Posts Tagged ‘mental health’

By Rachael Rettner

Many people tend to look back on the past with rose-colored glasses, remembering the good times and the good feelings…while forgetting the bad.

But a new study suggests that heavy marijuana users may have some trouble letting go of negative emotions tied to memories — a phenomenon that’s also seen in people with depression. Earlier research has also linked marijuana use with depression.

Although the new results are very preliminary, the findings, presented here on Friday (May 25) at the annual meeting of the Association for Psychological Science, may offer clues about the link between marijuana use and depression.

Rose-colored memories

The study explored a psychological phenomenon called “fading affect bias,” in which people tend to hold on to positive feelings tied to their memories more than they hold on to negative feelings. In other words, negative feelings related to our memories fade faster than positive ones.

Psychologists have hypothesized that this phenomenon, which is generally seen in people without mental health conditions, may serve as a sort of “psychological immune system,” said study lead author Daniel Pillersdorf, a graduate student in psychology at the University of Windsor in Ontario. This may be “so that we think more pleasantly in general, and don’t have that cognitive burden of holding on to negative emotions associated with memories,” Pillersdorf said.

Some previous studies have suggested that this fading affect bias may be different for people who use drugs, but no studies have looked at whether marijuana use could affect this phenomenon.

In the new study, the researchers analyzed information from 46 heavy marijuana users — most of whom used the drug at least four times a week — and 51 people who didn’t use marijuana. Participants were asked to recall, and provide written descriptions of, three pleasant memories and three unpleasant memories from the past year. The participants were then asked to rate the intensity of emotion tied to those memories, on a scale of negative 10, meaning extremely unpleasant, to positive 10, or extremely pleasant. They rated their emotions both at the time the memory was made, and at the current time. (Marijuana users were not under the influence at the time the researchers asked them the questions.)

The researchers found that both marijuana users and non-users showed fading affect bias, but for marijuana users, the fading was a lot less.

“They were hanging on to that unpleasant affect over time, much more” than non-users, Pillersdorf told Live Science. “They were less able … to shed that unpleasantness associated with their memories.”

The study also found that marijuana users tended to recall life events in more general terms than specific ones. For example, when asked about a happy event in the past year, marijuana users were more likely to respond with general or broad answers such as “I went on vacation,” rather than recalling a specific event or day, such as “I attended my college graduation.” This phenomenon is known as over-general autobiographical memory, and it’s also linked with depression, Pillersdorf said.

It’s important to note that the new study found only an association and cannot determine why marijuana users show less fading affect bias, and more overgeneral memory, than non-users.

Link with depression?

Even so, the new findings agree with previous research that has found a link between heavy marijuana use and depression. However, researchers don’t know why marijuana and depression are linked — it could be that marijuana use plays a role in developing depression, or that people who are already depressed are more likely to use the drug. [7 Ways Marijuana May Affect the Brain]

Based on the new findings, one hypothesis is that the decreased “fading” of negative memories in marijuana users could be contributing to the development or continuing of depression, Pillersdorf said. “It may be that, chronic or frequent cannabis use is putting [a person] more at risk for the development or continuing of depression,” he said. However, Pillersdorf stressed that this is just a hypothesis that would need to be investigated with future research.

To further investigate the link, researchers will need to study marijuana users and non-users over long periods of time. For example, researchers could start with people in their late teens or early 20s, who don’t have depression, and see if those who use marijuana frequently are more likely to eventually develop depression than non-users.

Additional studies could also investigate whether other substances have an effect on fading affect bias, Pillersdorf said.

The study has not yet been published in a peer-reviewed journal.

https://www.livescience.com/62679-marijuana-negative-memories.html?utm_source=notification

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Exposure to early life trauma can lead to poor physical and mental health in some individuals, which can be passed on to their children. Studies in mice show that at least some of the effects of stress can be transmitted to offspring via environmentally-induced changes in sperm miRNA levels.

A new epigenetics study raises the possibility that the same is true in humans. It shows for the first time that the levels of the same two sperm miRNAs change in both men and mice exposed to early life stress. In mice, the negative effects of stress are transmitted to offspring. The study is published On May 23rd in Translational Psychiatry.

“The study raises the possibility that some of the vulnerability of children is due to Lamarckian type inheritance derived from their parents’ experiences,” said Larry Feig, Ph.D., professor of Developmental, Molecular and Chemical Biology at Tufts University School of Medicine and member of the Cell, Molecular and Developmental Biology and Neuroscience programs at the Sackler School of Graduate Biomedical Sciences at Tufts.

The human part of the study utilized the Adverse Childhood Experiences (ACE) questionnaire as an indicator of men’s early life trauma. The ACE Study questionnaire includes 10 yes or no questions about one’s experiences until the age of 18, including physical, verbal, or sexual abuse, and physical or emotional neglect. Other questions relate to one’s family members. Four or more yes answers put one at significantly increased risk for future mental and physical health problems. According to a ChildTrends research brief published in 2014, a remarkably high percentage (~10 percent) of the population report scores at or above this cutoff.

miRNAs constitute a newly appreciated type of gene regulator, where each miRNA controls a distinct set of genes. Until recently, sperm from fathers were thought to contribute only DNA to the mother’s egg upon fertilization, but new data in mice indicate that sperm also contribute miRNAs that influence the next generation. Sperm miRNA expression in humans is known to be affected by environmental factors, such as smoking and obesity, but no human study to date has documented the effects of stress.

The new study found that among 28 Caucasian male volunteers, the expression of two highly related sperm miRNAs, miR-449 and miR-34, were inversely proportional to the men’s ACE scores. Men with the most extensive early abuse (highest ACE scores) had as much as a 300-fold reduction in the two sperm miRNAs compared to men with the least abuse.

The idea that these changes can affect the next generation is supported by additional findings in the study, e.g.:

the same sperm miRNA changes that take place in men with high ACE scores also occur in mice exposed to early life social instability stress, which Feig’s lab has shown previously leads to anxiety and sociability defects in female offspring of stressed males for at least three generations;
these two sets of miRNAs are known to work together in mice to allow proper development of the brain and sperm;
in humans, miR-34c has been implicated in promoting early embryo development;
the mouse studies showed that the decline in these sperm miRNA levels is transmitted to the next generation; and
when these embryos mature, these miRNAs are also reduced in the sperm of their male offspring who pass on stress behaviors to their female offspring.
“This is the first study to show that stress is associated with altered levels of sperm miRNAs in humans. We are currently setting up a new, larger study in men, and additional experiments in mice that could yield further support for the idea that changes in these sperm miRNAs do, in fact, contribute to an elevation of stress-related disorders across generations,” said David Dickson, an M.D./Ph.D. student at Tufts and first author of the study.

“Looking to the future, we may be able to figure out a way to restore the low miRNA levels found in men exposed to extreme trauma, because epigenetic changes, such as stress-induced decreases in sperm miRNA expression, are reversible, unlike genetic changes that alter the DNA sequence,” Dickson added.

For example, obesity has been shown to alter specific sperm miRNA levels in men, while bariatric surgery and subsequent weight loss can reverse the changes. In addition, Isabelle Mansuy’s lab has reversed some of the negative effects of stress in mice across generations by exposing mice to an “enriched environment” that involves extensive social interactions, exercise and opportunities to explore their surroundings.

Feig pointed out that in addition to focusing on the potential transgenerational effects of stress, there is a growing appreciation that physicians should collect information on childhood trauma for the sake of the patients who are experiencing this early trauma.

This is because “childhood abuse, trauma and dysfunction adds to the risk of future physical and psychiatric maladies, and significant exposure to abusive and/or dysfunctional families is remarkably common. Moreover, sensitivity to PTSD has been shown to correlate with ACE score, implying the ACE questionnaire could be used as a screening tool to identify people who should take extra precaution to avoid potentially traumatic experiences,” he said.

“However, some people may not answer the ACE survey accurately due to inaccurate recall or because of the sensitive nature of many of the questions, particularly in settings that do not allow anonymity and/or where their answers could affect their future. Thus, discovery of unbiased markers for early trauma, like specific sperm miRNA content, could complement ACE surveys in some clinical settings to bolster preventative medicine,” he concluded.

The authors note that the relatively small sample size limits their ability to more deeply explore the association between ACE scores and miRNA expression. In addition, a longitudinal study with information on behavioral and psychological factors throughout adulthood, with repeated measurements of sperm miRNA content, could allow for further exploration on the effect of cumulative exposure to childhood trauma on miRNA.

Additional authors are Jessica Paulus, Sc.D., Tufts Medical Center as well as Tufts University School of Medicine and the Sackler School; Virginia Mensah, M.D., formerly in Feig’s lab with Women & Infants Hospital and the Warren Alpert Medical School at Brown University and now with the Reproductive Science Center of New Jersey; Janis Lem, Ph.D., Tufts Medical Center; Lorena Saavedra-Rodriguez, Ph.D., formerly a postdoctoral fellow in Feig’s laboratory at Tufts and now with a biopharmaceutical company; and Adrienne Gentry, D.O. and Kelly Pagidas, M.D., University of Louisville School of Medicine.

This study was supported by awards from the National Institute of Mental Health of the National Institutes of Health (R01MH107536), as well as the Tufts Center for Neuroscience Research (National Institute of Neurological Disorders and Stroke of the NIH, P30NS047243). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or other funders.

Dickson, D.A., Paulus, J.K., Mensah, V., Lem, J., Saavedra-Rodriguez, L., Gentry, A., Pagidas, K., and Feig, L. A. (2018). Reduced levels of miRNAs 449 and 34 in sperm of mice and men exposed to early life stress. Translational Psychiatry. https://doi.org/10.1038/s41398-018-0146-2

https://now.tufts.edu/news-releases/early-life-trauma-men-associated-reduced-levels-sperm-micrornas


Pinpoint stimulation of a cluster of nerve cells in the brains of mice encouraged timid responses to a perceived threat, whereas stimulation of an adjacent cluster induced boldness and courage.

Researchers at the Stanford University School of Medicine have identified two adjacent clusters of nerve cells in the brains of mice whose activity level upon sighting a visual threat spells the difference between a timid response and a bold or even fierce one.

Located smack-dab in the middle of the brain, these clusters, or nuclei, each send signals to a different area of the brain, igniting opposite behaviors in the face of a visual threat. By selectively altering the activation levels of the two nuclei, the investigators could dispose the mice to freeze or duck into a hiding space, or to aggressively stand their ground, when approached by a simulated predator.

People’s brains probably possess equivalent circuitry, said Andrew Huberman, PhD, associate professor of neurobiology and of ophthalmology. So, finding ways to noninvasively shift the balance between the signaling strengths of the two nuclei in advance of, or in the midst of, situations that people perceive as threatening may help people with excessive anxiety, phobias or post-traumatic stress disorder lead more normal lives.

“This opens the door to future work on how to shift us from paralysis and fear to being able to confront challenges in ways that make our lives better,” said Huberman, the senior author of a paper describing the experimental results. It was published online May 2 in Nature. Graduate student Lindsey Salay is the lead author.

Perilous life of a mouse
There are plenty of real threats in a mouse’s world, and the rodents have evolved to deal with those threats as best they can. For example, they’re innately afraid of aerial predators, such as a hawk or owl swooping down on them. When a mouse in an open field perceives a raptor overhead, it must make a split-second decision to either freeze, making it harder for the predator to detect; duck into a shelter, if one is available; or to run for its life.

To learn how brain activity changes in the face of such a visual threat, Salay simulated a looming predator’s approach using a scenario devised some years ago by neurobiologist Melis Yilmaz Balban, PhD, now a postdoctoral scholar in Huberman’s lab. It involves a chamber about the size of a 20-gallon fish tank, with a video screen covering most of its ceiling. This overhead screen can display an expanding black disc simulating a bird-of-prey’s aerial approach.

Looking for brain regions that were more active in mice exposed to this “looming predator” than in unexposed mice, Salay pinpointed a structure called the ventral midline thalamus, or vMT.

Salay mapped the inputs and outputs of the vMT and found that it receives sensory signals and inputs from regions of the brain that register internal brain states, such as arousal levels. But in contrast to the broad inputs the vMT receives, its output destination points were remarkably selective. The scientists traced these outputs to two main destinations: the basolateral amygdala and the medial prefrontal cortex. Previous work has tied the amygdala to the processing of threat detection and fear, and the medial prefrontal cortex is associated with high-level executive functions and anxiety.

Further inquiry revealed that the nerve tract leading to the basolateral amygdala emanates from a nerve-cell cluster in the vMT called the xiphoid nucleus. The tract that leads to the medial prefrontal cortex, the investigators learned, comes from a cluster called the nucleus reuniens, which snugly envelopes the xiphoid nucleus.

Next, the investigators selectively modified specific sets of nerve cells in mice’s brains so they could stimulate or inhibit signaling in these two nerve tracts. Exclusively stimulating xiphoid activity markedly increased mice’s propensity to freeze in place in the presence of a perceived aerial predator. Exclusively boosting activity in the tract running from the nucleus reuniens to the medial prefrontal cortex in mice exposed to the looming-predator stimulus radically increased a response seldom seen under similar conditions in the wild or in previous open-field experiments: The mice stood their ground, right out in the open, and rattled their tails, an action ordinarily associated with aggression in the species.

Thumping tails

This “courageous” behavior was unmistakable, and loud, Huberman said. “You could hear their tails thumping against the side of the chamber. It’s the mouse equivalent of slapping and beating your chest and saying, ‘OK, let’s fight!’” The mice in which the nucleus reuniens was stimulated also ran around more in the chamber’s open area, as opposed to simply running toward hiding places. But it wasn’t because nucleus reuniens stimulation put ants in their pants; in the absence of a simulated looming predator, the same mice just chilled out.

In another experiment, the researchers showed that stimulating mice’s nucleus reuniens for 30 seconds before displaying the “looming predator” induced the same increase in tail rattling and running around in the unprotected part of the chamber as did vMT stimulation executed concurrently with the display. This suggests, Huberman said, that stimulating nerve cells leading from the nucleus reunions to the prefrontal cortex induces a shift in the brain’s internal state, predisposing mice to act more boldly.

Another experiment pinpointed the likely nature of that internal-state shift: arousal of the autonomic nervous system, which kick-starts the fight, flight or freeze response. Stimulating either the vMT as a whole or just the nucleus reuniens increased the mice’s pupil diameter — a good proxy of autonomic arousal.

On repeated exposures to the looming-predator mockup, the mice became habituated. Their spontaneous vMT firing diminished, as did their behavioral responses. This correlates with lowered autonomic arousal levels.

Human brains harbor a structure equivalent to the vMT, Huberman said. He speculated that in people with phobias, constant anxiety or PTSD, malfunctioning circuitry or traumatic episodes may prevent vMT signaling from dropping off with repeated exposure to a stress-inducing situation. In other experiments, his group is now exploring the efficacy of techniques, such as deep breathing and relaxation of visual fixation, in adjusting the arousal states of people suffering from these problems. The thinking is that reducing vMT signaling in such individuals, or altering the balance of signaling strength from their human equivalents of the xiphoid nucleus and nucleus reuniens may increase their flexibility in coping with stress.

Reference:
Salay, L. D., Ishiko, N., & Huberman, A. D. (2018). A midline thalamic circuit determines reactions to visual threat. Nature. doi:10.1038/s41586-018-0078-2

http://med.stanford.edu/news/all-news/2018/05/scientists-find-fear-courage-switches-in-brain.html


The study simulated long-term consumption of three cups of coffee a day.

It is well known that memory problems are the hallmarks of Alzheimer’s disease. However, this dementia is also characterized by neuro-psychiatric symptoms, which may be strongly present already in the first stages of the disorder. Known as Behavioural and Psychological Symptoms of Dementia (BPSD), this array of symptoms — including anxiety, apathy, depression, hallucinations, paranoia and sundowning (or late-day confusion) — are manifested in different manners depending on the individual patient, and are considered the strongest source of distress for patients and caregivers.


Coffee and caffeine: good or bad for dementia?

Caffeine has recently been suggested as a strategy to prevent dementia, both in patients with Alzheimer’s disease and in normal ageing processes. This is due to its action in blocking molecules — adenosine receptors — which may cause dysfunctions and diseases in old age. However, there is some evidence that once cognitive and neuro-psychiatric symptoms develop, caffeine may exert opposite effects.

To investigate this further, researchers from Spain and Sweden conducted a study with normal ageing mice and familial Alzheimer’s models. The research, published in Frontiers in Pharmacology, was conducted from the onset of the disease up to more advanced stages, as well as in healthy age-matched mice.

“The mice develop Alzheimer’s disease in a very close manner to human patients with early-onset form of the disease,” explains first author Raquel Baeta-Corral, from Universitat Autònoma de Barcelona, Spain. “They not only exhibit the typical cognitive problems but also a number of BPSD-like symptoms. This makes them a valuable model to address whether the benefits of caffeine will be able to compensate its putative negative effects.”

“We had previously demonstrated the importance of the adenosine A1 receptor as the cause of some of caffeine’s adverse effects,” explains Dr. Björn Johansson, a researcher and physician at the Karolinska University Hospital, Sweden.

“In this study, we simulated a long oral treatment with a very low dose of caffeine (0.3 mg/mL) — equivalent to three cups of coffee a day for a human — to answer a question which is relevant for patients with Alzheimer’s, but also for the ageing population in general, and that in people would take years to be solved since we would need to wait until the patients were aged.”

Worsened Alzheimer’s symptoms outweigh cognition benefits

The results indicate that caffeine alters the behavior of healthy mice and worsens the neuropsychiatric symptoms of mice with Alzheimer’s disease. The researchers discovered significant effects in the majority of the study variables — and especially in relation to neophobia (a fear of everything new), anxiety-related behaviors, and emotional and cognitive flexibility.

In mice with Alzheimer’s disease, the increase in neophobia and anxiety-related behaviours exacerbates their BPSD-like profile. Learning and memory, strongly influenced by anxiety, got little benefit from caffeine.

“Our observations of adverse caffeine effects in an Alzheimer’s disease model, together with previous clinical observations, suggest that an exacerbation of BPSD-like symptoms may partly interfere with the beneficial cognitive effects of caffeine. These results are relevant when coffee-derived new potential treatments for dementia are to be devised and tested,” says Dr. Lydia Giménez-Llort, researcher from the INc-UAB Department of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, and lead researcher of the project.

The results of the study form part of the PhD thesis of Raquel Baeta-Corral, first author of the article, and are the product of a research led by Lydia Giménez-Llort, Director of the Medical Psychology Unit, Department of Psychiatry and Legal Medicine and researcher at the UAB Institute of Neuroscience, together with Dr Björn Johansson, Researcher at the Department of Molecular Medicine and Surgery, Karolinska Institutet and the Department of Geriatrics, Karolinska University Hospital, Sweden, under the framework of the Health Research Fund project of the Institute of Health Carlos III.

Long-term caffeine worsens symptoms associated with Alzheimer’s disease

By Elizabeth Bernstein

You’re feeling depressed. What have you been eating?

Psychiatrists and therapists don’t often ask this question. But a growing body of research over the past decade shows that a healthy diet—high in fruits, vegetables, whole grains, fish and unprocessed lean red meat—can prevent depression. And an unhealthy diet—high in processed and refined foods—increases the risk for the disease in everyone, including children and teens.

Now recent studies show that a healthy diet may not only prevent depression, but could effectively treat it once it’s started.

Researchers, led by epidemiologist Felice Jacka of Australia’s Deakin University, looked at whether improving the diets of people with major depression would help improve their mood. They chose 67 people with depression for the study, some of whom were already being treated with antidepressants, some with psychotherapy, and some with both. Half of these people were given nutritional counseling from a dietitian, who helped them eat healthier. Half were given one-on-one social support—they were paired with someone to chat or play cards with—which is known to help people with depression.

After 12 weeks, the people who improved their diets showed significantly happier moods than those who received social support. And the people who improved their diets the most improved the most. The study was published in January 2017 in BMC Medicine. A second, larger study drew similar conclusions and showed that the boost in mood lasted six months. It was led by researchers at the University of South Australia and published in December 2017 in Nutritional Neuroscience.

And later this month in Los Angeles at the American Academy of Neurology’s annual meeting, researchers from Rush University Medical Center in Chicago will present results from their research that shows that elderly adults who eat vegetables, fruits and whole grains are less likely to develop depression over time.

The findings are spurring the rise of a new field: nutritional psychiatry. Dr. Jacka helped to found the International Society for Nutritional Psychiatry Research in 2013. It held its first conference last summer. She’s also launched Deakin University’s Food & Mood Centre, which is dedicated to researching and developing nutrition-based strategies for brain disorders.

The annual American Psychiatric Association conference has started including presentations on nutrition and psychiatry, including one last year by chef David Bouley on foods that support the peripheral nervous system. And some medical schools, including Columbia University’s Vagelos College of Physicians and Surgeons, are starting to teach psychiatry residents about the importance of diet on mental health.

Depression has many causes—it may be genetic, triggered by a specific event or situation, such as loneliness, or brought on by lifestyle choices. But it’s really about an unhealthy brain, and too often people forget this. “When we think of cardiac health, we think of strengthening an organ, the heart,” says Drew Ramsey, a psychiatrist in New York, assistant clinical professor of psychiatry at Columbia and author of “Eat Complete.” “We need to start thinking of strengthening another organ, the brain, when we think of mental health.”

A bad diet makes depression worse, failing to provide the brain with the variety of nutrients it needs, Dr. Ramsey says. And processed or deep-fried foods often contain trans fats that promote inflammation, believed to be a cause of depression. To give people evidenced-based information, Dr. Ramsey created an e-course called “Eat to Beat Depression.”

A bad diet also affects our microbiome—the trillions of micro-organisms that live in our gut. They make molecules that can alter the production of serotonin, a neurotransmitter found in the brain, says Lisa Mosconi, a neuroscientist, nutritionist and associate director of the Alzheimer’s Prevention Clinic at Weill Cornell Medical College in New York. The good and bad bacteria in our gut have complex ways to communicate with our brain and change our mood, she says. We need to maximize the good bacteria and minimize the bad.

So what should we eat? The research points to a Mediterranean-style diet made up primarily of fruits and vegetables, extra-virgin olive oil, yogurt and cheese, legumes, nuts, seafood, whole grains and small portions of red meat. The complexity of this diet will provide the nutrition our brain needs, regulate our inflammatory response and support the good bacteria in our gut, says Dr. Mosconi, author of “Brain Food: The Surprising Science of Eating for Cognitive Power.”

Can a good diet replace medicine or therapy? Not for everyone. But people at risk for depression should pay attention to the food they eat. “It really doesn’t matter if you need Prozac or not. We know that your brain needs nutrients,” Dr. Ramsey says. A healthy diet may work even when other treatments fail. And at the very least, it can serve as a supplemental treatment—one with no bad side effects, unlike antidepressants—that also has a giant upside. It can prevent other health problems, such as heart disease, obesity and diabetes.

Loretta Go, a 60-year-old mortgage consultant in Ballwin, Mo., suffered from depression for decades. She tried multiple antidepressants and cognitive behavioral therapy, but found little relief from symptoms including insomnia, crying jags and feelings of hopelessness. About five years ago, after her doctor wanted to prescribe yet another antidepressant, she refused the medicine and decided to look for alternative treatments.

Ms. Go began researching depression and learned about the importance of diet. When she read that cashews were effective in reducing depression symptoms, she ordered 100 pounds, stored them in the freezer, and started putting them in all her meals.

She also ditched processed and fried foods, sugar and diet sodas. In their place, she started to eat primarily vegetables and fruits, eggs, turkey and a lot of tofu. She bought a Vitamix blender and started making a smoothie with greens for breakfast each morning.

Within a few months, Ms. Go says she noticed a difference in her mood. She stopped crying all the time. Her insomnia went away and she had more energy. She also began enjoying activities again that she had given up when she was depressed, such as browsing in bookstores and volunteering at the animal shelter.

Ms. Go’s depression has never come back. “This works so well,” she says. “How come nobody else talks about this?”

https://www.wsj.com/articles/the-food-that-helps-battle-depression-1522678367

By Jane Ridley

Four years ago, Lillyth Quillan cowered behind a padlocked door as her teenage son, taller and stronger than she is, paced back and forth in a rage.

Suddenly he went quiet. “Don’t let me hurt you, Mom,” he said, his voice sounding chillingly calm.

It was the first time the high school freshman had used that particular tone, but he continued to deploy it as he menaced his mom and dad.

“He used the kind of language of abusive husbands — manipulating and controlling,” says Quillan, who had installed locks on every door in her house except her son’s bedroom. “I was terrified of what he was going to do next.”

The boy — whom Quillan chooses to call Kevin in her interview with The Post in reference to the unnerving Lionel Shriver novel “We Need To Talk About Kevin” about a school shooter in upstate New York — was out of control.

After years of cruel and violent behavior plus multiple suspensions and expulsions from school, psychiatrists finally diagnosed the then-14-year-old Kevin with “conduct disorder,” which, in its most extreme form, can be a precursor to psychopathy.

Psychopathy, which is often used interchangeably with the term sociopathy, is believed to affect 1 percent of adults. Key attributes that sociopaths and psychopaths have in common include a disregard for laws, social mores and the rights of others, a failure to feel remorse or guilt and, in some but not all cases, a tendency to violence.

The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) dictates that people under the age of 18 cannot be labelled psychopaths. However, in 2013 the American Psychiatric Association decided to include the condition “conduct disorder with callous and unemotional traits” for children ages 12 and over.

According to a 2001 report published in the journal American Family Physician, approximately 6 to 16 percent of boys and 2 to 9 percent of girls meet the diagnostic criteria for conduct disorder — only a fraction of which have the “callous and unemotional” label that can potentially lead to psychopathy in adulthood.

More than 50 studies have found that kids with the latter diagnosis are more likely to become criminals or display aggressive, psychopathic traits later in life. It has been reported that Nikolas Cruz, the 19-year-old who allegedly shot and killed 17 people at Marjory Stoneman Douglas High School in Parkland, Fla., last month showed classic signs of the disorder as a child, including abusing animals.

“Psychopaths don’t just appear when they are 20. They are always different from an early age,” Kent Kiehl, a psychology professor at the University of New Mexico and the author of “The Psychopath Whisperer,” tells The Post.

Characteristics to look for — as detailed in the widely used Hare Psychopathy Checklist Youth Version considered by clinicians and researchers to be the “gold standard” in assessing psychopathy — include lack of empathy, lack of guilt and regret, pathological lying, grandiose self-worth and failure to accept responsibility for actions such as fighting and bullying.

“Individuals who score high on those traits are more likely to produce further violence,” adds Kiehl. “If they are sanctioned but continue on the same path, it’s not a perfect indicator, but it’s enough to cause concern.”

Kiehl notes that research has shown that psychopathy is hereditary roughly half of the time. But his own breakthrough was the discovery that the psychopathic brain has a different structure than a “normal” one.

In 2014, he conducted a major study that found at least two abnormalities in the brains of adult psychopaths. There was a lack of gray matter in the section involved in processing emotions, while the area that reacts to excitement and thrills is overactive. Although the research has not been carried out yet, the pattern is likely to also occur in the brains of “callous and unemotional” children. “Brain science has helped us understand what is different about these kids,” adds Kiehl.

At the moment, there is no such thing as a “cure” for psychopathy or conduct disorder. But early intervention can be key for harm reduction, even with children as young as 2 or 3.

Paul Frick, a psychology professor at Louisiana State University and the author of “Conduct Disorder and Severe Antisocial Behavior,” recommends a range of therapies, most of which revolve around rewards systems rather than punishments.

“There are so-called ‘emotion coaching’ techniques that parents and therapists can employ to help children pay attention to the feelings of others,” he explains. “We find that they miss the cues that another child is upset.

“By saying: ‘Can you see how Johnny is feeling?’ [when a toy is snatched from him] and getting them to respond correctly, you can motivate them. You give them a star or a sticker as an incentive.

“Even though it doesn’t come naturally to them, they can learn others’ perspectives.”

Experts can identify a callous and unemotional child when they are as young as 3 or 4. Faced with a crying peer, typically developing children either try to comfort them or take flight. But those with the mental condition remain in place, showing apathy and coldness.

Remarkably, the psychology department at King’s College London has been able to trace the characteristics back to infancy. They tested more than 200 babies at 5 months old, tracking whether they preferred looking at a person’s face or at a red ball. The tots who favored the ball displayed more callous traits two and a half years later.

For Quillan, hindsight is 20/20, but she distinctly recalls the first signs that Kevin had behavioral issues at the age of just 8 months.

“He had teeth and would bite me while he was breast-feeding and he would laugh. He thought it was hilarious. I tried looking very sad and mimicking crying to show it was hurting me, but he would only laugh,” says Quillan, who ended up having to put him on formula.

“It didn’t occur to me until much later that this was a child for whom the amusement of my reaction when he bit me was a greater reward than food.”

Now 18, Kevin, who has had numerous run-ins with police, including for shoplifting, was made a ward of state and no longer lives with his parents. He lives in a residential school for “at-risk” youth in California, where he is on a waiting list to receive treatment, such as therapy, to build empathy.

“Because there is no real treatment for conduct disorder. All you can do is wait for your child to be arrested and enter the juvenile system and hope they get better,” says his 40-year-old homemaker mom.

“Luckily, Kevin is no longer violent and is actually cooperative.”

He is doing so well that he is about to receive his high school diploma, recently won an award for wrestling and has encouraged his mother to tell his story.

Now Quillian, who has no other kids, is focusing on advocacy and encouraging parents facing similar nightmares to hers. Three years ago, she formed a support group for families with kids with CD that has 420 members worldwide. More recently, she launched the Society for Treatment Options for Potential Psychopaths to bring awareness and to campaign for treatment for these children before they cause serious harm.

Adds Quillan: “As every news article came out about Parkland and Nikolas Cruz, I thought: ‘My God, this could easily be one of our kids.’”

https://nypost.com/2018/03/07/how-to-tell-if-your-child-is-a-future-psychopath/


3D reconstruction of a serotonin receptor generated by cryo-electron microscopy

by Rebecca Pool

Claiming a world first and using cryo-electron microscopy, researchers from Case Western Reserve University School of Medicine, US, have observed full-length serotonin receptors. The proteins are common drug targets, and the new images provide details about molecular binding sites that could lead to more precise drug design. Serotonin receptors, which reside in cell membranes throughout the body, are highly dynamic and difficult to image. In the past, the receptors have been sectioned into pieces to study, but by capturing full-length samples, researchers have revealed how different portions interact.

Dr Sandip Basak from Physiology and Biophysics, and colleagues, describe ‘a finely tuned orchestration of three domain movements’ that allows the receptors to elegantly control passageways across cell membranes. “The serotonin receptor acts as a gateway, or channel, from outside the cell to inside,” he says. “When serotonin binds onto the receptor, the channel switches conformation from closed to open. It eventually twists into a ‘desensitized’ state, where the channel closes but serotonin remains attached,” he adds. “This prevents it from being reactivated.”

For this study, the researchers used a FEI Titan Krios microscope, operating at 300 kV, and equipped with a Gatan K2-Summit direct detector camera, at the National Cryo-Electron Microscopy Facility in Frederick, Maryland.

“Successful design of safer therapeutics [for cancer therapies and gastrointestinal diseases] has slowed because there is currently a limited understanding of the structure of the serotonin receptor itself, and what happens after serotonin binds,” says research leader, Professor Sudha Chakrapani. “Our new structure of the serotonin receptor in the resting state has the potential to serve as a structural blueprint to drive targeted drug design and better therapeutic strategies.”

This research is published in Nature Communications.

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