Imagine seeing better by thinking differently. That’s a vision with a future, according to Harvard University psychologist Ellen Langer.
Eyesight markedly improved when people were experimentally induced to believe that they could see especially well, Langer and her colleagues report in the April Psychological Science. Such expectations actually enhanced visual clarity, rather than simply making volunteers more alert or motivated to focus on objects, they assert.
Langer’s new findings build on long-standing evidence that visual perception depends not just on relaying information from the eyes to the brain but on experience-based assumptions about what can be seen in particular situations. Those expectations lead people to devote limited attention to familiar scenes and, as a result, to ignore unusual objects and events.
In perhaps the most eye-popping of Langer’s new findings, 20 men and women who saw a reversed eye chart — arranged so that letters became progressively larger further down the chart, with a giant “E” at the bottom — accurately reported more letters from the smallest two lines than they did when shown a traditional eye chart with the big letters on top. All volunteers had normal eyesight.
These results reflect people’s expectation, based on experience with standard eye charts, that letters are easy to see at the top and become increasingly difficult to distinguish on lower lines, the researchers suggest.
Participants who said they thought that they could improve their eyesight with practice displayed a bigger vision boost on the reversed chart than those who didn’t think improvement was possible, but only for the next-to-smallest line. Both groups did equally well at reading the smallest, topmost line.
Another set of experiments included 63 members of the Reserve Officers’ Training Corps at MIT. Eye testing determined that their vision ranged from below average to excellent.
An experimenter told a group of 22 cadets to assume the role of a fighter pilot while operating a flight simulator. During this exercise, participants tried to identify letters shown on four plane wings of approaching aircraft. Each wing contained one of the bottom four lines of an eye chart.
Another 20 cadets performed the visual task while pretending to fly a plane in a simulator that they were told was broken. Ten other cadets read a motivational essay before the exercise. A final group of 11 cadets didn’t use a simulator but practiced eye exercises that researchers described as capable of improving eyesight before taking an eye test.
Vision improved substantially for nine of 22 simulator pilots compared with none of those who pretended to fly, two of 11 eye exercisers and one person in the motivational group. Simulator pilots did so well relative to the others because they more thoroughly adopted a mind-set of being real fighter pilots with presumably superior vision, the researchers posit. An initial survey of ROTC members found that they attributed particularly good vision to fighter pilots.
Simulator pilots with below-average vision displayed the biggest jumps in visual performance, perhaps because they had more room for improvement, the researchers suggest.
These results suggest that if eye exercise programs designed to improve vision work for some people, it’s not because of any physical effect on the eyes or brain. Such regimens “may be effective because they prime the belief that exercise improves vision,” Langer and her colleagues write.
Mind-set may boost visual performance without sharpening vision itself, comments psychologist Daniel Simons of the University of Illinois at Urbana-Champaign. Experimental manipulations in the new study, such as reversing the arrangement of an eye chart, may have made volunteers more willing to guess when they felt a bit unsure, Simons says. Such guesses stand a good chance of being right, in his view.
Blog Archive
A new study has come up empty-handed after pursuing a genetic explanation for why one identical twin developed multiple sclerosis while the other stayed healthy.
Researchers transcribed the complete genetic blueprints for a pair of identical twins, looking for differences that might explain why one has multiple sclerosis and the other does not. No trace of what caused the discrepancy appeared in the twins’ DNA. And scientists found no smoking gun when they compared levels of gene activity between the sick and well twin. The results appear in a report published April 29 in Nature.
“We looked under a lot of rocks and we found no differences that we could replicate,” says Stephen Kingsmore, a geneticist at the National Center for Genome Resources in Santa Fe, N.M., and leader of the new study. The finding “points to some novel environmental trigger that must be very important to the disease. We don’t know what it is.”
But the new study is small; it examines only three pairs of twins and one type of immune cell known to be involved in multiple sclerosis. A telling difference between sickness and health might be found in other types of cells, such as immune cells called B cells or in oligodendrocytes, which are cells that make the nerve cell insulation called myelin, says Esteban Ballestar of the Bellvitge Biomedical Research Institute in Barcelona, Spain. “They are closing a door here, but I think, perhaps, the door should be open,” he says.
In multiple sclerosis the immune system attacks and damages the myelin sheath that helps speed electrical communication between nerves, the equivalent of scraping the coating away from an electrical wire. The damage results in pain and symptoms such as loss of coordination and vision.
In the new study, Kingsmore and his colleagues determined the entire genetic makeup of immune cells called T cells from a pair of female twins. One of the women developed multiple sclerosis at age 30 while her twin remained healthy. The twins are now old enough that the healthy one is not likely to develop the disease.
Identical twins share the same genetic makeup, and the researchers confirmed that both women carried variants of genes already known to increase the risk of getting multiple sclerosis. Scientists had thought that maybe the sick twin had developed an additional mutation in her DNA that finally triggered the disease. But the team found no such mutations.
Another way to rev up the immune system and induce it to attack the body is to increase the activity of certain genes. Upping gene activity doesn’t necessarily involve changing the genes themselves, but can be done by altering chemical tags on the DNA. In two pairs of twins, the team examined more than 2 million DNA locations that had been tagged with a common label, known as a methyl group, that keeps gene activity in check.
In a previous study, Ballestar’s group found lower levels of methylated DNA when they compared people with lupus (SN: 1/16/2010, p.13) to their healthy identical twins. But Kingsmore and his colleagues found no similar differences that could account for just one twin developing MS.
The team also measured gene activity in three sets of identical twins, including the sisters who had their genomes sequenced. The researchers did find some minor differences, but none could explain why one twin got sick and the other didn’t.
Frogs have hopped onto the list of organisms that have had their genetic codes unraveled.
A new study, published April 30 in Science, lays out the genetic blueprint of the Western clawed frog, Xenopus tropicalis. A larger cousin of X. tropicalis, called Xenopus laevis, is a popular laboratory organism for studying development. But with a genome about half the size of X. laevis’, the Western clawed frog has easier DNA to decode, says Uffe Hellsten of the Department of Energy Joint Genome Institute in Walnut Creek, Calif.
Analysis of the Western clawed frog’s genome reveals that versions of 80 percent of genes that have been linked to disease in humans turn up in frogs.
Researchers hope that the genome sequence will help scientists track down the molecular steps that lead to amphibians’ high sensitivity to hormones and other toxins and offer clues to what is causing a worldwide decline of the animals.
People with post-traumatic stress disorder seem to accumulate an array of genetic changes different from those found in healthy people, researchers report online May 3 in the Proceedings of the National Academy of Sciences.
The new findings, while showing differences between people with and without PTSD, don't shed light on whether these differences might play a role in PTSD, says study coauthor Sandro Galea, a physician and epidemiologist at Columbia University in New York City.
Only a fraction of people who witness a traumatic event develop PTSD. In an attempt to identify what makes people who develop PTSD biologically different from those who don’t, Galea and his colleagues obtained blood samples from 100 people in the Detroit area. All had been exposed to at least one potentially traumatic event, and 23 were diagnosed with PTSD. The scientists tested 14,000 genes in these blood samples for chemical changes to DNA that can affect gene activity without altering the genetic information itself.
The researchers focused on the methylation of genes, a process in which a methyl molecule is added to DNA, typically turning off a gene and inhibiting production of the protein that the gene encodes. If people with PTSD have more or less methylation in specific genes, that might somehow contribute to PTSD, Galea says.
The team found that the people with PTSD showed less methylation in several immune system genes and more methylation in genes linked to the growth of brain cells. “There is evidence that PTSD is involved in immune dysfunction, and we suggest that that’s part of a larger process,” Galea says. Although previous studies have also suggested a PTSD link to immune gene activation, the connection is unclear.
“This is interesting data, but there are a lot of things still to do,” says Manel Esteller, a molecular geneticist at the Bellvitge Institute for Biomedical Research in Spain and the University of Barcelona who was not part of the study. “What’s missing is an explanation of how the traumatic stress really causes these changes in methylation — what is the mechanistic link?”
What’s more, the sample size of 23 patients is small, and PTSD diagnosis is tricky, says Naomi Breslau, a sociologist and epidemiologist who studies PTSD at Michigan State University in East Lansing. “I don’t believe this can be taken as a breakthrough.”
Galea agrees that finding the mechanisms involved will be the key to determining whether these methylation differences matter for PTSD. If further research clarifies how these changes play out in the body, he says, “that may allow us to eventually do something about it.”