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Is Metabolic Syndrome on Your Radar?

Metabolic syndrome is defined by the aggregation of hypertriglyceridemia, low high-density lipoprotein (HDL) levels, elevated fasting glucose, hypertension, and increased waist circumference. Metabolic syndrome confers an increased risk of developing diabetes and of dying from coronary artery disease. Cardiovascular disease is the leading cause of death among patients with schizophrenia, who have a life expectancy about 20 years shorter than the general population.

My colleagues and I conducted a study that was prompted by the observation that, in about 9,000 consecutive admissions to our psychiatric hospital, not once was the diagnosis of metabolic syndrome made. In a quality improvement intervention, the admission order set of the psychiatric hospital was changed to automatically trigger orders for waist circumference measurement, vital signs, and fasting HDL, triglyceride, and glucose tests. In addition, we created a computer program to automatically extract from the electronic medical records (EMR) the lab values required to make the diagnosis of metabolic syndrome. The diagnosis was flagged by the computer in the EMR, and, in our study, we asked, “Would the psychiatrists change their prescribing behavior, for example, by switching from a metabolically problematic second-generation antipsychotic (SGA) such as olanzapine to a more benign SGA such as aripiprazole or a first-generation antipsychotic (FGA)?”

The short answer is “no”; there was no change in prescribed SGAs from admission to discharge after the intervention for automatic detection of metabolic syndrome was initiated.

E-mail notification of the presence of metabolic syndrome did not improve the response of the psychiatrists. This intervention improved the documentation of metabolic syndrome in the EMR from 0% to 29%. However, there was no improvement in the treatment of the components of metabolic syndrome (by prescribing lipid-lowering, antiglycemic, and antihypertensive drugs).

These results are puzzling. Why wouldn’t psychiatrists proactively identify and treat metabolic syndrome? We speculate that psychiatrists may experience “cognitive dissonance”; they like to prescribe SGAs because of a perceived superiority of efficacy/tolerability over FGAs, although research has not supported this perception.

Another possible explanation is that the attitude in the inpatient psychiatric setting is “first things first”; ie, we need to get some relief for these patients and can’t worry too much about the long-term consequences. As a result, the patient is most likely discharged while taking SGAs, which are then likely to be continued by the outpatient psychiatrist, thus exposing the patient to increasing cumulative metabolic risk.

In our study, a small subgroup of patients experienced a very rapid increase in triglycerides in response to SGAs (about 100% to 400% increases in about 5 to 20 days). These patients may have a genetic predisposition to this adverse effect; pediatric patients with polymorphisms near the melanocortin 4 receptor gene were found to have very rapid weight gain and metabolic changes with SGAs.

For a more detailed discussion, I suggest watching a YouTube video that we have prepared.

Financial disclosure: Dr Raese had no relevant personal financial relationships to report. ​

Are Your Patients Receiving Unnecessary Antipsychotic Polypharmacy?

The recently published randomized, placebo-controlled trial (RCT) by my colleagues and me confirms what guidelines have been telling us for some time now—that the evidence does not support the use of antipsychotic polypharmacy. Yet the practice continues in about 1 in 4 patients. Are clinicians that indifferent to evidence-based medicine or do these figures reflect the fact that the issue is not so straightforward? I suggest the latter.

Such categorical positions rarely hold up in medicine; our own study reminds us of this. Indeed, a fellow clinical researcher at my center recently recalled aloud that one of his patients who participated in this trial experienced clinical worsening when the second antipsychotic was withdrawn. I could conjecture reasons for this; for example, in our study, discontinuation of the second antipsychotic was abrupt rather than gradual. It remains, though, that some individuals do seem to worsen when polypharmacy is changed to monotherapy, and unfortunately we have no way of accurately predicting who these individuals are (just as we have no clearly established rationale for why or how a change to monotherapy might benefit other patients). The net result is that we have many patients who are unnecessarily receiving combined antipsychotic therapy. This situation is not unlike the high-dose antipsychotic story. Almost every clinician working with patients who have schizophrenia can identify someone who has required high doses to maintain response, but this group of patients is far outweighed by those who fail to benefit from such a strategy.

That there are some individuals who might benefit from antipsychotic polypharmacy is less troublesome to me than how this practice plays out clinically. Evidence and my own clinical experience indicate that polypharmacy is routinely used before clozapine and, on occasion, clozapine is not even offered or only after endless trials and combinations to avoid its use. In addition, antipsychotic polypharmacy often seems to be implemented without a clear framework. What are the target symptoms, how will change be monitored, and when will the trial be terminated in the absence of clear improvement? As someone who deals predominantly with treatment resistance, I am taken aback by how often I see treatment combinations continued in the absence of any clear benefits. And, of course, these same issues exist after clozapine is tried.

In fairness, it is important to also view this process through the eyes of busy clinicians who are under pressure from a variety of sources, themselves included, to get people “better.” In a field in which our available treatments, including clozapine, demonstrate limited success, we still feel a need to be seen as “doing something.” Arguably, there are occasions when combined antipsychotics and/or high doses do work, but the evidence would indicate that these instances are, at best, infrequent. When using what can be considered desperate measures, the treatment plan needs to be held to the same (or even higher) standards as the previous, simpler strategies.

Financial disclosure: Dr Remington is a consultant for Neurocrine and Synchroneuron and is a member of the speakers/advisory board for Novartis. ​

What Do We Tell Patients About Marijuana?

In 23 states, medical use of marijuana is legal. Cannabis or marijuana refers to the plant cannabis sativa or cannabis indica, containing the psychoactive chemical delta-9-tetrahydrocannabinol or THC. In a meta-analysis of 79 trials involving 6,462 participants, the authors concluded that “moderate-quality evidence” supports the use of cannabinoids in chronic pain and spasticity, but they are associated with short-term adverse events.

One small retrospective study showed that marijuana improved the symptoms of PTSD according to scores on the Clinician Administered Posttraumatic Scale for DSM-IV (CAPS), but the authors stated that prospective, placebo-controlled studies were needed. A prospective study of 2,276 veterans showed that marijuana use was statistically significantly associated with a worse outcome in PTSD severity. Additionally, there was a higher incidence of violent behavior in the group using marijuana after discharge. The authors concluded, “Marijuana may actually worsen PTSD symptoms or nullify the effects of specialized, intensive treatment.”

In 2016, premium grade marijuana is more easily available than ever before. The marijuana available today appears to be more potent (ie, have greater THC content) than the marijuana of past decades. This greater potency results in not only an increase in euphoria but also increased adverse effects: short-term memory problems, motor incoordination, and psychotic reactions. Improved delivery systems such as “vaping” and “dabbing” only increase the risks. Liquid forms of marijuana can be placed in modified electronic smoking devices. When hash oil is vaporized, a highly concentrated THC is created. The use of a modified vaporizer pen effectively hides the telltale marijuana odor.

Whether or not marijuana has medicinal properties remains unclear. An interesting and provocative psychiatric question is, Does marijuana increase the risk for schizophrenia? An expert roundtable discussed this question for the CME Institute. The evidence pointed to an increased risk for psychosis among early, frequent users of cannabis, especially of a high-potency variety. Unfortunately, as Alan I. Greene, MD, stated, “The term medical marijuana makes it sound like a therapeutic agent, which may encourage more young people to use it.” Data from 2013–2014 indicated that about 7% of US youth aged 12 to 17 years used marijuana in the past month. Among full-time college students, data from 2002–2013 showed an average of about 1,000 new marijuana users per day.

Patients may self-titrate the drug because the general public perceives marijuana to be safe. Young people need a “clear head” in order to safely drive a vehicle, perform in school, and hold down a job without excessive absenteeism. It is up to the mental health professional to advise our patients or clients based on the clinical evidence.

Financial disclosure: Dr King and Mr King had no relevant personal financial relationships to report. ​

Expanding Our Understanding of OCD

Obsessive-compulsive disorder (OCD) is often portrayed by the media and educational training materials in a limited scope. Typically, when people think of OCD, they think of symptoms such as checking locks or the stove, frequently washing one’s hands, and arranging items to make them symmetrical and orderly. While these examples are common symptoms of OCD, the condition can manifest in many ways, and a limited understanding of these manifestations is problematic from a diagnostic and treatment perspective.

OCD occurs when an individual has an unwanted thought or image (obsession), and the presence of the obsession causes the person anxiety. In an attempt to get rid of the obsession, the individual performs mental and physical behaviors, also known as compulsions or rituals. Mental rituals include actions such as counting, saying safe words, or visualizing safe images. Physical rituals include behaviors such as touching, tapping, rewriting, and confessing.

The following examples of common obsessions are often unrecognized as symptoms of OCD by medical and mental health professionals:

  • Violent obsessions about hurting/killing others or oneself
  • Sexual obsessions regarding rape, pedophilia, incest
  • Sexual obsessions related to one’s sexual orientation
  • Religious obsessions about blasphemy

The ways in which OCD can manifest are essentially limitless. Below is a case example to highlight symptoms of someone with violent OCD obsessions.

Terry experiences unwanted thoughts about harming others. Constantly throughout the day, he thinks about the fact that he may take out his pocketknife and stab people whom he walks past. Since Terry is not sure if he actually has acted on his thoughts, he turns around each time after walking by a person to make sure the individual is still alive and well. When at work, Terry worries that he may intentionally spill hot coffee on his coworker; when having these thoughts, he can actually picture himself taking the coffee cup and splashing the boiling liquid in his colleague’s face. Terry used to love drinking coffee every morning but now avoids it. However, he can still see the office coffee pot from his desk and worries he may grab the pot one day and burn his colleague. At home, Terry is concerned that, when hugging his wife, he may intentionally hug so hard that he cracks all of her ribs. Whenever he hugs his wife, Terry says aloud, “I love you.” He believes that saying “I love you” will prevent him from hurting his wife.

Terry’s distressing thoughts/images are obsessions, while the checking, avoidance, and magical thinking are compulsions.

A more accurate understanding of OCD would benefit health care professionals, individuals with OCD, and society at large. Greater knowledge of the many ways in which OCD presents (including morally unacceptable thoughts) will hopefully lead to destigmatization and normalization of all symptom presentations of OCD and improve diagnosis and treatment.

Financial disclosure: Drs Glazier and McGinn have no personal affiliations with any commercial interest to disclose.​

Can Obesity Genes Affect Your Mood?

A bidirectional association between obesity and depression has been evidenced in longitudinal studies. In a meta-analysis of 15 longitudinal studies (N=55,745), obesity (body mass index [BMI] ≥ 30 kg/m2) at baseline was associated with a 1.55-fold increase in the incidence of depression at follow-up. Conversely, depression at baseline was associated with a 1.58-fold increase in the incidence of obesity over time. Environmental factors may account for part of this association (eg, weight increase as a consequence of antidepressant drug use). However, a heritability study suggested that shared genetic architecture may also account, at least in part, for the association between obesity and depression.

My colleagues and I previously reported an inverse association between depression and a gene variant linked to obesity; the obesity-risk FTO rs9939609 A gene variant was associated with an 8% decrease in the risk for depression in 6,561 people with depression and 21,932 controls. In a recent article published in The Journal of Clinical Psychiatry, we studied the effects of 21 additional obesity-predisposing gene variants on depression in the EpiDREAM study (3,209 people with depression and 14,195 controls), and we made two important discoveries. First, the TAL1 rs2984618 obesity risk allele was associated with an 11% higher risk of depression. Second, we identified an ethnic-specific pattern of association between an obesity gene variant and depression. While the BDNF rs1401635 obesity risk allele was associated with a 12% lower risk of depression in non-European populations, the same obesity risk allele was associated with an 11% higher risk of depression in European populations.

To render the picture more complex, five single-nucleotide polymorphisms in the FTO gene have been shown to interact with depression status to increase BMI in 2 independent European populations. Additionally, an interaction between the well-established obesity/type 2 diabetes–predisposing gene TCF7L2 and BMI in people with bipolar disorder has been recently reported.

Altogether, these recent discoveries demonstrate that susceptibility to obesity and depression share common molecular roots. In the long run, this research is expected to improve the prevention and treatment of depression and obesity, two frequent diseases on the rise at the global level.

Financial disclosure: Dr Meyre has no personal affiliations with any commercial interest to disclose.​

Recognizing and Attending to Obsessive-Compulsive Symptoms in Depression

A woman comes to your office complaining of feeling severely depressed and no longer wanting to live. You check off the symptoms of major depression one by one. Low energy? Yes. Lack of pleasure? Yes. Insomnia? Yes. Disinterest? Yes. Guilt? Yes. Poor concentration? Yes. Poor appetite? Yes. But, will you also ask her whether she worries that she might act or speak violently toward someone without meaning to? Or whether she frequently gets unwanted nasty thoughts? Or whether she checks to ensure that she has not already unknowingly harmed someone? These are taboo obsessive-compulsive symptoms (OCS), often comorbid with depression, that sufferers are unlikely to volunteer to clinicians for fear of stigmatization. Perhaps these patients’ fears are justified.

Three recent studies found that, although OCS involving contamination fears or symmetry concerns were usually correctly diagnosed by psychiatrists, psychologists, and primary care physicians—who provided appropriate first-line treatment recommendations of CBT and SSRI medications—these professionals consistently misdiagnosed vignettes of patients with OCS involving aggressive or sexual obsessions and were significantly less likely to recommend first-line treatment. Clinicians were more likely to recommend antipsychotic medication and, despite the extremely low risk of violence associated with this population, frequently included involuntary psychiatric admission and reports to child welfare agencies among treatment recommendations.

My colleagues and I recently sought to determine the frequency and impact of OCS in patients with major depression who participated in the NIMH Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, the largest study of depression treatment ever conducted, with over 4,000 participants from across the United States from 41 community, private practice, and academic sites. Although STAR*D has generated dozens of scientific papers, none had previously assessed OCS, likely because current primary obsessive-compulsive disorder was a STAR*D exclusion criterion. This study condition allowed us to conservatively estimate how often OCS were unattended to in these patients with major depression because any OCS that subjects reported on a self-report scale were either (a) not disclosed to the study doctors, or (b) not believed by the doctor to be significant clinical problems. Our results indicated that more than half of these depressed patients endorsed having one or more OCS, most commonly taboo obsessions of causing harm to someone. And, after controlling for depression severity, the presence of these unattended obsessions predicted both poorer rates of depression remission with SSRI treatment and elevated rates of suicidality.

I believe that many (perhaps most) OCS, particularly taboo obsessions, go unrecognized in the context of depression and are not adequately treated because patients do not volunteer them and are rarely asked about them. Thus, brief screening for OCS in patients with depression is an important first step. However, even when OCS are recognized, their treatment is often inappropriate, according to the studies cited above. We have much work to do in educating patients, as well as psychiatric and nonpsychiatric clinicians, about these disabling but treatable symptoms.

Financial disclosure: Dr Baer has no personal affiliations with any commercial interest to disclose.​

Exposure Therapy Helps Patients With OCD Who Don’t Benefit From Medication

When patients with obsessive-compulsive disorder (OCD) come to our clinic, they are almost always already on medication. Often, they have tried numerous doses and combinations of medications and have been taking medication for many years. Patients sometimes tell us that the medication they are taking has reduced their OCD symptoms, but rarely do we hear that it has made a really significant impact. Of course, many patients are helped a lot by OCD medication and don’t need additional treatment. We don’t see this group of patients at our clinic, so our sample is biased. But research backs up our clinical impression that OCD medications often fall short. Most patients who take serotonin reuptake inhibitors (SRIs), which are the most common medications prescribed for OCD, continue to have clinically significant symptoms that negatively affect their health, functioning, and quality of life. For these patients, adding an antipsychotic medication such as risperidone is the usual next step, but this strategy helps only a minority of patients, if any. So, how should we treat these patients? What can we do to help those who have already tried the first-line medication treatments for OCD and continue to have clinically significant symptoms?

This is the question that my colleagues aimed to answer in our recent study. Patients were 32 adults with OCD who were on a therapeutic dose of an SRI and completed an 8-week trial of augmentation with either risperidone or placebo. Basically, these were folks who had failed to achieve much benefit from either an SRI alone or an SRI with antipsychotic augmentation. In an open trial, we offered them a type of cognitive-behavioral therapy called exposure and response prevention, or EX/RP. EX/RP involves helping patients approach feared images and situations (ie, exposure) while simultaneously eliminating compulsive behaviors (ie, response prevention).

The results showed that EX/RP was effective in reducing OCD symptoms in these patients. After an average of 14 EX/RP sessions, 56% of patients were classified as treatment responders (≥ 25% reduction in symptoms), and 16% were classified as excellent responders, which means they had minimal symptoms. Excellent response is important because it is associated with long-term symptom remission, good quality of life, and a high-level of functioning. It means these patients are doing really well. While the effects of EX/RP in this study were good, they weren’t as strong as what we typically see for EX/RP as a stand-alone treatment. I think this is probably because the patients in our study were more treatment-resistant than patients in most other studies.

A large body of research supports the use of EX/RP for treating OCD. We already knew that this treatment works well. What makes the current findings important is that they tell us that EX/RP can help even when traditional medication treatments fail. Patients with OCD who have already tried standard medication treatments for OCD yet continue to suffer from symptoms (and this is not a small group) should take heart: we now have good reason to believe that our best psychotherapy, EX/RP, can help.

Financial disclosure: Dr McLean had no relevant personal financial relationships to report. ​

Quality of Antidepressant Treatment: What’s Improved and What Hasn’t

Beginning in the early 1990s mental health services researchers began studying the quality of antidepressant treatment in community practice. That research identified several specific gaps in care. First, many people with significant depression were not recognized or treated . Second, prescribed antidepressant doses were often too low to be effective. Third, many patients starting antidepressants discontinued them before they might have provided benefit. Fourth, many patients did not return for follow-up care. While some of the earliest research in this area focused on antidepressant treatment in primary care, subsequent research found similar gaps in treatment provided by community psychiatrists. Now, 25 years later, we can examine our progress in closing each of those gaps.

Regarding underrecognition of depression, we can point to fairly dramatic changes since the 1990s. Recognition and treatment of depression have increased dramatically, so that the proportion of US adults using antidepressant medications is now approximately 10%. This dramatic increase has raised the opposite concern of possible overprescription or unnecessary drug treatment for people with mild depression. The recent article by my colleagues and me in The Journal of Clinical Psychiatry suggests that concerns about overtreatment are probably overstated. Most antidepressant prescribing for depression falls reassuringly within what evidence-based guidelines recommend.

Regarding underdosing of depression, we can also point to significant progress, but physicians cannot take much credit. Underdosing was really a problem of the tricyclic antidepressant medication era. The greater tolerability of SSRIs and other newer antidepressants made gradual dose escalation less necessary than with tricyclics, leading to much simpler dosing schedules. Newer medications may not be more effective, but they are certainly easier to use (and harder to use ineffectively).

Unfortunately, the other two gaps in care have not shown much improvement. Early discontinuation of antidepressants remains common. The National Committee for Quality Assurance (NCQA) developed the Health Plan Employer Data and Information Set (HEDIS) in the 1990s to track health care quality, and the antidepressant medication management measures have shown very little progress in antidepressant adherence over the last decade. Frequency of follow-up visits typically falls far short of any recommended minimum. We should be a bit embarrassed that the original NCQA/HEDIS measure for depression follow-up visits was removed from our national “report card” because no health system could even approach a passing grade!

Financial disclosure: Dr Simon has received grant/research support from Novartis. ​

<span class="svspan"> Blog</span>Efficacy of Trauma-Informed Group Therapy for Intimate Partner Violence

Intimate partner violence (IPV) among military veterans and service members is a serious public health problem. Veterans with reported military trauma and elevated symptoms of posttraumatic stress disorder are at particularly increased risk for committing IPV. While more work in this area is needed, current theory and research suggest that the experience of trauma can alter the ways that people view themselves, others, and the world, which can then influence how they interact with others. For example, after a traumatic experience, one may develop a strong sense of mistrust in others. This mistrust may lead him or her to interpret others’ actions as being hostile or malicious, which can then escalate conflict and lead to violence.

Given the large number of US veterans returning from deployments, there is a pressing need for effective IPV intervention among this population. To try to meet this need, Taft and colleagues have developed the Strength at Home Men’s Program (SAH-M), which is a cognitive-behavioral, trauma-informed group therapy program designed to reduce and end IPV.

A recent randomized controlled clinical trial investigated the efficacy of SAH-M among a sample of 135 US veterans and service members. This study randomized participants to receive either SAH-M or enhanced treatment as usual (ETAU), in which participants were given clinical referrals for mental health and IPV services, as well as ongoing IPV assessment. A notable strength of the study is that it successfully incorporated collateral reports of IPV from veterans’ partners in the majority (82.2%) of cases.

This study found that SAH-M participants, relative to ETAU participants, showed greater reductions in physical and psychological IPV from pretreatment to posttreatment. When different forms of IPV were disaggregated, SAH-M appeared particularly effective at reducing behaviors that involve controlling one’s partner through monitoring and isolation.

Findings of this study provide support for the SAH-M program and are particularly exciting given that no prior randomized controlled trial has demonstrated the efficacy of an IPV intervention program among military or veteran populations. This study’s significant effects are also notable in the context of the larger literature on IPV intervention programs, in which intervention effects tend to be modest and not statistically significant, and rigorous research designs are scarce.

Some of the program’s success in reducing IPV may be due to its emphasis on trauma and its role in problematic social information processing (eg, hostile attributions of others’ behaviors). While all participants reported at least 1 trauma, not all of the distressing events reported were related to military service. Studies have found high rates of trauma exposure among samples of civilian men enrolled in IPV interventions, and certain forms of trauma (eg, witnessing interparental abuse in childhood) have long been discussed in the IPV literature. Thus, an important step for future research will be to examine whether the effects of this trauma-informed IPV intervention program generalize to civilian samples.

Financial disclosure: Mr LaMotte and Dr Taft had no relevant personal financial relationships to report.​

Improving Outcomes Through Pharmacogenetic Testing

Pharmacogenetic testing is the most exciting area I have encountered in psychiatric practice since the advent of the SSRIs/SNRIs and the atypical antipsychotics. These tests provide data that truly offer concrete assistance in selecting a pharmacotherapy that is more likely to have both efficacy and tolerability for a particular patient. Until recently, I have been selecting treatment based on diagnosis subtype, past treatment history, family history, and a few clinical pearls related to presentation. In the 40 or so patients with whom I have now used genetic testing, all but 1 patient had significant variations that contributed to my choice of treatment or a change in treatment.

I first used this testing only in patients with treatment-resistant depression, but, after seeing the impact, I have begun to use it more widely. I see a role for pharmacogenetic testing in patients with psychiatric conditions other than depression, including patients who are treated with antipsychotics and stimulants. Our patients are so ill and their quality of life is so impaired that they would benefit from the use of every tool at our disposal.

My colleagues and I reported 2 cases in which we used genetic testing. Mr B, the second patient we described, was able to return to a very competitive university in a challenging course of study once his medications were adjusted and his severe side effects abated. Of course, he still faces challenges because his depression and his ADHD are both chronic disorders. However, he graduated with a bachelor’s degree and a master’s degree at the same time and now has a highly coveted job with a national firm. As his treatment continues, his genetic profile will play a part in any ongoing selection of pharmacotherapy.

I suspect that, without careful parental observation and the genetic testing, Mr B would have become further depressed over his perceived lack of competence in his academic pursuits despite his superior intellectual ability.

One of the most challenging issues in the field of genetic testing is the lack of payer support, and I have made significant efforts to educate our local public sector payers. However, a challenge with insurers often relates to short-term versus long-term gains in a sizeable population. Both treating psychiatrists and patients can provide advocacy to accelerate the acceptance of this valuable testing. Also, further data on clinical outcomes and population cost-savings can be provided by companies engaged in this technology.

In my practice, I have found that reviewing the results of pharmacogenetic testing is a wonderful psychotherapeutic intervention for the demoralized patient who has tried many psychiatric treatments without success. Renewed hope is particularly evident with young adults who, along with their parents, have not understood their lack of treatment response and viewed it as a failure to expend enough effort to get better. I have found that this broader understanding of the link between heredity and treatment response can be a turning point with some patients. Additionally, noting that the parents are the source of the genetic mutations elicits comments about the parents’ psychiatric status.

I look forward to significant advances in the field of pharmacogenetics and the benefits those advances will bring.

Financial disclosure: Dr Rhea is a consultant for United Behavioral Health and Amerigroup. ​

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