TBD Meeting (5389-19)

CRYSTAL CITY, VA. – Borderline personality disorder has a genetic and neurobiological component, but researchers remain unable to discern exactly why specific genetic markers are attributed to the disease, Emil F. Coccaro, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“The neurobiology at this point gives us clues that what’s going on with borderline personality disorder isn’t simply developmental or environmental. That’s all that it tells us,” said Dr. Coccaro, director of the Clinical Neuroscience & Psychopharmacology Research Unit at the University of Chicago.

Similarly, studies in twins that show heritability of borderline personal disorder at rates between 31% and 49% “only show there’s something in the DNA,” he added. Dr. Coccaro called the evidence for the neurobiology of borderline personality disorder “hazy.” “The neurobiology of [borderline personality disorder] points to widespread brain network dysfunction affecting emotional processing and social cognition,” said Dr. Coccaro, also chairman of the university’s department of psychiatry and behavioral neuroscience.

That is true of a lot of disorders, he said, so only the details explain why patients with borderline personality disorder look different from those who might have “similar types of circuitry abnormalities,” he said.

For example, genomewide association studies have found links between borderline personality disorder and the genes DPYD and PKP4, indicating problems with pyrimidine metabolism and myelin production. The study also found a strong association between borderline personality disorder, bipolar disorder, major depression, and schizophrenia (Transl Psychiatry. 2017 Jun. doi: 10.1038/tp.2017.115). DPYD has been associated with schizophrenia, but the relationship between DPYD and borderline personality disorder is unknown, Dr. Coccaro said.

“These [associations] are suggestive of what’s going on genetically, but it hardly makes a story that’s coherent enough to sink your teeth into,” he said.

CRYSTAL CITY, VA. – Borderline personality disorder has a genetic and neurobiological component, but researchers remain unable to discern exactly why specific genetic markers are attributed to the disease, Emil F. Coccaro, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“The neurobiology at this point gives us clues that what’s going on with borderline personality disorder isn’t simply developmental or environmental. That’s all that it tells us,” said Dr. Coccaro, director of the Clinical Neuroscience & Psychopharmacology Research Unit at the University of Chicago.

Similarly, studies in twins that show heritability of borderline personal disorder at rates between 31% and 49% “only show there’s something in the DNA,” he added. Dr. Coccaro called the evidence for the neurobiology of borderline personality disorder “hazy.” “The neurobiology of [borderline personality disorder] points to widespread brain network dysfunction affecting emotional processing and social cognition,” said Dr. Coccaro, also chairman of the university’s department of psychiatry and behavioral neuroscience.

That is true of a lot of disorders, he said, so only the details explain why patients with borderline personality disorder look different from those who might have “similar types of circuitry abnormalities,” he said.

For example, genomewide association studies have found links between borderline personality disorder and the genes DPYD and PKP4, indicating problems with pyrimidine metabolism and myelin production. The study also found a strong association between borderline personality disorder, bipolar disorder, major depression, and schizophrenia (Transl Psychiatry. 2017 Jun. doi: 10.1038/tp.2017.115). DPYD has been associated with schizophrenia, but the relationship between DPYD and borderline personality disorder is unknown, Dr. Coccaro said.

“These [associations] are suggestive of what’s going on genetically, but it hardly makes a story that’s coherent enough to sink your teeth into,” he said.

CRYSTAL CITY, VA. – Borderline personality disorder has a genetic and neurobiological component, but researchers remain unable to discern exactly why specific genetic markers are attributed to the disease, Emil F. Coccaro, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“The neurobiology at this point gives us clues that what’s going on with borderline personality disorder isn’t simply developmental or environmental. That’s all that it tells us,” said Dr. Coccaro, director of the Clinical Neuroscience & Psychopharmacology Research Unit at the University of Chicago.

Similarly, studies in twins that show heritability of borderline personal disorder at rates between 31% and 49% “only show there’s something in the DNA,” he added. Dr. Coccaro called the evidence for the neurobiology of borderline personality disorder “hazy.” “The neurobiology of [borderline personality disorder] points to widespread brain network dysfunction affecting emotional processing and social cognition,” said Dr. Coccaro, also chairman of the university’s department of psychiatry and behavioral neuroscience.

That is true of a lot of disorders, he said, so only the details explain why patients with borderline personality disorder look different from those who might have “similar types of circuitry abnormalities,” he said.

For example, genomewide association studies have found links between borderline personality disorder and the genes DPYD and PKP4, indicating problems with pyrimidine metabolism and myelin production. The study also found a strong association between borderline personality disorder, bipolar disorder, major depression, and schizophrenia (Transl Psychiatry. 2017 Jun. doi: 10.1038/tp.2017.115). DPYD has been associated with schizophrenia, but the relationship between DPYD and borderline personality disorder is unknown, Dr. Coccaro said.

“These [associations] are suggestive of what’s going on genetically, but it hardly makes a story that’s coherent enough to sink your teeth into,” he said.

CRYSTAL CITY, VA. – Insomnia is a neuropsychiatric disorder of hyperarousal that should be evaluated as a disorder and treated with any associated comorbid conditions, Karl Doghramji, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Karen Winton/iStockphoto

“When I was a resident, I used to say insomnia is never a disorder. It’s always a symptom; you’ve got to find the primary disorder to know what the insomnia is caused by,” said Dr. Doghramji, medical director of the Jefferson Sleep Disorders Center at Jefferson Medical College, Philadelphia. “We no longer believe that. Throw that out the window.”

According to the new definition under the DSM-5, insomnia is characterized by dissatisfaction with sleep quality or quantity in the presence of adequate opportunity for sleep that causes significant distress or impairment for more than 3 nights per week over a period of 3 months. A survey of almost 7,500 U.S. health plan subscribers conducted a few years ago found that the prevalence of insomnia was estimated at 23.2% (Sleep. 2011 Sep 1;34[9]:1161-71).

Insomnia is also not well identified in clinical practice: In results published from his own group, Dr. Doghramji and colleagues evaluated 97 patients who were administered the Insomnia Severity Index; of those patients, 79.4% met the criteria for insomnia, but there was no mention of insomnia in the discharge notes for those patients (J Nerv Ment Dis. 2018 Oct;206[10]:765-9).

Many cognitive impairments can occur as a result of insomnia, which affects performance at work; decreases enjoyment of social activities; can lead to motor vehicle accidents or falls; and can affect health in the form of diabetes, hypertension, and increased mortality. Insomnia also can predict the risk of future depression and is a risk factor for suicide, Dr. Doghramji said at the meeting presented by Global Academy for Medical Education.

Adults can have insomnia for many reasons, including genetics, stress, negative conditioning, intrapsychic conflict, and bad habits, as well as medical and psychiatric conditions. While knowledge surrounding insomnia has advanced under a hyperarousal model, “It is really a hyperarousal disturbance which defies psychological understanding,” said Dr. Doghramji, who is also professor of psychiatry, neurology, and medicine at the university.

Evaluating the type of insomnia a patient is experiencing should be the first step in managing the disorder, followed by determining whether the insomnia is contributing to daytime impairment or decreased quality of life for the patient. From there, the insomnia can be treated with behavioral or pharmacotherapy. However, if insomnia is associated with another comorbid condition, the condition should be treated alongside the insomnia.

Sleep is highly comorbid with psychiatric and medical conditions (Sleep Med Clin. 2019 Jun;14[2]:167-75). Initial insomnia is more likely to be associated with delayed sleep phase disorder and restless legs syndrome, while middle insomnia is associated with sleep apnea and depression. Patients who wake early and are unable to go back to sleep (terminal insomnia) are likely to have depression, shift work disorder, or advanced sleep phase disorder.

“Once you identify [insomnia], there are all sorts of wonderful ways to manage it, including behavioral and pharmacological therapy,” said Dr. Doghramji. The comorbid condition also should be considered when deciding how to treat insomnia. For example, a patient with gastroesophageal reflux disease and insomnia would be more suited to cognitive-behavioral therapy than pharmacologic agents to help with sleep, because being able to wake up during the night from acid building in the esophagus is the body’s defense mechanism for the disease, Dr. Doghramji said.

Dr. Doghramji reported serving as a consultant for Eisai, Merck, and Pfizer. He also receives research funding from and owns stock in Merck.

Global Academy for Medical Education, Current Psychiatry, and this news organization are owned by the same company.

CRYSTAL CITY, VA. – Insomnia is a neuropsychiatric disorder of hyperarousal that should be evaluated as a disorder and treated with any associated comorbid conditions, Karl Doghramji, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Karen Winton/iStockphoto

“When I was a resident, I used to say insomnia is never a disorder. It’s always a symptom; you’ve got to find the primary disorder to know what the insomnia is caused by,” said Dr. Doghramji, medical director of the Jefferson Sleep Disorders Center at Jefferson Medical College, Philadelphia. “We no longer believe that. Throw that out the window.”

According to the new definition under the DSM-5, insomnia is characterized by dissatisfaction with sleep quality or quantity in the presence of adequate opportunity for sleep that causes significant distress or impairment for more than 3 nights per week over a period of 3 months. A survey of almost 7,500 U.S. health plan subscribers conducted a few years ago found that the prevalence of insomnia was estimated at 23.2% (Sleep. 2011 Sep 1;34[9]:1161-71).

Insomnia is also not well identified in clinical practice: In results published from his own group, Dr. Doghramji and colleagues evaluated 97 patients who were administered the Insomnia Severity Index; of those patients, 79.4% met the criteria for insomnia, but there was no mention of insomnia in the discharge notes for those patients (J Nerv Ment Dis. 2018 Oct;206[10]:765-9).

Many cognitive impairments can occur as a result of insomnia, which affects performance at work; decreases enjoyment of social activities; can lead to motor vehicle accidents or falls; and can affect health in the form of diabetes, hypertension, and increased mortality. Insomnia also can predict the risk of future depression and is a risk factor for suicide, Dr. Doghramji said at the meeting presented by Global Academy for Medical Education.

Adults can have insomnia for many reasons, including genetics, stress, negative conditioning, intrapsychic conflict, and bad habits, as well as medical and psychiatric conditions. While knowledge surrounding insomnia has advanced under a hyperarousal model, “It is really a hyperarousal disturbance which defies psychological understanding,” said Dr. Doghramji, who is also professor of psychiatry, neurology, and medicine at the university.

Evaluating the type of insomnia a patient is experiencing should be the first step in managing the disorder, followed by determining whether the insomnia is contributing to daytime impairment or decreased quality of life for the patient. From there, the insomnia can be treated with behavioral or pharmacotherapy. However, if insomnia is associated with another comorbid condition, the condition should be treated alongside the insomnia.

Sleep is highly comorbid with psychiatric and medical conditions (Sleep Med Clin. 2019 Jun;14[2]:167-75). Initial insomnia is more likely to be associated with delayed sleep phase disorder and restless legs syndrome, while middle insomnia is associated with sleep apnea and depression. Patients who wake early and are unable to go back to sleep (terminal insomnia) are likely to have depression, shift work disorder, or advanced sleep phase disorder.

“Once you identify [insomnia], there are all sorts of wonderful ways to manage it, including behavioral and pharmacological therapy,” said Dr. Doghramji. The comorbid condition also should be considered when deciding how to treat insomnia. For example, a patient with gastroesophageal reflux disease and insomnia would be more suited to cognitive-behavioral therapy than pharmacologic agents to help with sleep, because being able to wake up during the night from acid building in the esophagus is the body’s defense mechanism for the disease, Dr. Doghramji said.

Dr. Doghramji reported serving as a consultant for Eisai, Merck, and Pfizer. He also receives research funding from and owns stock in Merck.

Global Academy for Medical Education, Current Psychiatry, and this news organization are owned by the same company.

CRYSTAL CITY, VA. – Insomnia is a neuropsychiatric disorder of hyperarousal that should be evaluated as a disorder and treated with any associated comorbid conditions, Karl Doghramji, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Karen Winton/iStockphoto

“When I was a resident, I used to say insomnia is never a disorder. It’s always a symptom; you’ve got to find the primary disorder to know what the insomnia is caused by,” said Dr. Doghramji, medical director of the Jefferson Sleep Disorders Center at Jefferson Medical College, Philadelphia. “We no longer believe that. Throw that out the window.”

According to the new definition under the DSM-5, insomnia is characterized by dissatisfaction with sleep quality or quantity in the presence of adequate opportunity for sleep that causes significant distress or impairment for more than 3 nights per week over a period of 3 months. A survey of almost 7,500 U.S. health plan subscribers conducted a few years ago found that the prevalence of insomnia was estimated at 23.2% (Sleep. 2011 Sep 1;34[9]:1161-71).

Insomnia is also not well identified in clinical practice: In results published from his own group, Dr. Doghramji and colleagues evaluated 97 patients who were administered the Insomnia Severity Index; of those patients, 79.4% met the criteria for insomnia, but there was no mention of insomnia in the discharge notes for those patients (J Nerv Ment Dis. 2018 Oct;206[10]:765-9).

Many cognitive impairments can occur as a result of insomnia, which affects performance at work; decreases enjoyment of social activities; can lead to motor vehicle accidents or falls; and can affect health in the form of diabetes, hypertension, and increased mortality. Insomnia also can predict the risk of future depression and is a risk factor for suicide, Dr. Doghramji said at the meeting presented by Global Academy for Medical Education.

Adults can have insomnia for many reasons, including genetics, stress, negative conditioning, intrapsychic conflict, and bad habits, as well as medical and psychiatric conditions. While knowledge surrounding insomnia has advanced under a hyperarousal model, “It is really a hyperarousal disturbance which defies psychological understanding,” said Dr. Doghramji, who is also professor of psychiatry, neurology, and medicine at the university.

Evaluating the type of insomnia a patient is experiencing should be the first step in managing the disorder, followed by determining whether the insomnia is contributing to daytime impairment or decreased quality of life for the patient. From there, the insomnia can be treated with behavioral or pharmacotherapy. However, if insomnia is associated with another comorbid condition, the condition should be treated alongside the insomnia.

Sleep is highly comorbid with psychiatric and medical conditions (Sleep Med Clin. 2019 Jun;14[2]:167-75). Initial insomnia is more likely to be associated with delayed sleep phase disorder and restless legs syndrome, while middle insomnia is associated with sleep apnea and depression. Patients who wake early and are unable to go back to sleep (terminal insomnia) are likely to have depression, shift work disorder, or advanced sleep phase disorder.

“Once you identify [insomnia], there are all sorts of wonderful ways to manage it, including behavioral and pharmacological therapy,” said Dr. Doghramji. The comorbid condition also should be considered when deciding how to treat insomnia. For example, a patient with gastroesophageal reflux disease and insomnia would be more suited to cognitive-behavioral therapy than pharmacologic agents to help with sleep, because being able to wake up during the night from acid building in the esophagus is the body’s defense mechanism for the disease, Dr. Doghramji said.

Dr. Doghramji reported serving as a consultant for Eisai, Merck, and Pfizer. He also receives research funding from and owns stock in Merck.

Global Academy for Medical Education, Current Psychiatry, and this news organization are owned by the same company.

CRYSTAL CITY, VA. – Individuals with mood disorders might have an altered microbiome, but more information is needed to understand how the microorganisms that make up the microbiome affect patients’ health, an expert said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“An increased understanding of the neurobiology of the microbiome is required so that the benefit that these microorganisms serve to human health can be fully harnessed,” said Emily G. Severance, PhD, assistant professor of pediatrics at John Hopkins University, Baltimore.

Diseases that involve the microbiome include those with a single identifiable infectious agent that produces persistent inflammation, central nervous system diseases with mucosal surface involvement, and diseases with “variable response to antibiotic and anti-inflammatory agents.”

“It’s becoming clear that [the microbiome is] integral for the modulation of the central nervous system,” which occurs through neurotransmitter production, Dr. Severance said at the meeting presented by Global Academy for Medical Education.

“We have an extensive enteric nervous system that has the very same receptors that the brain does,” she said. “If you have those receptors activated in the gut or [are] having the neurotransmitters produced in the gut, and if there’s a way for those neurotransmitters to reach the brain, that’s a very powerful mechanism to illustrate the gut-brain axis.”

In addition to neuropsychiatric diseases, the microbiome also can be involved in inflammatory gastrointestinal, systemic rheumatoid and autoimmune, chronic inflammatory lung, and periodontal diseases, as well as immune-mediated skin disorders. Mood disorders in particular have evidence for dysbiosis in low-level inflammation and leaky gut pathology, which is present in patients with depression, Dr. Severance said. “All these data suggest that there’s a viable rationale to try to harness the functional significance of the microbial community. We can do that because gut bacteria are easily accessed and can be altered through probiotics, prebiotics, diet, and fecal transplant, and in patients, Lactobacillus and Bifidobacterium combinations may improve mood, reduce anxiety, and enhance cognitive function.”

In addition, epidemiological studies show that antibiotic exposure can be a risk factor for developing mood disorders. One recent study found that anti-infective agents, particularly antibiotics, increased the risk of schizophrenia (hazard rate ratio, 2.05; 95% confidence interval, 1.77-2.38) and affective disorders (HRR, 2.59; 95% CI, 2.31-2.89), which the researchers attributed to brain inflammation, the microbiome, and environmental factors (Acta Psychiatr Scand. 2016 Nov 21. doi: 10.1111/acps.12671). In mice, other researchers found that those that received a fecal transplant with a “depression microbiota” showed symptoms of major depressive disorder, compared with mice that received a “healthy microbiota.” Those results suggest that change in microbiota can induce mood disorders (Mol Psychiatry. 2016 Apr 12. doi: 10.1038/mp.2016.44).


The evidence for probiotics is mixed, primarily because the study population in trials are so heterogeneous, but there is evidence for its efficacy in patients with mood disorders, Dr. Severance said. Probiotics have been shown to prevent rehospitalization for patients in mania. For example, one study showed reduced rehospitalization in patients with mania (8 of 33 patients) who received probiotics, compared with placebo (24 of 33 patients). Also, probiotic use was associated with fewer days of rehospitalization (Bipolar Disord. 2018 Apr 25. doi: 10. 1111/bdi.12652).

Meanwhile, a pilot study analyzing patients with irritable bowel syndrome and mild to moderate anxiety and/or depression found use of B. longum in this population reduced depression scores, but not anxiety or irritable bowel syndrome symptoms, compared with placebo (Gastroenterology. 2017 May 5. doi: 10.1053/j.gastro.2017.05.003).

Probiotic efficacy can be variable for patients with mood disorders, but the intervention is a “relatively low-risk, potentially high reward” option for these patients, Dr. Severance said. “Clinicians should inquire about patient GI conditions and overall GI health. Dietary interventions and the use of probiotics and their limitations should be discussed as supplemental therapeutic options.”

Dr. Severance reported no relevant financial disclosures.

Global Academy and this news organization are owned by the same parent company.

CRYSTAL CITY, VA. – Individuals with mood disorders might have an altered microbiome, but more information is needed to understand how the microorganisms that make up the microbiome affect patients’ health, an expert said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“An increased understanding of the neurobiology of the microbiome is required so that the benefit that these microorganisms serve to human health can be fully harnessed,” said Emily G. Severance, PhD, assistant professor of pediatrics at John Hopkins University, Baltimore.

Diseases that involve the microbiome include those with a single identifiable infectious agent that produces persistent inflammation, central nervous system diseases with mucosal surface involvement, and diseases with “variable response to antibiotic and anti-inflammatory agents.”

“It’s becoming clear that [the microbiome is] integral for the modulation of the central nervous system,” which occurs through neurotransmitter production, Dr. Severance said at the meeting presented by Global Academy for Medical Education.

“We have an extensive enteric nervous system that has the very same receptors that the brain does,” she said. “If you have those receptors activated in the gut or [are] having the neurotransmitters produced in the gut, and if there’s a way for those neurotransmitters to reach the brain, that’s a very powerful mechanism to illustrate the gut-brain axis.”

In addition to neuropsychiatric diseases, the microbiome also can be involved in inflammatory gastrointestinal, systemic rheumatoid and autoimmune, chronic inflammatory lung, and periodontal diseases, as well as immune-mediated skin disorders. Mood disorders in particular have evidence for dysbiosis in low-level inflammation and leaky gut pathology, which is present in patients with depression, Dr. Severance said. “All these data suggest that there’s a viable rationale to try to harness the functional significance of the microbial community. We can do that because gut bacteria are easily accessed and can be altered through probiotics, prebiotics, diet, and fecal transplant, and in patients, Lactobacillus and Bifidobacterium combinations may improve mood, reduce anxiety, and enhance cognitive function.”

In addition, epidemiological studies show that antibiotic exposure can be a risk factor for developing mood disorders. One recent study found that anti-infective agents, particularly antibiotics, increased the risk of schizophrenia (hazard rate ratio, 2.05; 95% confidence interval, 1.77-2.38) and affective disorders (HRR, 2.59; 95% CI, 2.31-2.89), which the researchers attributed to brain inflammation, the microbiome, and environmental factors (Acta Psychiatr Scand. 2016 Nov 21. doi: 10.1111/acps.12671). In mice, other researchers found that those that received a fecal transplant with a “depression microbiota” showed symptoms of major depressive disorder, compared with mice that received a “healthy microbiota.” Those results suggest that change in microbiota can induce mood disorders (Mol Psychiatry. 2016 Apr 12. doi: 10.1038/mp.2016.44).


The evidence for probiotics is mixed, primarily because the study population in trials are so heterogeneous, but there is evidence for its efficacy in patients with mood disorders, Dr. Severance said. Probiotics have been shown to prevent rehospitalization for patients in mania. For example, one study showed reduced rehospitalization in patients with mania (8 of 33 patients) who received probiotics, compared with placebo (24 of 33 patients). Also, probiotic use was associated with fewer days of rehospitalization (Bipolar Disord. 2018 Apr 25. doi: 10. 1111/bdi.12652).

Meanwhile, a pilot study analyzing patients with irritable bowel syndrome and mild to moderate anxiety and/or depression found use of B. longum in this population reduced depression scores, but not anxiety or irritable bowel syndrome symptoms, compared with placebo (Gastroenterology. 2017 May 5. doi: 10.1053/j.gastro.2017.05.003).

Probiotic efficacy can be variable for patients with mood disorders, but the intervention is a “relatively low-risk, potentially high reward” option for these patients, Dr. Severance said. “Clinicians should inquire about patient GI conditions and overall GI health. Dietary interventions and the use of probiotics and their limitations should be discussed as supplemental therapeutic options.”

Dr. Severance reported no relevant financial disclosures.

Global Academy and this news organization are owned by the same parent company.

CRYSTAL CITY, VA. – Individuals with mood disorders might have an altered microbiome, but more information is needed to understand how the microorganisms that make up the microbiome affect patients’ health, an expert said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“An increased understanding of the neurobiology of the microbiome is required so that the benefit that these microorganisms serve to human health can be fully harnessed,” said Emily G. Severance, PhD, assistant professor of pediatrics at John Hopkins University, Baltimore.

Diseases that involve the microbiome include those with a single identifiable infectious agent that produces persistent inflammation, central nervous system diseases with mucosal surface involvement, and diseases with “variable response to antibiotic and anti-inflammatory agents.”

“It’s becoming clear that [the microbiome is] integral for the modulation of the central nervous system,” which occurs through neurotransmitter production, Dr. Severance said at the meeting presented by Global Academy for Medical Education.

“We have an extensive enteric nervous system that has the very same receptors that the brain does,” she said. “If you have those receptors activated in the gut or [are] having the neurotransmitters produced in the gut, and if there’s a way for those neurotransmitters to reach the brain, that’s a very powerful mechanism to illustrate the gut-brain axis.”

In addition to neuropsychiatric diseases, the microbiome also can be involved in inflammatory gastrointestinal, systemic rheumatoid and autoimmune, chronic inflammatory lung, and periodontal diseases, as well as immune-mediated skin disorders. Mood disorders in particular have evidence for dysbiosis in low-level inflammation and leaky gut pathology, which is present in patients with depression, Dr. Severance said. “All these data suggest that there’s a viable rationale to try to harness the functional significance of the microbial community. We can do that because gut bacteria are easily accessed and can be altered through probiotics, prebiotics, diet, and fecal transplant, and in patients, Lactobacillus and Bifidobacterium combinations may improve mood, reduce anxiety, and enhance cognitive function.”

In addition, epidemiological studies show that antibiotic exposure can be a risk factor for developing mood disorders. One recent study found that anti-infective agents, particularly antibiotics, increased the risk of schizophrenia (hazard rate ratio, 2.05; 95% confidence interval, 1.77-2.38) and affective disorders (HRR, 2.59; 95% CI, 2.31-2.89), which the researchers attributed to brain inflammation, the microbiome, and environmental factors (Acta Psychiatr Scand. 2016 Nov 21. doi: 10.1111/acps.12671). In mice, other researchers found that those that received a fecal transplant with a “depression microbiota” showed symptoms of major depressive disorder, compared with mice that received a “healthy microbiota.” Those results suggest that change in microbiota can induce mood disorders (Mol Psychiatry. 2016 Apr 12. doi: 10.1038/mp.2016.44).


The evidence for probiotics is mixed, primarily because the study population in trials are so heterogeneous, but there is evidence for its efficacy in patients with mood disorders, Dr. Severance said. Probiotics have been shown to prevent rehospitalization for patients in mania. For example, one study showed reduced rehospitalization in patients with mania (8 of 33 patients) who received probiotics, compared with placebo (24 of 33 patients). Also, probiotic use was associated with fewer days of rehospitalization (Bipolar Disord. 2018 Apr 25. doi: 10. 1111/bdi.12652).

Meanwhile, a pilot study analyzing patients with irritable bowel syndrome and mild to moderate anxiety and/or depression found use of B. longum in this population reduced depression scores, but not anxiety or irritable bowel syndrome symptoms, compared with placebo (Gastroenterology. 2017 May 5. doi: 10.1053/j.gastro.2017.05.003).

Probiotic efficacy can be variable for patients with mood disorders, but the intervention is a “relatively low-risk, potentially high reward” option for these patients, Dr. Severance said. “Clinicians should inquire about patient GI conditions and overall GI health. Dietary interventions and the use of probiotics and their limitations should be discussed as supplemental therapeutic options.”

Dr. Severance reported no relevant financial disclosures.

Global Academy and this news organization are owned by the same parent company.

CRYSTAL CITY, VA. – As technology advances and the population becomes older, clinicians should understand how modest age-related declines in cognition affect older adults’ ability to learn new technological skills, Philip D. Harvey, PhD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

©AlexRaths/thinkstockphotos.com

According to the U.S. Census Bureau, the number of adults in the United States above age 65 is slated to increase over the next several decades, and by 2030, one in five adults in the United States will be at retirement age. By 2050, “a significant number of people” in the United States are expected to be age 90, Dr. Harvey said at the meeting, presented by Global Academy for Medical Education.

“What we need to do is to understand what are the normal things that happen to people as they become 90 years of age,” said Dr. Harvey, of the department of psychiatry and behavioral sciences at the University of Miami.

Within the technology industry, significant advancements were made over the last 40 years with the advent of the personal computer in the 1980s, mobile phones in the 1990s, and wireless Internet, smartphones, and wireless devices in the 2000s. Many interactions that used to be person-to-person are now performed online, and it is feasible for a 90-year-old living today to never have encountered this technology during their careers. “Utilizing technology is a central requirement for independent living today,” Dr. Harvey said.

Most people passively adapt to these new changes in technology. However, Dr. Harvey noted that adults in their 80s and 90s who are retired can have difficulty using or learning about new technology as they age. “Human-technology interaction involves information processing, and places demands on memory and other cognitive abilities,” he said. “Age is associated with declines specifically in the kind of abilities that are required to master new technology.”

Learning about and using technology requires different elements of cognition that include different types of memory, such as working, episodic, declarative, procedural, semantic, long-term factual, and emotional. A decline in any of those kinds of memory could result in failures in forgetting, learning or recalling material, and learning new motor skills, among other problems. Crystallized intelligence is more likely to be retained over time, but fluid cognition in the form of processing speed, working and episodic memory, and the ability to solve abstract problems tend to decline over time as people age, Dr. Harvey said.

Base cognitive abilities do play a role in how crystallized and fluid cognition decline over time. For example, while vocabulary might increase as one ages, a person’s working memory, processing speed, and episodic memory decline over time. Evidence also suggests that speed training and exercise appear to improve cognition. In the ACTIVE trial, 2,832 adults with a baseline age of 73.6 years who underwent 10 cognitive training sessions to improve memory showed better cognitive scores that remained at 10-year follow-up (J Am Geriatr Soc. 13 Jan 2014. doi: 10.1111/jgs.12607).

Cyrus Raji, MD, PhD, and colleagues also explored the relationship between caloric expenditure and gray matter volume in the Cardiovascular Health Study, and found that exercise of various types improved gray matter volume and reduced the risk of dementia in people aged 65 or older. Furthermore, Dr. Raji and colleagues found, caloric expenditures, rather than intensity of exercise, may alone predict increases in gray matter volume (J Alzheimers Dis. 2016. doi: 10.3233/JAD-160057).

“If you want to improve your memory, grow your hippocampus,” Dr. Harvey said at the meeting.

Dr. Harvey reported serving as a consultant for Alkermes, Boehringer-Ingelheim, Lundbeck, Otsuka Digital Health, Sanofi, Sunovion Pharmaceuticals, Takeda, and Teva. He also reported receiving a grant from Takeda, and is the founder and CSO of i-Function.

Global Academy and this news organization are owned by the same parent company.

CRYSTAL CITY, VA. – As technology advances and the population becomes older, clinicians should understand how modest age-related declines in cognition affect older adults’ ability to learn new technological skills, Philip D. Harvey, PhD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

©AlexRaths/thinkstockphotos.com

According to the U.S. Census Bureau, the number of adults in the United States above age 65 is slated to increase over the next several decades, and by 2030, one in five adults in the United States will be at retirement age. By 2050, “a significant number of people” in the United States are expected to be age 90, Dr. Harvey said at the meeting, presented by Global Academy for Medical Education.

“What we need to do is to understand what are the normal things that happen to people as they become 90 years of age,” said Dr. Harvey, of the department of psychiatry and behavioral sciences at the University of Miami.

Within the technology industry, significant advancements were made over the last 40 years with the advent of the personal computer in the 1980s, mobile phones in the 1990s, and wireless Internet, smartphones, and wireless devices in the 2000s. Many interactions that used to be person-to-person are now performed online, and it is feasible for a 90-year-old living today to never have encountered this technology during their careers. “Utilizing technology is a central requirement for independent living today,” Dr. Harvey said.

Most people passively adapt to these new changes in technology. However, Dr. Harvey noted that adults in their 80s and 90s who are retired can have difficulty using or learning about new technology as they age. “Human-technology interaction involves information processing, and places demands on memory and other cognitive abilities,” he said. “Age is associated with declines specifically in the kind of abilities that are required to master new technology.”

Learning about and using technology requires different elements of cognition that include different types of memory, such as working, episodic, declarative, procedural, semantic, long-term factual, and emotional. A decline in any of those kinds of memory could result in failures in forgetting, learning or recalling material, and learning new motor skills, among other problems. Crystallized intelligence is more likely to be retained over time, but fluid cognition in the form of processing speed, working and episodic memory, and the ability to solve abstract problems tend to decline over time as people age, Dr. Harvey said.

Base cognitive abilities do play a role in how crystallized and fluid cognition decline over time. For example, while vocabulary might increase as one ages, a person’s working memory, processing speed, and episodic memory decline over time. Evidence also suggests that speed training and exercise appear to improve cognition. In the ACTIVE trial, 2,832 adults with a baseline age of 73.6 years who underwent 10 cognitive training sessions to improve memory showed better cognitive scores that remained at 10-year follow-up (J Am Geriatr Soc. 13 Jan 2014. doi: 10.1111/jgs.12607).

Cyrus Raji, MD, PhD, and colleagues also explored the relationship between caloric expenditure and gray matter volume in the Cardiovascular Health Study, and found that exercise of various types improved gray matter volume and reduced the risk of dementia in people aged 65 or older. Furthermore, Dr. Raji and colleagues found, caloric expenditures, rather than intensity of exercise, may alone predict increases in gray matter volume (J Alzheimers Dis. 2016. doi: 10.3233/JAD-160057).

“If you want to improve your memory, grow your hippocampus,” Dr. Harvey said at the meeting.

Dr. Harvey reported serving as a consultant for Alkermes, Boehringer-Ingelheim, Lundbeck, Otsuka Digital Health, Sanofi, Sunovion Pharmaceuticals, Takeda, and Teva. He also reported receiving a grant from Takeda, and is the founder and CSO of i-Function.

Global Academy and this news organization are owned by the same parent company.

CRYSTAL CITY, VA. – As technology advances and the population becomes older, clinicians should understand how modest age-related declines in cognition affect older adults’ ability to learn new technological skills, Philip D. Harvey, PhD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

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According to the U.S. Census Bureau, the number of adults in the United States above age 65 is slated to increase over the next several decades, and by 2030, one in five adults in the United States will be at retirement age. By 2050, “a significant number of people” in the United States are expected to be age 90, Dr. Harvey said at the meeting, presented by Global Academy for Medical Education.

“What we need to do is to understand what are the normal things that happen to people as they become 90 years of age,” said Dr. Harvey, of the department of psychiatry and behavioral sciences at the University of Miami.

Within the technology industry, significant advancements were made over the last 40 years with the advent of the personal computer in the 1980s, mobile phones in the 1990s, and wireless Internet, smartphones, and wireless devices in the 2000s. Many interactions that used to be person-to-person are now performed online, and it is feasible for a 90-year-old living today to never have encountered this technology during their careers. “Utilizing technology is a central requirement for independent living today,” Dr. Harvey said.

Most people passively adapt to these new changes in technology. However, Dr. Harvey noted that adults in their 80s and 90s who are retired can have difficulty using or learning about new technology as they age. “Human-technology interaction involves information processing, and places demands on memory and other cognitive abilities,” he said. “Age is associated with declines specifically in the kind of abilities that are required to master new technology.”

Learning about and using technology requires different elements of cognition that include different types of memory, such as working, episodic, declarative, procedural, semantic, long-term factual, and emotional. A decline in any of those kinds of memory could result in failures in forgetting, learning or recalling material, and learning new motor skills, among other problems. Crystallized intelligence is more likely to be retained over time, but fluid cognition in the form of processing speed, working and episodic memory, and the ability to solve abstract problems tend to decline over time as people age, Dr. Harvey said.

Base cognitive abilities do play a role in how crystallized and fluid cognition decline over time. For example, while vocabulary might increase as one ages, a person’s working memory, processing speed, and episodic memory decline over time. Evidence also suggests that speed training and exercise appear to improve cognition. In the ACTIVE trial, 2,832 adults with a baseline age of 73.6 years who underwent 10 cognitive training sessions to improve memory showed better cognitive scores that remained at 10-year follow-up (J Am Geriatr Soc. 13 Jan 2014. doi: 10.1111/jgs.12607).

Cyrus Raji, MD, PhD, and colleagues also explored the relationship between caloric expenditure and gray matter volume in the Cardiovascular Health Study, and found that exercise of various types improved gray matter volume and reduced the risk of dementia in people aged 65 or older. Furthermore, Dr. Raji and colleagues found, caloric expenditures, rather than intensity of exercise, may alone predict increases in gray matter volume (J Alzheimers Dis. 2016. doi: 10.3233/JAD-160057).

“If you want to improve your memory, grow your hippocampus,” Dr. Harvey said at the meeting.

Dr. Harvey reported serving as a consultant for Alkermes, Boehringer-Ingelheim, Lundbeck, Otsuka Digital Health, Sanofi, Sunovion Pharmaceuticals, Takeda, and Teva. He also reported receiving a grant from Takeda, and is the founder and CSO of i-Function.

Global Academy and this news organization are owned by the same parent company.

CRYSTAL CITY, VA. – Some patients experience consistent suicidal ideation – but most do not, an expert said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Highwaystarz-Photography/Thinkstock

“In most patients, the ideation tends to go up and down – which means you ask the patient about the most severe example of suicidal ideation … in the last week or 2,” J. John Mann, MD, said. Getting a handle on patients’ worst suicidal ideation also can provide clues into the range of suicidal behavior they might be subject to, he added.

U.S. suicide rates have increased dramatically since 2000, and most people who die by suicide had depression, said Dr. Mann, the Paul Janssen Professor of Translational Neuroscience (in psychiatry and in radiology) at Columbia University, New York. However, those patients who are depressed tend to attempt suicide early in their depression.

“Most people with a major depressive episode never attempt suicide,” said Dr. Mann, who also is affiliated with the New York State Psychiatric Institute. “Suicidal behavior is not a ‘wear and tear’ phenomenon.”

When assessing risk of suicide clinically, patients most at risk include those with past history of suicide attempts, a family history of suicide, and those who have the worst suicidal ideation.

About half of the predisposition to suicidal behavior is genetic and independent of genetic risk associated with major psychiatric disorders. This genetic risk affects the diathesis each patient has for suicidal behavior. In the stress-diathesis model for suicidal behavior, stress from major depressive episodes and life events contributes to the patient’s perception of stress, which in turn contributes to that patient’s response to stress. Rather than depression itself being a suicidal trigger, these stressors in the form of adverse life events appear to be the trigger for suicide attempts, Dr. Mann noted.

“All of the risk is pretty much accounted for by whether the patient was in or out of an episode of major depression,” said Dr. Mann. “If they were in an episode of major depression, all the risk was accounted for by the major depression, and the stressors counted for enough. When they’re out of an episode of major depression, the risk fell right away and the stressors didn’t matter much.”

In the stress-diathesis model, trait components of suicidal behavior include mood and emotion dysregulation and perception; misreading social signals; reactive or impulsive aggressive traits of decision making or delayed discounting; and altered learning, memory, and problem solving. However, clinicians should look to the patients for whom depression appears more painful in subjective scores, because going by these trait components alone will not distinguish between patients at risk for suicide and those who will not make an attempt.

According to the Columbia Classification Algorithm of Suicide Assessment, suicide is distinguished by whether a patient wished to die, if an attempt is stopped by themselves or another person before harm has begun, and whether a patient prepared for the act beyond verbalizing or thinking of suicide but before harm has begun.

In addition to prescribing antidepressants, treatments with evidence for preventing suicide include means restriction and cognitive-behavioral therapy. For patients with borderline personality disorder, dialectical behavior therapy has proven effective. School interventions that educate students about mental health also have shown effectiveness. Other strategies include educating reporters about media guidelines on writing about suicide. Internet outreach interventions are promising, he said, but more evidence is needed to determine whether they work.

Among antidepressant options for patients with suicidal ideation, fluoxetine appears best for adolescents, and data show that venlafaxine is effective in adults. The Food and Drug Administration originally put a black box warning on selective serotonin reuptake inhibitors in 2004; however, recent data have shown that the increased risk of suicidal ideation brought on by those medications tapers off after the first week on the medication. Meanwhile, in the case of ketamine, there is “rapid and robust improvement” in depressive symptoms and suicidal ideation, which targets the diathesis, Dr. Mann said at the meeting presented by Global Academy for Medical Education.

“We need to identify rapidly acting antisuicidal medications, and we now see there’s a clear path forward to do that” with treatments like ketamine, he said.

Dr. Mann’s presentation was based on research funded by the National Institute of Mental Health and the Brain & Behavior Research Foundation. He reported receiving royalties from the Research Foundation for Mental Hygiene for commercial use of the Columbia-Suicide Severity Rating Scale.

Global Academy for Medical Education, Current Psychiatry, and this publication are owned by the same company.

CRYSTAL CITY, VA. – Some patients experience consistent suicidal ideation – but most do not, an expert said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Highwaystarz-Photography/Thinkstock

“In most patients, the ideation tends to go up and down – which means you ask the patient about the most severe example of suicidal ideation … in the last week or 2,” J. John Mann, MD, said. Getting a handle on patients’ worst suicidal ideation also can provide clues into the range of suicidal behavior they might be subject to, he added.

U.S. suicide rates have increased dramatically since 2000, and most people who die by suicide had depression, said Dr. Mann, the Paul Janssen Professor of Translational Neuroscience (in psychiatry and in radiology) at Columbia University, New York. However, those patients who are depressed tend to attempt suicide early in their depression.

“Most people with a major depressive episode never attempt suicide,” said Dr. Mann, who also is affiliated with the New York State Psychiatric Institute. “Suicidal behavior is not a ‘wear and tear’ phenomenon.”

When assessing risk of suicide clinically, patients most at risk include those with past history of suicide attempts, a family history of suicide, and those who have the worst suicidal ideation.

About half of the predisposition to suicidal behavior is genetic and independent of genetic risk associated with major psychiatric disorders. This genetic risk affects the diathesis each patient has for suicidal behavior. In the stress-diathesis model for suicidal behavior, stress from major depressive episodes and life events contributes to the patient’s perception of stress, which in turn contributes to that patient’s response to stress. Rather than depression itself being a suicidal trigger, these stressors in the form of adverse life events appear to be the trigger for suicide attempts, Dr. Mann noted.

“All of the risk is pretty much accounted for by whether the patient was in or out of an episode of major depression,” said Dr. Mann. “If they were in an episode of major depression, all the risk was accounted for by the major depression, and the stressors counted for enough. When they’re out of an episode of major depression, the risk fell right away and the stressors didn’t matter much.”

In the stress-diathesis model, trait components of suicidal behavior include mood and emotion dysregulation and perception; misreading social signals; reactive or impulsive aggressive traits of decision making or delayed discounting; and altered learning, memory, and problem solving. However, clinicians should look to the patients for whom depression appears more painful in subjective scores, because going by these trait components alone will not distinguish between patients at risk for suicide and those who will not make an attempt.

According to the Columbia Classification Algorithm of Suicide Assessment, suicide is distinguished by whether a patient wished to die, if an attempt is stopped by themselves or another person before harm has begun, and whether a patient prepared for the act beyond verbalizing or thinking of suicide but before harm has begun.

In addition to prescribing antidepressants, treatments with evidence for preventing suicide include means restriction and cognitive-behavioral therapy. For patients with borderline personality disorder, dialectical behavior therapy has proven effective. School interventions that educate students about mental health also have shown effectiveness. Other strategies include educating reporters about media guidelines on writing about suicide. Internet outreach interventions are promising, he said, but more evidence is needed to determine whether they work.

Among antidepressant options for patients with suicidal ideation, fluoxetine appears best for adolescents, and data show that venlafaxine is effective in adults. The Food and Drug Administration originally put a black box warning on selective serotonin reuptake inhibitors in 2004; however, recent data have shown that the increased risk of suicidal ideation brought on by those medications tapers off after the first week on the medication. Meanwhile, in the case of ketamine, there is “rapid and robust improvement” in depressive symptoms and suicidal ideation, which targets the diathesis, Dr. Mann said at the meeting presented by Global Academy for Medical Education.

“We need to identify rapidly acting antisuicidal medications, and we now see there’s a clear path forward to do that” with treatments like ketamine, he said.

Dr. Mann’s presentation was based on research funded by the National Institute of Mental Health and the Brain & Behavior Research Foundation. He reported receiving royalties from the Research Foundation for Mental Hygiene for commercial use of the Columbia-Suicide Severity Rating Scale.

Global Academy for Medical Education, Current Psychiatry, and this publication are owned by the same company.

CRYSTAL CITY, VA. – Some patients experience consistent suicidal ideation – but most do not, an expert said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Highwaystarz-Photography/Thinkstock

“In most patients, the ideation tends to go up and down – which means you ask the patient about the most severe example of suicidal ideation … in the last week or 2,” J. John Mann, MD, said. Getting a handle on patients’ worst suicidal ideation also can provide clues into the range of suicidal behavior they might be subject to, he added.

U.S. suicide rates have increased dramatically since 2000, and most people who die by suicide had depression, said Dr. Mann, the Paul Janssen Professor of Translational Neuroscience (in psychiatry and in radiology) at Columbia University, New York. However, those patients who are depressed tend to attempt suicide early in their depression.

“Most people with a major depressive episode never attempt suicide,” said Dr. Mann, who also is affiliated with the New York State Psychiatric Institute. “Suicidal behavior is not a ‘wear and tear’ phenomenon.”

When assessing risk of suicide clinically, patients most at risk include those with past history of suicide attempts, a family history of suicide, and those who have the worst suicidal ideation.

About half of the predisposition to suicidal behavior is genetic and independent of genetic risk associated with major psychiatric disorders. This genetic risk affects the diathesis each patient has for suicidal behavior. In the stress-diathesis model for suicidal behavior, stress from major depressive episodes and life events contributes to the patient’s perception of stress, which in turn contributes to that patient’s response to stress. Rather than depression itself being a suicidal trigger, these stressors in the form of adverse life events appear to be the trigger for suicide attempts, Dr. Mann noted.

“All of the risk is pretty much accounted for by whether the patient was in or out of an episode of major depression,” said Dr. Mann. “If they were in an episode of major depression, all the risk was accounted for by the major depression, and the stressors counted for enough. When they’re out of an episode of major depression, the risk fell right away and the stressors didn’t matter much.”

In the stress-diathesis model, trait components of suicidal behavior include mood and emotion dysregulation and perception; misreading social signals; reactive or impulsive aggressive traits of decision making or delayed discounting; and altered learning, memory, and problem solving. However, clinicians should look to the patients for whom depression appears more painful in subjective scores, because going by these trait components alone will not distinguish between patients at risk for suicide and those who will not make an attempt.

According to the Columbia Classification Algorithm of Suicide Assessment, suicide is distinguished by whether a patient wished to die, if an attempt is stopped by themselves or another person before harm has begun, and whether a patient prepared for the act beyond verbalizing or thinking of suicide but before harm has begun.

In addition to prescribing antidepressants, treatments with evidence for preventing suicide include means restriction and cognitive-behavioral therapy. For patients with borderline personality disorder, dialectical behavior therapy has proven effective. School interventions that educate students about mental health also have shown effectiveness. Other strategies include educating reporters about media guidelines on writing about suicide. Internet outreach interventions are promising, he said, but more evidence is needed to determine whether they work.

Among antidepressant options for patients with suicidal ideation, fluoxetine appears best for adolescents, and data show that venlafaxine is effective in adults. The Food and Drug Administration originally put a black box warning on selective serotonin reuptake inhibitors in 2004; however, recent data have shown that the increased risk of suicidal ideation brought on by those medications tapers off after the first week on the medication. Meanwhile, in the case of ketamine, there is “rapid and robust improvement” in depressive symptoms and suicidal ideation, which targets the diathesis, Dr. Mann said at the meeting presented by Global Academy for Medical Education.

“We need to identify rapidly acting antisuicidal medications, and we now see there’s a clear path forward to do that” with treatments like ketamine, he said.

Dr. Mann’s presentation was based on research funded by the National Institute of Mental Health and the Brain & Behavior Research Foundation. He reported receiving royalties from the Research Foundation for Mental Hygiene for commercial use of the Columbia-Suicide Severity Rating Scale.

Global Academy for Medical Education, Current Psychiatry, and this publication are owned by the same company.