The Diagnostic and Statistical Manual of Mental Disorders (DSM), long the master reference work in psychiatry, is seriously flawed and needs radical change from its current “field guide” form, according to an essay by two Johns Hopkins psychiatrists published in the May 17 issue of the New England Journal of Medicine.

“A generation ago it served useful purposes, but now it needs clear alterations,” says Paul R. McHugh, M.D., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and co-author of the paper with Phillip R. Slavney, M.D., a professor emeritus in the same department. “They say they can’t do any better. We disagree and can show how.”

The original DSM, published in the 1950s, was intended as a public health service documenting the incidence and prevalence of mental illnesses. By its third edition in 1980 (DSM-III), however, it had evolved into a reference book prescribing how clinicians should identify and classify psychiatric disorders.

Today, the Johns Hopkins psychiatrists say, DSM provides checklists of symptoms, offering few clues to the underlying causes of mental disease and making it difficult to direct treatment or investigate the disorders it details. A new edition, DSM-5, is due out in 2013.

The manual, put together by the American Psychiatric Association, currently identifies hundreds of conditions via lists of diagnostic criteria and symptoms, functioning exactly as does a naturalist’s field guide but for mental illness. It offers no way to make sense of mental disorders and no way to distinguish illnesses that appear to be similar but actually are quite different and require different treatments, the psychiatrists argue.

“If you just name things and don’t explain what the causes are, you do not know how to rationally treat or study the diseases,” says McHugh, former director of Hopkins’ psychiatry department. “The DSM gives everything a name but not a nature.”

Before DSM-III, McHugh and Slavney say, psychiatrists typically used a “bottom-up” method of diagnosis, based on a detailed life history, painstaking examination of mental status and corroboration from third parties. The new emphasis on symptoms, they say, has unfortunately encouraged a cursory “top-down” method that relies on checklists and ignores much of the narrative of the patients’ lives.

The causes of psychiatric disorders derive from four interrelated but separable categories: brain diseases, personality dimensions, motivated behaviors and life encounters, write McHugh and Slavney. The two physicians suggest that organizing mental illnesses based on these four causalities would “promote fruitful thought and, consequently, progress.”

“Psychiatrists would start moving toward the day when they address psychiatric disorders in the same way that internists address physical disorders, explaining the clinical manifestations as products of nature to be comprehended not simply by their outward show but by the causal processes and generative mechanisms that provoke them,” they write. “Only then will psychiatry come of age as a medical discipline and a field guide cease to be its master work.”

ᔥJohns Hopkins Medicine

Doctors for the Family’s claims aren’t based on scientific evidence. Flickr/Poes In Boots

The evidence is clear that children who grow up in a family with a mother and a father do better in all parameters than children without.” That’s according to the Doctors for the Family’s submission to the Senate Inquiry into Marriage Equality. And it’s rightly generated a lot of criticism over the past few days.

It’s unfortunate that a group of 150 doctors, which doesn’t represent the academic consensus on the issue, has been given such a high profile. The Conversation’s medical blogger, Michael Vagg, has already critiqued the sources of the group’s so-called “evidence”. But what does the research really show?

We need only look back to 2007 to find a review by the Australian Psychological Society. The academic literature on lesbian, gay, bisexual and transgendered families states that the “research does not support negative assumptions about the experiences or outcomes of children of lesbian mothers.”

This view was foreshadowed by the American Academy of Pediatrics which concluded in 2002 that there was no systematic difference in the psychological well-being of children with same-sex attracted parents. It’s the quality and type of relationship – both between and with parents – that matters most.

Kids with same-sex parents tend to have better relationships with their parents than heterosexual families. nettsu

Kids with same-sex parents tend to have better relationships with their parents than heterosexual families. nettsu

A synthesis of research from numerous studies followed in 2004 and suggested that parent-child relationships were slightly better in same-sex families.

Longitudinal research from the United Kingdom has shown that social acceptance, close friendships and peer relationships were no different for children with lesbian mothers when compared with other families. And population-based studies from the United States have even suggested that these children were more connected at school.

This is just a snapshot of a continuing body of research. Critics highlight the small sample sizes across all these studies and the almost universal focus on lesbian mothers. What’s needed now is a broader approach that accurately reflects the complex issues at play and incorporates all forms of parenting by same-sex attracted people.

That’s what we’re aiming to do with the Australian Study of Child Health in Same-Sex Families. For the first time we’re capturing the complete physical, mental and social well-being of up to 750 children with at least one same-sex attracted parent. We’re currently recruiting families with children aged under 18 where at least one parent identifies as being same-sex attracted. So this includes bisexual and transgender parents.

Our research is not about marriage equality; although the stability that this might bring to same-sex families can only be a good thing. Our study is about optimising the health and well-being of children and aims to provide a strong evidence base from which this can be achieved.

Doctors for the Family's submission to the Senate Inquiry into Marriage Equality isn't based on evidence. nettsu

As public health researchers, we recognise the weight of evidence that demonstrates children with same-sex attracted parents are generally doing very well. But we also acknowledge concerns about the impact that stigma and discrimination could potentially have on these children. In countries where there’s a lot of perceived stigma – most notably, the United States – children face definite challenges coping with homophobic attitudes.

Groups such as Doctors for the Family only serve to propagate such stigma and discrimination. Contrary to their stated objective to “ensure a healthy future for our children,” they’re harming the very people they claim to protect.

As doctors, we’re trained to critically appraise evidence. And it’s our responsibility to present this information, in a balanced manner, to the public. To state that there is clear evidence that children who grow up in a family with a mother and a father do better in all parameters than children without is failing in this duty.

If you’re interested in being part of the Australian Study of Child Health in Same-Sex Families, please email me at admin@achess.org.au or visit our website. The study is part of the Jack Brockhoff Child Health and Wellbeing Program at the McCaughey VicHealth Centre in the Melbourne School of Population Health.

This article was originally published at The Conversation.
Read the original article.

A powerful and moving video ~ Michael French has frontotemporal dementia, for which there is no treatment. As his condition deteriorated, his wife, Ruth, had to move him to a nursing home, where she spends most days.

New York Times

Image: istockphoto

Several weeks after mild brain ischemia, mice display a depressive-like syndrome characterized by increased anxiety, inactivity and “cheerlessness”. These symptoms of depression following a stroke are associated with the delayed loss of nerve cells in the brain’s reward regions. This is the major finding of a study published in the current issue of Biological Psychiatry.

Scientists at Charité – Universitätsmedizin Berlin collaborating with researchers from Bochum, Magdeburg and Boston were able to show that delayed treatment of laboratory mice with cipramil, an antidepressant of the selective serotonin reuptake inhibitor (SSRI) family, not only prevented the development of depression, but also attenuated the subacute degeneration of nerve cells in the brain’s reward system after stroke. At the same time, the area in the brain directly affected by the stroke turned out to be smaller in those mice which had received the antidepressant. “These results indicate that antidepressants from the SSRI group protect nerve cells. This effect can also be harnessed even when medication is started days after the stroke,” explains psychiatrist Prof. Golo Kronenberg, who works on the subject of “Depression after Stroke” at the Center for Stroke Research Berlin (CSB) at Charité.

Poststroke depression is of great clinical relevance. Not only do symptoms of depression occur frequently after stroke, they also negatively impact stroke outcome with increased morbidity and mortality and worse functional outcome. The neurobiological mechanisms underlying the development of depression after a stroke have hardly been examined on the molecular or cellular levels. Conversely, the effects of commonly prescribed antidepressants on stroke outcome have only sparsely been investigated.

“These results may be of considerable clinical significance because until now it was assumed that the window for effective treatment options after a stroke is limited to a few hours. However, this study shows that a treatment even when started several days after the stroke may still prove effective,” says Prof. Matthias Endres, the Director of the Department of Neurology at Charité.

Based on these experimental findings, the phenomenon of delayed nerve cell loss will also be studied in human stroke patients using neuroimaging. Furthermore, within the framework of the Clinic for Affective Disorders that is currently being set up at the Experimental and Clinical Research Center (ECRC) in Berlin-Buch, special consultation hours for patients suffering from poststroke depression will be scheduled.

http://www.charite.de Exofocal Dopaminergic Degeneration as Antidepressant Target in Mouse Model of Poststroke Depression. Kronenberg G, Balkaya M, Prinz V, Gertz K, Ji S, Kirste I, Heuser I, Kampmann B, Hellmann-Regen J, Gass P, Sohr R, Hellweg R, Waeber C, Juckel G, Hörtnagl H, Stumm R, Endres M. Biol Psychiatry (2012). doi:10.1016/j.biopsych.2012.02.026

The peak risk for misusing prescription pain relievers occurs in mid-adolescence, specifically about 16 years old and earlier than many experts thought, according to a new study by Michigan State University researchers.

The results, based on recent nationwide surveys of nearly 120,000 U.S. adolescents, suggest prevention programs may need to be introduced earlier, in childhood and early adolescence, said James C. Anthony of MSU’s Department of Epidemiology and Biostatistics.

Recent trends show clinicians and public health professionals are prescribing more pain relievers, and research suggests an increased misuse of these drugs and increased rates of overdose deaths, said Anthony, who supervised the research of postdoctoral fellow Elizabeth Meier and graduate student Jonathan Troost.

“While much of the previous thinking was that misuse of these drugs emerged in the final year of high school and during the college-age years, we found that for adolescents the peak risk of starting to misuse these painkillers generally occurs earlier, not during the postsecondary school years,” Anthony said. “We suspect many physicians, other prescribing clinicians and public health professionals, will share our surprise in this finding.”

The study, supported by grants from the National Institute on Drug Abuse and MSU, was published today in the Archives of Pediatrics & Adolescent Medicine, a network publication of the Journal of the American Medical Association.

The team of researchers analyzed data from the 2004 through 2008 National Surveys on Drug Use and Health to identify when young people are most likely to start using prescription pain relievers to get high or for other unapproved uses. The results show about 1 in 60 young people between 12 and 21 years old starts using prescription pain relievers each year, outside the boundaries of what a prescriber has intended.

Peak risk is concentrated at about 16 years, when roughly 1 in 30 to 40 youth start to use painkillers to get high, or for other reasons not intended by the prescriber.

“Getting a firm grasp of when the first onset occurs is very important when we try to take public health action to prevent first occurrence,” Anthony said. “With the peak risk at age 16 years and a notable acceleration in risk between ages 13 and 14 years, any strict focus on college students or 12th graders might be an example of too little too late.”

The results reveal a need to strengthen prescribing guidelines for clinicians and introduce early school-based prevention programs such as effective school-based alcohol and tobacco initiatives, he said.

Other types of prevention programs include peer-resistance programs such as the popular “Just Say No” campaigns. There also is an opportunity to work with pharmaceutical specialists who sometimes can reformulate these drugs so their effects are blunted when misused.

As for clinicians with a public health perspective, Anthony said that non-opioid pain relievers such as ibuprofen can be quite effective, and that when opioid pain killers are prescribed for adolescents or in reach of teens, the number of tablets can be limited or kept under lock and key.

“Patients in transient pain are often given a larger opioid prescription than is needed. It can end up stacked in the medicine cabinet, available to anyone in or visiting the household,” he said

To read the full journal article, go to http://bit.ly/ISxsmN.

When children with autism were randomly compared with typically developing children or children with other developmental disorders, biomarkers correctly identified more than thirty percent of autistic children without incorrectly identifying a single non-autistic child. Image: istockphoto

Now a team of University of Washington  and Battelle scientists have identified metabolites in urine that could potentially predict young children at risk of developing autism.

The varying degrees and manifestations of this developmental brain condition are collectively called autistic spectrum disorder.  ASD is characterized by impaired social interactions, difficulty in communicating, and repetitive behaviors. Many other symptoms also can be present, including anxiety, depression, learning disabilities, sleep disorders, and gastrointestinal problems.

Currently, diagnosing a child with ASD requires a thorough evaluation by a team of health professionals from a wide range of specialties. Early intervention often can reduce or prevent the more severe symptoms and disabilities associated with ASD.

Autism specialists and many other people look forward to a day when a test for a  biological marker might detect autism risk in young children. To this end, Seattle researchers evaluated porphyrins in the urine of children to determine if the levels of these metabolites could predict ASD.

The research team included James Woods, professor of environmental and occupational health sciences at the UW School of Public Health, and Nicholas Heyer and Diana Echeverria, senior scientists at Battelle Centers for Public Health Research and Evaluation

While porphyrins are found in everyone’s urine, the research team observed that certain kinds of these metabolic byproducts are much higher in  the urine of some children with autism, compared with typically developing, non-autisitic children of the same age.

Additionally, when children with autism were randomly compared with typically developing children or children with other developmental disorders, the porphyrin biomarkers correctly identified more than thirty percent of autistic children without incorrectly identifying a single non-autistic child.

The ability to detect porphyrins in a urine sample opens new clinical possibilities. Simple urine tests, if they prove effective, could become a rapid, low-cost, widely available  way to screen young children for this type of autism risk.

“The significance of this biomarker is not only that it may facilitate earlier detection of autism risk,” said Woods, “but also that it might help identify those ASD children whose symptoms are specifically associated with altered porphyrin metabolism.”

He added, “When validated in a larger study, this biomarker could help to identify a specific subset of ASD kids and improve the search for more focused treatment options for these children.”

The findings were published in this month’s edition of Autism Research to coincide with Autism Awareness Month. The paper can be found online.

Partial funding for this research was provided by the National Institute of Environmental Health Sciences. Additional funding was provided by the Autism Research Institute and the Wallace Research Foundation.

Source: University of Washington

The flavanoids in strawberries and blueberries could help delay dementia. EPA/Bilawal Arbab

People who eat greater amounts of blueberries and strawberries could delay their cognitive ageing by years, according to data from a large-scale study conducted over more than three decades.

In a paper published in the journal Annals of Neurology, German and US researchers report that cognitive decline could be delayed by up to 2½ years in elderly people who eat more of the flavonoid-rich berries.

Flavonoids are compounds found in fruits, nuts and vegetables that have been linked to disease prevention through their antioxidant and anti-inflammatory properties. Berries are particularly high in a type of flavonoid called anthocyanidins, which can cross the blood–brain barrier to areas of learning and memory.

The research team used data from the Nurses’ Health Study, which has collected information about the diet of 121,700 female, registered nurses since 1980. Between 1995 and 2001, the team measured cognitive function in 16,010 women over the age of 70, at two-year intervals.

Those who ate more berries experienced a delayed cognitive decline by up to 2½ years. But the authors stressed that while they did control for health factors in the modelling, they could not exclude the possibility that participants with preserved cognition may also have been affected by lifestyle choices, such as exercise.

Study leader Elizabeth Devore, from Brigham and Women’s Hospital and Harvard Medical School in Boston, said that because the US population was ageing, understanding the health issues facing the elderly was vital. “Our findings have significant public health implications as increasing berry intake is a fairly simple dietary modification to test cognition protection in older adults,” Dr Devore said.

Bryce Vissel, Head of the Neurodegeneration Research Laboratory at the Garvan Institute of Medical Research in Sydney, said the public policy implications of the research were “sufficiently important to merit further study. However, the implications are further reaching, as they show that research offers the possibility to identify ways to slow dementia. Most importantly, if research can show that lifestyle affects cognitive decline, then it seems logical to suggest that research will also deliver effective treatments that slow cognitive decline, given the chance.”

Dr Vissel added: “The potential implications of this type of research are that simple berries could potentially reduce the time before elderly people may need care. However, the broader point is that more research is needed and it is needed urgently.”

Flavonoids appeared not only to influence cognitive function but also visual function, said Peter Howe, a Research Professor in Nutritional Physiology at the University of South Australia.

“What I think is happening here, which is not considered in this paper, is that the flavonoids are acting on the blood vessels in the brain and the eyes to improve the circulation. We’re conducting research at the Nutritional Physiology Research Centre looking at how foods rich in flavonoids, like the ones present in these berries, are able to improve blood flow in the brain, because that may be the key to their cognitive benefits.”

Shawn Somerset, an Associate Professor of Public Health at the Australian Catholic University in Brisbane, said that in elderly Australians the most likely source of flavonoids was wine. Berries were expensive, he said, and there were other good sources of anthocyanadins, such as aubergine. “Australian intake of vegetables is inferior to fruit, therefore vegetable consumption needs to be promoted above fruit consumption.

“The most sensible advice is to consume a wide range of flavonoids, rather than large amounts of specific ones, since excessive amounts of some are problematic. This translates to consuming a range of vegetables and fruits, not just one type.”

This article was originally published at The Conversation.
Read the original article.

Commonly prescribed anti-depressants appear to be doing patients more harm than good, say researchers who have published a paper examining the impact of the medications on the entire body.
“It’s important because millions of people are prescribed anti-depressants each year, and the conventional wisdom about these drugs is that they’re safe and effective.”

“We need to be much more cautious about the widespread use of these drugs,” says Paul Andrews, an evolutionary biologist at McMaster University and lead author of the article, published today in the online journal Frontiers in Psychology.

Andrews and his colleagues examined previous patient studies into the effects of anti-depressants and determined that the benefits of most anti-depressants, even taken at their best, compare poorly to the risks, which include premature death in elderly patients.
 
Anti-depressants are designed to relieve the symptoms of depression by increasing the levels of serotonin in the brain, where it regulates mood. The vast majority of serotonin that the body produces, though, is used for other purposes, including digestion, forming blood clots at wound sites, reproduction and development.

What the researchers found is that anti-depressants have negative health effects on all processes normally regulated by serotonin.

The findings include these elevated risks:

• developmental problems in infants
• problems with sexual stimulation and function and sperm development in adults
• digestive problems such as diarrhea, constipation, indigestion and bloating
• abnormal bleeding and stroke in the elderly

The authors reviewed three recent studies showing that elderly anti-depressant users are more likely to die than non-users, even after taking other important variables into account. The higher death rates indicate that the overall effect of these drugs on the body is more harmful than beneficial.

“Serotonin is an ancient chemical. It’s intimately regulating many different processes, and when you interfere with these things you can expect, from an evolutionary perspective, that it’s going to cause some harm,” Andrews says.
Millions of people are prescribed anti-depressants every year, and while the conclusions may seem surprising, Andrews says much of the evidence has long been apparent and available.

“The thing that’s been missing in the debates about anti-depressants is an overall assessment of all these negative effects relative to their potential beneficial effects,” he says. “Most of this evidence has been out there for years and nobody has been looking at this basic issue.”
In previous research, Andrews and his colleagues had questioned the effectiveness of anti-depressants even for their prescribed function, finding that patients were more likely to suffer relapse after going off their medications as their brains worked to re-establish equilibrium.

With even the intended function of anti-depressants in question, Andrews says it is important to look critically at their continuing use.
“It could change the way we think about such major pharmaceutical drugs,” he says. “You’ve got a minimal benefit, a laundry list of negative effects – some small, some rare and some not so rare. The issue is: does the list of negative effects outweigh the minimal benefit?”

ᔥMcMaster University The journal article: http://bit.ly/I88RKb

A new blood test diagnoses major depression in teens—an approach that offers an objective diagnosis by measuring a specific set of genetic markers.

The current method of diagnosing depression is subjective. It relies on the patient’s ability to recount his or her symptoms and the physician’s ability and training to interpret them.

Diagnosing teens is an urgent concern because they are highly vulnerable to depression and difficult to accurately diagnose due to normal mood changes during this age period.

The test also is the first to identify subtypes of depression. It distinguished between teens with major depression and those with major depression combined with anxiety disorder. This is the first evidence that it’s possible to diagnose subtypes of depression from blood, raising the hope for tailoring care to the different types.

“Right now depression is treated with a blunt instrument,” says Eva Redei, a professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine and lead investigator of the study, published in Translational Psychiatry.

“It’s like treating type 1 diabetes and type 2 diabetes exactly the same way. We need to do better for these kids.
“This is the first significant step for us to understand which treatment will be most effective for an individual patient,” adds Redei. “Without an objective diagnosis, it’s very difficult to make that assessment. The early diagnosis and specific classification of early major depression could lead to a larger repertoire of more effective treatments and enhanced individualized care.”

The estimated rates of major depressive disorder jump from 2 to 4 percent in pre-adolescent children to 10 to 20 percent by late adolescence. Early onset of major depression in teens has a poorer prognosis than when it starts in adulthood.

Untreated teens with this disease experience increases in substance abuse, social maladjustment, physical illness, and suicide. Their normal development is derailed, and the disease persists into adulthood.

The depressed teens in the study were patients of Kathleen Pajer, a co-first author of the study, and her colleagues from the Research Institute of Nationwide Children’s Hospital in Columbus, Ohio.
The study subjects included 14 adolescents with major depression who had not been clinically treated and 14 non-depressed adolescents, all between 15 to 19 years old. The depressed and control subjects were matched by sex and race.

Redei’s lab tested the adolescents’ blood for 26 genetic blood markers she had identified in previous research. She discovered 11 of the markers were able to differentiate between depressed and non-depressed adolescents. In addition, 18 of the 26 markers distinguished between patients that had only major depression and those who had major depression combined with anxiety disorder.

The blood analysis was done by Brian Andrus from Redei’s lab, the other co-first author of the study, who was blind to the diagnoses of the subjects.

“These 11 genes are probably the tip of the iceberg because depression is a complex illness,” Redei says. “But it’s an entree into a much bigger phenomenon that has to be explored. It clearly indicates we can diagnose from blood and create a blood diagnosis test for depression.”

Redei first isolated and identified the genetic blood markers for depression and anxiety based on decades of research with severely depressed and anxious rats. The rats mirror many behavioral and physiological abnormalities found in patients with major depression and anxiety.
Further indicating the challenge in working with depressed adolescents, none of the teens who were diagnosed with depression opted for treatment.

“Everybody, including parents, are wary of treatment, and there remains a social stigma around depression, which in the peer-pressured world of teenagers is even more devastating,” Redei says. “Once you can objectively diagnose depression as you would hypertension or diabetes, the stigma will likely disappear.”
The human research was funded by grants from the Research Institute of Nationwide Children’s Hospital in Columbus, Ohio. Animal research was supported by grants from the Davee Foundation, the RD Foundation, and the National Institutes of Health.

ᔥFuturity
Read the original study

A five year study conducted with thousands of local teenagers by University of Montreal researchers reveals that those who used speed (meth/ampthetamine) or ecstasy (MDMA) at fifteen or sixteen years of age were significantly more likely to suffer elevated depressive symptoms the following year. “Our findings are consistent with other human and animal studies that suggest long-term negative influences of synthetic drug use,” said co-author Frédéric N. Brière of the School Environment Research Group at the University of Montreal. “Our results reveal that recreational MDMA and meth/amphetamine use places typically developing secondary school students at greater risk of experiencing depressive symptoms.” Ecstasy and speed-using grade ten students were respectively 1.7 and 1.6 times more likely to be depressed by the time they reached grade eleven.

The researchers worked with data provided by 3,880 students enrolled at schools in disadvantaged areas of Quebec. The participants were asked a series of questions that covered their drug use – what they had used in the past year or ever in their life – and their home life. Depressive symptoms were established by using a standard epidemiological evaluation tool. 310 respondents reported using MDMA (8%) and 451 used meth/amphetamines (11.6%). 584 of all respondents were identified as having elevated depressive symptoms (15.1%). The range of questions that the researchers asked enabled them to adjust their statistics to take into account other factors likely to affect the psychological state of the student, such as whether there was any conflict between the parents and the participant. “This study takes into account many more influencing factors than other research that has been undertaken regarding the association between drugs and depression in teenagers,” Brière said. “However, it does have its limitations, in particular the fact that we cannot entirely rule out the effects of drug combinations and that we do not know the exact contents of MDMA and meth/amphetamine pills.”

The study’s authors would like to do further research into how drug combinations affect a person’s likelihood to suffer depression and they are keen to learn more about the differences between adults and adolescents in this area. “Our study has important public health implications for adolescent populations,” said Jean-Sébastien Fallu, a professor at the University of Montreal and study co-author. “Our results reinforce the body of evidence in this field and suggest that adolescents should be informed of the potential risks associated with MDMA and meth/amphetamine use.”

ᔥ University of Montreal