Allergic to orgasms? Man's sad story has happy ending

Brian Alexander 01.21.2011

Poor Mr. A! He’s a 50-year-old married man, who, since the age of 19, has been plagued with a litany of unpleasant ailments every time he ejaculates.

On cue, after any orgasm, the beleaguered man would experience fever, weakness, exhaustion, loss of initiative, headache, disordered speech, irritability, forgetfulness and frightening dreams, not to mention swollen lips and throat.

The symptoms were so severe that he and his wife planned intercourse for Fridays so he’d have two days to recover before returning to work on Monday. He also suffered from premature ejaculation, so the problem was no picnic for Mrs. A, either. It’s a miracle they had two children.

We know all this because Mr. A’s condition is detailed in a just-published paper in the Journal of Sexual Medicine in which Dutch doctors describe what they call Post Orgasmic Illness Syndrome, or POIS.

POIS was first identified by the same team of doctors in 2002. Initially it was thought the cause might be psychological, possibly related to a syndrome called “dhat” that is sometimes reported among men in India and Sri Lanka that leaves them fearful of ejaculating.

Then, doctors in the United Kingdom noted similar symptoms in two men, including one whose problem improved dramatically by taking non-steroidal anti-inflammatory drugs just before and for two days after ejaculating. That seemed to indicate the problem was caused by some sort of immune system reaction.

The Dutch doctors figured POIS might lie in a man’s reaction to his own semen. They conducted skin prick testing, a common way to test for allergies, on 33 of the 45 men they’ve identified with potential POIS so far. When the men were exposed to their own semen this way, 29 of them had classic allergic reactions. Mr. A was one.

They tried treating him the way allergists sometimes treat food allergies, with “hyposensitization,” a technique that uses the allergen itself to treat the condition.

The doctors began a long series of treatments, first diluting the semen 40,000 times, inoculating him with it, and then, over a period of 31 months, gradually working up to a dilution of 1-to-20.

Amazingly, it worked. Mr. A eventually was able to ejaculate without debilitating illness. His symptoms did not disappear entirely, but they were much milder and lasted only a short time. Lead author Marcel Waldinger, of the Department of Psychiatry and Neurosexology at Haga Hospital in The Hague, said the results “contradict the idea that the complaints have a psychological cause.”

That’s good to know, but why, we may ask, is Mr. A allergic to his own semen at all? Women have been known to have allergic reactions to men’s emissions, but that’s entirely different.

Scientists aren’t sure, but they believe that a gap in the seminal plumbing somehow allows the semen to contact immune cells called T-lymphocytes which, in turn, sets off immune system alarm bells. With repeated exposure, the reaction becomes intense.

Whatever the cause, Mr. A is relieved that his problem has eased. Doctors report he is now “quite contented” at both home and work.

As a side benefit, the premature ejaculation stopped, too, so we can only surmise that Mrs. A is content as well.

Why Does Schizophrenia Appear in Young Adults?

Recent research explores the effects of a schizophrenia risk factor (DISC1) and its influence over the onset of the disease

By Christie Nicholson
Saturday, February 27, 2010

Schizophrenia typically shows up in young adults. For men it tends to emerge around 20 to 28 years and peak onset for women is between 26 to 32 years. But what triggers the disease during this time? Well past studies have shown that mutations in a gene called DISC1 are linked to schizophrenia. DISC1 enables a guide to new nerve cells—sort of like a traffic cop—sending them to the right place to make the right connections to other cells. But recently, researchers partially shut off DISC1 in lab mice to see what happens when there is no traffic cop. And what they saw is a steady decrease in the size and number of dendritic spines, the tiny branches of the nerve cell that receive messages from nearby cells. Their results are published in the March issue of Nature Neuroscience. Connections between cells are constantly broken and forged throughout our lives but there’s an amazingly large amount of so-called “pruning” during adolescence. So if this breaking of connections goes awry, as it does when DISC1 is shut off, then one might be at high risk for schizophrenia. And so while the defective gene may be there at birth, its effect does not show up until many years into one’s life, post adolescence in young adulthood.

Journal’s Paper on ESP Expected to Prompt Outrage

By BENEDICT CAREY

One of psychology’s most respected journals has agreed to publish a paper presenting what its author describes as strong evidence for extrasensory perception, the ability to sense future events.

The decision may delight believers in so-called paranormal events, but it is already mortifying scientists. Advance copies of the paper, to be published this year in The Journal of Personality and Social Psychology, have circulated widely among psychological researchers in recent weeks and have generated a mixture of amusement and scorn.

The paper describes nine unusual lab experiments performed over the past decade by its author, Daryl J. Bem, an emeritus professor at Cornell, testing the ability of college students to accurately sense random events, like whether a computer program will flash a photograph on the left or right side of its screen. The studies include more than 1,000 subjects.

Some scientists say the report deserves to be published, in the name of open inquiry; others insist that its acceptance only accentuates fundamental flaws in the evaluation and peer review of research in the social sciences.

“It’s craziness, pure craziness. I can’t believe a major journal is allowing this work in,” Ray Hyman, an emeritus professor of psychology at the University Oregon and longtime critic of ESP research, said. “I think it’s just an embarrassment for the entire field.”

The editor of the journal, Charles Judd, a psychologist at the University of Colorado, said the paper went through the journal’s regular review process. “Four reviewers made comments on the manuscript,” he said, “and these are very trusted people.”

All four decided that the paper met the journal’s editorial standards, Dr. Judd added, even though “there was no mechanism by which we could understand the results.”

But many experts say that is precisely the problem. Claims that defy almost every law of science are by definition extraordinary and thus require extraordinary evidence. Neglecting to take this into account — as conventional social science analyses do — makes many findings look far more significant than they really are, these experts say.

“Several top journals publish results only when these appear to support a hypothesis that is counterintuitive or attention-grabbing,” Eric-Jan Wagenmakers, a psychologist at the University of Amsterdam, wrote by e-mail. “But such a hypothesis probably constitutes an extraordinary claim, and it should undergo more scrutiny before it is allowed to enter the field.”

Dr. Wagenmakers is co-author of a rebuttal to the ESP paper that is scheduled to appear in the same issue of the journal.

In an interview, Dr. Bem, the author of the original paper and one of the most prominent research psychologists of his generation, said he intended each experiment to mimic a well-known classic study, “only time-reversed.”

In one classic memory experiment, for example, participants study 48 words and then divide a subset of 24 of them into categories, like food or animal. The act of categorizing reinforces memory, and on subsequent tests people are more likely to remember the words they practiced than those they did not.

In his version, Dr. Bem gave 100 college students a memory test before they did the categorizing — and found they were significantly more likely to remember words that they practiced later. “The results show that practicing a set of words after the recall test does, in fact, reach back in time to facilitate the recall of those words,” the paper concludes.

In another experiment, Dr. Bem had subjects choose which of two curtains on a computer screen hid a photograph; the other curtain hid nothing but a blank screen.

A software program randomly posted a picture behind one curtain or the other — but only after the participant made a choice. Still, the participants beat chance, by 53 percent to 50 percent, at least when the photos being posted were erotic ones. They did not do better than chance on negative or neutral photos.

“What I showed was that unselected subjects could sense the erotic photos,” Dr. Bem said, “but my guess is that if you use more talented people, who are better at this, they could find any of the photos.”

In recent weeks science bloggers, researchers and assorted skeptics have challenged Dr. Bem’s methods and his statistics, with many critiques digging deep into the arcane but important fine points of crunching numbers. (Others question his intentions. “He’s got a great sense of humor,” said Dr. Hyman, of Oregon. “I wouldn’t rule out that this is an elaborate joke.”)

Dr. Bem has generally responded in kind, sometimes accusing critics of misunderstanding his paper, others times of building a strong bias into their own re-evaluations of his data.

In one sense, it is a historically familiar pattern. For more than a century, researchers have conducted hundreds of tests to detect ESP, telekinesis and other such things, and when such studies have surfaced, skeptics have been quick to shoot holes in them.

But in another way, Dr. Bem is far from typical. He is widely respected for his clear, original thinking in social psychology, and some people familiar with the case say his reputation may have played a role in the paper’s acceptance.

Peer review is usually an anonymous process, with authors and reviewers unknown to one another. But all four reviewers of this paper were social psychologists, and all would have known whose work they were checking and would have been responsive to the way it was reasoned.

Perhaps more important, none were topflight statisticians. “The problem was that this paper was treated like any other,” said an editor at the journal, Laura King, a psychologist at the University of Missouri. “And it wasn’t.”

Many statisticians say that conventional social-science techniques for analyzing data make an assumption that is disingenuous and ultimately self-deceiving: that researchers know nothing about the probability of the so-called null hypothesis.

In this case, the null hypothesis would be that ESP does not exist. Refusing to give that hypothesis weight makes no sense, these experts say; if ESP exists, why aren’t people getting rich by reliably predicting the movement of the stock market or the outcome of football games?

Instead, these statisticians prefer a technique called Bayesian analysis, which seeks to determine whether the outcome of a particular experiment “changes the odds that a hypothesis is true,” in the words of Jeffrey N. Rouder, a psychologist at the University of Missouri who, with Richard D. Morey of the University of Groningen in the Netherlands, has also submitted a critique of Dr. Bem’s paper to the journal.

Physics and biology, among other disciplines, overwhelmingly suggest that Dr. Bem’s experiments have not changed those odds, Dr. Rouder said.

So far, at least three efforts to replicate the experiments have failed. But more are in the works, Dr. Bem said, adding, “I have received hundreds of requests for the materials” to conduct studies.

Anger at God common, even among atheists

By: Elizabeth Landau - CNN.com Health Writer/Producer

If you're angry at your doctor, your boss, your relative or your spouse, you can probably sit down and have a productive conversation about it. God, on the other hand, is probably not available to chat.

And yet people get angry at God all the time, especially about everyday disappointments, finds a new set of studies in the Journal of Personality and Social Psychology.

It's not just religious folks, either. People unaffiliated with organized religion, atheists and agnostics also report anger toward God either in the past, or anger focused on a hypothetical image - that is, what they imagined God might be like - said lead study author Julie Exline, Case Western Reserve University psychologist.

In studies on college students, atheists and agnostics reported more anger at God during their lifetimes than believers. A separate study also found this pattern among bereaved individuals. This phenomenon is something Exline and colleagues will explore more in future research, which is open to more participants.

It seems that more religious people are less likely to feel angry at God and more likely to see his intentions as well-meaning, Exline's research found.

And younger people tend to be angrier at God than older people, Exline said. She says some of the reasons she's seen people the angriest at God include rejection from preferred colleges and sports injuries preventing high schoolers from competing.

The age difference may have to do with cultural norms, she said. Perhaps previous generations were taught to not question God, whereas younger people today don't have any qualms about it. On the other hand, it might be that as people get older, they learn how to handle these types of feelings better.

Anger at God can strongly resemble feelings you may have against another person, Exline found. God may seem treacherous or cruel when bad things happen, just like another individual might. Your anger may fester even more when there's no good reason for the negative event, such as a natural disaster or a disease, to occur. And strong, longstanding negative emotions of any kind can lead to physical ailments.

Moreover, distress at God is associated with mental health symptoms. Exline and colleagues found that among cancer survivors interviewed once and then again a year later, those who were angry at God at both points in time had the poorest mental and physical health. But the study cannot prove whether anger at God made them feel worse or that feeling worse made them more angry at God.

Just like with people in your life, you can respect and feel anger toward God at the same time. And you can move toward forgiveness by reframing the way you view the negative event: Perhaps God was not responsible for it or that he acted in that way for a reason.

"When people trust that God cares about them and has positive intentions toward them, even if they can’t understand what those intentions or meanings are, it tends to help to resolve anger," she said.

Granted, these studies aren't definitive; they are steps forward in this emerging field of inquiry and not the final word on the subject.

But we see it in the real world, too. Jeff Crim listens to people's anger at God all the time - specifically, people who are dying. He's a chaplain and bereavement coordinator North Star Hospice in Calhoun, Georgia, and has found that it's important to find a way to express your anger at God in order to deal with it.

Expressing anger can be cathartic, and help you move on, but how you do it is deeply personal, Crim said. Crim himself will speak aloud to God, but others find solace in a trusted spiritual leader or other person to confide in about their anger at a higher power.

"What they need is a safe place to express their anger, to know that their anger has been heard and listened to," he said.

SAD: When seasons change how you feel

By Elizabeth Landau, CNN

(CNN) -- By 10 a.m. every day during the winters, Rachelle Strauss felt like she could go back to bed. She used to be a morning person, but that all changed about 10 years ago when she started to feel exhausted as the darkest days dragged on.

"As soon as March came 'round and we hit spring, I was back to my bouncy self. It's almost like being two people for two different seasons of the year," said Strauss, 38, of Gloucestershire, England.

Strauss is not alone. In Northern Europe, an estimated 12 million people suffer from seasonal affective disorder. Over here in the United States, about 4% to 6% of the population may have it, but 10% to 20% might have milder winter blues, according to the Cleveland Clinic.

The condition tends to strike mainly women in their 20s, 30s and 40s, although men can also have it. Children and adolescents may also develop it, and it is less common in adults of older ages.

Seasonal affective disorder can be expected in regions of the world that are farther away from the equator and thus experience seasonal changes in daylight hours more dramatically, said Simon Rego, psychologist at Albert Einstein College of Medicine and Montefiore Medical Center in the Bronx, New York.

Scientists aren't sure why some people get seasonal affective disorder and others don't. One theory is that sufferers may have a biological predisposition to it, and the symptoms get triggered in particular ways.

Symptoms of SAD

For Strauss, the symptoms of lack of energy and depression formed a vicious cycle, where she wouldn't exercise or socialize, and then became irritable and cranky.

"I got depressed because I couldn't do the things I wanted to do," she said. "Certainly this total exhaustion is very debilitating after awhile."

Alison Kero of Denver, Colorado, can relate. Before moving from New York, her energy dropped off in the winter, and she would go to sleep at 6 p.m.

Anxiety, suicidal thoughts and poor concentration can also accompany seasonal affective disorder, said Dr. Tracy Latz, psychiatrist in Mooresville, North Carolina.

A hallmark of the condition is that symptoms get worse when daylight saving time ends. If you're feeling down fairly consistently for two weeks or more, and the feelings recur during the same time every year, there's reason to suspect that it's seasonal affective disorder, she said.

More rarely, seasonal affective disorder can flare up with warm, sunny weather. In these people, anxiety, insomnia and irritability can worsen in the spring and summer. And others exhibit a form of bipolar disorder called "reverse seasonal affective disorder," with hyperactivity, agitation and inappropriate enthusiasm in the spring and summer.

When it's not necessarily SAD

For the patients whose moods suffer in the summertime, there may be longstanding issues contributing to the problem, such as bad childhood memories of staying at home when school let out, Latz said.

"If we came to dread a certain time of the year every year as kids because of our family dynamics or the environment that we were in, then we can carry that into this subconscious dread of that time of the year," she said.

Personal experiences are a major component of how the seasons can influence how you feel, said Dr. John Sharp, author of "The Emotional Calendar." Anyone, regardless of whether they have seasonal affective disorder, may get into particular moods because of environmental, psychological and cultural forces that occur at various times of the year.

If you once had an amazing experience one year in the early part of December, you'll likely feel positively when seasonal changes such as snow, crackling fireplaces and hot chocolate bring back those good memories.

The anniversary of a major loss, on the other hand, can throw a dark cloud over any time of year. Sharp noted that Mark Madoff, son of convicted Ponzi-schemer Bernie Madoff, took his own life on December 10, the two-year anniversary of his father's arrest.

Cultural norms can also drive seasonal changes in mood, he said. It has been documented that there are peaks in suicides in the spring. The reason for that has not been pinned down.

Sharp posits that as the days get longer, many people tend to appear more active and carefree, which makes sufferers of depression feel worse. The cultural experiences of the winter holidays can also be a burden for adults, with the stress of family gatherings, whereas for children they were times of joy.

What are the treatments?

Seasonal affective disorder has to do primarily with environment; specifically, how much light you're getting. That's why one of most iconic therapies for seasonal affective disorder is the light box.

Light therapy imitates light from the outdoors and triggers changes in the brain that can help elevate mood. It doesn't work for everyone, but many people such as Strauss have found relief from sitting in front of a bright light box. Strauss uses hers during breakfast, and it helps her get through the day. There are also dawn simulators, which mimic the sunrise as you wake up, and light visors that look like baseball caps that you can wear to get light exposure.

Since moving to Denver, which tends to see more sun than New York, Kero feels like she doesn't have to use her light box anymore, but 15 to 30 minutes a day did help her back East.

"It's a deep biological reality that our brains sense the amount of sunlight we're exposed to with great sensitivity. It adds up to become a big drain when we don't have enough light," Sharp said.

But light therapy doesn't work for everyone.

Some people need medications that depression patients would receive: anti-depressants called selective serotonin reuptake inhibitors. Anxiety, suicidal thoughts and poor concentration because of excessive worry are all signs that there could be an issue with serotonin, a brain chemical involved in mood, Latz said.

Lack of energy is a sign of a problem with the brain's levels of dopamine, another brain chemical, she said. Exercise can help stimulate this system and help you feel more awake.

In mild cases, certain nutrients and herbs may help. Omega-3 fatty acids have been shown to relieve some symptoms of anxiety, Latz said, which are found in oily fish. The American College of Physicians considers St. John's wort an option for mild depression, but be aware it can interact with many drugs and might cause oversensitivity to light. Strauss, whose website Little Green Blog discusses natural remedies, recommends uplifting essential oils such as lavender. Kero suggests surrounding yourself with positive people.

And if there are issues you're having besides the weather, try talking to a mental health professional. Cognitive behavioral therapy is one form of talk therapy that can help you confront negative thought patterns.

"Obviously if there's something to talk about, if you're having frustrations with some aspect of life, counseling is quite good as a potential way forward," Sharp said.

Seek help if you're entertaining suicidal thoughts and feeling like life isn't worth living. Call the National Suicide Hotline at 1-800-784-2433 if you need immediate assistance.

Slipping the 'Cognitive Straitjacket' of Psychiatric Diagnosis

Psychiatry's diagnostic bible meets the awkward facts of genetics
By Steven E. Hyman |

It can fairly be said that modern psychiatric diagnosis was “born” in a 1970 paper on schizophrenia.

The authors, Washington University psychiatry professors Eli Robins and Samuel B. Guze, rejected the murky psychoanalytic diagnostic formulations of their time. Instead, they embraced a medical model inspired by the careful 19th-century observational work of Emil Kraepelin, long overlooked during the mid-20th-century dominance of Freudian theory. Mental disorders were now to be seen as distinct categories, much as different bacterial and viral infections produce characteristic diseases that can be seen as distinct “natural kinds.”

Disorders, Robins and Guze argued, should be defined based on phenomenology: clinical descriptions validated by long-term follow-up to demonstrate the stability of the diagnosis over time. With scientific progress, they expected fuller validation of mental disorders to derive from laboratory findings and studies of familial transmission.

This descriptive approach to psychiatric diagnosis -- based on lists of symptoms, their timing of onset, and the duration of illness -- undergirded the American Psychiatric Association’s widely disseminated and highly influential Diagnostic and Statistical Manual of Mental Disorders, first published in 1980. Since then, the original “DSM-III” has yielded two relatively conservative revisions, and right now, the DSM-5 is under construction. Sadly, it is clear that the optimistic predictions of Robins and Guze have not been realized.

Four decades after their seminal paper, there are still no widely validated laboratory tests for any common mental illness. Worse, an enormous number of family and genetic studies have not only failed to validate the major DSM disorders as natural kinds, but instead have suggested that they are more akin to chimaeras. Unfortunately for the multitudes stricken with mental illness, the brain has not given up its secrets easily.

That is not to say that we have made no progress. DNA research has begun to illuminate the complex genetics of mental illness. But what it tells us, I would argue, is that, at least for the purposes of research, the current DSM diagnoses do not work. They are too narrow, too rigid, altogether too limited. Reorganization of the DSM is hardly a panacea, but science cannot thrive if investigators are forced into a cognitive straitjacket.

Before turning to the scientific evidence of fundamental problems with the DSM, let’s first take note of an important problem that the classification has produced for clinicians and patients alike: An individual who receives a single DSM diagnosis very often meets criteria for multiple additional diagnoses (so-called co-occurrence or “comorbidity”), and the pattern of diagnoses often changes over the lifespan. Thus, for example, children and adolescents with a diagnosis of an anxiety disorder often manifest major depression in their later teens or twenties. Individuals with autism spectrum disorders often receive additional diagnoses of attention deficit hyperactivity disorder, obsessive-compulsive disorder, and tic disorders.

Of course, there are perfectly reasonable explanations for comorbidity. One disorder could be a risk factor for another just as tobacco smoking is a risk factor for lung cancer. Alternatively, common diseases in a population could co-occur at random. The problem with the DSM is that many diagnoses co-occur at frequencies far higher than predicted by their population prevalence, and the timing of co-occurrence suggests that one disorder is not likely to be causing the second. For patients, it can be confusing and demoralizing to receive multiple and shifting diagnoses; this phenomenon certainly does not increase confidence in their caregivers.

Family studies and genetics shed light on the apparently high rate of co-occurrence of mental disorders and suggest that it is an artifact of the DSM itself. Genetic studies focused on finding variations in DNA sequences associated with mental disorders have repeatedly found shared genetic risks for both schizophrenia and bipolar disorder. Other studies have found different sequence variations within the same genes to be associated with schizophrenia and autism spectrum disorders.

An older methodology, the study of twins, continues to provide important insight into this muddy genetic picture. Twin studies generally compare the concordance for a disease or other trait within monozygotic twin pairs, who share 100% of their DNA, versus concordance within dizygotic twin pairs, who share on average 50% of their DNA. In a recent article in the American Journal of Psychiatry, a Swedish team of researchers led by Paul Lichtenstein studied 7,982 twin pairs. They found a heritability of 80% for autism spectrum disorders, but also found substantial sharing of genetic risk factors among autism, attention deficit hyperactivity disorder, developmental coordination disorder, tic disorders, and learning disorders.

In another recent article in the American Journal of Psychiatry, Marina Bornovalova and her University of Minnesota colleagues studied 1,069 pairs of 11-year-old twins and their biological parents. They found that parent-child resemblance was accounted for by shared genetic risk factors: in parents, they gave rise to conduct disorder, adult antisocial behavior, alcohol dependence, and drug dependence; in the 11-year-olds these shared factors were manifest as attention deficit hyperactivity disorder, conduct disorder, and oppositional-defiant disorder. (Strikingly, attention deficit disorder co-occurs in both the autism spectrum cluster and disruptive disorder cluster.)

These and many other studies call into question two of the key validators of descriptive psychiatry championed by Robins and Guze. First, DSM disorders do not breed true. What is transmitted across generations is not discrete DSM categories but, perhaps, complex patterns of risk that may manifest as one or more DSM disorders within a related cluster. Second, instead of long-term stability, symptom patterns often change over the life course, producing not only multiple co-occurring diagnoses but also different diagnoses at different times of life.

How can these assertions be explained? In fairness to Robins and Guze, they could not have imagined the extraordinary genetic complexity that produces the risk of many common human ills, including mental disorders. What this means is that common mental disorders appear to be due to different combinations of genes in different families, acting in combination with epigenetics -- gene expression varies even if the underlying DNA sequence is the same -- and non-genetic factors.

In some families, genetic risk for mental disorders seems to be due to many, perhaps hundreds, of small variations in DNA sequence -- often single “letters” in the DNA code. Each may cause a very small increment in risk, but, in infelicitous combinations, can lead to illness. In other families, there may be background genetic risk, but the coup de grace arrives in the form of a relatively large DNA deletion, duplication, or rearrangement. Such “copy number variants” may occur de novo in apparently sporadic cases of schizophrenia or autism.

In sum, it appears that no gene is either necessary or sufficient for risk of a common mental disorder. Finally, a given set of genetic risks may produce different symptoms depending on broad genetic background, early developmental influences, life stage, or diverse environmental factors.

The complex nature of genetic risk offers a possible explanation for comorbidity: what the DSM treats as discrete disorders, categorically separate from health and from each other, are not, in fact, discrete. Instead, schizophrenia, autism-spectrum disorders, certain anxiety disorders, obsessive-compulsive disorder, attention deficit hyperactivity disorder, mood disorders, and others represent families of related disorders with heterogeneous genetic risk factors underlying them. I would hypothesize that what is shared within disorder families, such as the autism spectrum or the obsessive-compulsive disorder spectrum, are abnormalities in neural circuits that underlie different aspects of brain function, from cognition to emotion to behavioral control, and that these circuit abnormalities do not respect the narrow symptoms checklists within the DSM.

The first DSM had many important strengths, but I would argue that part of what went wrong with it was a fairly arbitrary decision: the promulgation of a large number of disorders, despite the early state of the science, and the conceptualization of each disorder as a distinct category. That decision eschewed the possibility that some diagnoses are better represented in terms of quantifiable dimensions, much like the diagnoses of hypertension and diabetes, which are based on measurements on numerical scales.

These fundamental missteps would not have proven so problematic but for the human tendency to treat anything with a name as if it is real. Thus, a scientifically pioneering diagnostic system that should have been treated as a set of testable hypotheses was instead virtually set in stone. DSM categories play a controlling role in clinical communication, insurance reimbursement, regulatory approval of new treatments, grant reviews, and editorial policies of journals. As I have argued elsewhere, the excessive reliance on DSM categories, which are poor mirrors of nature, has limited the scope and thus the utility of scientific questions that could be asked. We now face a knotty problem: how to facilitate science so that DSM-6 does not emerge a decade or two from now a trivially revised descendant of DSM-III, but without disrupting the substantial clinical and administrative uses to which the DSM system is put.

I believe that the most plausible mechanism for repairing this plane while it is still flying is to give new attention to overarching families of disorders, sometimes called meta-structure. In previous editions of the DSM, the chapters were almost an afterthought compared with the individual disorders. It should be possible, without changing the criteria for specific diagnoses, to create chapters of disorders that co-occur at very high rates and that appear to share genetic risk factors based on family, twin, and molecular genetic studies.

This will not be possible for the entire DSM-5, but it would be possible for certain neurodevelopmental disorders, anxiety disorders, the obsessive-compulsive disorder spectrum, so-called externalizing or disruptive disorders (such as antisocial personality disorder and substance use disorders), and others. Scientists could then be invited by funding agencies and journals to be agnostic to the internal divisions within each large cluster, to ignore the over-narrow diagnostic categories. The resulting data could then yield a very different classification by the time the DSM-6 arrives.

Psychiatry has been overly optimistic about progress before, but I would predict that neurobiologically based biomarkers and other objective tests will emerge from current research, along with a greater appreciation of the role of neural circuits in the origins of mental disorders. I would also predict that discrete categories will give way, where appropriate, to quantifiable dimensions. At the very least, the science of mental disorders should be freed from the unintended cognitive shackles bequeathed by the DSM-III experiment.

Can Psychological Trauma Be Inherited?

By Rick Nauert PhD
Senior News Editor, PsychCentral

Can Psychological Trauma Be Inherited?An emerging topic of investigation looks to determine if post-traumatic stress disorder (PTSD) can be passed to subsequent generations.

Scientists are studying groups with high rates of PTSD, such as the survivors of the Nazi death camps. Adjustment problems of the children of the survivors — the so-called “second generation” — is topic of study for researchers.

Studies suggested that some symptoms or personality traits associated with PTSD may be more common in the second generation than the general population.

It has been assumed that these transgenerational effects reflected the impact of PTSD upon the parent-child relationship rather than a trait passed biologically from parent to child.

However, Dr. Isabelle Mansuy and colleagues provide new evidence in the current issue of Biological Psychiatry that some aspects of the impact of trauma cross generations and are associated with epigenetic changes, i.e., the regulation of the pattern of gene expression, without changing the DNA sequence.

They found that early-life stress induced depressive-like behaviors and altered behavioral responses to aversive environments in mice.

Importantly, these behavioral alterations were also found in the offspring of males subjected to early stress even though the offspring were raised normally without any stress. In parallel, the profile of DNA methylation was altered in several genes in the germline (sperm) of the fathers, and in the brain and germline of their offspring.

“It is fascinating that clinical observations in humans have suggested the possibility that specific traits acquired during life and influenced by environmental factors may be transmitted across generations. It is even more challenging to think that when related to behavioral alterations, these traits could explain some psychiatric conditions in families,” said Dr. Mansuy.

“Our findings in mice provide a first step in this direction and suggest the intervention of epigenetic processes in such phenomenon.”

“The idea that traumatic stress responses may alter the regulation of genes in the germline cells in males means that these stress effects may be passed across generations. It is distressing to think that the negative consequences of exposure to horrible life events could cross generations,” commented Dr. John Krystal, editor of Biological Psychiatry.

“However, one could imagine that these types of responses might prepare the offspring to cope with hostile environments. Further, if environmental events can produce negative effects, one wonders whether the opposite pattern of DNA methylation emerges when offspring are reared in supportive environments.”