Maiden shows signs of TB-like infection

As if being a human sacrifice weren’t bad enough, a teenager may have been fighting off tuberculosis before being killed on top of a South American volcano 500 years ago.
As she climbed to her death, the immune system of a 15-year-old Incan girl known as the Maiden was combating a bacterial infection caused by a type of Mycobacterium, an analysis indicates. Angelique Corthals, a forensic anthropologist at the City University of New York, and colleagues report the findings online July 25 in PLoS One.
La Doncella, as the Maiden is called in Spanish, was one of three children whose mummified remains were found near the summit of Llullaillaco volcano in Argentina in 1999. She, a younger girl and young boy were probably sacrificed in a ritual called Capacocha. But the exact cause of the children’s deaths has remained a mystery; their perfectly preserved mummies show no signs of violent trauma.
Corthals wanted to know whether the children were given a fermented corn drink called chicha, which was used to numb sacrifice victims as part of the Capacocha ritual. The alcohol in the drink would have evaporated almost immediately, but the children might still have traces of corn clinging to their lips, she reasoned. Researchers swabbed blood and saliva from the lips of the Maiden and the boy, and snipped off a small piece of the boy’s blood-soaked cloak for testing using a technique that identifies proteins contained in the samples. The younger girl’s face was damaged by a lightning strike after burial, so the researchers couldn’t include her in the study.
Coauthor Antonius Koller of the State University of New York Stony Brook Medical Center and his colleagues determined which proteins were present in the samples. There was no sign of corn liquor, Corthals says, but the protein profile indicated clearly what the two mummies’ immune systems had been up to at the time of death.
The Maiden’s immune system was more active than the boy’s was, and her swabs contained immune system proteins indicating a chronic lung infection. Modern people fighting off Mycobacterium diseases such as tuberculosis make similar proteins. DNA evidence showed that the girl was carrying some type of Mycobacterium, although the researchers can’t yet nail down which species of the bacterium was infecting her.
The new findings are consistent with radiological exams showing signs of lung and sinus inflammation in the Maiden. The boy showed no signs of active infection.
Other researchers are sure to latch onto the new research approach described in the study, says Robert DeSalle, of the American Museum of Natural History in New York City. “It is going to be the first paper among probably a lot to come looking at infectious diseases among dead people,” he says. He predicts that examining the immune systems of long-dead creatures may also help solve some archaeological debates, such as whether woolly mammoths were victims of overhunting or disease.

North African Diaspora written in genes

Historical Jewish migrations out of the Middle East about 2,000 years ago can also be traced in the DNA of people living in Africa and Southwest Asia today.
These distinctive genetic signatures bolster historical accounts that there were waves of Jewish migration out of the Middle East into neighboring regions. Human geneticist Harry Ostrer of Albert Einstein College of Medicine in New York City and colleagues report their analysis of 509 people from 15 Jewish populations online August 6 in the Proceedings of the National Academy of Sciences, focusing their attention on communities in North Africa, Ethiopia, Yemen and the Caucasus.
Geneticists have previously traced movements of Jewish groups in Europe and the Middle East (SN: 7/3/10, p. 13; SN: 1/3/09, p. 12), but few studies have focused on Diaspora groups in other regions.
Jews settled in Tunisia more than 2,000 years ago, and genetic signatures carried from the Middle East are still evident in Tunisian Jews today, the researchers found. Together with Djerban and Libyan Jews, the Tunisian Jews form a separate genetic branch from Moroccan and Algerian Jews.
Jews in Morocco and Algeria bear genetic signatures characteristic of Sephardic Jews, who once lived in Spain and Portugal. The Spanish Inquisition caused the expulsion of Sephardic Jews from the Iberian Peninsula and many went to North Africa, carrying their genetic heritage with them.
DNA signatures found in Ethiopian Jews indicate that they are genetically different from Middle Eastern Jews and from the other people living in Ethiopia. The genetic evidence can’t confirm the origin tale that Ethiopian Jews are descendants of King Solomon and the Queen of Sheba, but the findings are consistent with historical accounts that local people were converted to Judaism, then spent more than 2,000 years in cultural and genetic isolation.
Yemenite Jewish people also form a separate genetic group from other Jews, consistent with conversions. “I like to think of it as both the flow of ideas as well as genes that contribute to Jewishness,” Ostrer says.
In the Caucasus, Georgian Jews are an offshoot of groups that first moved from Palestine to present-day Iran and Iraq, the new analysis shows.
Although the new study is the most in-depth of its kind, it certainly doesn’t determine who is a Jew, says Francesc Calafell, a population geneticist at the Institute of Evolutionary Biology in Barcelona. Palestinians have a similar genetic makeup to Jewish people, he points out. “Genetics is only a facet of identity.”

Psychopaths get time off for bad brains

A callous, manipulative psychopath convicted of a brutal crime can count on a long prison stint. But a judge may issue a slightly shorter sentence if presented with a biological explanation for the criminal’s psychopathic personality.
Supplying judges with scientific evidence about suspected brain deficits in psychopathy led to a reduction in prison sentences from about 14 years to 13 years, researchers report in the Aug. 17 Science. The results come from a nationwide, online survey of state judges given a hypothetical scenario about a psychopath convicted of what lawyers call aggravated battery.
Judges taking the survey tended to view psychopathic criminals as dangerous, whether or not scientific evidence was introduced, say psychologist Lisa Aspinwall, lawyer Teneille Brown and philosopher James Tabery, all of the University of Utah in Salt Lake City. A hypothetical psychopath in the new study got sent to the slammer for longer than the average nine-year sentence given to non-psychopaths found guilty of aggravated battery in real courts.
Aspinwall and her colleagues informed judges that clinicians use psychopathy — which is not an official psychiatric diagnosis — to refer to individuals who are impulsive, emotionally shallow, outwardly charming, lacking in empathy or remorse, chronic liars and callous manipulators (SN: 12/9/06, p. 379). Judges were told that psychopathy is incurable.
But any tendency toward reduced sentences for psychopathic convicts in a survey would be weaker in actual courtrooms where judges hear evidence contested by prosecutors and defense attorneys, says psychologist Jennifer Skeem of the University of California, Irvine.
“It is premature to apply neuroscience on psychopathy to decisions about criminal responsibility and sentencing,” Skeem says.
It’s hard to know whether defense attorneys could win reduced prison sentences for actual psychopathic offenders by introducing brain evidence, Tabery acknowledges. Even in the new 19-state survey, evidence about biological contributions to psychopathy led to substantially reduced sentences in two states (Utah and Maryland), slightly reduced or unchanged sentences in six states and slightly increased sentences in three states (Colorado, New York and Tennessee). The remaining eight states included too few participants to determine statewide trends.
“No one knows if real-world sentencing of psychopathic defendants works as it does in this study, or even whether most judges consider psychopathy when imposing sentences,” says lawyer and psychologist Stephen Morse of the University of Pennsylvania Law School in Philadelphia.
Aspinwall’s group can’t say whether psychological or social explanations for a psychopath’s crime would affect sentencing decisions as much as biological evidence did, Morse adds.
In the online study, 181 judges read a scenario in which a man beat a store clerk with a gun during a robbery, causing brain damage to the victim. All judges saw evidence that the criminal was a psychopath. In addition, 90 judges received scientific findings from either the prosecution or the defense about psychopathy’s biological roots. Prosecutors argued that biological evidence supported a longer sentence; defenders sought a reduced sentence.
About 87 percent of judges listed at least one factor, such as the crime’s seriousness, as relevant to lengthening the sentence. When judges received biological explanations of psychopathy from the defense, the proportion taking at least one sentence-reducing factor into account rose from around 30 percent to 66 percent.
For unclear reasons, the judges didn’t rate psychopaths as having less free will or being less responsible after hearing evidence about brain influences on the condition.

Anti-inflammatories tied to cardiac risk

People who have survived a heart attack seem to increase their risk of having another one, or of dying, by taking common painkillers called NSAIDs, a popular class of drugs that includes ibuprofen.
The unsettling link between non-steroidal anti-inflammatory drugs and heart attack risk is not new. The American Heart Association released guidelines in 2007 discouraging the use of any NSAIDs among people with a history of cardiovascular disease. Researchers in Denmark now bolster that link with the largest study to date of NSAID use in heart patients. The findings appear September 10 in Circulation.
In conducting the analysis, the scientists mined a huge database to identify every first-time heart attack in people 30 years old or older that occurred in the country between 1997 and 2009, nearly 100,000 people in all. The researchers then cross-checked this information with death records, subsequent heart attacks and NSAID prescriptions. (Most NSAIDs in Denmark are prescribed.) About 44 percent of people were prescribed an NSAID during the five years following a first heart attack.
Compared with people who didn’t get NSAIDs via prescription, those who did were 63 percent more likely to die over the next five years and 41 percent more likely to die specifically of a heart problem or to have another heart attack.
“This is the biggest study, no question, in terms of numbers and completeness,” to address the NSAID/heart risk question, says Vibeke Strand, a rheumatologist at Stanford University School of Medicine.
While the study shows that NSAIDs as a group seem to boost heart attack risk, certain NSAIDs, such as diclofenac (Voltaren), appear worse than others. While the drug is sold by prescription only in the United States and Denmark, it is offered over the counter in other parts of Europe, says study coauthor Anne-Marie Schjerning Olsen, a physician at the University of Copenhagen. “I think it’s a huge problem,” she says.
Ibuprofen, which is marketed as Advil and Motrin, seemed to impart a consistent risk as well. The apparent risk from naproxen, sold as Aleve, was equivocal in these data, particularly after a patient had gotten past the first year post–heart attack.
Strand says the researchers have compiled “very impressive data.” But she notes that the researchers were unable to track use of aspirin, which is sold over the counter in Denmark. Daily low-dose aspirin limits heart attacks by reducing the blood’s clotting ability. “If you don’t take aspirin regularly, or if you take it simultaneously with NSAIDs, you lose that aspirin benefit,” Strand says. NSAIDs bind to the same molecular pocket on blood platelets as aspirin does, crowding out the aspirin. While NSAIDs have some ability to limit clotting caused by platelet aggregation, this capacity fades as the drugs wear off, she notes. In contrast, when aspirin binds to a platelet, its effect is irreversible, which is how daily aspirin suppresses stickiness in the population of platelets even as they are replenished.
“Some people think that if they are taking NSAIDs, they don’t need aspirin,” Strand says. “That’s absolutely wrong.” Patients who need NSAIDs for pain or inflammation, yet who have risk factors for heart disease, should take aspirin at least a few hours before taking an NSAID, she says.
Reducing aspirin’s protective effect might explain part of why NSAIDs seem to add to heart risk. NSAIDs have also been linked to increased blood pressure and atrial fibrillation, a heart rhythm disorder.