Yeast Infection May Be Linked To High Risk For Bipolar Disorder, Schizophrenia

schizophrenia-addictionHaving a yeast infection is associated with a higher risk of developing schizophrenia and bipolar disorder, a new study has shown.

Researchers from the Johns Hopkins University have found that incidence of bipolar disorder and schizophrenia is higher in individuals with a history of Candida infections.

The researchers, however, warned that their study finding does not establish causal relationship but only shows that immune system susceptibility, lifestyle, and brain and gut association all contribute to memory and psychiatric health impairment.

Emily Severance, member of the university’s School of Medicine’s Stanley Division of Developmental Neurovirology and assistant professor of pediatric, said there is not enough evidence to say whether yeast infection alone can cause psychiatric illness. But it would be very crucial if doctors treating these patients become aware of such infections because it can be easily treated in its early stages.



Severance and her colleagues tried to establish whether or not an association exists between the infection and psychiatric illness particularly because new evidence suggests that schizophrenia could be due to immune system susceptibility.

To establish the connection, the researchers collected blood samples from 808 people from the Sheppard Pratt Health System. The group, with ages ranging from 18 to 65 years old, were divided into three groups: the control group included 277 individuals not diagnosed with any mental illness; the second group included 261 schizophrenic patients, and the third group had 270 individuals with bipolar disorder.

Blood samples were used to measure the presence of IgG antibodies, which are an indication of a past yeast infection. Other factors that may affect their findings such as age, medications, socioeconomic status, and race were accounted for.

The researchers found that having antibodies against Candida is not associated with mental illness. However, by isolating the numbers for men, they identified that 26 percent of individuals with schizophrenia had the antibodies compared with only 14 percent of the control group. No significant difference was found in the data collected from women, which may suggest that women have an increased protection for the infection.

It is also significant to note that male individuals with bipolar disorder were also more likely to have previous yeast infection at 26.4 percent compared to the control group at 14 percent. Researchers believe these numbers could be due to homelessness. They reasoned that changes in mood, diet and sanitation, and stress while out on the streets predispose someone to develop yeast infection.

The same could not be said for schizophrenia and the yeast infection, however.



Based on an earlier study that suggested neurological problems can arise from parasites and other infections, Severance and the team asked the participants to complete a cognitive task. The 30-minute assessment aimed to measure attention, language and visual-spatial skills, and immediate and delayed memory.

The team also found that in the control group, with or without yeast infection in the past, cognition was not different between men and women. But they noted that women with either bipolar disorder or schizophrenia and past yeast infection had poor memory recall compared to those with mental illness but without previous infection.

“Although we cannot demonstrate a direct link between Candida infection and physiological brain processes, our data show that some factor associated with Candida infection, and possibly the organism itself, plays a role in affecting the memory of women with schizophrenia and bipolar disorder, and this is an avenue that needs to be further explored,” said Severance.


 

Taken From TechTimes.Com


 

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Could We Soon Diagnose Autism And Schizophrenia By People’s Hand Movements?

autismJust the subtlest of differences in the movement of our hands could reveal our inherent personality traits, research has revealed.

By analysing and classifying these movements, health professionals could one day treat mental health conditions such as autism and schizophrenia.

Researchers have shown we all have an individual motor signature (IMS) but people who display similar behavioural characteristics tend to move in a similar way.


A team of experts from the universities of Exeter, Bristol, Montpellier and Naples Federico II, studied how people mirrored each other and themselves as an avatar on a screen.

They suggest everyone has an IMS, or blueprint of the subtle differences in the way we move compared to someone else.


Krasimira Tsaneva-Atanasova, who specialises in mathematics in healthcare at the University of Exeter, told MailOnline: ‘What we found is that each individual has their own preferred style of movement, or velocity profile.’

She said this was the case when participants were tested weeks and even months apart, so in the future individuals may be able to be identified simply by how they move.

The differences may be in the speed or weight of movement, but the study, published in the Royal Society journal Interface, does not go as far as classifying specific movements associated with certain personality traits




‘Although human movement has been well studied, what is far less well understood is the differences each of us displays when we move – whether it is faster, or lighter, or smoother for example,’ said Dr Tsaneva-Atanasova said.

However, she said ‘velocity is one of the main features and is sufficient to get a signature’.

Using a plain mirror game, in which two ‘players’ are asked to imitate each other’s movements, the team showed that while people’s movements were unique, those using similar movements tended to display ‘more organised collective behaviour’ to complete the mirroring task better.

They believe these findings indicate that people with comparable movement blueprints find it easier to coordinate with each other during interpersonal interactions.

‘This study shows that people who move in a certain way, will also react in similar ways when they are performing joint tasks,’ Dr Tsaneva-Atanasova said.

‘Essentially, our movements give an insight into our inherent personality traits.

‘What we demonstrate is that people typically want to react and interact with people who are similar to themselves.

‘But what our study also shows is that movement gives an indication of a person’s behavioural characteristics.’

The researchers think a person’s IMS, together with how they interact with others, could give experts an insight into their mental health and could pave the way for personalised prediction, diagnosis or treatments in the future.

So those who move in a distinctly different way, may have a condition not shared with the majority of a population.

People with autism or schizophrenia, for example, could potentially be diagnosed by performing a simple tactile task, rather than undergoing more invasive tests such as lying in CT scanners, Dr Tsaneva-Atanasova, said.

The research could lead to new therapeutic therapies being developed, such as a computer program where people shy of interaction with others could learn to mimic movements made by an avatar to improve their communication.

‘It could help people with social phobias become more interactive,’ Dr Tsaneva-Atanasova said.

The research is part of a wider EU-funded project called Alter Ego, which is still ongoing.

In the future, the team hopes to study the movements of healthy people and those with schizophrenia.



Taken from DailyMail.Co.Uk

The Neuroscientist Who Lost Her Mind

Struck by a brain tumour, she truly grasped how terrifying life can be for the mentally ill

 

brain-circulation-110818-02As the director of the human brain bank at the United States National Institute of Mental Health, I am surrounded by brains, some floating in jars of formalin and others icebound in freezers. As part of my work, I cut these brains into tiny pieces and study their molecular and genetic structure.

My speciality is schizophrenia, a devastating disease that often makes it hard for the patient to discern what is real and what is not.

I examine the brains of people with schizophrenia whose suffering was so acute that they committed suicide.

I always did my work with great passion, but I don’t think I really understood what was at stake until my own brain stopped working.

Early last year, I was sitting at my desk when something freakish happened. I extended my arm to turn on the computer and, to my astonishment, my right hand “disappeared” when I moved it to the right lower quadrant of the keyboard. I tried again, and the same thing happened: The hand disappeared completely as if it had been cut off at the wrist. Stricken with fear, I kept trying to find my right hand, but it was gone.

I had battled breast cancer in 2009 and melanoma in 2012, but I had never considered the possibility of a brain tumour. I knew immediately that this was the most logical explanation for my symptoms, and yet I quickly dismissed the thought.

Instead, I headed to a meeting with my colleagues. We were supposed to review new data on the molecular composition of schizophrenia patients’ frontal cortex, a region that shapes who we are – our thoughts, emotions, memories.

But I couldn’t focus because the other scientists’ faces kept vanishing. Thoughts about a brain tumour crept quietly into my consciousness again, then screamed for attention.

An MRI scan later in the day showed that I indeed had a small brain tumour – it was bleeding and blocking my right visual field. I was told it was metastatic melanoma and was given what was, in effect, a death sentence. I was a scientist, a triathlete, a wife, a mother and a grandmother. Then one day my hand vanished, and it was over.

Almost right away, I had brain surgery, which removed the tumour and the blood. I quickly regained my vision. Unfortunately, new lesions were popping up throughout my brain, small but persistent. I started radiation treatments. In the spring, I entered an immunotherapy clinical trial. Shortly before the end of this treatment, my brain really went awry.

It was difficult, at first, to pinpoint the changes in my behaviour because they came on slowly. I didn’t suddenly become someone else. Rather, some of my normal traits and behaviours became exaggerated and distorted, as if I were turning into a caricature of myself.

I had always been very active but, now, I was rushing about frantically. I had no time for anything – not even for the things I really enjoyed, like talking to my children and my sister on the telephone. I cut them off mid-sentence, running off somewhere to do something of great importance, though what exactly, I couldn’t say. I became rude and snapped at anyone who threatened to distract me. I would read a paragraph and forget it instantly. I got lost driving home from work along a route I had taken for decades. I went running in the woods outside my house, barely dressed.

Yet, I wasn’t worried. Like many patients with mental illness, whose brains I had studied for a lifetime, I was losing my grasp on reality.

I came up with elaborate justifications for my behaviour.

I had reasons for everything I did and, even if I couldn’t articulate these reasons, my certainty that they existed reinforced my belief that I was perfectly sane.

I kept sending my doctor detailed e-mail about how great I was feeling. I was excited that I had completed immunotherapy. I felt certain that there was nothing wrong with my brain. This wasn’t just wishful thinking or extreme denial; my world view made perfect sense to me. I still saw myself as a scientist – a master of the rational – and was, in fact, still working hard on other people’s brains, not able to see that my own was crashing.

One day, when I was acting particularly strangely, my family took me to the emergency room. A brain scan showed many new tumours, inflammation and severe swelling. My frontal cortex was especially affected. I had studied this area of the brain for 30 years; I knew what that kind of swelling meant, and yet I showed no interest in the scans. Instead, I believed that my doctor and my family were scheming behind my back and making a mistake by giving in to unreasonable panic. I was frustrated that no one saw the world as clearly as I did.

Despite my conviction that there was nothing really wrong with me, I took the drugs prescribed. Steroids reduced the swelling and inflammation. Then the visible tumours were destroyed by radiation. I was also placed on a new drug regimen intended to kill the melanoma cells in my body.

Gradually, my brain began to work again. Memories started coming back, as if I had awakened from a deep sleep. I could tell the days apart. I could find my way home from work. I began apologising left and right for my strange actions and insensitive behaviour. But the more I remembered, the more frightened I became that I might lose my mind again.



The underlying causes of mental illness are rarely as clear as metastatic brain cancer. And yet I felt I understood for the first time what many of the patients I study go through – the fear and confusion of living in a world that doesn’t make sense; a world in which the past is forgotten and the future is utterly unpredictable. I had tried to fill the gaps with guesses. But when my guesses were wrong, conspiracy theories crawled in.

As terrifying as it was for me, it was even more terrifying for my family. For them, it was not just the prospect of my death that was shockingly painful, but the possibility that my persona, who I was – my brain – might change so profoundly that I would, in effect, vanish before I was truly gone. Or as my daughter put it: “Mum, I thought I had already lost you.”

My latest MRI scan shows that almost all the tumours in my brain have disappeared or shrunk considerably. Against all odds, the combination of treatments has been effective. I still scrutinise my emotions and behaviours, examining my mind over and over for any loose ends. It remains an obsession.

But I am learning to delight in the fact that my brain works again. I can see the sunny street outside and make total sense of it. I can ever so casually extend my arm and call my children, and they will recognise my voice and sigh with relief.

I can flick on my computer and get back to work.


 

  • Barbara K. Lipska, a neuroscientist, is the director of the Human Brain Collection Core at the National Institute of Mental Health.

Taken from StraitsTimes.Com

Why Risk Of Schizophrenia Is Three Times Higher In Refugees

refugees schizophrenia 1Much commentary in politics and the media refers to refugees as a problem or threat, without much acknowledgement of their suffering. A large study from Sweden published in the BMJ illustrates part of that human cost. It reported that refugees in Sweden were about twice as likely to experience schizophrenia and other psychoses compared to non-refugee migrants and three times as likely as native born Swedes.

As the article points out, Sweden grants more asylum applications per capita than any other high income country. It also has a system of linked registers, which provide anonymised data on individuals from multiple sources and make it possible to do detailed research on the health problems associated with immigration and refugee status. This study focused on schizophrenia.

It is well established that being an immigrant is a risk factor for schizophrenia. Schizophrenia affects around 1% of people in their lifetime and often results in lifelong social problems and a reduced life expectancy. A widely accepted model of schizophrenia is that each individual has a genetically determined degree of predisposition (the diathesis-stress model). This can result in illness when they are subjected to a particular level of stress.

The experience of migration and of living as part of a minority are thought to cause stress which results in more frequent cases of schizophrenia in these populations. The authors of this study wanted to know whether refugees, who have been given asylum on the basis of a “well founded fear of persecution” – and so by definition have experienced a lot of stress – show even higher frequency of schizophrenia than other migrants.

The study included a total of 1.3m people, of which 24,123 were refugees, 132,663 non-refugee migrants and the rest born in Sweden to two Swedish-born parents. The result was quite clear: the refugees had roughly double the incidence of schizophrenia in non-refugee migrants and triple the incidence found in the Swedish-born. This is very much what you would expect from the diathesis-stress model, and gives an indication of the lasting burden that the experience of having to flee creates for individuals.

The ratios sound large, but you have to keep in mind that they come from differences between fairly small numbers. There were, for example, 93 cases among the 24,000 refugees – so it doesn’t mean that there will be huge numbers of schizophrenics among refugees.



The period studied ended in 2011, and so predates the current wave of refugees from Syria, although the largest proportion did come from the Middle East, and it’s reasonable to expect a similar result among the latest refugees.

There are some differences when refugees of different origins are compared: the difference between refugees and non-refugee migrants is most pronounced in those of Eastern European and Russian origin, and absent in those of Sub-Saharan African origin where the incidence in both groups is particularly high. This may be due to conditions in the countries of origin, or to possibly different social reception in Sweden.

The study compares refugees with non-refugee migrants from similar origins, so the “refugee effect” is clearly not due to genetic differences between populations. It is possible that different populations also have differing distributions of genetic predisposition.

Although our understanding of the genetics of schizophrenia is advancing rapidly, we don’t have the ability to determine whether this is the case at the moment. We cannot directly compare incidence of mental illness across countries with widely different medical systems and customs. Of course, if we had a full understanding of genetic predisposition we could predict schizophrenia risk accurately from genetic data, but we are not that far advanced, especially for comparing different populations. But we can conclude that the Swedish study supports the idea that stress increases the risk of schizophrenia.


Taken from TheConversation.Com

Scientists Find Gene Fault That Raises Schizophrenia Risk 35-Fold

schizophrenia brainScientists say they have conclusive evidence that changes to a gene called SETD1A can dramatically raise the risk of developing schizophrenia – a finding that should help the search for new treatments.

The team, led by researchers at Britain’s Wellcome Trust Sanger Institute, said damaging changes to the gene happen very rarely but can increase the risk of schizophrenia 35-fold.

Changes in SETD1A also raise the risk of a range of neurodevelopmental disorders, the researchers said.

In a study published in the journal Nature Neuroscience, the team found that mutations that remove the function of SETD1A are almost never found in the general population, but affect 1 in 1,000 people with schizophrenia.

While this gene fault explains only a very small fraction of all schizophrenia patients, it provides an important clue to the wider biology of the disorder, they said.

Schizophrenia is a severe and common psychiatric illness that affects around one in 100 people worldwide. Symptoms include disruptions in thinking, language and perception, and patients can also suffer psychotic experiences such as hearing voices or having delusions.

While the exact causes of schizophrenia are unknown, research to date suggests a combination of physical, genetic, psychological and environmental factors can make people more likely to develop it.

Jeff Barrett, who led the study for the Sanger Institute, said its results were surprising and exciting.

“Psychiatric disorders are complex diseases involving many genes, and it is extremely difficult to find conclusive proof of the importance of a single gene,” he said.



NEW PATHWAYS

Mike Owen, a Cardiff University expert in neuropsychiatric genetics and genomics, said the so-far limited understanding of schizophrenia’s causes has hampered efforts to develop new treatments.

“Current drugs are only effective in alleviating some of the symptoms, can lead to troubling side effects and are ineffective in a sizeable minority of cases,” he said.

This new finding about defects in the SETD1A gene – although only explaining a small fraction of cases – may guide researchers toward new pathways that could be targets for treatments or medicines in a larger number of cases, Owen said.

The study analyzed the genome sequences of more than 16,000 people from Britain, Finland and Sweden, including those from 5,341 people with schizophrenia.

Damage to the SETD1A gene was found in 10 of the schizophrenia patients, and surprisingly also in six other people with other developmental and neuropsychiatric disorders such as intellectual disability, the scientists said.

This shows the same gene is involved in both schizophrenia and developmental disorders and suggests they may share common biological pathways.


Taken from Reuters.Com



When People With Schizophrenia Hear Voices, They’re Really Hearing Their Own Subvocal Speech

Unlike most people, they just can’t tell it’s themselves.

electromyography .jpg.CROP.article250-mediumMy first encounter with a schizophrenic patient was as a medical student in my third week of a neurology rotation. The attending neurologist and I were called to consult on a psychiatric inpatient who had just had a seizure. “Have you taken psychiatry yet?” the doctor asked. I hadn’t. The neurologist insisted that it would be a valuable educational experience for me to see the patient on my own, listen to his story and medical history, and report back. So I headed alone to the psych ward, through the two sets of remote-activated metal doors, and into Room 621, where I met Brandon, a paranoid schizophrenic who suffered from frequent auditory hallucinations.

At 28 years old, Brandon was a graduate of Cornell University with a degree in history but had been unemployed for years afterward. He had a fresh-looking, boyish face and floppy brown hair, a look that conflicted with the disturbing history I had read in his chart. When first hospitalized three weeks earlier, Brandon repeatedly chased down staff members and yanked their earlobes. He said he was trying to “shake out their spy recorders.” In the short time he had been on the ward, he threatened to attack his nurse twice, once with a pen and once with a pair of tweezers, claiming that she was an FBI agent sent to do the work of Satan. Before his seizure that morning, he had been ranting that the nursing staff was “making him crazy” and that they were “putting the angry thoughts in his head” to make him look bad. After getting the information I needed about his seizure, I asked Brandon about his hallucinations.



“Usually I hear him when I’m alone,” he said.

“Who do you hear?” I asked.

“Gerald. He’s such an asshole. He works for the FBI. He spies on me all the time. He knows everything. It happened when I was a kid—you know, when he put the spy chip in my brain—but the doctors here say that they don’t see it on their brain scans.”

“What’s he saying now?”

Brandon leaned forward and locked eyes with me. “He’s talking about you. The devil! He sees the devil in your eyes!”

This seemed like a good time to end the interview, but still my mind was flooded with questions. Why does Brandon hear a voice in his head? Where does it come from? Why does it say what it says?

* * *

Imagine you are standing in the lobby of an unfamiliar building, various unmarked corridors and elevator banks swimming all around you, and you scratch your head as you attempt to understand the directions in your hand that are supposed to lead you to the main conference room: “Proceed down the second hallway to the left, go through the double doors, and take Elevator C to the fifth floor, Suite 511.” As you ponder which hallway is “second to the left,” and even begin to question the integrity of your navigational skills, you feel a tap on your shoulder.

“Elevator C is down that way.” A friendly passer-by points you in the right direction. Apparently you were thinking so intently about the directions that you began mumbling them out loud. You intended for this mental dialogue to remain only in your mind, and yet you ended up broadcasting your thoughts to a complete stranger.

This phenomenon is called subvocal speech, and it happens all the time. Our brains process all language, even the private language in our minds, using its distinct linguistic regions and vast neural pathways that transmit instructions to the muscles of speech. Our thoughts turn into subvocal speech when that mechanism goes as far as to rouse those muscles to contract, even though that stimulation is usually too weak to generate a voice that anyone could actually hear.

The psychiatrist Louis Gould wanted to know whether auditory hallucinations in schizophrenia have anything to do with the phenomenon of subvocal speech. Are the experiences that schizophrenics describe as having “voices in their heads” merely the unintentional mutterings of the speech muscles? If so, why would schizophrenics happen to notice their subvocal speech while healthy people do not? Gould designed an experiment using a technique called electromyography, or EMG, which measures muscle activation through time. He gathered a group of schizophrenic and healthy patients and, one by one, recorded their vocal muscle activity. When Gould compared the EMG recordings of schizophrenic patients as they experienced auditory hallucinations to those of nonhallucinating patients, he found that, when the patients were hearing voices, their EMG recordings showed greater vocal muscle activation. This result meant that when the schizophrenics were hearing voices in their heads, their vocal muscles were contracting—they were engaging in subvocal speech.

Subvocal speech is an activation of the vocal muscles even though no voice is heard. But why isn’t it heard? Is no voice produced at all or is the voice just very, very quiet? If no voice at all were produced, then subvocal speech couldn’t be the source of the hallucinated voice. But what if subvocal speech was just very quiet, and nobody but the patient could hear it? Could it help explain why schizophrenics hear voices?

Gould decided to look for the answer in one of his patients, whom we will call Lisa, a 46-year-old woman with paranoid schizophrenia. He thought to himself: If subvocal speech is a slight activation of the vocal muscles, leading to the production of extremely quiet sound, what if we were to make it louder? It should be possible, in theory, to amplify the unheard sound using a microphone. Gould pressed a small microphone to the skin of Lisa’s throat, and to his astonishment, the subvocal, previously inaudible voice emerged as a soft whisper: Airplanes… Yes, I know who they are… Also… Yes, she knows it so well. Lisa had just been telling Gould about her recent dream about airplanes. The voice continued:

Whisper: She knows I’m here. What are you going to do? She’s a voice I know. I don’t see where she goes. I know she is a wise woman. She doesn’t know what I want. She’s wise all right. People will think she is someone else.

Lisa: I’m hearing the voices again.

Whisper: She knows. She’s the most wicked thing in the whole wide world. The only voice I hear is hers. She knows everything. She knows all about aviation.

Lisa: I heard them say I have a knowledge of aviation.

 



Gould was taken aback. Whenever Lisa reported hearing the voice in her head, he heard whispers emanating from the microphone. What’s more, when asked about what the voice told her, Lisa’s description matched the content of the amplified speech word for word. The voice in Lisa’s head spoke at the same time, and said the same things, as the subvocal speech she herself generated.

Years later, a research group had a similar interaction with a 51-year-old male patient, whom we will call Roy, who often described his communication with an entity in his mind named Miss Jones. Just like in Gould’s experiment, researchers placed a microphone against Roy’s throat and recorded the following exchange:

Whisper: If you’re in his mind, you come out of there, but if you’re not in his mind you won’t come out of there. You want to stay there.

Examiner: Who said that?

Roy: Er she said…

Whisper: I said that.

Examiner: Are you talking to yourself?

Roy: No I don’t.  [To himself:] What is it?

Whisper: Mind your own business darling, I don’t want him to know what I was doing.

Roy: See that, I spoke to her to ask what she was doing and she said mind your own business.

Yet again, the timing and content of the hallucination matched the patient’s subvocal speech, words that were articulated using his own mind, lungs, and muscles. Despite how frighteningly real the “voice in his head” seemed to Roy, Miss Jones did not exist. Apparently, the voice he was hearing all along was his own.

But why doesn’t he know that?

* * *

We mumble under our breath all the time. Usually, we don’t notice it, but even if we do, we still recognize that it’s our own voice we are hearing, not that of some shady figure trespassing into our minds. So, what is it about schizophrenic patients that renders them helpless to recognize that they themselves are the ones talking?

Whenever a person hears her own voice, an unconscious recognition circuit lights up in the brain. It works by comparing the sound she hears with the expected sound of her voice, a prediction honed through years of experience with conversation. If the actual voice matches the prediction, the brain concludes that the voice was self-generated. Alternatively, if the heard voice doesn’t match the prediction, the brain concludes that someone else is speaking.

Schizophrenic patients like Brandon are believed to have a defect in this circuit. When Brandon hears his own voice, the unconscious matching system incorrectly identifies a mismatch (false negative) and prevents him from consciously recognizing that it is his own speech that he’s experiencing. His brain is left to reconcile two seemly contradictory pieces of information: on the one hand he hears a voice that isn’t his own. On the other hand, there’s nobody else in the room. So, whose voice is it?

The brain tries to generate the most logical explanation it can. Who could project a voice into Brandon’s mind who isn’t in his vicinity? Perhaps someone with access to impressive technologies—someone with the means and motivation to spy on him. Someone from the FBI? That’s possible. If an agent had implanted a chip in his brain, that would explain the voice in his head. If the agent has been spying on Brandon for a while, that would explain why the voice seems to know so much about him.

The brain is a master storyteller, designed to make sense of the chaos of our lives. It compensates for the presence of auditory hallucinations, caused by a defect in self-recognition, by writing a narrative to account for them. It’s no accident that schizophrenic patients reach for spy agencies, religious entities, or supernatural forces when describing the voices in their heads. These are theories that the brain concocts to explain how a foreign voice could infiltrate a mind, know it intimately, and torment its victim with relentless surveillance. Faced with such bewildering circumstances, the explanation the brain generates is surprisingly logical.

Excerpted fromNeuroLogic: The Brain’s Hidden Rationale Behind Our Irrational Behavior by Eliezer Sternberg, M.D. Out now from Pantheon.


Taken from Slate.Com