Evolutionary Psychology: A New Approach to Understand Crime

Relative new branch of Psychology addresses crime towards a comprehensive explanation of Punishment, Public Policy, and Prevention

Crime is responsible for a significant amount of human suffering in society. The lives of victims and their families can be adversely affected; often in profound ways. Crime can erode social trust in communities and lead to fear amongst the residents. Crime is expensive for police and even more expensive to prosecute and contain. Perpetrators, too, suffer from the effects of their actions as their lives are altered, often permanently, and typically for the worse. It’s important to analyze an evolutionary approach, which will be invaluable for advancing our understanding of why crime occurs and what accounts for the main patterns in offending that we observed.

We need to keep in mind that problematic behaviors can arise as a result of evolved psychological mechanisms operating as they were “designed” by natural and sexual selection. A significant amount of male to male aggression, for instance, reflects selection for intra-sexual competition amongst males because success in such context advances reproductive success. Male to male violence reflects the operation of evolved adaptation working as they were designed to. Problem behaviors can also arise through the operation of conditional adaptations operating as they were designed by natural and sexual selection in response to specific social and ecological environments.



Before we begin considering specific approaches for preventing crime, we think it is useful to recognize three general points regarding an evolutionary approach towards reducing problematic behaviors. First, where it is possible, programs and policies should work with “human nature” rather than against it. Even if we recognize that humans are enormously flexible in their behavioral repertories, there are likely to be certain practices, policies, and social arrangements that work too crudely against the grain of evolved predisposition and proclivities. Hence, this will likely lead to ineffectiveness. A second related point is that it can often be possible to affect “workarounds” that act on the same evolved motivations that lead to problematic behavior, but instead, channeling the behavior along more societally desirable paths is ideal.

Police officers can’t help but think they have a magical effect on the flow of traffic as all they have to do is enter a stream of vehicles in a marked patrol car and the cars around them immediately slow down and become more cautious. Of course there is no magic involved: human behavior is enormously flexible and will change in predictable ways to different features of the situation as they emerge.

There are two interesting strategies (increasing the effort and reducing the rewards of offending) that are fairly explicable from both a rational choice and evolutionary perspective. If a good deal of offending is related to the pursuit of social status, then changing the reward structure of the environment will alter the relative value of criminal actions as a means to increase social standing. Better locks, bars, screens, security measures and so forth. Simple means that offenders find it harder to obtain the rewards of offending.



Efforts to increase the risk of offending such as the implementation of closed-circuit television, improved street lighting, and better opportunity for natural surveillance have shown to be effective in reducing certain types of offending . Strategies to remove excuses for offending such as instructions, signs, notices, and techniques for altering the conscience of individuals have been evaluated less rigorously. However, we suggest that both of these situational crime prevention strategies can be effective for largely the same reasons. Both strategies provide ecological context that enhance prosocial behavior by reinforcing social and moral norms and alerting individuals to the risk of punishment.

There are a large number of different social crime prevention programs that have been developed and are subject to formal evaluations. Most of these programs focus on addressing the known risk factors for offending and there is a good deal of evidence that properly developed and implemented social crime prevention programs that can be effective in reducing offending. From an evolutionary perspective, the importance of developmental focused social crime prevention initiatives cannot be emphasized enough.



Approaches to interventions that largely focus on merely preventing or stopping risky behavior without any consideration of the ‘function’ of that behavior are not likely to be effective. We think that the key contribution of an evolutionary approach is to help us to go beyond our understanding of the developmental risk factors for offending to identify the key causal processes that are most likely to be implicated. For example, prevention programs like education and home visitation provide information about proper prenatal and antenatal care, parenting practices, and health care which create less harsh intrauterine and early childhood environments that, in turn, can promote the development of slower life history strategies.

An evolutionary perspective suggests that the existence of punishment is essential for the viable functioning of any society, small or large. Without the existence of the third-party punishment of individuals who violate important social and moral norms, there will almost certainly be a substantial reduction in cooperation and an increase in unsanctioned punishment. We are not simply suggesting that we should punish norm transgressions because that is how we have evolved to respond to such transgression. Rather, any attempt to abolish punishment is likely to have unintended negative consequences given our evolved predispositions and the evolutionary function of punishment.



Psychological and behavioral adaptations along with cultural practices have evolved in tandem in response to the violation of significant moral norms. One result of this dynamic and evolving interaction of biology and human nature has been a suite of normative systems and institutions specifically designed to prevent, and if necessary, manage serious wrongdoing (crime).
A problem with groups or individuals seeking revenge without the mediation of an impartial agency is that it can lead to a seemingly endless cycle of harmful actions and counteractions that destabilize social networks.

Punishment can be defined loosely as the intentional infliction of sanctions by the state on individuals who have unjustifiably harmed other people. There are numerous normative justifications of punishment including retributivism, consequentialism, and communicative justification.

The focus of the communicative justification of punishment on the well-being of a community means that relationships between moral stakeholders are of critical importance and the role of individual entitlements and duties assumes lesser importance. It is a collectivist approach to resolving disputes between people and arriving towards solutions to ethical problems such as crime. The process of reconciliation involves forgiveness and the willingness of individuals and the state to look beyond the imposition of punishment, or vengeance, to the moral task of repairing damaged relationships between offenders, victims, and the community.

Because humans are cultural species whose behavior is strongly influenced by social and moral norms and the ecological contexts in which they are embedded, changes in these norms can affect significant changes in behavior that can be sustained through cultural and ecological inheritance. Sustained efforts to support and facilitate the development of pro-social norms and change norms that support or facilitate antisocial behavior, are therefore, likely to be one essential component of efforts to reduce the harmful effects of crime. Changes in legal practices have an important role to play in this context. An evolutionary perspective does not provide all the answers. It does offer a coherent, theoretical framework for integrating the basic and applied sciences in a way that can foster the development of a science of intentional change that has implications for our efforts to reduce offending and the various harms that arise from crime and its management.
By: Jaime F. Adriazola
American Graduate University, Washington DC
References:
Evolutionary Criminology, Russil Durrant / Tony Ward
The Psychology of criminal conduct; New Providence NJ, Mathew Bender & Company Inc.
Missing the Revolution: Darwinism for social Scientists, Oxford: University Press
Handbook of evolutionary psychology, D. M. Buss
Why evolution is true; New York: Viking
The evolutionary psychology of violence; Psicothema

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Nonverbal Influence and Forensic Psychology

How Police Witnesses could be misled by a Simple Wave of the Hand
Hand it over.

How easy do you think it would be for someone to convince you that you’d seen something that never really happened? What about them doing this without actually saying anything misleading? That would almost be impossible, surely? Well, research into verbal and nonverbal influence suggests this can happen, and that we’re actually far more suggestible than we might like to think.

We know that people easily can be misled through words, and that changing the way we phrase a question can affect how somebody answers it. For instance, if you ask someone “how tall was the man?” they will probably say he was taller on average than if you asked “how short was the man?” A cleverly-worded question that implies something was present can make people believe they saw it, and biased questions can implant false memories in people, causing them to remember something fictional as if it were real.

But speech isn’t the only way we communicate with people. We also give lots of information away through our nonverbal behavior, especially our hand gestures. When we talk, we tend to gesture a lot, and the people we’re speaking to can use these gestures to make sense of what we’re saying.



Handy hints
Imagine you’re telling a friend that you hurt your arm recently. You might say “I hurt myself last week” and rub your arm while doing so. Here, you communicate part of the message through your speech (“hurt”) and the other part through your gesture (“arm”). A listener will combine these two pieces of information to get one full story, and probably won’t even realize the information came from two different places.

Giving somebody helpful information through gesture is one thing, but what about if we gave them some misleading information? Could a misleading gesture implant a suggestion in someone, and cause them to believe something that isn’t true? These questions sparked my research into the “gestural misinformation effect”.

In one of my first academic studies, I wanted to see if people would misremember seeing something if false information was given to them through a hand gesture. To test this, I showed participants a video (a man coming into my office and stealing a phone from my desk) and arranged for them to be interviewed on what they could remember afterwards.



After softening them up with a few distractor questions, the interviewer asked if they could describe the man’s face. We found that if the interviewer stroked his chin while asking this, significantly more participants would claim that the man had a beard or stubble than if he didn’t gesture.

We tried this with other questions, too. If the interviewer pinched his finger while asking if the man was wearing any jewelry, the participants remembered him wearing a ring. If he grasped his wrist, they remembered a watch. People seemed to remember parts of the video differently according to what was suggested to them through the interviewer’s hand gestures.

In my original set of studies, our participants were largely psychology students but, since then, we’ve replicated the effect in children, members of the general public and even lawyers. In light of this, the gestural misinformation effect seems to be quite robust.

But are people aware of how much influence these gestures have on them? Even if we can remember what has been said to us in speech, we often cannot identify when extra information has been given to us through gestures, so nonverbal influence is a bit more subtle. Typically, we’re not really aware of when we gesture, and listeners don’t generally see our gestures either.



Because of this, people can extract information from gestures without even realizing it. In a follow-up study, I found suggestions made through gesture can be just as effective as those made through speech, but that people were less likely to know when they’d been misled by a gesture compared to speech.

Forensic implications
The fact that people can be misled through gesture so easily is very interesting (if not a little scary), but there are some clear implications for this research, particularly in forensic psychology, too. Because witnesses are so prone to misleading questions, police officers have to be very careful not to suggest any leading information to them through their questions.

To make sure no unwanted influence has occurred, interviews are also audio-recorded. However, currently, there is very little training on how our gestures can influence others in interviews and, without a video recording of an interview it’s possible for a witness to be misled by gestures without a record of this happening.

These findings on nonverbal suggestion can extend to any interview situation, or any dialogue between two people. There may be times when we’ve been influenced by someone’s hand gestures, and without even knowing it. Because of this, we should be aware of the power of nonverbal suggestion and how susceptible we can be to its effects.
Source: Daniel Gurney - The Conversation, Academic -Journal

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Model of Anorexia Created Using Stem Cells

Though often viewed as a non-biological disorder, new research suggests 50 to 75 percent of risk for AN may be heritable; with predisposition driven primarily by genetics and not, as sometimes presumed, by vanity, poor parenting or factors related to specific groups of individuals. NeuroscienceNews.com image is for illustrative purposes only.

Findings suggest a strong genetic factor could predispose people to anorexia and other eating disorders. Technique suggests novel gene may contribute to eating disorder.

An international research team, led by scientists at University of California San Diego School of Medicine, has created the first cellular model of anorexia nervosa (AN), reprogramming induced pluripotent stem cells (iPSCs) derived from adolescent females with the eating disorder.

Writing in the March 14th issue of Translational Psychiatry, the scientists said the resulting AN neurons — the disease in a dish — revealed a novel gene that appears to contribute to AN pathophysiology, buttressing the idea that AN has a strong genetic factor. The proof-of-concept approach, they said, provides a new tool to investigate the elusive and largely unknown molecular and cellular mechanisms underlying the disease.

“Anorexia is a very complicated, multifactorial neurodevelopmental disorder,” said Alysson Muotri, PhD, professor in the UC San Diego School of Medicine departments of Pediatrics and Cellular and Molecular Medicine, director of the UC San Diego Stem Cell Program and a member of the Sanford Consortium for Regenerative Medicine. “It has proved to be a very difficult disease to study, let alone treat. We don’t actually have good experimental models for eating disorders. In fact, there are no treatments to reverse AN symptoms.”



Primarily affecting young female adolescents between ages 15 and 19, AN is characterized by distorted body image and self-imposed food restriction to the point of emaciation or death. It has the highest mortality rate among psychiatric conditions. For females between 15 and 24 years old who suffer from AN, the mortality rate associated with the illness is 12 times higher than the death rate of all other causes of death.

Though often viewed as a non-biological disorder, new research suggests 50 to 75 percent of risk for AN may be heritable; with predisposition driven primarily by genetics and not, as sometimes presumed, by vanity, poor parenting or factors related to specific groups of individuals.

But little is actually known about the molecular, cellular or genetic elements or genesis of AN. In their study, Muotri and colleagues at UC San Diego and in Brazil, Australia and Thailand, took skin cells from four females with AN and four healthy controls, generated iPSCs (stem cells with the ability to become many types of cells) from these cells and induce these iPSCs to become neurons.



(Previously, Muotri and colleagues had created stem cell-derived neuronal models of autism and Williams syndrome, a rare genetic neurological condition.)

Then they performed unbiased comprehensive whole transcriptome and pathway analyses to determine not just which genes were being expressed or activated in AN neurons, but which genes or transcripts (bits of RNA used in cellular messaging) might be associated with causing or advancing the disease process.

No predicted differences in neurotransmitter levels were observed, the researchers said, but they did note disruption in the Tachykinin receptor 1 (TACR1) gene. Tachykinins are neuropeptides or proteins expressed throughout the nervous and immune systems, where they participate in many cellular and physiological processes and have been linked to multiple diseases, including chronic inflammation, cancer, infection and affective and addictive disorders.

The scientists posit that disruption of the tachykinin system may contribute to AN before other phenotypes or observed characteristics become obvious, but said further studies employing larger patient cohorts are necessary.



“But more to the point, this work helps make that possible,” said Muotri. “It’s a novel technological advance in the field of eating disorders, which impacts millions of people. These findings transform our ability to study how genetic variations alter brain molecular pathways and cellular networks to change risk of AN — and perhaps our ability to create new therapies.”
Source: NEUROSCIENCE NEWS

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New MIT-developed System can make Webpages load 34 per cent Faster in any Browser

Students walk across the MIT campus, where the program was developed Joe Raedle/Getty Images

The 'Polaris' system could help counter the browser-slowing effects of complex webpages

Computer scientists at the world-famous Massachusetts Institute of Technology (MIT) have developed a system that can reliably make websites load 34 per cent faster.

As internet speeds have increased, websites have got more complex, leaving some pages sluggish and unresponsive. This is a problem for companies like Amazon, who say that for every one-second delay in loading time, their profits are cut by one per cent.
But a team of researchers, working at the university's Computer Science and Artificial Intelligence Laboratory, may have found the solution.



Named Polaris, the system cuts load-times by determining the best way to 'overlap' the downloading of different parts of a webpage.

When you visit a new page, your browser reaches across the internet to fetch 'objects' like pictures, videos, and HTML files. The browser then evaluates the objects and puts them on the page.

However, some objects are dependent on others, and browsers can't see all of these dependencies until they come across them.

Polaris works by tracking all of these relationships and dependencies between objects on the page and turning the information into a 'dependency graph' that can be interpreted by your browser.

Polaris essentially gives the browser a roadmap of the page, with all the details of the best and quickest way to load it.

PhD student Ravi Netravali, who worked on Polaris, explained: "It can take up to 100
milliseconds each time a browser has to cross a mobile network to fetch a piece of data."
"As pages increase in complexity, they often require multiple trips that create delays that really add up. Our approach minimizes the number of round trips so that we can substantially speed up a page's load-time."



The researchers tested Polaris across a range of network conditions on some of the world's most popular websites, and found it made them load an average of 34 per cent faster when compared to a normal browser.

Polaris could be used on any website and with unmodified browsers, and when tech companies like Google and Amazon are working hard to improve load-times, a similar system might appear on your device soon.

Source: Massachusetts Institute Of Technology, Computer Science

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MIT desarrolla un Nuevo Sistema que Revolucionará las Páginas Web

Los estudiantes caminan por el campus del MIT, donde se desarrolló el programa Joe Raedle / Getty Images

El sistema 'Polaris' podría ayudar a contrarrestar los efectos de desaceleración del navegador de páginas web complejas

Científicos de computación del famoso Instituto de Tecnología de Massachusetts (MIT) han desarrollado un sistema que puede hacer que los sitios web, de forma fiable, carguen un 34 por ciento más rápido.

Como las velocidades del Internet han aumentado, los sitios web se han vuelto más complejos, dejando algunas páginas lentas e insensibles. Este es un problema para las empresas como Amazon, que dicen que por cada segundo de retraso en el tiempo de carga, sus beneficios se reducen en un uno por ciento.

Pero un equipo de investigadores, que trabaja en el Laboratorio de Informática e Inteligencia Artificial de la universidad, ha logrado encontrado la solución.

Nombrado Polaris, el sistema reduce los tiempos de carga determinando la mejor manera de "superponerse" a la descarga de diferentes partes de una página web.



Cuando visita una página nueva, su navegador llega a través del Internet para buscar "objetos" como imágenes, videos y archivos HTML. A continuación, el navegador evalúa los objetos y los coloca en la página.

Sin embargo, algunos objetos son dependientes de otros, y los navegadores no pueden ver todas estas dependencias hasta que se encuentran con ellos.

Polaris funciona mediante el seguimiento de todas estas relaciones y dependencias entre los objetos en la página y convertir la información en un "gráfico de dependencia" que puede ser interpretado por su navegador.
Polaris esencialmente da al navegador una hoja de ruta de la página, con todos los detalles de la mejor y más rápida forma de cargarlo.



El estudiante de PhD, Ravi Netravali, que trabajó en Polaris, explicó: "Se puede tomar hasta 100 milisegundos cada vez que un navegador tiene que cruzar una red móvil, a buscar una pieza de datos."
"
A medida que las páginas aumentan en complejidad, a menudo requieren viajes múltiples que crean retrasos que realmente se van sumando. Nuestro enfoque minimiza el número de viajes de ida y vuelta para que podamos aumentar sustancialmente el tiempo de carga de una página".
Los investigadores probaron Polaris a través de una amplia gama de condiciones de red, en algunos de los sitios web más populares del mundo, y encontraron que les hacía cargar un promedio de un 34 por ciento más rápido, en comparación con un navegador normal.

Polaris podría ser utilizado en cualquier sitio web, en los navegadores no modificados, y cuando las empresas de tecnología como Google y Amazon estén trabajando fuerte para mejorar la carga de los tiempos, un sistema similar podría aparecer en el dispositivo, prontamente.
Fuente: Instituto de Tecnología de Massachusetts, Ciencias de la Computación

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Genetics Play a Role in Social Anxiety Disorder, Study Finds

The serotonin transporter gene “SLC6A4” is linked to social anxiety disorder.

Researchers at the Institute of Human Genetics at the University of Bonn in Germany recently discovered that a specific serotonin transporter gene called “SLC6A4” is strongly correlated with someone's odds of suffering from social anxiety disorder (SAD). The initial findings of this research were published online ahead of print March 9 in the journal Psychiatric Genetics.

Social anxiety disorder (or social phobia) is a common and heritable psychiatric disorder that is driven by a combination of genetic and environmental factors. Until now, genetic studies on SAD have been rare. According to the researchers, "This is the largest association study so far into social phobia."
For this study the German’s researcher genotyped 321 patients with SAD and 804 controls without social phobia. Then, they carried out a single-marker analysis to identify a quantitative association between SAD and avoidance behaviors. Their results provide evidence that the serotonin transporter gene SLC6A4 is frequently correlated with anxiety-related traits.

Notably, selective-serotonin reuptake inhibitors (SSRIs) are often prescribed to treat depression and anxiety disorders. SSRIs are believed to target the serotonin transporter gene SLC6A4.



People with social anxiety tend to avoid larger groups and situations in which they fearbeing judged by others. SAD is marked by symptoms such as increased heart rate, sweaty palms, shakiness, shortness of breath, etc.

The physiological discomfort of social anxiety reinforces avoidance behaviors and a withdrawal from face-to-face social contact. The fear of social encounters can lead to isolation and loneliness that snowballs. Unfortunately, people with social anxiety who rely excessively on social media to maintain a sense of connectedness may actually exacerbate their feelings of perceived social isolation, according to a recent study by researchers at the University of Pittsburgh, School of Medicine.

In 1948, when Maurice M. Rapport first isolated the chemical serotonin (5-hydroxytryptamine, 5-HT) in the human body and brain, serotonin was initially classified as a “serum agent that affected vascular tone.” Today, serotonin is commonly viewed as a neurotransmitter that helps to maintain mood balance.

Although there is a strong link between serotonin, depression, and social anxiety disorders; scientists remain uncertain about which comes first in terms of driving the correlation vs. causation dynamic between serotonin and psychiatric disorders. For example: Do low levels of serotonin contribute to social anxiety or does social phobia trigger a decrease in serotonin levels?

Interestingly, a 2015 study, "Serotonin Synthesis and Reuptake in Social Anxiety Disorder,“ published in JAMA Psychiatry reported that Individuals with social phobia have too much serotonin—not too little.

Surprisingly, the researchers found that the more serotonin someone with SAD self-produced, the more anxious he or she became in social situations. This raises doubt about the common assumption that selective serotonin reuptake inhibitor (SSRIs) help to lower social anxiety by keeping more serotonin in circulation.
In a statement, co-author Andreas Frick, a doctoral student at Uppsala University Department of Psychology said,



"Not only did individuals with social phobia make more serotonin than people without such a disorder, they also pump back more serotonin. We were able to show this in another group of patients using a different tracer which itself measures the pump mechanism.
We believe that this is an attempt to compensate for the excess serotonin active in transmitting signals. Serotonin can increase anxiety and not decrease it as was previously often assumed."

Taken together, all of this new research marks a significant leap forward when it comes to identifying changes in the brain's chemical messengers in people who suffer from social anxiety disorders. That said, much more research is needed to fully understand the enigmatic and complex workings of serotonin and transporter gene SLC6A4.

"There is still a great deal to be done in terms of researching the genetic causes of this illness," Andreas Forstner from the Institute of Human Genetics at the University of Bonn concluded.

If you would like to get involved in the genetic research on social anxiety disorder, Forstner and colleagues are encouraging the general public to participate in their research online by visiting their website: Social Phobia Research. The more people that get involved in the study of social anxiety disorder, serotonin, and SLC6A4, the more precisely the researchers will be able to decode these complex mechanisms.
References: Psychology Today
Andreas J. Forstner, Stefanie Rambau, Nina Friedrich, Kerstin U. Ludwig, Anne C. Böhmer, Elisabeth Mangold, Anna Maaser, Timo Hess, Alexandra Kleiman, Antje Bittner, Markus M. Nöthen, Jessica Becker, Franziska Geiser, Johannes Schumacher, Rupert Conrad.

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Understanding the Obsessive Compulsive Disorder: Conceptual Background and Brain Etiology

Patients suffering from obsessive–compulsive disorder (OCD) experience a combination of anxiety-producing obsessive thought patterns and related compulsive behaviors designed to reduce the distress associated with the obsessions.

Obsessions are recurrent thoughts, impulses, or images that are threatening because they are perceived as either unacceptable or leading to a dreaded outcome, and thus cause marked anxiety. Common obsessional ‘themes’ include contamination (thinking one has contacted dangerous germs or toxins), aggression (image or urge to drive into oncoming traffic or stab one’s spouse), accidental harm (fear that one has hit a pedestrian or doubting whether one turned off the stove), blasphemy (thinking one has offended God by doing a religious ritual incorrectly), and sexuality (intrusive images of having sex with a child or parent). Sometimes an obsession is vague, yet still evokes a looming sense of danger: a ‘bad feeling’ that occurs during an action, or the inexplicable sense that a behavior has not been done correctly. Multiple types of obsessions are found in most affected individuals and can change over time.



Compulsions include behaviors (e.g., hand washing, checking, ordering, or arranging things) and mental actions (e.g., praying, counting, repeating words silently) that are aimed at preventing or neutralizing the threat associated with the obsession, and thus temporarily reduce anxiety. This relief from the distress is highly reinforcing, resulting in the persistent use of compulsions. Compulsive behaviors are often repeated (checking the stove 15 times), or have to be performed according to rules that must be applied rigidly (a sterilization ritual for plates and silverware before meals).

Sometimes compulsions are ‘logically’ linked to the obsessions, as in the case of washing one’s hands in response to a contamination obsession, or driving back to a spot where one fears they may have hit someone. Done once, such behavior might seem reasonable; it is the repetitive, time-consuming, and rigid quality that distinguishes compulsions. Sometimes there is no ‘logical’ action to prevent the obsessional threat so, compulsions develop that are more akin to superstitious rituals. For example, going through doorways can often trigger an obsession (‘bad feeling’). Given no clear antidote to the vague threat, individuals may develop a ritualized compulsion aimed at neutralizing the obsession in some magical way. This might involve having to go through the door on the left side, touching both sides of the threshold 3 times, or passing through the doorway repeatedly until it is accomplished without any ‘bad thoughts.’



Individuals with OCD generally have some degree of insight that their symptoms are excessive or unreasonable. Nonetheless, the disorder is time-consuming, distressing, and severely impairing within the realms of both social and occupational functioning. It is also associated with increased risk of suicide. OCD has an estimated, lifetime prevalence in the general US population of 2–3%, and is equally common in both males and females. The age of onset follows a bimodal distribution: early onset (prepubescent, the majority of cases) and late onset (early 20s). Early-onset cases are more likely to be male, have a family history of OCD, greater symptom severity, and co-occurring tics, OCD spectrum (discussed in section Differential Diagnosis), and disruptive behavioral disorders (e.g., attention deficit hyperactivity disorder).

Differential Diagnosis
It is important to distinguish OCD from worry, intrusive thoughts, and compulsions seen in everyday life. OCD obsessions are experienced as unwanted and anxiety-producing, whereas worry functions more as a mental coping strategy that provides a sense of control and preparation for a perceived future threat. Intrusive thoughts (i.e., suddenly envisioning a family member falling off a cliff while hiking together) are common, but in OCD they occur at a higher frequency, and are experienced as having unusual importance, so are more distressing to the affected individual. Compulsive behaviors are also frequently seen in normal populations in the form of superstitious behavior and repetitive checking. The diagnosis of OCD is made only if they are time consuming or if they result in significant psychosocial impairment or distress.

There are a number of disorders that share the features of OCD, and are sometimes considered as ‘OCD spectrum disorders.’ Disorders such as body dysmorphic disorder, hypochondriasis, and hoarding and eating disorders include obsessive-like fears (that one has a serious illness or is fat), but the thoughts are not experienced themselves as highly intrusive and inappropriate. Derma-tillomania (skin picking) and trichotillomania (hair pulling) have repetitive behaviors that may bring some anxiety relief, but they are neither triggered by obsessions nor have the magical or ritualistic quality of OCD compulsions. Although impulse-control disorders such as kleptomania, pyromania, and pathological gambling also have recurrent thoughts and behaviors that are difficult to resist, the drive tends to be more pleasure-seeking than distress reducing.



Schizophrenia is often characterized by strongly held beliefs that are clearly false (delusions) as well as by stereotyped behaviors. Individuals with OCD, however, generally show considerable insight into their symptoms. In major depression, the depressed individual may have distressing, repetitive thoughts, but these are rarely resisted, and are often focused on a past incident rather than on a current or future threat. Although it has a similar name, obsessive–compulsive personality disorder is actually quite different from OCD. Obsessive–compulsive personality disorder does not involve obsessions or compulsions; rather, it is characterized by a pervasive pattern of maladaptive orderliness, perfectionism, and control.

Other disorders may mimic OCD. Tics and stereotyped movements are similar to compulsions in their appearance but not in their function. Generally, the cognitive elements involved in OCD compulsions are much more complex, whereas in tics and stereotypic movements, the individual does not report any specific reason for the behavior, but only a nonspecific tension that builds until the behavior is performed. Of note, Tourette’s syndrome and OCD are frequently co-occurring disorders, and individuals with Tourette’s should be routinely asked about the presence of obsessions and compulsions.



Etiology
There is converging evidence that OCD involves dysfunction of the corticostriatal-thalamic circuits, which help integrate cognitive and sensorimotor functions, and in particular initiate automatic, procedural behaviors. The high co-occurrence of OCD with Tourette’s – a disorder involving cortical and striatal pathways – is suggestive of a similar etiology. There are also data supporting an association between an autoimmune response to Group A β-hemolytic Streptococcus, affecting the striatal regions, and the acute emergence of OCD, often with tic symptoms (including Tourette’s). The term pediatric autoimmune neuropsychiatric disorder associated with Streptococcus refers to a group of children with this presumed immunological etiology. The role of serotonin in the corticostriatal-thalamic circuits is thought to be important, and several studies suggest that serotonin reuptake inhibitors may normalize activity in these pathways. Medications that boost serotonin activity reliably reduce OCD symptoms. Research also suggests that abnormalities in the glutamate and dopamine systems are involved in OCD as well.

The evidence for a genetic contribution is supported by the monozygotic twin studies showing a concordance rate from 63% to 87%, and first-degree relatives showing rates of OCD in the range of 10–22.5%. No candidate gene has been identified that can reliably account for the broad phenotype of OCD. Animal models of OCD, such as those found naturally in dogs or induced in laboratory mice identify the potential genes for further study.



From the standpoint of neuroimaging, OCD is one of the most investigated illnesses in the anxiety cluster. As of yet, it remains impossible to attribute causality to particular brain structures in the cognitions and clinical features of OCD. In animal models, abnormalities in the orbitofronto-striatal circuits are associated with an impaired ability to modify behavior in response to new information, for example: impaired inhibition of previously important, but now inappropriate response to stimuli. Humans with injuries to the striatum, or areas to which it projects, often develop obsessive –compulsive behaviors. Nevertheless, no consistent structural abnormality has been identified in patients meeting the criteria for OCD. This may suggest that the causative abnormalities are present at the level of a system or network, not at the level of isolated neuroanatomical structures, or because of a marked heterogeneity within the diagnosis. Illnesses with components of compulsive and impulsive behaviors, such as Tourette’s syndrome and trichotillomania, tend to occur in comorbidity with OCD, or cluster with OCD within families. Further research into these disorders of overlapping end phenotype may serve to illuminate the rest of the OCD picture as it relates to the brain structure.
Source: Vimen L. Beckner, University of California San Francisco, and San Francisco Group for Evidence-Based Psychotherapy, San Francisco, CA, USA.

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How humans bond: The Brain Chemistry Revealed

In a new study researches found for the first time that dopamine is involved in human bonding bringing the brain’s reward into understanding of how we form human attachments.

In new research published Monday in the journal Proceedings of the National Academy of Sciences, Northeastern University psychology professor Lisa Feldman Barrett found, for the first time, that the neurotransmitter dopamine is involved in human bonding, bringing the brain's reward system into our understanding of how we form human attachments. The results, based on a study with 19 mother-infant pairs, have important implications for therapies addressing postpartum depression as well as disorders of the dopamine system such as Parkinson's disease, addiction, and social dysfunction.



"The infant brain is very different from the mature adult brain -- it is not fully formed," says Barrett, University Distinguished Professor of Psychology and author of the forthcoming book How Emotions Are Made: The Secret Life of the Brain. "Infants are completely dependent on their caregivers. Whether they get enough to eat, the right kind of nutrients, whether they're kept warm or cool enough, whether they're hugged enough and get enough social attention, all these things are important to normal brain development. Our study shows clearly that a biological process in one person's brain, the mother's, is linked to behavior that gives the child the social input that will help wire his or her brain normally. That means parents' ability to keep their infants cared for leads to optimal brain development, which over the years results in better adult health and greater productivity."

To conduct the study, the researchers turned to a novel technology: a machine capable of performing two types of brain scans simultaneously -- functional magnetic resonance imaging, or fMRI, and positron emission tomography, or PET.

fMRI looks at the brain in slices, front to back, like a loaf of bread, and tracks blood flow to its various parts. It is especially useful in revealing which neurons are firing frequently as well as how different brain regions connect in networks. PET uses a small amount of radioactive chemical plus dye (called a tracer) injected into the bloodstream along with a camera and a computer to produce multidimensional images to show the distribution of a specific neurotransmitter, such as dopamine or opioids.



Barrett's team focused on the neurotransmitter dopamine, a chemical that acts in various brain systems to spark the motivation necessary to work for a reward. They tied the mothers' level of dopamine to her degree of synchrony with her infant as well as to the strength of the connection within a brain network called the medial amygdala network that, within the social realm, supports social affiliation.

"We found that social affiliation is a potent stimulator of dopamine," says Barrett. "This link implies that strong social relationships have the potential to improve your outcome if you have a disease, such as depression, where dopamine is compromised. We already know that people deal with illness better when they have a strong social network. What our study suggests is that caring for others, not just receiving caring, may have the ability to increase your dopamine levels."



Before performing the scans, the researchers videotaped the mothers at home interacting with their babies and applied measurements to the behaviors of both to ascertain their degree of synchrony. They also videotaped the infants playing on their own.

Once in the brain scanner, each mother viewed footage of her own baby at solitary play as well as an unfamiliar baby at play while the researchers measured dopamine levels, with PET, and tracked the strength of the medial amygdala network, with fMRI.

The mothers who were more synchronous with their own infants showed both an increased dopamine response when viewing their child at play and stronger connectivity within the medial amygdala network. "Animal studies have shown the role of dopamine in bonding but this was the first scientific evidence that it is involved in human bonding," says Barrett. "That suggests that other animal research in this area could be directly applied to humans as well."

The findings, says Barrett, are "cautionary." "They have the potential to reveal how the social environment impacts the developing brain," she says. "People's future health, mental and physical, is affected by the kind of care they receive when they are babies. If we want to invest wisely in the health of our country, we should concentrate on infants and children, eradicating the adverse conditions that interfere with brain development."
Source: Materials provided by Northeastern University, original written by Thea Singer.

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