Join us Friday, May 3, from 11 am to noon EST, for a discussion of attention deficit hyperactivity disorder (ADHD) to help commemorate National Children’s Mental Health Awareness DayExternal Link: Please review our disclaimer. on May 9. NIMH’s own Ben Vitiello, M.D, from the Child and Adolescent Treatment and Preventive Intervention Research Branch, will field questions regarding ADHD in children and teens.
It’s normal for children to be inattentive, hyperactive or impulsive sometimes, but these behaviors are more severe and frequent in children with ADHD. This common mental disorder in children and adolescents continues through adulthood. Although treatments relieve many of the disorder’s symptoms, there is no cure. With treatment, most people with ADHD can be successful in school and lead productive lives. Researchers are developing more effective treatments and interventions, and using new tools such as brain imaging, to better understand the disorder and to find more effective ways to treat and prevent it.
National Children’s Mental Health Awareness Day is a national campaign coordinated by the Substance Abuse and Mental Health Services Administration to increase public awareness that positive mental health is essential for a child’s development. Local, state and federal partners include advocacy groups, government agencies, service organizations, professional groups and affiliates. This year SAMHSA hopes to increase community involvement by engaging local groups in a national conversation about the importance of children's social and emotional well-being. Local groups are also encouraged to offer individuals attending Awareness Day events an opportunity to become a "hero of hope" by making a pledge to take action to help a child or youth.
You can find this discussion under #NIMHchats. An archive of the chat will be posted shortly after the event.
To learn more about these disorders that lead to childhood rapid-onset of OCD, please join us Wednesday, May 8, from 11 am to noon ET for a Twitter chat. Sue Swedo, M.D., and her colleague, Paul Grant, M.D., both at the Pediatrics and Developmental Neuroscience Branch at NIMH, will be online to answer questions. Dr. Swedo and her team were the first to identify PANDAS, and more recently PANS, as a subset of childhood OCD. The chat is part of an ongoing campaign to acknowledge National Children’s Mental Health Awareness DayExternal Link: Please review our disclaimer. and National Mental Health Awareness Month.External Link: Please review our disclaimer.
You can find this discussion under #NIMHchats. An archive of the chat will be posted shortly after the event.
National Children’s Mental Health Awareness Day is a national campaign coordinated by the Substance Abuse and Mental Health Services Administration to increase public awareness of children’s mental health. Positive mental health is essential for a child’s development. Local, state and federal partners include advocacy groups, government agencies, service organizations, professional groups and affiliates. This year SAMHSA hopes to increase community involvement by engaging local groups in a national conversation about the importance of children's social and emotional well-being. Local groups are also encouraged to offer individuals attending Awareness Day events an opportunity to become a "hero of hope" by making a pledge to take action to help a child or youth.
President Barack Obama proclaimed May as National Mental Health Awareness Month. He called upon citizens, government agencies, organizations, health care providers and research institutions to “redouble our efforts to address mental health problems in America.” Tens of millions of Americans are living with a mental health problem yet only half receive available treatment.
Pregnant mothers’ exposure to the flu was associated with a nearly fourfold increased risk that their child would develop bipolar disorder in adulthood, in a study funded by the National Institutes of Health. The findings add to mounting evidence of possible shared underlying causes and illness processes with schizophrenia, which some studies have also linked to prenatal exposure to influenza.
This colorized transmission electron micrograph shows H1N1 influenza virus particles. Surface proteins on the virus particles are shown in black. Source: NIAID
“Prospective mothers should take common sense preventive measures, such as getting flu shots prior to and in the early stages of pregnancy and avoiding contact with people who are symptomatic,” said Alan Brown, M.D., M.P.H, of Columbia University and New York State Psychiatric Institute, a grantee of the NIH’s National Institute of Mental Health (NIMH). “In spite of public health recommendations, only a relatively small fraction of such women get immunized. The weight of evidence now suggests that benefits of the vaccine likely outweigh any possible risk to the mother or newborn.”
Brown and colleagues reported their findings online May 8, 2013 in JAMA Psychiatry.
Although there have been hints of a maternal influenza/bipolar disorder connection, the new study is the first to prospectively follow families in the same HMO, using physician-based diagnoses and structured standardized psychiatric measures. Access to unique Kaiser-Permanente, county and Child Health and Development StudyExternal Link: Please review our disclaimer. databases made it possible to include more cases with detailed maternal flu exposure information than in previous studies.
Among nearly a third of all children born in a northern California county during 1959-1966, researchers followed 92 who developed bipolar disorder, comparing rates of maternal flu diagnoses during pregnancy with 722 matched controls.
The nearly fourfold increased risk implicated influenza infection at any time during pregnancy, but there was evidence suggesting slightly higher risk if the flu occurred during the second or third trimesters. Moreover, the researchers linked flu exposure to a nearly sixfold increase in a subtype of bipolar disorder with psychotic features.
A previous study, by Brown and colleagues, in a related northern California sample, found a threefold increased risk for schizophrenia associated with maternal influenza during the first half of pregnancy. Autism has similarly been linked to first trimester maternal viral infections and to possibly related increases in inflammatory molecules.
“Future research might investigate whether this same environmental risk factor might give rise to different disorders, depending on how the timing of the prenatal insult affects the developing fetal brain,” suggested Brown.
Bipolar disorder shares with schizophrenia a number of other suspected causes and illness features, the researchers note. For example, both share onset of symptoms in early adulthood, susceptibility genes, run in the same families, affect nearly one percent of the population, show psychotic behaviors and respond to antipsychotic medications.
Increasing evidence of such overlap between traditional diagnostic categories has led to the NIMH Research Domain Criteria (RDoC) project, which is laying the foundation for a new mental disorders classification system based on brain circuits and dimensional mechanisms that cut across traditional diagnostic categories.
The research was also funded by NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
Reference
Gestational Influenza and bipolar Disorder in Adult Offspring. Parboosing R, Bao Y, Shen L, Schaefer CA, Brown AS. JAMA Psychiatry, May 8, 2013.
The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website.
The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the NICHD website.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit the NIH website.
In a few weeks, the American Psychiatric Association will release its new edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). This volume will tweak several current diagnostic categories, from autism spectrum disorders to mood disorders. While many of these changes have been contentious, the final product involves mostly modest alterations of the previous edition, based on new insights emerging from research since 1990 when DSM-IV was published. Sometimes this research recommended new categories (e.g., mood dysregulation disorder) or that previous categories could be dropped (e.g., Asperger’s syndrome).1
The goal of this new manual, as with all previous editions, is to provide a common language for describing psychopathology. While DSM has been described as a “Bible” for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been “reliability” – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.
Patients with mental disorders deserve better. NIMH has launched the Research Domain Criteria (RDoC) project to transform diagnosis by incorporating genetics, imaging, cognitive science, and other levels of information to lay the foundation for a new classification system. Through a series of workshops over the past 18 months, we have tried to define several major categories for a new nosology (see below). This approach began with several assumptions:
A diagnostic approach based on the biology as well as the symptoms must not be constrained by the current DSM categories,
Mental disorders are biological disorders involving brain circuits that implicate specific domains of cognition, emotion, or behavior,
Each level of analysis needs to be understood across a dimension of function,
Mapping the cognitive, circuit, and genetic aspects of mental disorders will yield new and better targets for treatment.
It became immediately clear that we cannot design a system based on biomarkers or cognitive performance because we lack the data. In this sense, RDoC is a framework for collecting the data needed for a new nosology. But it is critical to realize that we cannot succeed if we use DSM categories as the “gold standard.”2 The diagnostic system has to be based on the emerging research data, not on the current symptom-based categories. Imagine deciding that EKGs were not useful because many patients with chest pain did not have EKG changes. That is what we have been doing for decades when we reject a biomarker because it does not detect a DSM category. We need to begin collecting the genetic, imaging, physiologic, and cognitive data to see how all the data – not just the symptoms – cluster and how these clusters relate to treatment response.
That is why NIMH will be re-orienting its research away from DSM categories. Going forward, we will be supporting research projects that look across current categories – or sub-divide current categories – to begin to develop a better system. What does this mean for applicants? Clinical trials might study all patients in a mood clinic rather than those meeting strict major depressive disorder criteria. Studies of biomarkers for “depression” might begin by looking across many disorders with anhedonia or emotional appraisal bias or psychomotor retardation to understand the circuitry underlying these symptoms. What does this mean for patients? We are committed to new and better treatments, but we feel this will only happen by developing a more precise diagnostic system. The best reason to develop RDoC is to seek better outcomes.
RDoC, for now, is a research framework, not a clinical tool. This is a decade-long project that is just beginning. Many NIMH researchers, already stressed by budget cuts and tough competition for research funding, will not welcome this change. Some will see RDoC as an academic exercise divorced from clinical practice. But patients and families should welcome this change as a first step towards "precision medicine,” the movement that has transformed cancer diagnosis and treatment. RDoC is nothing less than a plan to transform clinical practice by bringing a new generation of research to inform how we diagnose and treat mental disorders. As two eminent psychiatric geneticists recently concluded, “At the end of the 19th century, it was logical to use a simple diagnostic approach that offered reasonable prognostic validity. At the beginning of the 21st century, we must set our sights higher.”3
The major RDoC research domains:
Negative Valence Systems Positive Valence Systems Cognitive Systems Systems for Social Processes Arousal/Modulatory Systems
1Mental health: On the spectrum. Adam D. Nature. 2013 Apr 25;496(7446):416-8. doi: 10.1038/496416a. No abstract available. PMID: 23619674
For carriers of a BRCA1 mutation, the lifetime risk for invasive breast cancer is 65 per cent. What is that based on? It's based on very large studies of thousands of women. When we're counselling people, we give them average numbers because they're the most robust.
Angelina Jolie said her lifetime risk was 87 per cent, where did that figure come from? That 87 per cent number is from some of the earlier studies. The BRCA1 and BRCA2 genes were discovered in the mid-90s and the earliest research mostly studied very striking families who came to doctors because everybody had cancer. When you look at those families, you're going to make a very high estimate of risk. But then when you do bigger studies, the average risk is lower.
So that 87 per cent figure is probably not a calculation of her personal risk? I am not involved with her care, but I doubt it's a personal assessment. I see that number often and in general think of it as coming from slightly older, smaller studies. Most of us in this field tend to use the newer numbers from the larger studies.
From that 65 per cent average, what makes an individual carrier of a BRCA1 mutation more or less likely to get breast cancer? That's the million-dollar question. There's great interest in understanding why one person with a BRCA1 mutation might develop cancer in their 30s whereas another might never get cancer at all.
But if a woman has a BRCA1 mutation and most of her relatives have developed very early breast cancer, I worry about her a little bit more than a woman in a family with a BRCA1 mutation where, for whatever reason, they don't seem to have as many cancers.
Is there a way to accurately calculate someone's individual lifetime risk of developing invasive breast cancer? I don't think we're quite there yet. The BRCA decision tool we developed makes the average estimate based on large numbers, because that is the safest thing to do.
The tool then compares different options a person might choose. For example, one might choose preventive mastectomy, like Angelina Jolie did; other women might choose a very intensive screening strategy. Our tool helps to compare those different options and what they would provide in terms of survival and quality of life.
Not everyone currently has access to – or can afford – BRCA screening tests. Do you think they should be offered to all women? I'd certainly like to see expanded access to healthcare of all kinds. But I don't think that every woman needs to be tested for BRCA mutations because they're rare. On average, if you pull people in off the street, about one in 400 would carry a BRCA mutation.
But I think when there are red flags – like early breast cancer, multiple breast cancers, ovarian cancer or male breast cancer – all of those families should be offered genetic testing.
As a geneticist specialising in breast cancer, were you glad to see Angelina Jolie share her experience of being someone with a BRCA1 mutation? Absolutely, I think she was extremely courageous. I think it greatly increases the opportunity that we would diagnose people who are at high risk and offer them life-saving interventions. I'm very impressed; it's a very generous thing to do.
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Thomas R. Insel, M.D., Director, NIMH Jeffrey A. Lieberman, M.D., President-elect, APA
NIMH and APA have a shared interest in ensuring that patients and health providers have the best available tools and information today to identify and treat mental health issues, while we continue to invest in improving and advancing mental disorder diagnostics for the future.
Today, the American Psychiatric Association's (APA) Diagnostic and Statistical Manual of Mental Disorders (DSM), along with the International Classification of Diseases (ICD) represents the best information currently available for clinical diagnosis of mental disorders. Patients, families, and insurers can be confident that effective treatments are available and that the DSM is the key resource for delivering the best available care. The National Institute of Mental Health (NIMH) has not changed its position on DSM-5. As NIMH's Research Domain Criteria (RDoC) project website states, "The diagnostic categories represented in the DSM-IV and the International Classification of Diseases-10 (ICD-10, containing virtually identical disorder codes) remain the contemporary consensus standard for how mental disorders are diagnosed and treated."
Yet, what may be realistically feasible today for practitioners is no longer sufficient for researchers. Looking forward, laying the groundwork for a future diagnostic system that more directly reflects modern brain science will require openness to rethinking traditional categories. It is increasingly evident that mental illness will be best understood as disorders of brain structure and function that implicate specific domains of cognition, emotion, and behavior. This is the focus of the NIMH’s Research Domain Criteria (RDoC) project. RDoC is an attempt to create a new kind of taxonomy for mental disorders by bringing the power of modern research approaches in genetics, neuroscience, and behavioral science to the problem of mental illness.
The evolution of diagnosis does not mean that mental disorders are any less real and serious than other illnesses. Indeed, the science of diagnosis has been evolving throughout medicine. For example, subtypes of cancers once defined by where they occurred in the body are now classified on the basis of their underlying genetic and molecular causes.
All medical disciplines advance through research progress in characterizing diseases and disorders. DSM-5 and RDoC represent complementary, not competing, frameworks for this goal. DSM-5, which will be released May 18, reflects the scientific progress seen since the manual's last edition was published in 1994. RDoC is a new, comprehensive effort to redefine the research agenda for mental illness. As research findings begin to emerge from the RDoC effort, these findings may be incorporated into future DSM revisions and clinical practice guidelines. But this is a long-term undertaking. It will take years to fulfill the promise that this research effort represents for transforming the diagnosis and treatment of mental disorders.
By continuing to work together, our two organizations are committed to improving outcomes for people with some of the most disabling disorders in all of medicine.
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The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit the NIH website.
Scientists funded by the National Institutes of Health have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer’s disease. It’s based on unclogging removal of toxic debris that accumulates in patients’ brains, by blocking activity of a little-known regulator protein called CD33.
“Too much CD33 activity appears to promote late-onset Alzheimer’s by preventing support cells from clearing out toxic plaques, key risk factors for the disease,” explained Rudolph TanziExternal Link: Please review our disclaimer., Ph.D., of Massachusetts General Hospital and Harvard University, a grantee of the NIH’s National Institute of Mental Health (NIMH) and National Institute on Aging (NIA). “Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.”
Tanzi and colleagues report on their findings April 25, 2013 in the journal Neuron.
“These results reveal a previously unknown, potentially powerful mechanism for protecting neurons from damaging toxicity and inflammation,” said NIMH Director Thomas R. Insel, M.D. “Given increasing evidence of overlap between brain disorders at the molecular level, understanding such workings in Alzheimer’s disease may also provide insights into other mental disorders.”
Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer’s-affected families, reported by Tanzi and colleagues in 2008. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer’s, the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.
They found over-expression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset Alzheimer’s disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid protein and plaques – damaging debris – had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from Alzheimer’s conspicuously showed reduced amounts of CD33 on the surface of microglia and less beta-amyloid.
Brain levels of beta-amyloid and plaques were also markedly reduced in mice engineered to under-express or lack CD33. Microglia cells in these animals were more efficient at clearing out the debris, which the researchers traced to levels of CD33 on the cell surface.
Evidence also suggested that CD33 works in league with another Alzheimer’s risk gene in microglia to regulate inflammation in the brain.
The study results – and those of a recent rat study that replicated many features of the human illness – add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer’s pathology. They come at a time of ferment in the field, spurred by other recent contradictory evidenceExternal Link: Please review our disclaimer. suggesting that these presumed culprits might instead play a protective role.
Since increased CD33 activity in microglia impaired beta-amyloid clearance in late onset Alzheimer’s, Tanzi and colleagues are now searching for agents that can cross the blood-brain barrier and block it.
Activity of a regulator protein called CD33 (green) clogs removal of brain-damaging debris, beta-amyloid protein (red), by support cells, microglia. Left: Microglia of normal control mice (A”) show more CD33 and less beta-amyloid than mice in which CD33 expression is experimentally knocked-out (B”). Right: Little beta-amyloid can be seen in microglia of a mouse line in which CD33 is over-expressed (C”), compared to microglia of mice in which CD33 is experimentally inactivated (D”). Evidence from post-mortem human brains indicates that CD33 is similarly over-active in Alzheimer’s disease, suggesting that a treatment that impedes it might help treat or prevent the disease. Source: Rudolph Tanzi, Ph.D.External Link: Please review our disclaimer., of Massachusetts General Hospital and Harvard University
NIH-funded scientists have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer’s disease. It’s based on unclogging removal of toxic debris that accumulates in patients’ brains, by blocking activity of a little-known regulator protein called CD33. Too much CD33 activity may promote late-onset Alzheimer’s by preventing support cells from clearing out toxic plaques. Future medications that impede CD33 activity might help prevent or treat the disorder. Dr. Thomas Lehner, director of NIMH’s Office of Genomics Research Coordination, explains the significance of the new findings. Credits: Microglia photo -- Sam Listwak, Ph.D., Miles Herkenham, Ph.D., NIMH Section on Functional Neuroanatomy CD33 photo -- Rudolph Tanzi, Ph.DExternal Link: Please review our disclaimer., Massachusetts General Hospital and Harvard University Video animation – National Institute on Aging, National Human Genome Research Institute
Alzheimer’s disease risk gene CD33 inhibits microglial uptake of amyoid beta. Griciuc A, Serrano-Pozo A, Parrado AR, Lesinski AN, Asselin CN, Mullin K, Hooli B, Choi SH, Hyman BT, Tanzi RE. Neuron, April 25, 2013.
The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website.
The NIA leads the federal government effort conducting and supporting research on aging and the health and well-being of older people. It provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer’s Disease Education and Referral (ADEAR) Center at http://www.nia.nih.gov/Alzheimers. For expanded information on Alzheimer’s care and resources, please visit the federal government’s portal website http://www.alzheimers.govExternal Link: Please review our disclaimer.. Information on health and on aging generally can be found at http://www.nia.nih.gov. To sign up for e-mail alerts about new findings or publications, please visit either NIA website.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit the NIH website.
A rethink is needed in terms of how we view mental illness, stated National Institute of Mental Health Director Thomas Insel, M.D., in a recent TEDx talkExternal Link: Please review our disclaimer. at the California Institute of Technology (Caltech) in Pasadena.
Deaths from medical causes such as leukemia and heart disease have decreased over the past 30 years. The same cannot be said of the suicide rate, which has remained the same. A vast majority of suicides—90 percent—are related to mental illnesses such as depression and schizophrenia.
Insel believes part of the problem is that mental illness is referred to either as a mental or behavioral disorder. “We need to think of these as brain disorders,” he said, adding that for these brain disorders, behavior is the last thing to change.
Insel walked the audience through recent advances in neuroscience, including the Human Connectome, which indicates that mental illness may be more of a neuronal connection or circuit disorder. The earlier these circuits are identified, he said, the earlier preventive treatments could be used to save the lives of people with mental illnesses.
“If we waited for the ‘heart attack,’ we would be sacrificing 1.1 million lives every year in this country,” he said. “That is precisely what we do today when we decide that everyone with one of these brain disorders, brain circuit disorders, has a behavior disorder. We wait until the behavior emerges. That’s not early detection, that’s not early prevention.”
Brief episodes of stress could be good for us, protecting us from the effects of ageing – as long as we're not too frazzled to begin with. That's the surprise finding of a study measuring stress-related damage inside cells.
One reason for this is that the body responds to stress by burning fuel to release energy. While this helps us respond to a threat, it also swamps cells with toxic free radicals produced during metabolism. Switched on long-term, this response damages DNA, RNA and other molecules, ageing us before our time.
Kirstin Aschbacher of the University of California, San Francisco, and her colleagues wanted to test whether a short period of intense stress is more damaging if we are already living through a stressful period. They took a group of women chronically stressed by caring for close relatives with dementia, and made them give a speech in front of a sceptical panel of judges. A group of unstressed women performed the same task to act as a control group.
The researchers asked the women to say how stressful they found the test. They also measured their levels of the stress hormone cortisol, plus biochemical markers of damage inside their cells.
Unexpected effect
For the stressed women, the extra challenge indeed proved particularly harmful: the threat of the test caused more cellular damage than in the non-stressed controls. Perhaps more intriguing, though, was an unexpected effect Aschbacher and her colleagues found within the control group.
Among these normally relaxed women, those who found the task moderately stressful had lower levels of cellular damage than those who did not find it stressful at all. In other words, while chronic stress can have knock-on effects that damage cellular structures, short bursts of stress can reduce such damage and protect our health in some circumstances.
The idea that being under pressure helps to focus attention and makes us better at cognitive tasks has been around for almosta century. But Aschbacher's study is a first step to showing how it can sometimes make us physically healthier as well – although exactly what is going on at the cellular level to explain the result is still unclear.
"It's like weightlifting, where we build muscles over time," says Aschbacher. As long as there is time to recover in between, short bursts of psychological stress "might allow us to become stronger".
Bruce McEwen, who studies the physiology of stress at the Rockefeller University in New York City, describes the research as "provocative", and says it is starting to untangle the mechanisms by which stress can have positive effects. "Mother Nature put these things there to help us adapt and survive," he says.
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Your article on my research into the environmental and genetic factors that cause high rates of mesothelioma in the Turkish region of Cappadocia was excellent (13 April, p 34).
But contrary to your headline, the Cappadocian villagers are not "the damned". There are reasons for these proud, religious and dignified people to be optimistic.
I hope that in Cappadocia the incidence of mesothelioma caused by the local mineral erionite will decrease and possibly disappear thanks to a new erionite-free village built in response to our findings. We are also identifying new mesothelioma biomarkers and developing more sensitive tests for early diagnosis and better therapies; I anticipate profound positive impacts for those with the condition.
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