilitation, 90(3), 407-412.

Sattar, N., Wannamethee, G., Sarwar, N., Chernova, J., Lawlor, D. A., Kelly, A., et al. (2009). Leptin and coronary heart disease: Prospective study and systematic review. Journal of the American College of Cardiology, 53(2), 167-175.

Saylor, P. J., & Smith, M. R. (2009). Metabolic complications of androgen deprivation therapy for prostate cancer. The Journal of Urology, 181(5), 1998-2006; discussion 2007-8.

Scanu, A. M., & Bamba, R. (2008). Niacin and lipoprotein(a): Facts, uncertainties, and clinical considerations. The American Journal of Cardiology, 101(8A), 44B-47B.

Sheridan, M.J., Cooper, J.N., Erario, M. & Cheifetz, C.E. (2007).  Pistachio nut consumption and serum lipd levels. Journal of the American College of Nutrition, 26, (2), 141-148.

Sood, N., Baker, W. L., & Coleman, C. I. (2008). Effect of glucomannan on plasma lipid and glucose concentrations, body weight, and blood pressure: Systematic review and meta-analysis. The American Journal of Clinical Nutrition, 88(4), 1167-1175.

Steiner, G. (2007). Atherosclerosis in type 2 diabetes: A role for fibrate therapy. Diabetes and Vascular Disease Research, 4, (4), 368-374.

Strunz, C.C., Oliveira, T.V., Vinagre, J.C., Lima, A., Cozzolino, S., & Maranhao, R.C. (2008). Brazil nut ingestion increased plasma selenium but had minimal effects on lipids, apolipoproteins, and high-desnity lipoprotein function in human subjects. Nutrition Research, 28, (3), 151-155.

Superko, H. R., Garrett, B. C., King, S. B.,3rd, Momary, K. M., Chronos, N. A., & Wood, P. D. (2009). Effect of combination nicotinic acid and gemfibrozil treatment on intermediate density lipoprotein, and subclasses of low density lipoprotein and high density lipoprotein in patients with combined hyperlipidemia. The American Journal of Cardiology, 103(3), 387-392.

Thorp, A. A., Howe, P. R., Mori, T. A., Coates, A. M., Buckley, J. D., Hodgson, J., et al. (2008). Soy food consumption does not lower LDL cholesterol in either equol or nonequol producers. The American Journal of Clinical Nutrition, 88(2), 298-304.

Underberg, J. A., & Hays, R. (2007). Bridging the gap in treatment options for patients with hypertriglyceridemia. The Journal of Family Practice, 56(12 Suppl New), S24-31.

Williams, K. J. (2008). Molecular processes that handle -- and mishandle -- dietary lipids. The Journal of Clinical Investigation, 118(10), 3247-3259.

Yassine, H. N., Marchetti, C. M., Krishnan, R. K., Vrobel, T. R., Gonzalez, F., & Kirwan, J. P. (2009). Effects of exercise and caloric restriction on insulin resistance and cardiometabolic risk factors in older obese adults--a randomized clinical trial. The Journals of Gerontology.Series A, Biological Sciences and Medical Sciences, 64(1), 90-95.

Zambon, D., Sabate, J., Munoz, S., Campero, B. Casals, E., Merlos, M. et al. Substituting walnuts for monosaturated fat improves serum lipid profile of hypercholesteremic men and women. A randomized crossover trial. Annals of Internal Medicine, 132(7), 538-546.

Zibaeenezhad, M.J., Shamsnia, S.J. & Khorasani, M. (2005). Walnut consumption in hyperlipidemic patients. Angiology, 56, (5), 581-583.

Zittermann, A., Frisch, S., Berthold, H. K., Gotting, C., Kuhn, J., Kleesiek, K., et al. (2009). Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers. The American Journal of Clinical Nutrition, 89(5), 1321-1327.

H1N1 2009: The Swine Flu is Not About the Pigs. It’s About Viral Recombination Possible in Many Animals Including Man, and Can Be Combated with Sensible Precautions & Good Science

The current bout of swine flu, more properly 2009 H1N1,  appears to have originated in Mexico, but neither pigs per se nor Mexicans  “caused it.”

 

Killing  all the pigs, infected and uninfected,  (much as has been mandated in Egypt) and quarantining all Mexico would not stop the further spread of the virus.

 

Uninfected pigs cannot give H1N1 to other uninfected pigs or to humans.

 

Although ironically, infected humans can give it to pigs.

 

Only infected creatures, human or otherwise, can spread it, and only they should be quarantined in all cases.

 

It does makes some sense to quarantine those persons (or pigs) who have been in very close contact with those who are sick.

 

 

And the quarantine times that seem to be working out now for animals or humans that have been in close contact with infected animals or humans appears to be limited: 10 days to two weeks are about the longest spans this author has seen mentioned.

 

Eating well-cooked pork is absolutely not a cause of this so-called swine flu.

 

 

It would seems likely that being a swine farmer, veterinarian,  or pork meat packer who may come into contact with infected pigs is at increased risk.

However, the vast majority of H1N1 cases in the US have come from people infected by other people not by contact with pigs.

 

Indeed, some people may become alarmed at  news reports that tens of thousands of pigs (mainly in Mexican feedlots)  have been found to be affected, but this should be put into the context.

 

Each year over 130,000,000 hogs are processed in the US, and this increasingly centralized industry has an incredible financial incentive to keep their hogs infection-free.

 

Under the current system of raising hogs in the US, a high percentage of hogs are owned by the pork processors or otherwise supplied to pork processors by contract growers who have swine herd veterinarians on retainer precisely to avoid or root out any illnesses that could cause injury to the health of humans or to the sale of pork.

 

The pork industry already is fighting the misconception held by some that pork may be somehow be intrinsically unhealthy when compared to other proteins sources, like chicken breast, hence the “Pork: the other White Meat” campaign. They are on top of this flu situation.

 

 

The cause of this new flu is in essence genetic recombination that happens in nature, whether or not man intervenes.

 

It is now realized that many flu viruses can be in circulation at the same time, in humans and/or  in pigs, and it appears most likely that avian, human, and swine viruses came into contact with one another, and nucleic acid fragments from one or more of these sources apparently interpolated themselves in nucelic acid sequences within individual infected pigs, within larger  pig herds during the span of 2005-2009.

 

Those recombinant viruses then successfully were spread from pig to pig and then from pig to human, and then from human to human , and yes, from human to pig.

 

This H1N1 strain may actually be older than the stated 2009 date of origin.

 

Because kits for its specific testing were not developed, or when available, were not utilized, it was not detected in sufficient numbers to make the headlines we now see, as if it were something entirely unexpected  and unstoppable.

 

How can we put the morbidity and lethality of this alleged swine flu into perspective?

 

If you want to worry about an animal that will cause you harm, don’t look with fear at pigs, look at your neighborhood dog. The CDC reports that annually there are about 4,500,000 reported cases of dog bite in the US. Over 800,000 of them result in trips to the hospital and over 30,000 result in reconstructive plastic surgery.

 

Or, let us compare the lethality of H1N1 with garden variety seasonal flu.

 

In 2009, how many people in the US have died of seasonal flu as of  today(May 13, 2009)? Over 13,000. How many have died of H1N1? 3.

 

And unless you are very old, very young, or suffer from a chronic medical condition that compromises your body’s ability to fight infections of practically any kind, you are very likely to survive an H1N1 infection, should you get it, with no long term sequelae.

 

 

Is there other good news in this story. Sure. While some strains of flu have developed resistance, two drugs appear to be working effectively: Oseltamivir and Zanamivir.

 

Are there still mysteries and dilemmas yet unresolved about H1N1?

 

While there are doubtlessly a great many, there are two being increasingly mentioned.

 

First, it appears that many H1N1 patients are having bouts of severe diarrhea, and that hand contamination  with a potential for virus spreading from repeated toileting  is a concern, that is added to the usual worry about contamination of hands through coughing and sneezing of mucus droplets that contain the virus.

 

The solution to both  newer and well-established routes of transmission is practical and literally at hand: Vigorous hand washing with soap and water and/or use of alcohol-based cleansing gels.

 

Second, there is some worry that the virus will further mutate and/or  recombinate and return with a vengeance next Fall. This must be recognized as a possibility, and scientists will doubtlessly be on the lookout.

 

But their focus will not be soley on pigs, but on any animal, including humans, within which  this might occur, and on sensible means to contain and counteract it.

 

Tony Stankus, FSLA tstankus@uark.edu Life Sciences Librarian & Professor

University of Arkansas Libraries MULN 223 East

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Voice: 479-575-4031

Fax:  470-575-4592

Altman, L.K. (May 12, 2009). Many swine flu cases have no fever. New York Times www.nytimes.com/2009/05/13fever.html

Baden, L.R., Drazen, J.M., Kritek, P.A., Curfman, Morrissey, S. & Campion, E.W. (2009). H1N1 influenza A  disease – Information for health professionals. New England Journal of Medicine, e-published  ahead of print at www.NEJM.org May 7, 2009 (10.1056/NEJMe0903992)

Centers for Disease Control and Prevention. 2009. Interim guidance on antiviral recommendations for patients with novel influenza A (H1N1) virus infection and their close contacts. www.cdc.gov/h1n1flu/recommendations.htm

 Dharan, N.J., Gubareva, L.V., Meyer, J.J., Okomo-Adhiambo, M., McClinton, R.C., Marshall, S.A., et al. (2009). Infections with oseltamivir-resistant influenza A (H1N1) virus in the United States. JAMA, 301, (10), 1034-1041.

Gooskens, J. JOnges, M., Claas, E.C.J., Meijer, A., Van Den Vroek, P.J. & Kroes, A.C.M. Morbidity and mortality associated with nosocomial transmission of oseltamivir-resistant influenza A(H1N1) virus. JAMA, 301 (10), 1042-1046.

Irvine, R.M. & Brown, I.H. (May 9, 2009). Novel H1N1 influenza in people: Global spread from an animal source? The Veterinary Record, 577-578.

Novel Swine Origin Influenza A (H1N1) Virus Investigation Team. 2009. Emergence of a novel swine-origin influenza A (H1N1) virus in humans. New England Journal of Medicine, e-published ahead of print at www.NEJM.org May 7, 2009 (10.1056/NEJMoa0903810)

Shinde, V., Bridges, C.B., Uyeki, T.M., Shu, B., Balish, A, Xu, X., et al. 2009. Triple-reassortment swine influenza A (H1) in Humans in the United States, 2005-2009. New England Journal of Medicine , e- published ahead of print  at www.nejm.org  May 7, 2009 (10.1056/NEJMoa0903812)

Weinstock, D.M. & Zuccotti, G. 2009. The evolution of influenza resistance and treatment. JAMA, 301, (10), 1066-1069.

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 tstankus@uark.edu Life Sciences Librarian & Professor

The University of Arkansas Libraries MULN 223 East

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Voice:  479-575-4031

Fax: 470-575-4592

Becchio, C. (2007). Motor contagion from gaze: The case of autism. Brain, 130, (9), 2401-2411.

Clifford, S. M., & Dissanayake, C. (2008). The early development of joint attention in infants with autistic disorder using home video observations and parental interview. Journal of Autism and Developmental Disorders, 38(5), 791-805.

Clifford, S., Young, R., & Williamson, P. (2007). Assessing the early characteristics of autistic disorder using video analysis. Journal of Autism and Developmental Disorders, 37(2), 301-313.

Darwin, C. 1998. The Expression Of Emotions In Man And Animals, With An Introduction, Afterword, And Commentaries By Paul Ekman And Essays On The History Of The Illustrations By Phillip Prodger. 3^rd ed., NY: Oxford University Press.

De Jong, M. C., van Engeland, H., & Kemner, C. (2008). Attentional effects of gaze shifts are influenced by emotion and spatial frequency, but not in autism. Journal of the American Academy of Child & Adolescent Psychiatry, 47(4), 443-454.

Deruelle, C., Rondan, C., Gepner, B. & Tardif, C. (2004). Spatial frequency and face processing in children with autism and Asperger’s Syndrome. Journal of Autism and Developmental Disorders, 34, (2004): 199-210.

Ekman, P. (1973). Darwin and Facial Expression: A Century of Research in Review. New York: Academic Press.

Ekman, P. Emotions Revealed: Recognizing Faces and Feelings to Improve Communication and Emotional Life. New York: Times Books.

Elsabbagh, M., Volein, A., Csibra, G., Holmboe, K., Garwood, H., Tucker, L., et al. (2009). Neural correlates of eye gaze processing in the infant broader autism phenotype. Biological Psychiatry, 65(1), 31-38.

Fletcher-Watson, S., Leekam, S. R., Findlay, J. M., & Stanton, E. C. (2008). Brief report: Young adults with autism spectrum disorder show normal attention to eye-gaze information--evidence from a new change blindness paradigm. Journal of Autism and Developmental Disorders, 38(9), 1785-1790.

Goldberg, M. C., Mostow, A. J., Vecera, S. P., Larson, J. C. G., Mostofsky, S. H., Mahone, E. M., et al. (2008). Evidence for impairments in using static line drawings of eye gaze cues to orient visual-spatial attention in children with high functioning autism. Journal of Autism and Developmental Disorders, 38(8), 1405-1413.

Gulsrud, A. C., Kasari, C., Freeman, S., & Paparella, T. (2007). Children with autism's response to novel stimuli while participating in interventions targeting joint attention or symbolic play skills. Autism, 11(6), 535-546.

Hubert, B., Wicker, B., Moore, D.G., Monfardini, E., Duverger, H., DaFonseca, D. & Deruelle, C. (2007). Recognition of emotional and non-emotional biological motion in individuals with Autistic Spectrum Disorders. Journal of Autism and  Developmental Disorders, 37, (1386-1392.  

Ibanez, L. V., Messinger, D. S., Newell, L., Lambert, B., & Sheskin, M. (2008). Visual disengagement in the infant siblings of children with an Autism Spectrum Disorder (ASD). Autism, 12(5), 473-485.

Jones, E.A., & Carr, E.G. (2004).  Joint attention in children with autism: Theory and intervention. Focus on Autism and Other Developmental Disabilities, 19 (1): 13-26.

Joseph, R. M., Ehrman, K., McNally, R., & Keehn, B. (2008). Affective response to eye contact and face recognition ability in children with ASD. Journal of the International Neuropsychological Society, 14(6), 947-955.

Klin, A. (2008). In the eye of the beholden: Tracking developmental psychopathology. Journal of the American Academy of Child & Adolescent Psychiatry, 47(4), 362-363.

Klin, A., Lin, D.J., Gorrindo, P., Ramsay, G. & Jones, W. (2009). Two-year-olds with autism orient to non-social contingencies rather biological motion. Nature, 458, (7237), 1-7.

Milne, E., Sweettenham, J., Hansen, P., Campbell, R. Jeffries, H. & Plaisted, K. (2002) High motion coherence thresholds in children with autism. Journal of Child Psychology and Psychiatry, 43, 255-263.

Nation, K., & Penny, S. (2008). Sensitivity to eye gaze in autism: Is it normal? Is it automatic? is it social? Development and Psychopathology, 20 ( 1), 79-97.

Parron, C., DaFonseca, D., Santos, A., Moore, D.G., Monfardini, E. & Deruelle, C. (2008).  Recognition of biological motion in children with autistic spectrum disorders. Autism, 12, 261-274.

Pollick, F.E., Hill, H., Calder, A. & Patterson, H. (2003). Recognizing facial expression from spatially and temporally modified movements. Perception, 32, 813-826.

Robel, L., Ennouri, K., Piana, H., Vaivre-Douret, L. Perier, A., Flament, M.F., Mouren-Simeoni, M.C. (2004). Discrimination of face identities and expressions in children with autism: Same or different? European Child and Adolescent Psychaitry 13, 227-233.

Rondan, C. & Deruelle, C. (2004) Face processing in high functioning autistic adults: A look into spatial frequencies and the Inversion Effect. Jounal of Cognitive and Behavioral Psychotherapies, 4, 149-164.

Sasson, N. J., Turner-Brown, L., Holtzclaw, T. N., Lam, K. S. L., & Bodfish, J. W. (2008). Children with autism demonstrate circumscribed attention during passive viewing of complex social and nonsocial picture arrays. Autism, 12,  (1), 31-42.

Senju, A., Kikuchi, Y., Hasegawa, T., Tojo, Y., & Osanai, H. (2008). Is anyone looking at me? direct gaze detection in children with and without autism. Brain and Cognition, 67(2), 127-139.

Van der Geest, J.N., Kemner, C., Campfferman, G., Verbaten, M.N. & Van Engeland, H. (2002). Looking at images with human figures: Comparison between autistic and normal children. Journal of Autism and Developmental Disorders, 32 (2), 69-75.

Van der Geest, J.N., Kemner C., Verbaten, M.N. & Van Engeland. (2002) Gaze behavior of children with pervasive developmental disorder toward human faces: A fixation time study. Journal of Child Psychology and Psychiatry, 43 (5): 669-678.

Do Snake Venoms Evolve According to the Prey They Are Intended to Kill, Or Do Snakes Just Dial Up the Dosage or Concentration of Whatever Venom They Have to the Size of the Prey in their Sights?

Snake venoms are overwhelmingly composed  of dissolved protein  mixtures which typically exert their action on a victim in one of the following three ways, and sometimes in combination:

·        Hemotoxins. Depending on their mix of proteins, these can either cause the blood to clot precipitously, causing cardiovascular blockages (essentially heart attacks) in extreme cases, or alternatively, cause it to thin so quickly that the victim bleeds out.  This is one of the  modes of action of rattlesnake venoms.

 

·        Neurotoxins.  These disrupt either or both the voluntary and autonomic nervous system of the victim, rendering it incapable of escape, and in extreme cases, cause the victim to stop breathing or to convulse. This is the primary  mode of action of cobra venoms.

 

·         Tissue Necrotizers:  These basically break down the muscular and connective tissue at the site of the bite, and basically cause an ever expanding dead zone until the toxin is so diluted as to lose effect. Often the victim dies before this can happen. This is the mode of action of the fer-de-lance the most prominent perpetrator of poisonous snake bites in Latin America.

The popularity of proteomics and the wider availability of its instrumentation  leads to “venomics” & confirms evolutionary relationships & distinctions  among the many differing families  of poisonous snakes

 

Can you tell a venomous snake just by a chemical analysis of its venom?

The short, and historically most orthodox answer,  is, yes.

For most of the history of snake venom studies , the relatively small number of total analyses achieved indicated that most snakes tend to have signature venom protein mixes.

Now, given the widespread use of automated proteomics analyzers and advances in protein sequence informatics, much of this  old work is being confirmed with more  complete analyses of more venoms from more snakes and especially from differing families of snakes. Indeed, you can now search a variety of biomedical, chemical and pharmaceutical  databases under “Venomics” for on-point papers.

 And the new results can be extended to say that snakes that are in the same genus tend to have rather similar, if not always quite identical, cocktails of toxins.

Such variations as are found, are thought to be minor,  the results of random genetic drift, and to be incidental to the  study of  either the lineage, the  or day-to-day functioning of the snake.

There is  some thought that evolutionary relationships suggested by traditional morphological characters or modern genomics ,  can predict,  with reasonable certainty what venom toxins given families of snakes are likely to share, even before all their members are tested.

As a kind of real-world proof of the all-in-the-family nature  of protein toxins , consider that snake antivenoms (which work on biochemical recognition and disabling of venom proteins through binding them up)  work best when customized to the type of specific snake that does the biting. Such antitoxins are called monovalents, and are the treatment of choice whenever available.

But  given that maintaining a large and varied collection of monovalent antivenoms  is not always practical in areas where there are many possible different poisonous snakes which bite, some polyvalent vaccines have had to be developed which counteract, to some degree,  venoms from a variety of unrelated species.

Despite their polyvalent intent, their comparative effectiveness is positively correlated  with snakebites  that are evolutionarily related to the species from which the original pharmaceutical venom/vaccine was drawn.  In other words, antivenom that derives from a specific type of cobra,  is likely to work better with other persons bitten by somewhat different cobras, than it is to work on people bitten by rattlesnakes.

The prevalent theory is that the biosynthesis of toxins is likely to be highly conserved  over many generations and over differing populations of snake families  because their venom seems so central to the function of the snake, and that even incidental variations in toxins caused my random mutations could come at a cost to the snake in reduced prey killing capacity.

But  the dismissal of the significance of small differences in toxin blends within related snakes  is now being challenged,  and variations are being seen as having some meaningful function, and not just being blips in encoding that have no real life meaning to the snake.

Why have differing toxins within the same family of snakes? Couldn’t the snake just adjust the dosage to the size of the prey?

Differing types of snakes have differing quantities of venom available for hunting or defense, but certain general rules can predict among populations of the same snakes which will have more venom on average.

Generally, the older the snake of a given species is , the larger it is, and therefore the larger its storage and potential supply of venom for “envenomation, ”  when compared to younger and smaller snakes of the same species.

Furthermore female snakes generally have significantly more venom than males for two  readily  understood reasons: They are generally larger than males and have larger heads, and the head is where most of the venom production and storage is confined in all but a tiny handful of snake species.

But, it turns out that many adult snakes, whether large or small,  are actually thrifty in their use of venom.

They adjust the amount of venom to the size of their prey.  A mouse might get less venom per bite  than a gopher, for example.

Although as a general rule, given a choice between small and large prey , larger snakes will choose larger prey, and are willing to “spend the venom”  in order to get the larger meal.

The saw-scaled viper family and their venoms

A particularly  interesting comparison test of the venoms of four kinds of  saw-scaled vipers done by Barlow et al. (2009, cited below).

These four related viper species  are a genuine menace to public health in that they cause the majority of snakebite cases in North Africa and the adjacent Middle East.

 (The fact that some of them kill harmful vermin, may, of course be an offsetting factor, before deciding that they all should be wiped out indiscriminately.)

A comparison of the  electrophoretic separations of major toxin proteins  from the four different types of saw-scaled viper  showed that they were indeed, matching in the major protein bands,  something predictable owing to conventional thinking about the molecular evolution of snake venoms.

But there was a surprising amount of variation in the minor bands.

And this was also reflected in the fact that in the Middle East and in Northern Africa, saw scale viper antivenoms were markedly more effective against  Middle Eastern saw scale viper bites than they were against the bites of  the North African saw scale vipers that were presumed to be their evolutionarily closest relatives.

The drop off in effectiveness is notable in clinical terms and makes follow-up injections or IV drips of antivenom necessary more often in North Africa than they were in the Middle East.

A question arose:  Beyond any clinical significance, did these  variant protein toxins  have a purpose in the life of the snake?  Or, were they just the result of geographic isolation and random genetic drift?

Prey size vs. prey type: Which  plays a bigger role in the  evolution of venoms?

One competing theory of comparative venom toxicity  is that snakes within the same general family of snakes that prey on larger animals will eventually evolve   not only to produce more of the same general type of venom,  but also evolve higher, and therefore more potent concentrations of venom, with which to immobilize and kill their “big game.”

Its principal rival theory  is that differing prey  specialists within the same general family of snakes are more likely to require,  and eventually develop over succeeding generations venoms that gradually become more distinct, depending for success in killing prey, not so much on increasing the amount or the concentration of venom injected,   but rather on matching  the prey’s particular susceptibility to the venom.

Saw scale vipers represent a wonderful set of relatives upon which to test these competing outlooks.

Several types of saw scaled vipers have become small mammal specialists (usually eating rodents)  in terms of their prey.  Most of these are in the Middle East.

Others have a mixed diet of rodents and invertebrates.

(Most commonly in the Middle East and Africa, the invertebrates are various types of scorpions. )

Still others are almost exclusively scorpion feeders. These vipers are found only in North Africa.

It should be understood that even the biggest scorpions are but a fraction of the size and weight of the mice and rats typically consumed by either the rodent specialist,  or the mixed-diet-consuming saw scale  vipers.

Consequently “big game venom” should actually be more toxic to little game, because of its overall increased potency.

In other words, it may not be necessary to shoot a big-game venom cannon ball to kill a scorpion, but if it were to happen,  the cannon ball should surely be lethal to the scorpion.

Using ingenious methods, such as directly injecting carefully calibrated, matching fluid amounts of venom directly into  test scorpions from all four types of saw scale viper, and then seeing which venoms were, “ounce for ounce” more deadly, the team found something unexpected.

The “big game hunters”  of rats and mice, who would presumably need more toxicity to bring down their big game, actually  had venom that was notably less toxic to the small size game of scorpions, than the venom   of the mixed-bag-diet hunters.

And even more  intriguingly,   the mixed-bag-hunter venom was still less toxic to the scorpions than that of the specialized scorpion hunters.

The most toxic & effective venoms against the small game of scorpions, came from scorpion specialists, not from big-game or mixed-game specialists, who routinely had to knock down and kill bigger game.

In other words, the venom of North African scorpion specialists had become distinct enough through evolutionary adaptation to its prey, to make a difference in the life of its particular type of saw scale viper.

And maybe that distinction was now big enough to explain why Middle Eastern antivenom vaccines against North African saw scale vipers were seeing decreased efficiency.

Are the prey utterly without their own evolutionary defenses against specially  evolved snake venom?

This would seem to be the case, but in a number of settings, various ground squirrels, gophers and badgers, whose paths frequently intersect with predatory snakes like rattlers, seem to have grown immune to the local venom (see, for example Hayes, Lavin-Murcio & Kardong, 1995, cited below). This is also the case with some eels that live alongside sea snakes that hunt for eels (Heatwole & Pran, 1995).

Whether or not this leads to the evolutionary  alteration of the local snake venom to make if effective once again, has not yet been studied.

But in a particularly intriguing case, a poisonous sea snake that has become a fish egg eating specialists, and therefore has no need to immobilize and kill its prey (the eggs don’t run away and are not guarded by their parent fish) has actually evolved venom of greatly reduced toxicity, seeming to spare itself unnecessary toxin protein production (Li, Fry & Manjunatha Kini, 2005).

 

Tony Stankus tstankus@uark.edu Life Sciences Librarian & Professor

University of Arkansas Libraries MULN 223 E

365 North McIIroy Avenue

Fayetteville, AR 72701-4002

Voice: 479-575-4031

Fax: 479-575-4592

 

Aird, S. D. (2008). Snake venom dipeptidyl peptidase IV: Taxonomic distribution and quantitative variation. Comparative Biochemistry and Physiology B-Biochemistry & Molecular Biology, 150(2), 222-228.

Alape-Giron, A., Sanz, L., Escolano, J., Flores-Diaz, M., Madrigal, M., Sasa, M., et al. (2008). Snake venomics of the lancehead pitviper Bothrops asper : Geographic, individual, and ontogenetic variations. Journal of Proteome Research, 7(8), 3556-3571.

Andrade, D.V. & Abe, A.S. 1999. Relationship of venom ontogeny and diet in Bothrops.  Herpetologica, 55, 200-204.

Biardi, J. E., Chien, D. C., & Coss, R. G. (2006). California ground squirrel (Spermophilus beecheyi) defenses against rattlesnake venom digestive and hemostatic toxins. I. Journal of Chemical Ecology, 32(1), 137-154.

Biardi, J. E., Chien, D. C., & Coss, R. G. (2005). California ground squirrel (Spermophilus beecheyi) defenses against rattlesnake venom digestive and hemostatic toxins. II.  Journal of Chemical Ecology, 31(11), 2501-2518.

Calvete, J. J., Escolano, J., & Sanz, L. (2007). Snake venomics of bitis species reveals large intragenus venom toxin composition variation: Application to taxonomy of congeneric taxa. Journal of Proteome Research, 6(7), 2732-2745.

Chander, R., Batra, M., Singh, D., Kumar, Y., Rawat, S., & Kumar, S. (2006). A new in-vitro agglutination technique for potency estimation of antisnake venom serum (ASVS). Toxicon, 48(8), 1011-1017.

Chang, L., Wang, J., Cheng, Y., & Chou, W. (2008). Genetic organization of Bungarus multicinctus protease inhibitor-like proteins. Toxicon, 51(8), 1490-1495.

Chen, H., Tsai, H., Wang, Y., & Tsai, I. (2008). P-III hemorrhagic metalloproteinases from Russell's viper venom: Cloning, characterization, phylogenetic and functional site analyses. Biochimie, 90(10), 1486-1498.

Chippaux, J.P., Williams, V. & White, J. 1991. Snake venom variability: Methods of study, results and interpretation. Toxicon, 29, 1279-1303.

Chippaux, J.P. (1998). Snake-bites: Appraisal of the global situation. Bulletin of the World Health Organization, 76, 515-524.

Daltry, J.C., Wuster, W. & Thorpe, R.S. 1996. Diet and snake venom evolution. Nature, 379, 537-540.

Furtado, M. F. D., Travaglia-Cardoso, S. R., & Rocha, M. M. T. (2006). Sexual dimorphism in venom of Bothrops jararaca (serpentes : Viperidae). Toxicon, 48(4), 401-410.

Galan, J. A., Sanchez, E. E., Bashir, S., & Perez, J. C. (2005). Characterization and identification of disintegrins in Crotalus horridus venom by liquid chromatography and tandem matrix-assisted laser desorption ionization-quadrupole ion trap time-of-flight (MALDI-QIT-TOF) mass spectrometry. Canadian Journal of Chemistry-Revue Canadienne De Chimie, 83(8), 1124-1131.

Gibbs, H. L., & Rossiter, W. (2008). Rapid evolution by positive selection and gene gain and loss: PLA(2) venom genes in closely related Sistrurus rattlesnakes with divergent diets. Journal of Molecular Evolution, 66(2), 151-166.

Gibbs, H. L., Sanz, L., & Calvete, J. J. (2009). Snake population venomics: Proteomics-based analyses of individual variation reveals significant gene regulation effects on venom protein expression in Sistrurus rattlesnakes. Journal of Molecular Evolution, 68(2), 113-125.

Gutierre, J.M., Theakston, R.D., & Warrell, D.A. (2006). Confronting the neglected problem of snake bite envenoming: The need for a global partnership. PLoS Medicine, 3, article number  e150.

Hayes, W.K., Lavin-Murcio, P. & Kardong, K.V. 1995. Northern Pacific rattlesnakes (Crotalus viridis oreganus) meter venom when feeding on prey of different sizes. Copeia, 1995, 337-343.

Heatwole, H. & Pran, N.S. 1995. Resistance of sympatric and allopathetic eels to sea snake venoms. Copeia, 1995, 136-147.

Jurado, J. D., Rael, E. D., Lieb, C. S., Nakayasu, E., Hayes, W. K., Bush, S. P., et al. (2007). Complement inactivating proteins and intraspecies venom variation in Crotalus oreganus helleri. Toxicon, 49(3), 339-350.

King, R.B., Bittner, T.D. Queral &-Regil, A. & Cline, J.H. (1999).  Sexual dimorphism in neonate and adult snakes. Journal of Zoology, 247, 19-28.

Kordis, D. & Gubensek, F. 2000. Adaptive evolution of animal toxin multigene families. Gene, 261, 43-52.

Li, M. Fry, B.G. & Manjunatha Kini, R. 2005. Eggs-only diet: Its implication for the toxin changes and ecology of the marbled sea snake (Aipysurus eydouxii). Molecular Biology & Evolution, 22, (4), 934-941.

Mackessy, S. P., Sixberry, N. A., Heyborne, W. H., & Fritts, T. (2006). Venom of the brown treesnake, Boiga irregularis: Ontogenetic shifts and taxa-specific toxicity. Toxicon, 47(5), 537-548.

Markland, F.S. (1998). Snake venoms and the hemostatic system. Toxicon, 36: 1749-1800.

Menezes, M. C., Furtado, M. F., Travaglia-Cardoso, S. R., Camargo, A. C. M., & Serrano, S. M. T. (2006). Sex-based individual variation of snake venom proteome among eighteen Bothrops jararaca siblings. Toxicon, 47(3), 304-312.

Mora, J., Mora, R., Lomonte, B. & Gutierrez, J.M. (2008). Effects of Bothrops asper snake venom on lymphatic vessels: Insights into a hidden aspect of envenomation. PLoS Neglected Tropical Diseases, 2,  (10), article number 318.

Pahari, S., Bickford, D., Fry, B. G., & Kini, R. M. (2007). Expression pattern of three-finger toxin and phospholipase A(2) genes in the venom glands of two sea snakes, Lapemis curtus and Acalyptophis peronii: Comparison of evolution of these toxins in land snakes, sea kraits and sea snakes. BMC Evolutionary Biology, 7, 175.

Pimenta, D. C., Prezoto, B. C., Konno, K., Melo, R. L., Furtado, M. F., Camargo, A. C. M., et al. (2007). Mass spectrometric analysis of the individual variability of Bothrops jararaca venom fraction. evidence for sex-based variation among the bradykinin-potentiating peptides. Rapid Communications in Mass Spectrometry, 21(6), 1034-1042.

Powell, R. L., Reyes, S. R., & Lannutti, D. I. (2006). Molecular barcoding, DNA from snake venom, and toxinological research: Considerations and concerns. Toxicon, 48(8), 1095-1097.

Queiroz, G. P., Pessoa, L. A., Portaro, F. C. V., Furtado, M. d. F. D., & Tambourgi, D. V. (2008). Interspecific variation in venom composition and toxicity of Brazilian snakes from Bothrops genus. Toxicon, 52(8), 842-851.

Salazar, A. M., Rodriguez-Acosta, A., Giron, M. E., Aguilar, I., & Guerrero, B. (2007). A comparative analysis of the clotting and fibrinolytic activities of the snake venom (Bothrops atrox) from different geographical areas in Venezuela. Thrombosis Research, 120(1), 95-104.

Sanz, L., Gibbs, H. L., Mackessy, S. P., & Calvete, J. J. (2006). Venom proteomes of closely related Sistrurus rattlesnakes with divergent diets. Journal of Proteome Research, 5(9), 2098-2112.

Siegel, R.A. & Collins, J.T., eds.  (1993). Snakes: Ecology and Behavior. New York McGraw-Hill.

Soto, J. G., Powell, R. L., Reyes, S. R., Wolana, L., Swanson, L. J., Sanchez, E. E., et al. (2006). Genetic variation of a disintegrin gene found in the American copperhead snake (Agkistrodon contortrix). Gene, 373, 1-7.

Soto, J. G., White, S. A., Reyes, S. R., Regalado, R., Sanchez, E. E., & Perez, J. C. (2007). Molecular evolution of PIII-SVMP and RGD disintegrin genes from the genus Crotalus. Gene, 389(1), 66-72.

Steuten, J., Winkel, K., Carroll, T., Williamson, N. A., Ignjatovic, V., Fung, K., et al. (2007). The molecular basis of cross-reactivity in the Australian snake venom detection kit (SVDK). Toxicon, 50(8), 1041-1052.

Thorpe, R. S., Pook, C. E., & Malhotra, A. (2007). Phylogeography of the Russell's viper (Daboia russelii) complex in relation to variation in the colour pattern and symptoms of envenoming. Herpetological Journal, 17(4), 209-218.

Tsai, I., Tsai, H., Saha, A., & Gomes, A. (2007). Sequences, geographic variations and molecular phylogeny of venom phospholipases and three finger toxins of eastern india Bungarus fasciatus and kinetic analyses of its Pro31 phospholipases A(2). FEBS Journal, 274(2), 512-525.

Tsai, I., Tsai, H., Wang, Y., Tun-Pe, & Warrell, D. A. (2007). Venom phospholipases of Russell's vipers from Myanmar and eastern India - cloning, characterization and phylogeographic analysis. Biochimica Et Biophysica Acta-Proteins and Proteomics, 1774(8), 1020-1028.

Wagstaff, S. C., Laing, G. D., Theakston, R. D. G., Papaspyridis, C., & Harrison, R. A. (2006). Bioinformatics and multiepitope DNA immunization to design rational snake antivenom. PLoS Medicine, 3(6), 832-844.

Warrell, D.A. (2004). Clinical toxicology of snakebite in Africa and the Middle East/ Arabian  peninsula. . In,Meier, J. & White, J.,  eds., Handbook of Clinical Toxicology of Animal Venoms and Poisons. Boca Raton, FL: CRC Press, 433-492.