Archive for July 27th, 2012

The Great DSM Hoax


I have been reading Marilyn Wedge’s excellent Pills Are Not for Preschoolers and it moved me to write again about the extent to which the DSM, the “diagnostic manual” used by the psychotherapeutic professional class, is an utter hoax.

You may be familiar with complaints surrounding the American Psychiatric Association’s DSM as those complaints have mounted in recent months in connection with the imminent appearance of the next version of the DSM, the DSM-V, which is scheduled to appear in 2013. In that volume a slew of new “mental disorders,” created out of whole cloth for profit, will appear. Many people, including thousands of mental health professionals, have pushed back. But too few are willing to call the whole thing the hoax it is.

The DSM is a disease-mongering naming game where collections of disparate painful thoughts and feelings and unwanted or distressing behaviors are given profit-seeking labels. That is all the DSM does. It tells a story about life, that behaviors like restlessness and feelings like sadness are medical problems, without ever announcing its premises or its motives. It doesn’t just name or label: it imputes. By calling sadness “depression” or restlessness “attention deficit disorder” it secretly imputes biological causes for which there is no evidence. They want us to believe that biological abnormality is at play, so that they can prescribe drugs, without having to frankly say that there are biological abnormalities at play, which might require that they prove their assertions.  

It is one thing to say that when you see the numeral 2 you are to call it “two.” It is a rather similar thing to say that when you see a bird with feathers of this color and a beak of this sort you are to call it an oriole. That is simple naming for the sake of communication and convenience. But when you assert that when you see an oak, a rose, or a giraffe you are to call them “God’s handiwork,” that is not naming. That is imputing. That is telling a loaded story under the guise of naming. The DSM, which has sometimes been criticized as a naturalist’s guide to mental disorders, is far worse than that. It doesn’t just name: it imputes causes it is completely unjustified in ascribing.

Calling the sadness you feel because your parents are fighting or calling your entirely understandable boredom at school a “mental disorder” is not just naming. The causes of your “disorder” are being ascribed without anyone saying anything overt. The DSM tells a secret, silent, never-explained story as it gets from “a restless child who gets up six times at school but never gets up when he visits his grandmother who lets him play video games” to “attention deficit disorder.” How did it get there? Just by using language in a way that too many people find plausible and seductive.

You will agree that a label like “attention deficit disorder” seems to be positing some biological malfunctioning? Yet the American Psychiatric Association’s own current definition of a mental disorder contains not a word about biology, defining a mental disorder as a “psychological or behavioral syndrome.” It is rather amazing that in the definition of a mental disorder the psychotherapeutic professional class admits that they do not believe for an instant that there are biological irregularities going on, even though their labels are imputing precisely those causes.

They probably feel free to admit it there, in the definition of a “mental disorder,” because they know that no one, not even members of their professional class, will ever actually look at the definition. So they are safe in admitting a bit of the truth there. Then, when questioned in Heaven, they will be able to say, “Look we never said that this has anything to do with biology. We can’t help it that people thought we did and that they thought that because we were prescribing medication that there was something biologically wrong with them. That’s their fault, not ours. Look, we clearly defined a ‘mental disorder’ as a ‘psychological or behavioral syndrome.’ We never said that biology was involved. We have no clue where they got that idea.”

For indeed the current definition of “mental disorder” says nothing about biology. Ah, but perhaps because of the scrutiny being put on the DSM-V creators, who maybe now fear that someone will actually look at their definition, they have proposed a massive change to the definition of “mental disorder” to include biology. They intend it now to read: “A Mental Disorder is a health condition characterized by significant dysfunction in an individual’s cognitions, emotions, or behaviors that reflects a disturbance in the psychological, biological, or developmental processes underlying mental functioning.”

One might sensibly ask: what, did you forget to include “biology” in the current definition, in the one that every mental health provider supposedly is using right this minute? Did “biology” escape your mind or your notice? Did you have a “blind-to-biology disorder”? And are you now saying that the current definition, which makes no mention of biology, is untrue? Are you saying that it is a mistake? If it is a mistake, is it not dangerous and perhaps even actionable to let it just stand? Please tell us which one is right!  

Just ask yourself: how can you drop “biology” into the definition of a “mental disorder” as if you had added a comma or a semi-colon? Either the current definition is incorrect or the prospective definition is incorrect. They can’t both be correct. They can indeed both be incorrect, and they are, but they can’t both be correct. So which is the correct one, DSM creators, and what is your justification for dubbing the one correct and the other incorrect? Have you just “changed your mind,” as your predecessors did when they changed their mind about homosexuality being a mental disorder?    

Is the proposed definition of a “mental disorder” a truer definition than the previous one? No, it is the same hoax: and in fact the creators of the DSM blithely announce that they are unconcerned about whether or not their definition of a “mental disorder” is true. They explain that “The diagnosis of a mental disorder should have clinical utility,” not that it should be true. There you go. Since they do not mean by clinical utility that a diagnosis be either valid or reliable, they must mean that it be profitable.

In fact, tellingly enough, as a prospective client you do not to meet their own proposed criteria in order to receive treatment. They explain: “Clinicians may thus encounter individuals who do not meet full criteria for a mental disorder, but who demonstrate a clear need for treatment or care. The fact that some individuals do not show all symptoms indicative of a diagnosis in these individuals should not be used to justify limiting their access to appropriate care.”

Wow! Isn’t that a clever sentence? Orwell would have loved it. This translates as: “We say that we are using this manual to diagnose you but since our labeling scheme is a hoax and our criteria are trumped up to begin with, it certainly doesn’t matter to us whether you meet them or not—we are happy to medicate you simply by virtue of you having walked through the door.”

There can be no real change in this procedure until politicians intervene; and they will not intervene because of the power of Big Pharma. Perhaps when some senator notices that her six-year-old son, who is on an antidepressant, an anticonvulsant, and an antipsychotic, has suffered a psychotic break that will cost him his whole adult life, she will be moved to say, “I don’t care how much Big Pharma is paying me, I’m sick of this lie.” Perhaps then some questions will get asked by people with the clout to demand real answers. Until then the hoax will continue.   

**

Eric Maisel, Ph.D., is a psychotherapist, bestselling author of 40 books, and widely regarded as America’s foremost creativity coach. His latest book is Rethinking Depression: How to Shed Mental Health Labels and Create Personal Meaning (New World Library, February, 2012) and is available here. Dr. Maisel is the founder of natural psychology, the new psychology of meaning. Please visit Dr. Maisel at http://www.ericmaisel.com or contact him at ericmaisel@hotmail.com. You can learn more about natural psychology at http://www.infinitemeaningclass.com.

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Fluoxetine — a.k.a., Prozac — is effective as an anti-viral, study suggests


ScienceDaily (July 27, 2012) — UCLA researchers have come across an unexpected potential use for fluoxetine — commonly known as Prozac — which shows promise as an antiviral agent. The discovery could provide another tool in treating human enteroviruses that sicken and kill people in the U.S. and around the world.

Human enteroviruses are members of a genus containing more than 100 distinct RNA viruses responsible for various life threatening infections, such as poliomyelitis and encephalitis. While immunization has all but eliminated the poliovirus, the archetype for the genus, no antiviral drugs currently exist for the treatment of enterovirus infections, which are often severe and potentially fatal. In view of its favorable pharmacokinetics and safety profile of fluoxetine — which is in a class of compounds typically used in the treatment of depression, anxiety disorders and some personality disorders — the research team found that it warrants additional study as a potential antiviral agent for enterovirus infections.

Using molecular screening, the UCLA research team from the Department of Pediatrics, the California NanoSystems Institute and the Department of Molecular and Medical Pharmacology found that fluoxetine was a potent inhibitor of coxsackievirus replication. This is one of the viruses that include polio and echovirus that is found in the gastrointestinal tract. Exposure to the virus causes other opportunistic infections and diseases.

“The discovery of unexpected antiviral activity of fluoxetine is scientifically very significant and draws our attention to previously overlooked potential targets of fluoxetine and other psychogenic drugs,” said Robert Damoiseaux, scientific director of the Molecular Screening Shared Resource at the California NanoSystems Institute. “Part of our follow-up work will be the discovery of these unconventional targets for fluoxetine and other drugs of the same class and how these targets intersect with the known targets of this drug class.”

Paul Krogstad, professor of pediatrics and molecular and medical pharmacology, added that understanding the mechanisms of action of fluoxetine and norfloxetine against coxsackieviruses “will add to our understanding of enterovirus replication and lead to assessment of their potential clinical utility for the future treatment of serious enterovirus infections.”

The research team found that fluoxetine did not interfere with either viral entry or translation of the viral genome. Instead, fluoxetine and norfluoxetine markedly reduced the production of viral RNA and protein.

The study was published on July 2 in the journal of Antimicrobial Agents and Chemotherapy. Study authors also include Jun Zuo, Kevin K. Quinn, Steve Kye, and Paige Cooper from the Department of Pediatrics. The study was supported by grants from the Today’s and Tomorrow’s Children’s Fund and the UCLA Department of Pediatrics Nanopediatrics Program.

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The above story is reprinted from materials provided by University of California – Los Angeles. The original article was written by Jennifer Marcus.

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Journal Reference:

  1. J. Zuo, K. K. Quinn, S. Kye, P. Cooper, R. Damoiseaux, P. Krogstad. Fluoxetine is a Potent Inhibitor of Coxsackievirus Replication. Antimicrobial Agents and Chemotherapy, 2012; DOI: 10.1128/AAC.00983-12

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Tumor cells’ inner workings predict cancer progression


ScienceDaily (July 27, 2012) — Using a new assay method to study tumor cells, researchers at the University of California, San Diego School of Medicine and UC San Diego Moores Cancer Center have found evidence of clonal evolution in chronic lymphocytic leukemia (CLL). The assay method distinguishes features of leukemia cells that indicate whether the disease will be aggressive or slow-moving, a key factor in when and how patients are treated.

The findings are published in the July 26, 2012 First Edition online issue of Blood.

The progression of CLL is highly variable, dependent upon the rate and effects of accumulating monoclonal B cells in the blood, marrow, and lymphoid tissues. Some patients are symptom-free for years and do not require treatment, which involves the use of drugs that can cause significant side effects and are not curative. In other patients, however, CLL is relatively aggressive and demands therapeutic intervention soon after diagnosis.

“Our study shows that there may not be a sharp dividing line between the more aggressive and less aggressive forms of CLL,” said Thomas J. Kipps, MD, PhD, Evelyn and Edwin Tasch Chair in Cancer Research and senior author of the study. “Instead, it seems that over time the leukemia cells of patients with indolent disease begin to use genes similar to those that are generally used by CLL cells of patients with aggressive disease. In other words, prior to requiring therapy, the patterns of genes expressed by CLL cells appear to converge, regardless of whether or not the patient had aggressive versus indolent disease at diagnosis.”

Existing markers for aggressive or indolent disease are mostly fixed and have declining predictive value the longer the patient is from his or her initial diagnosis. When the blood sample is collected, these markers cannot reliably predict whether a CLL patient will need therapy soon, particularly when the patient has had the diagnosis of CLL for many years.

Kipps and colleagues studied thousands of genes, particularly those that code for proteins, in a group of 130 CLL patients with varying risks of disease progression. They identified 38 prognostic subnetworks of interacting genes and proteins that, at the time of sample collection, indicate the relative the aggressiveness of the disease and predict when the patient will require therapy. They confirmed their work using the method on two other, smaller CLL patient cohorts in Germany and Italy.

The subnetworks offer greater predictive value because they are based not on expression levels of individual genes or proteins, but on how they dynamically interact and change over time, influencing the course of the CLL and patient symptoms.

“In a sense, we looked at families rather than individuals,” said Kipps. “If you find in an interconnected family where most genes or proteins are expressed at higher levels, it becomes more likely that these genes and proteins have functional significance.”

He added that while the subnetworks abound in data, their complexity actually makes them easy to interpret and understand. “It’s like when you look out of a window and see the sky, clouds, trees, people, cars. You’re getting tremendous amounts of information that individually doesn’t tell you much. But when you look at the scene as a whole, you see patterns and networks. This work is similar. We’re taking all of the individual gene expression patterns and making sense of them as a whole. We’re more able to more clearly see how they control and regulate function.”

The findings help define how CLL — and perhaps other cancers — evolve over time, becoming more aggressive and deadly. “It’s as if each tumor has a clock which determines how frequently it may acquire the chance changes that make it behave more aggressively. Although the rates can vary, it appears that tumors march down similar pathways, which converge over time to a point where they become aggressive enough to require therapy.”

The study may alter how scientists think about CLL and how clinicians treat the disease: whether it is better to wait for later stages of the disease when tumor cells are more fragile and easier to kill, or treat early-stage indolent tumor cells aggressively, when they are fewer in number but harder to find and more resistant to therapy.

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The above story is reprinted from materials provided by University of California – San Diego, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Han-Yu Chuang, Laura Rassenti, Michelle Salcedo, Kate Licon, Alexander Kohlmann, Torsten Haferlach, Robin Foà, Trey Ideker, and Thomas J. Kipps. Subnetwork-based analysis of chronic lymphocytic leukemia identifies pathways that associate with disease progression. Blood, July 26, 2012 DOI: 10.1182/blood-2012-03-416461

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Novel therapy may prevent damage to the retina in diabetic eye diseases


ScienceDaily (July 27, 2012) — Researchers at the University of Michigan Kellogg Eye Center have identified a compound that could interrupt the chain of events that cause damage to the retina in diabetic retinopathy. The finding is significant because it could lead to a novel therapy that targets two mechanisms at the root of the disease: inflammation and the weakening of the blood barrier that protects the retina.

To date, treatments for diabetic retinopathy, the leading cause of blindness among working-age Americans, have been aimed largely at one of those mechanisms.

In diabetic retinopathy, damage to the retina results, in part, from the activity of vascular endothelial growth factor (VEGF), a protein that weakens the protective blood-retinal barrier. Recent drugs targeting VEGF have exhibited good response for nearly half of the patients with diabetic retinopathy. But researchers believe that there is also an inflammatory component that may contribute to the disease process.

The study, published in the Biochemical Journal, June 2012 [epub ahead of print] identifies a specific protein common to both pathways as an important target in regulating the disease process in which blood vessels become leaky, and provides a drug that may be developed into a therapeutic intervention for patients in which anti-VEGF treatment alone is not sufficient.

“In diabetic retinopathy and a host of other retinal diseases, increases in VEGF and inflammatory factors — some of the same factors that contribute to the response to an infection — cause blood vessels in the eye to leak which, in turn, results in a buildup of fluid in the neural tissue of the retina,” says David A. Antonetti, Ph.D., Professor, Department of Ophthalmology and Visual Sciences and Molecular and Integrative Physiology, who has also been awarded a Jules and Doris Stein Professorship from Research to Prevent Blindness. “This insidious form of modified inflammation can eventually lead to blindness.”

The compound targets atypical protein kinase C (aPKC), required for VEGF to make blood vessels leak. Moreover, Antonetti’s laboratory has demonstrated that the compound is effective at blocking damage from tumor necrosis factor also elevated in diabetic retinopathy that comprises part of the inflammation. Benefits of this compound could extend to therapies for uveitis, or changes to the brain blood vessels in the presence of brain tumors or stroke.

“This is a great leap forward,” says Antonetti. “We’ve identified an important target in regulating blood vessel leakage in the eye and we have a therapy that works in animal models. Our research is in the early stages of development. We still have a long way to go to demonstrate effectiveness of this compound in humans to create a new therapy but the results are very promising.”

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The above story is reprinted from materials provided by University of Michigan Health System, via Newswise.

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Journal Reference:

  1. Paul Titchenell, Cheng-Mao Lin, Jason Keil, Jeffrey Sundstrom, Charles Smith, David Antonetti. Novel Atypical PKC Inhibitors Prevent Vascular Endothelial Growth Factor-Induced Blood-Retinal Barrier Dysfunction. Biochemical Journal, 2012; DOI: 10.1042/BJ20111961

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Researchers find link between childhood abuse and age at menarche


ScienceDaily (July 27, 2012) — Researchers from Boston University School of Medicine (BUSM) have found an association between childhood physical and sexual abuse and age at menarche. The findings are published online in the Journal of Adolescent Health.

Researchers led by corresponding author, Renée Boynton-Jarrett, MD, assistant professor of pediatrics at BUSM, found a 49 percent increase in risk for early onset menarche (menstrual periods prior to age 11 years) among women who reported childhood sexual abuse compared to those who were not abused. In addition, there was a 50 percent increase in risk for late onset menarche (menstrual periods after age 15 years) among women who reported severe physical abuse in childhood. The participants in the study included 68,505 women enrolled in the Nurses’ Health Study II, a prospective cohort study.

“In our study child abuse was associated with both accelerated and delayed age at menarche and importantly, these associations vary by type of abuse, which suggest that child abuse does not have a homogenous effect on health outcomes,” said Boynton-Jarrett. “There is a need for future research to explore characteristics of child abuse that may influence health outcomes including type, timing and severity of abuse, as well as the social context in which the abuse occurs.”

Child abuse is associated with a significant health burden over the life course. Early menarche has been associated with risks such as cardiovascular disease, metabolic dysfunction, cancer and depression, while late menarche has been associated with lower bone mineral density and depression.

“We need to work toward better understanding how child abuse influences health and translate these research findings into clinical practice and public health strategies to improve the well-being of survivors of child abuse,” added Boynton-Jarrett.

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The above story is reprinted from materials provided by Boston University Medical Center, via EurekAlert!, a service of AAAS.

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Journal Reference:

  1. Renée Boynton-Jarrett, Rosalind J. Wright, Frank W. Putnam, Eileen Lividoti Hibert, Karin B. Michels, Michele R. Forman, Janet Rich-Edwards. Childhood Abuse and Age at Menarche. Journal of Adolescent Health, 2012; DOI: 10.1016/j.jadohealth.2012.06.006

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Adolescent Girls More Likely To Be Depressed Than Boys


Editor’s Choice
Main Category: Depression
Also Included In: Pediatrics / Children’s Health
Article Date: 27 Jul 2012 – 9:00 PDT

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In the past year, the percentage of girls aged 12 and 15 years who experienced a major depressive episode has tripled from 5.1% to 15.2%, according to a report by the Substance Abuse and Mental Health Services Administration (SAMHSA).

The report, which is based on combined data from the 2008 to 2010 SAMHSA National Survey on Drug Use and Health (NSDUH), also revealed that each year, an average of 1.4 million adolescent girls aged between 12 to 17 years suffers from a major depressive episode, which is three times higher, i.e. 12% than the risk of their male counterparts (4.%). The NSDUH is a scientifically conducted annual US-wide survey that involves around 67,500 individuals above the age of 12 years.

According to criteria listed in its Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), the American Psychiatric Association has defined a major depressive episode as a person suffering a period of depressed mood or loss of interest/pleasure that lasts 2 weeks or longer, in addition to suffering from at least four other symptoms that indicate a change in functional behavior, including sleeping problems, problems with eating, concentration, energy and with their self-image.

Pamela S. Hyde, SAMHSA Administrator, states:

“It is crucial that we provide adolescent girls the coping skills and social supports they need to avoid the onset of depression, and to offer behavioral health services that foster resilience and recovery if they experience it. These efforts are a sound investment in girls’ health and well-being and in our nation’s future.”

SAMHSA provides various successful programs designed to effectively promote the recovery of adolescent girls suffering from depression. One of their programs, the Child Mental Health Initiative, offers everyone with regular contact to young people, including parents, family members, teachers, coaches, friends, etc., comprehensive and coordinated services and care across all of the systems. The program has been successful in considerable reducing depression rates in young adults, helping them to lead full and productive lives.

Another key finding in the report showed that older adolescent girls with major depressive episodes tended to receive more treatment than their younger peers, with around two fifth of girls aged 15 to 17 years receiving therapy compared with only one thirds of those in the 12 to 14-age group.

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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The longer you’re awake, the slower you get


ScienceDaily (July 27, 2012) — Anyone that has ever had trouble sleeping can attest to the difficulties at work the following day. Experts recommend eight hours of sleep per night for ideal health and productivity, but what if five to six hours of sleep is your norm? Is your work still negatively affected? A team of researchers at Brigham and Women’s Hospital (BWH) have discovered that regardless of how tired you perceive yourself to be, that lack of sleep can influence the way you perform certain tasks.

This finding is published in the July 26, 2012 online edition of The Journal of Vision.

“Our team decided to look at how sleep might affect complex visual search tasks, because they are common in safety-sensitive activities, such as air-traffic control, baggage screening, and monitoring power plant operations,” explained Jeanne F. Duffy, PhD, MBA, senior author on this study and associate neuroscientist at BWH. “These types of jobs involve processes that require repeated, quick memory encoding and retrieval of visual information, in combination with decision making about the information.”

Researchers collected and analyzed data from visual search tasks from 12 participants over a one month study. In the first week, all participants were scheduled to sleep 10-12 hours per night to make sure they were well-rested. For the following three weeks, the participants were scheduled to sleep the equivalent of 5.6 hours per night, and also had their sleep times scheduled on a 28-hour cycle, mirroring chronic jet lag. The research team gave the participants computer tests that involved visual search tasks and recorded how quickly the participants could find important information, and also how accurate they were in identifying it. The researchers report that the longer the participants were awake, the more slowly they identified the important information in the test. Additionally, during the biological night time, 12 a.m. -6 a.m., participants (who were unaware of the time throughout the study) also performed the tasks more slowly than they did during the daytime.

“This research provides valuable information for workers, and their employers, who perform these types of visual search tasks during the night shift, because they will do it much more slowly than when they are working during the day,” said Duffy. “The longer someone is awake, the more the ability to perform a task, in this case a visual search, is hindered, and this impact of being awake is even stronger at night.”

While the accuracy of the participants stayed the fairly constant, they were slower to identify the relevant information as the weeks went on. The self-ratings of sleepiness only got slightly worse during the second and third weeks on the study schedule, yet the data show that they were performing the visual search tasks significantly slower than in the first week. This finding suggests that someone’s perceptions of how tired they are do not always match their performance ability, explains Duffy.

This research was supported by NIH grant P01 AG09975 and was conducted in the BWH CCI, part of the Harvard Catalyst Clinical and Translational Science Center (UL1 RR025758-01), formerly a GCRC (M01RR02635). Development and implementation of the visual search task was supported in part by NIH grant R21 AT002571. JFD was supported in part by the BWHBRI Fund to Sustain Research Excellence; MM was supported by fellowships from the La-Roche and Novartis Foundations (Switzerland) and Jazz Pharmaceuticals (USA); SWC was supported in part by a fellowship from the Natural Sciences and Engineering Research Council of Canada.

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The above story is reprinted from materials provided by Brigham and Women’s Hospital.

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Journal Reference:

  1. Marc Pomplun, Edward J. Silva, Joseph M. Ronda, Sean W. Cain, Mirjam Y. Münch, Charles A. Czeisler, and Jeanne F. Duffy. The effects of circadian phase, time awake, and imposed sleep restriction on performing complex visual tasks: Evidence from comparative visual search. The Journal of Vision, July 26, 2012 DOI: 10.1167/12.7.14

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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