Posts Tagged ‘mental health’

by Drake Baer, Senior writer at Thrive Global covering the brain and social sciences.

Teachers, parents and policymakers are finally started to realize that academic success depends on more than just “booksmarts,” the kind of fluid intelligence captured by IQ tests and the like. The importance of “soft” or “non-cognitive” skills like grit and emotional intelligence is growing rapidly. But there’s a deeper question here: where do these soft skills come from? According to a new paper in Psychological Science, it’s your mom.

The research team, lead by Lilian Dindo, a clinical psychologist at the Baylor College of Medicine, crossed disciplines and decades to discover what they describe as an “adaptive cascade” that happens in three parts, drawing a line from the relational experiences we have as infants to the academic achievements we have later on. “That having a supportive responsive caregiving environment can actually provide these inner resources that will foster something like effortful control, and that this in turn can actually promote better functioning in school is the new thing here,” she tells Thrive Global.

The first part of that cascade is “secure attachment.” Tots—in this study, one cohort of 9-month olds and another of two-to-three year olds—get strongly influenced by their primary caregivers, implicitly learning how relationships work (often called attachment in the psychology field).

In this study, the mothers rated their children’s security of attachment using a widely used assessment tool. “If a child is distressed and shows distress to a parent and the parent responds to the distress in sensitive and loving and reassuring ways the child then feels secure in their knowledge that they can freely express this negative emotion,” Dindo explained. “Learning in that way is very different than learning that if I express negative emotion then I will be rejected or minimized or ignored or ridiculed. And so the child will learn not to express the negative emotions, to inhibit that negative emotion, or to actually act up even more to try to get that response. Either way they’re learning that expressing this negative emotion will not be responded to in a sensitive or loving way.”

Think of it this way: if you ate at a restaurant and it made you sick, you’d be unlikely to go back; if you expressed hurt and your mom rejected it, you’d minimize that pain next time. Even very early in life, kids are already observing cause and effect.

Step two in the cascade is effortful control, or the ability to delay gratification and inhibit a response to something when it’s in your best interest to do so—it’s the toddler-aged forerunner of things like grit and conscientiousness. In this study, effortful control in toddlers was examined experimentally—for example, in a “snack delay” task where tykes are presented with a cup of Goldfish crackers and instructed to wait to eat them until the experimenter rings a bell—and through parental ratings of how well the kids controlled themselves at home.

Then comes the third part of the cascade: academic achievement. More than a decade after the first experiments, Dindo tracked down the mother-child duos. About two-thirds of each cohort participated in the follow-up, where moms sent in their now 11 to 15-year-old kids’ scores on a couple of academic different standardized tests. The researchers crunched the data from all of the experiments and found quite the developmental chain: secure attachment was associated with effortful control in toddlers, and in turn, effortful control at age 3 predicted better test scores in early adolescence.

While this study doesn’t explain the mechanics of that three-part cascade, Dindo thinks it has to do with how we learn to regard our own inner emotional lives from the way our moms (or primary caregivers) regard us. If mom is soothing and dependable, you learn to consistently do the same for yourself—you learn that you’re going to be okay even if you feel anxious in the moment, like when tackling homework or a test. To Dindo, this shows how coming from a psychologically or emotionally deprived environment can have long-term consequences: if you don’t get the loving attentiveness you need when you’re little, it’s going to be harder to succeed as you grow up.

In very hopeful news though, other studies out this year—like here (https://www.ncbi.nlm.nih.gov/pubmed/28401843) and here (https://www.ncbi.nlm.nih.gov/pubmed/28401847) —show that when parents get attachment interventions, or are coached to be more attentive to their toddlers, the kids’ effortful control scores go up, which should, in turn, lead to greater achievement down the line. Because as this line of research is starting to show, just like plants need sunlight to grow into their fullest forms, humans need skillful love to reach their full potential.

https://www.thriveglobal.com/stories/15459-this-is-how-you-raise-successful-teens

https://www.ncbi.nlm.nih.gov/pubmed/29023183

Psychol Sci. 2017 Oct 1:956797617721271. doi: 10.1177/0956797617721271. [Epub ahead of print]

Attachment and Effortful Control in Toddlerhood Predict Academic Achievement Over a Decade Later.

Dindo L, Brock RL, Aksan N, Gamez W, Kochanska G, Clark LA.

Abstract

A child’s attachment to his or her caregiver is central to the child’s development. However, current understanding of subtle, indirect, and complex long-term influences of attachment on various areas of functioning remains incomplete. Research has shown that (a) parent-child attachment influences the development of effortful control and that (b) effortful control influences academic success. The entire developmental cascade among these three constructs over many years, however, has rarely been examined. This article reports a multimethod, decade-long study that examined the influence of mother-child attachment and effortful control in toddlerhood on school achievement in early adolescence. Both attachment security and effortful control uniquely predicted academic achievement a decade later. Effortful control mediated the association between early attachment and school achievement during adolescence. This work suggests that attachment security triggers an adaptive cascade by promoting effortful control, a vital set of skills necessary for future academic success.

KEYWORDS: academic performance; attachment; effortful control; longitudinal; temperament

PMID: 29023183 DOI: 10.1177/0956797617721271

Advertisements

by Amanda Oldt

Recent findings suggest that treatment with psilocybin may “reset” brain connectivity in patients with treatment-resistant depression.

“Several of our patients described feeling ‘reset’ after the treatment and often used computer analogies. For example, one said he felt like his brain had been ‘defragged’ like a computer hard drive, and another said he felt ‘rebooted,’” Robin L. Carhart-Harris, PhD, of Imperial College London, said in a press release. “Psilocybin may be giving these individuals the temporary ‘kick start’ they need to break out of their depressive states and these imaging results do tentatively support a ‘reset’ analogy. Similar brain effects to these have been seen with electroconvulsive therapy.”

To assess psilocybin for treatment-resistant depression, researchers used functional MRI to measure cerebral blood flow (CBF) and blood oxygen-level dependent resting-state functional connectivity before and after psilocybin treatment among 16 patients with treatment-resistant depression.

One week after treatment, all patients exhibited decreased depressive symptoms.

At 5 weeks, 47% of the cohort met criteria for treatment response.

Whole-brain analyses indicated decreases in CBF in the temporal cortex, including the amygdala, following treatment with psilocybin.

Decreased CBF in the amygdala was associated with decreased depressive symptoms.

Posttreatment, resting-state functional connectivity was increased in the default-mode network.

Treatment response at 5 weeks was predicted by increased resting-state functional connectivity in the ventromedial prefrontal cortex-bilateral inferior lateral parietal cortex and decreased resting-state functional connectivity in the parahippocampal prefrontal cortex.

“Through collecting these imaging data we have been able to provide a window into the after effects of psilocybin treatment in the brains of patients with chronic depression,” Carhart-Harris said in the release. “Based on what we know from various brain imaging studies with psychedelics, as well as taking heed of what people say about their experiences, it may be that psychedelics do indeed ‘reset’ the brain networks associated with depression, effectively enabling them to be lifted from the depressed state.”

Carhart-Harris RL, et al. Sci Rep. 2017;doi:10.1038/s41598-017-13282-7.

https://www.healio.com/psychiatry/depression/news/online/%7B3089a96c-7e81-494d-abd8-248d77aefbab%7D/magic-mushrooms-may-reset-brain-connectivity-in-depression?utm_source=selligent&utm_medium=email&utm_campaign=psychiatry%20news&m_bt=1162769038120

Regular use of nicotine may normalize brain activity impairments linked with schizophrenia, according to a study using a mouse model, published online in Nature Medicine. The finding may explain why up to 90% of people with schizophrenia smoke—most of them heavily.

“Basically the nicotine is compensating for a genetically determined impairment,” said researcher Jerry Stitzel, PhD, of the University of Colorado Boulder. “No one has ever shown that before.”

Dr. Stitzel is part of an international research team that investigated whether a variant in the CHRNA5 gene, which is believed to increase schizophrenia risk, is associated with a reduction of neural firing in the brain’s prefrontal cortex, or hypofrontality. Researchers also examined whether nicotine could interrupt the effect.

In mice with the CHRNA5 gene variant, brain images confirmed hypofrontality, researchers reported. Behavioral tests further revealed that the mice shared key characteristics of people with schizophrenia, such as an inability to suppress a startle response and aversion to social interaction. The findings, they explained, suggest the CHRNA5 gene variant plays a role in schizophrenia by causing hypofrontality.

Nicotine, however, seemed to reverse hypofrontality. When researchers gave the mice daily nicotine, their sluggish brain activity improved within 2 days. Within a week, it was normal.

Researchers believe the nicotine corrected the impaired brain activity by acting on nicotinic receptors in regions important for healthy cognitive function.

Noting that hypofrontality is also linked with addiction, attention deficit hyperactivity disorder, bipolar disorder, and other psychiatric conditions, researchers believe the discovery could lead to new nonaddictive, nicotine-based medications.

“This defines a completely novel strategy for medication development,” said lead author Uwe Maskos, PhD, of Institut Pasteur, Paris, France.

—Jolynn Tumolo

References:

Koukouli F, Rooy M, Tziotis D, et al. Nicotine reverses hypofrontality in animal models of addiction and schizophrenia. Nature Medicine. 2017 January 23;[Epub ahead of print].

Nicotine normalizes brain deficits key to schizophrenia [press release]. Boulder, CO: University of Colorado Boulder; January 23, 2017.

Supplementation with taurine, the additive found in many energy drinks, may improve the symptoms in young people suffering a first episode of psychosis (FEP), according to a new study presented at the International Early Psychosis Association (IEPA) meeting.

Taurine, an amino acid naturally occurring in the body, exhibits an inhibitory neuro-modulatory effect in the nervous system and also functions as a neuroprotective agent. The authors devised a study to analyze the efficacy of taurine supplementation in improving symptoms and cognition in patients with FEP.

The study included 86 individuals with FEP between the ages of 18 and 25 years. It was conducted by Dr. Colin O’Donnell, Donegal Mental Health Service, Co. Donegal, Ireland, and Professor Patrick McGorry and Dr. Kelly Allott, Orygen, The National Centre of Excellence in Youth Mental Health, Australia, and colleagues. Each participant was taking a low dose antipsychotic medication and was attending Orygen.

Forty-seven participants received 4g of taurine daily, while 39 received placebo. Symptoms were assessed Using the scoring system called BPRS (Brief Psychiatric Rating Scale) and cognition was assessed with the MCCB tool (MATRICS consensus cognitive battery).

Results showed that taurine significantly improved symptoms on the BPRS scale, in overall score and in psychosis specific analysis, however, there was no difference between the treatment and placebo group regarding cognition. Depression symptoms (rated by the Calgary Depression Scale for Schizophrenia) and general overall functioning also improved in the taurine group.

“The use of taurine warrants further investigation in larger randomised studies, particularly early in the course of psychosis,” concluded the authors, who themselves, are planning to conduct further studies into the potential benefits of taurine in the treatment of psychosis.

http://www.empr.com/news/energy-drink-additive-could-potentially-improve-psychosis-symptoms/article/567497/?DCMP=EMC-MPR_Charts_rd&cpn=&hmSubId=&NID=&c_id=&dl=0&spMailingID=16159114&spUserID=MzI5NTMwMzQ0NDIyS0&spJobID=921765029&spReportId=OTIxNzY1MDI5S0


St. Jude Children’s Research Hospital scientists have linked disruption of a brain circuit associated with schizophrenia to an age-related decline in levels of a single microRNA in one brain region

St. Jude Children’s Research Hospital scientists have identified a small RNA (microRNA) that may be essential to restoring normal function in a brain circuit associated with the “voices” and other hallucinations of schizophrenia. The microRNA provides a possible focus for antipsychotic drug development. The findings appear today in the journal Nature Medicine.

The work was done in a mouse model of a human disorder that is one of the genetic causes of schizophrenia. Building on previous St. Jude research, the results offer important new details about the molecular mechanism that disrupts the flow of information along a neural circuit connecting two brain regions involved in processing auditory information. The findings also provide clues about why psychotic symptoms of schizophrenia are often delayed until late adolescence or early adulthood.

“In 2014, we identified the specific circuit in the brain that is targeted by antipsychotic drugs. However, the existing antipsychotics also cause devastating side effects,” said corresponding author Stanislav Zakharenko, M.D., Ph.D., a member of the St. Jude Department of Developmental Neurobiology. “In this study, we identified the microRNA that is a key player in disruption of that circuit and showed that depletion of the microRNA was necessary and sufficient to inhibit normal functioning of the circuit in the mouse models.

“We also found evidence suggesting that the microRNA, named miR-338-3p, could be targeted for development of a new class of antipsychotic drugs with fewer side effects.”

There are more than 2,000 microRNAs whose function is to silence expression of particular genes and regulate the supply of the corresponding proteins. Working in a mouse model of 22q11 deletion syndrome, researchers identified miR-338-3p as the microRNA that regulates production of the protein D2 dopamine receptor (Drd2), which is the prime target of antipsychotics.

Individuals with the deletion syndrome are at risk for behavior problems as children. Between 23 and 43 percent develop schizophrenia, a severe chronic disorder that affects thinking, memory and behavior. Researchers at St. Jude are studying schizophrenia and other brain disorders to improve understanding of how normal brains develop, which provides insights into the origins of diseases like cancer.

The scientists reported that Drd2 increased in the brain’s auditory thalamus when levels of the microRNA declined. Previous research from Zakharenko’s laboratory linked elevated levels of Drd2 in the auditory thalamus to brain-circuit disruptions in the mutant mice. Investigators also reported that the protein was elevated in the same brain region of individuals with schizophrenia, but not healthy adults.

Individuals with the deletion syndrome are missing part of chromosome 22, which leaves them with one rather than the normal two copies of more than 25 genes. The missing genes included Dgcr8, which facilitates production of microRNAs.

Working in mice, researchers have now linked the 22q11 deletion syndrome and deletion of a single Dgcr8 gene to age-related declines in miR-338-3p in the auditory thalamus. The decline was associated with an increase in Drd2 and reduced signaling in the circuit that links the thalamus and auditory cortex, a brain region implicated in auditory hallucination. Levels of miR-338-3p were lower in the thalamus of individuals with schizophrenia compared to individuals of the same age and sex without the diagnosis.

The miR-338-3p depletion did not disrupt other brain circuits in the mutant mice, and the findings offer a possible explanation. Researchers found that miR-338-3p levels were higher in the thalamus than in other brain regions. In addition, miR-338-3p was one of the most abundant microRNAs present in the thalamus.

Replenishing levels of the microRNA in the auditory thalamus of mutant mice reduced Drd2 protein and restored the circuit to normal functioning. That suggests that the microRNA could be the basis for a new class of antipsychotic drugs that act in a more targeted manner with fewer side effects. Antipsychotic drugs, which target Drd2, also restored circuit function.

The findings provide insight into the age-related delay in the onset of schizophrenia symptoms. Researchers noted that microRNA levels declined with age in all mice, but that mutant mice began with lower levels of miR-338-3p. “A minimum level of the microRNA may be necessary to prevent excessive production of the Drd2 that disrupts the circuit,” Zakharenko said. “While miR-338-3p levels decline as normal mice age, levels may remain above the threshold necessary to prevent overexpression of the protein. In contrast, the deletion syndrome may leave mice at risk for dropping below that threshold.”

The study’s first authors are Sungkun Chun, Fei Du and Joby Westmoreland, all formerly of St. Jude. The other authors are Seung Baek Han, Yong-Dong Wang, Donnie Eddins, Ildar Bayazitov, Prakash Devaraju, Jing Yu, Marcia Mellado Lagarde and Kara Anderson, all of St. Jude.

https://www.stjude.org/media-resources/news-releases/2016-medicine-science-news/small-rna-identified-that-offers-clues-for-quieting-the-voices-of-schizophrenia.html

mdma

By DAVE PHILIPPS

After three tours in Iraq and Afghanistan, C. J. Hardin wound up hiding from the world in a backwoods cabin in North Carolina. Divorced, alcoholic and at times suicidal, he had tried almost all the accepted treatments for post-traumatic stress disorder: psychotherapy, group therapy and nearly a dozen different medications.

“Nothing worked for me, so I put aside the idea that I could get better,” said Mr. Hardin, 37. “I just pretty much became a hermit in my cabin and never went out.”

Then, in 2013, he joined a small drug trial testing whether PTSD could be treated with MDMA, the illegal party drug better known as Ecstasy.

“It changed my life,” he said in a recent interview in the bright, airy living room of the suburban ranch house here, where he now lives while going to college and working as an airplane mechanic. “It allowed me to see my trauma without fear or hesitation and finally process things and move forward.”

Based on promising results like Mr. Hardin’s, the Food and Drug Administration gave permission Tuesday for large-scale, Phase 3 clinical trials of the drug — a final step before the possible approval of Ecstasy as a prescription drug.

If successful, the trials could turn an illicit street substance into a potent treatment for PTSD.

Through a spokeswoman, the F.D.A. declined to comment, citing regulations that prohibit disclosing information about drugs that are being developed.

“I’m cautious but hopeful,” said Dr. Charles R. Marmar, the head of psychiatry at New York University’s Langone School of Medicine, a leading PTSD researcher who was not involved in the study. “If they can keep getting good results, it will be of great use. PTSD can be very hard to treat. Our best therapies right now don’t help 30 to 40 percent of people. So we need more options.”

But he expressed concern about the potential for abuse. “It’s a feel-good drug, and we know people are prone to abuse it,” he said. “Prolonged use can lead to serious damage to the brain.”

The Multidisciplinary Association for Psychedelic Studies, a small nonprofit created in 1985 to advocate the legal medical use of MDMA, LSD, marijuana and other banned drugs, sponsored six Phase 2 studies treating a total of 130 PTSD patients with the stimulant. It will also fund the Phase 3 research, which will include at least 230 patients.

Two trials here in Charleston focused on treating combat veterans, sexual assault victims, and police and firefighters with PTSD who had not responded to traditional prescription drugs or psychotherapy. Patients had, on average, struggled with symptoms for 17 years.

After three doses of MDMA administered under a psychiatrist’s guidance, the patients reported a 56 percent decrease of severity of symptoms on average, one study found. By the end of the study, two-thirds no longer met the criteria for having PTSD. Follow-up examinations found that improvements lasted more than a year after therapy.

“We can sometimes see this kind of remarkable improvement in traditional psychotherapy, but it can take years, if it happens at all,” said Dr. Michael C. Mithoefer, the psychiatrist who conducted the trials here. “We think it works as a catalyst that speeds the natural healing process.”

The researchers are so optimistic that they have applied for so-called breakthrough therapy status with the Food and Drug Administration, which would speed the approval process. If approved, the drug could be available by 2021.

Under the researchers’ proposal for approval, the drug would be used a limited number of times in the presence of trained psychotherapists as part of a broader course of therapy. But even in those controlled circumstances, some scientists worry that approval as a therapy could encourage more illegal recreational use.

“It sends the message that this drug will help you solve your problems, when often it just creates problems,” said Andrew Parrott, a psychologist at Swansea University in Wales who has studied the brains of chronic Ecstasy users. “This is a messy drug we know can do damage.”

Allowing doctors to administer the drug to treat a disorder, he warned, could inadvertently lead to a wave of abuse similar to the current opioid crisis.

During initial studies, patients went through 12 weeks of psychotherapy, including three eight-hour sessions in which they took MDMA. During the sessions, they lay on a futon amid candles and fresh flowers, listening to soothing music.

Dr. Mithoefer and his wife, Ann Mithoefer, and often their portly terrier mix, Flynn, sat with each patient, guiding them through traumatic memories.

“The medicine allows them to look at things from a different place and reclassify them,” said Ms. Mithoefer, a psychiatric nurse. “Honestly, we don’t have to do much. Each person has an innate ability to heal. We just create the right conditions.”

Research has shown that the drug causes the brain to release a flood of hormones and neurotransmitters that evoke feelings of trust, love and well-being, while also muting fear and negative emotional memories that can be overpowering in patients with post-traumatic stress disorder. Patients say the drug gave them heightened clarity and ability to address their problems.

For years after his combat deployments, Mr. Hardin said he was sleepless and on edge. His dreams were marked with explosions and death. The Army gave him sleeping pills and antidepressants. When they didn’t work, he turned to alcohol and began withdrawing from the world.

“I just felt hopeless and in the dark,” he said. “But the MDMA sessions showed me a light I could move toward. Now I’m out of the darkness and the world is all around me.”

Since the trial, he has gone back to school and remarried.

The chemist Alexander Shulgin first realized the euphoria-inducing traits of MDMA in the 1970s, and introduced it to psychologists he knew. Under the nickname Adam, thousands of psychologists began to use it as an aid for therapy sessions. Some researchers at the time thought the drug could be helpful for anxiety disorders, including PTSD, but before formal clinical trails could start, Adam spread to dance clubs and college campuses under the name Ecstasy, and in 1985, the Drug Enforcement Administration made it a Schedule 1 drug, barring all legal use.

Since then, the number of people seeking treatment for PTSD has exploded and psychiatry has struggled to keep pace. Two drugs approved for treating the disorder worked only mildly better than placebos in trials. Current psychotherapy approaches are often slow and many patients drop out when they don’t see results. Studies have shown combat veterans are particularly hard to treat.

In interviews, study participants said MDMA therapy had not only helped them with painful memories, but also had helped them stop abusing alcohol and other drugs and put their lives back together.

On a recent evening, Edward Thompson, a former firefighter, tucked his twin 4-year-old girls into bed, turned on their night light, then joined his wife at a backyard fire.

“If it weren’t for MDMA … ” he said.

“He’d be dead,” his wife, Laura, finished.

They both nodded.

Years of responding to gory accidents left Mr. Thompson, 30, in a near constant state of panic that he had tried to numb with alcohol and prescription opiates and benzodiazepines.

By 2015, efforts at therapy had failed, and so had several family interventions. His wife had left with their children, and he was considering jumping in front of a bus.

A member of a conservative Anglican church, Mr. Thompson had never used illegal drugs. But he was struggling with addiction from his prescription drugs, so he at first rejected a suggestion by his therapist that he enter the study. “In the end, I was out of choices,” he said.

Three sessions with the drug gave him the clarity, he said, to identify his problems and begin to work through them. He does not wish to take the drug again.

“It gave me my life back, but it wasn’t a party drug,” he said. “It was a lot of work.”

http://mobile.nytimes.com/2016/11/29/us/ptsd-mdma-ecstasy.html

A pair of new studies links childhood cat ownership and infection with the parasite Toxoplasma gondii (T. gondii) with later onset schizophrenia and other mental illness. Researchers published their findings in the online Schizophrenia Research and Acta Psychiatrica Scandinavica.

In the Schizophrenia Research study, investigators compared two previous studies that suggested childhood cat ownership could be a possible risk factor for schizophrenia or another serious mental illness with a third, even earlier survey on mental health to see if the finding could be replicated.

“The results were the same,” researchers reported, “suggesting that cat ownership in childhood is significantly more common in families in which the child later becomes seriously mentally ill.”

If accurate, the researchers expect the culprit to be infection with T. gondii, a parasite commonly carried by cats. At this point, though, they are urging others to conduct further studies to clarify the apparent link between cat ownership and schizophrenia.

The Acta Psychiatrica Scandinavica study was a meta-analysis of 50 previously published studies to investigate the prevalence of t. gondii infection in people diagnosed with psychiatric disorders compared with healthy controls.

In cases of schizophrenia, researchers said evidence of an association with T. gondii was “overwhelming,” CBS News reported. Specifically, people infected with T. gondii were nearly twice as likely to be diagnosed with schizophrenia as people never infected with the parasite, according to the report.

The meta-analysis also suggested associations between T. gondii infection and bipolar disorder, obsessive-compulsive disorder, and addiction. No association, however, was found for major depression.

—Jolynn Tumolo

References

1. Fuller Torrey E, Simmons W, Yolken RH. Is childhood cat ownership a risk factor for schizophrenia later in life? Schizophrenia Research. 2015 April 18. [Epub ahead of print].

2. Sutterland AL, Fond G, Kuin A, et al. Beyond the association. Toxoplasma gondii in schizophrenia, bipolar disorder, and addiction: systematic review and meta-analysis. Acta Psychiatrica Scandinavica. 2015 April 15. [Epub ahead of print].

http://www.psychcongress.com/article/studies-link-cat-ownership-schizophrenia-other-mental-illness