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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. ​

<span class="svspan"> Blog</span>How Can We Help Persons With SMI and SUD Permanently Exit Homelessness?

During my psychiatry training, I worked at a community service agency, treating chronically homeless patients with serious mental illness (SMI) and substance use disorders (SUD) as they transitioned into supported housing. Naively, I equated supported housing to a path that would universally allow my patients to permanently exit homelessness. Instead, I witnessed a diverse range of housing outcomes and discovered a dearth of knowledge surrounding factors affecting exits from homelessness. Today, as a psychiatrist on an assertive community treatment team for veterans who have experienced homelessness, my patients continue to inspire important research questions: What are the long-term housing outcomes of persons who have experienced homelessness? What factors allow us to predict these housing outcomes? What services are needed to facilitate permanent exits from homelessness?

My colleagues and I aimed to answer these questions in our recent study. We used VA administrative data to identify persons with SMI and SUD who had experienced homelessness. For 36 of these individuals, we gathered retrospective housing histories over an average of 2.5 years. We also collected information on a range of factors that might predict housing outcomes, like psychiatric symptoms, community supports, and cognition (eg, memory, attention, planning abilities, and speed of information processing).

Each of the individuals we studied fell into 1 of 3 long-term housing outcomes. Some achieved stable housing—they were able to successfully exit homelessness. That is, they spent most days in stable housing arrangements, like their own apartments or permanent residences with family or friends. Others were unstably housed, spending most days vacillating between settings not intended for people to live in (like vehicles or abandoned buildings) or short-term housing arrangements (like homeless shelters or transitional housing). The third group was continuously enrolled in a housing program, sequentially enrolling in different housing programs on VA grounds.

In statistical analyses, we found that 2 salient factors predicted which of these housing outcomes an individual achieved. Those who were continuously enrolled in a housing program had very poor cognition. Among individuals with better cognition, those in stable housing had fewer difficulties interacting with other people than persons who were unstably housed.

In clinical practice, many of our patients with SMI and/or SUD who have trouble achieving stable housing have cognitive problems like difficulty with planning, attention, or memory. Many also have labile mood, psychotic symptoms, and related challenges that impair interaction with peers, family/friends, and treatment providers. Our study findings suggest a potential role for cognitive and/or social skills training to help this vulnerable population successfully exit homelessness. These treatment approaches are not commonly found within services for homeless consumers; future research may allow us to effectively integrate these services to add to our "toolbox" of treatments for people with mental illness who have experienced homelessness.

Financial disclosure: Dr Gabrielian has received grant/research support from VA Health Services Research and Development. ​

<span class="svspan"> Blog</span>Does Medicinal Marijuana Help People With PTSD?

Medicinal marijuana . . . it is all over the media. Some people are for it, some against. But do we actually know whether or how it works in the treatment of various diseases? The reality is that marijuana, especially as a form of medicine, is still in the very early stages of research. Yes, people have been studying it for many decades, but the Drug Enforcement Administration label of schedule 1 has made conducting meaningful research limited and difficult. It is no surprise, then, that we now find ourselves in this state of confusion as to whether marijuana is a medicine or just a recreational drug. In a recent article, I sought to succinctly summarize one small area of the knowledge base: the use of medicinal marijuana in posttraumatic stress disorder (PTSD).

With the increasing number of persons, particularly veterans, diagnosed with PTSD and the rampant rates of suicide within this population, it is not surprising that people are looking to what some consider to be nontraditional forms of treatment. Although federal agencies have not approved its use, medicinal marijuana is now an approved treatment for PTSD in some US states. Registry data from 2011 showed that, in a state that allowed the use of medicinal marijuana, PTSD was the primary indication for which people used it. Why? Well, it appears that it may help. One study suggested that medicinal marijuana resulted in a 75% decrease in clinical symptoms of PTSD, especially traumatic intrusions, hyperarousal, and overall anxiety. Another study found a significant relationship between PTSD symptom severity and coping-motivated use of marijuana.

How is medicinal marijuana thought to work? Cannabinoid receptors are widespread in the brain. According to the Peters and Mechoulam chapter in the book Professional Perspectives On Addiction Medicine: Beyond Medical Marijuana, the areas of the brain with the highest number of cannabinoid receptors are those involved in memory formation (hippocampus), motor coordination (cerebellum), and emotionality (prefrontal cortex). Perhaps unsurprisingly, this distribution correlates with a number of known side effects of marijuana. Combinations of animal and human research have begun to shed light on possible mechanisms to explain the reported improvement of PTSD symptoms with marijuana. To name a few, potential correlations exist between cannabinoid receptors in the amygdala, an area known for modulating “fight or flight,” and decreased hyperarousal, hypervigilance, and anxiety, and cannabinoids may also play a role in so-called extinction response, the forgetting of traumatic memories.

While this research sounds promising, nothing conclusive can be said at this time. Most of the evidence has come from either animal or observational studies rather than from large-scale, randomized, controlled studies, which are considered the gold standard of science. Also, marijuana has potential problems such as pulmonary issues from smoking, sleep disturbances from chronic use, and possible development of cannabis use disorder. While not an exhaustive list of potential concerns, it does emphasize that medicinal marijuana is not without risks. Patients and clinicians need to be aware of these and other risks, as well as of the limitations of the evidence for efficacy, prior to undertaking marijuana treatment for PTSD.

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

Cocaine Use in Older Adults

Since the time of Sigmund Freud, psychiatry has had a complicated affair with cocaine. Besides the field of psychiatry, the entertainment field has also been linked with cocaine use. Los Angeles has been called a “coke town,” with celebrities reporting cocaine use as being casual and common, whether at parties or during daily life. Famously, cocaine and other illicit substances have long been associated with the Rock ‘n’ Roll movement (and other music genres since); from almost the very beginning, the two have been intertwined. Pulling out records (cassettes, CDs, mp3s) from those times, one will have no trouble finding songs written about cocaine. Famous musicians like Keith Richards, Neil Young, Eric Clapton, Stevie Nicks, Bob Dylan, and Johnny Cash and bands such as Lynyrd Skynyrd, Guns ‘n’ Roses, The Eagles, The Grateful Dead, and The Rolling Stones all wrote songs “about, influenced by, and more than likely written on clouds of Peruvian marching powder.” Many of these artists have been to substance use disorder rehabilitation (some multiple times), and some musicians, actors, and others in the entertainment field have died as a result of their substance use.

What is perhaps less well known is what happened to all of the less famous people who grew up with these cultural influences. The Baby Boomer generation, born from 1946 to 1964, lived through Woodstock, the disco revolution, cocaine parties of the 1980s, the prescription drug boom, and the general acceptance of the “sex, drugs, and rock and roll” mentality, so it should come as no surprise that a large percentage of Baby Boomers have tried illicit drugs. Compared with earlier generations, many Baby Boomers have experienced life-long issues with substance use, including alcohol, cocaine, and heroin. Some Boomers never stopped using substances, while others exhibited a chronic pattern of sobriety and relapse.

Illicit substance use, cocaine in particular, in advanced age is a relatively novel trend. Prior to the Baby Boomer generation, substance use disorders had primarily been seen as a disease of younger people and something that many outgrew. The latest data, described in my recent review article, however, paint a different picture. Increasingly, older individuals are presenting for substance abuse treatment, with some studies estimating upwards of 5.7 million older individuals needing treatment for a substance use disorder by 2020. Cocaine use in older age also carries significant health risks, including increased rates of heart attacks, strokes, and cognitive impairment. Despite these risks, this population largely goes unidentified because physicians often assume older persons do not use cocaine. As the population ages, more individuals will need treatment. Clinicians should be aware of the need for screening and identification of substance use in older individuals. Additionally, as a society, we should question whether the existing infrastructure is ready to handle this population with diverse social, medical, spiritual, and practical problems not typically accounted for in current treatment paradigms.

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

Is Bipolar Disorder Partly a Vascular Disease?

Heather is 43-year-old woman with bipolar disorder attending her follow-up appointment in your clinic. You have been treating her since her first hospitalization for mania a decade ago. Whether it is depression, mania, anxiety, or the occasional intervals of excessive alcohol use, each appointment brings a new treatment target. Thankfully, Heather has finally enjoyed an extended recovery from her mood symptoms for the past 2 years. You are surprised to learn that, since your last appointment, Heather has, despite her young age, experienced a relatively significant myocardial infarction.

The above scenario is not as uncommon as we might hope, according to data from a recent study that my colleagues and I conducted of the incidence of new-onset cardiovascular disease in a large, representative, epidemiologic sample of the United States population. In this study, adults with bipolar I or II disorder were markedly more likely than either adults without mood disorders or those with major depressive disorder to be diagnosed with new-onset cardiovascular disease between baseline and 3-year follow-up. Additionally, new-onset cardiovascular disease occurred extremely prematurely among adults with bipolar disorder—on average, 8–11 years earlier than in adults with major depressive disorder and 14–17 years earlier than in adults without mood disorders. The question arises, why?

Among people with bipolar disorder, rates of cardiovascular risk factors, such as smoking and obesity, are higher than in the general population. The physiologic strain of mania and depression may contribute to the excessive burden of heart disease in bipolar disorder. Many of the medications used to treat bipolar disorder also precipitate weight gain and other metabolic disturbances that contribute to cardiovascular risk. But maybe all of these considerations are only part of the story. Maybe bipolar disorder and cardiovascular disease have shared etiopathology, ie, they are geographic strangers but mechanistic family.

In our study, many people with bipolar disorder had never received treatment for their condition, and most had never received antimanic medications, suggesting that these findings cannot be explained by medications alone. This was not a highly distilled sample of patients in tertiary care settings but rather a representative community sample. The large sample afforded us the rare luxury of controlling for many potential confounding variables. Even after taking into account demographic variables, smoking, obesity, hypertension, and alcohol and drug use disorders, the odds of people with bipolar disorder developing cardiovascular disease were twice that of people with major depressive disorder and over two and a half times that of the general population without mood disorders.

What does this all mean? Clearly, we need to help patients optimize their lifestyle, and we need to minimize the metabolic burden conferred by our medications. But we also need to recognize—in our conceptualizing of bipolar disorder, in our advocacy efforts toward reducing stigma, and in the design of envelope-pushing clinical trials and biological research—that bipolar disorder is in part a vascular disease and needs to be approached as such.

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

Prevention of Perinatal Mood and Anxiety Disorders

During the last few years, many articles have been written on the etiology of postpartum depression (PPD) and other perinatal mood and anxiety disorders (PMADs). Biochemical and psychosocial causes have been noted in much of the research. Interestingly, a paucity of information remains regarding how to lower the incidence of, decrease the severity of, and possibly prevent these illnesses. That is where my focus lies. Why not attempt to circumvent the suffering in the first place?

For almost 3 decades, stemming from my own personal experiences with suicidal depression following the births of my children, my message has been one of hope. Not only are PPD and related illnesses completely treatable with proper help, their incidence rates can be minimized, and in some cases they can even be prevented so that the nightmare never begins. In Postpartum Depression For Dummies, I outlined many preventive steps for women who know they are at high risk for a bout of illness following a delivery.

Although chemical and life factors place women at high risk for PPD and other PMADs, no one is immune. Even women with no previous personal or family mental health issue can be hit hard. Therefore, regardless of risk factors, every new mother should arrange certain pieces of a wellness strategy, ideally before the baby comes. These basic steps can help to ward off emotional and psychological problems after delivery. The first 7 steps are for all mothers, and the last 2 are for those who are already suffering or know they are at high risk.

  1. Have realistic expectations of motherhood—throw out the myths and fantasies.
  2. Discuss wishes and concerns with your partner—communicate expectations and make an agreeable plan together.
  3. Pay attention to nutrition (including supplements) to feed the body and brain, such as the right proteins, complex carbohydrates, omega-3 fatty acid, vitamin D, folate, etc.
  4. Plan for nighttime sleep to protect brain chemistry—even a breastfeeding mom can get a few hours of uninterrupted nighttime sleep with a good plan.
  5. Exercise or use special breathing to oxygenate the brain.
  6. Find emotional support, ie, people to lean on and be “real” with.
  7. Find logistical support, ie, people to give you regular breaks to nurture yourself and “recharge your batteries.”
  8. Seek psychotherapy with a professional who specializes in perinatal disorders (if you are at high risk).
  9. Take medication or alternative/complementary treatments (if necessary).

When a pregnant woman or new mom contacts me with concerns that she will develop depression, anxiety, or another PMAD, we develop an individualized wellness plan using the above steps. Each woman needs a plan that will work with her particular circumstances, beliefs, chemistry, and level of support. So much unnecessary suffering can be avoided when these basics are in place!

Financial disclosure: Dr Bennett is a perinatal psychologist ( and is the author of Postpartum Depression For Dummies; she had no other relevant personal financial relationships to report.​

The Business of Medicine

Most psychiatrists (and physicians in general) receive little information in their training about the business of medicine. This is particularly problematic if one decides to go into private practice, as I did.

Issues that enter one's life in private practice include learning where to get the best loans, finding an office, buying office equipment, hiring and managing staff, handling accounting records, selecting malpractice policies, and dealing with health insurers like Medicare (including becoming 'approved' by insurers and facing the hassle of prior authorizations). Throughout one’s time in practice, questions arise such as which insurers reimburse better and in a timely way, what electronic billing/prescribing/charting companies are the best, what should I look for in joining another practice or taking on an associate, and should I continue to take insurance or go to cash only.

By virtue of finishing medical school and training, doctors believe ourselves smart … and we are. But being smart does not mean we know everything. Generally, I have found doctors to be among the worst businesspeople because we make dumb mistakes in areas where we really don't have much expertise.

I know one young doctor who, when I asked how his practice was going, became indignant. He felt that talking about the business side of his practice was beneath him.

"I'm here to help people," he bristled. I know he's dedicated and well intentioned. We all become physicians so we might help people. That's not the issue.

Someone once said to me, "No one watches your money better than you do." We can be dedicated to helping, but we also need to be circumspect in how we run our practices as well as informed about how we (and accountants and financial advisers) manage our hard-earned money (eg, paying off loans, investing, building our savings, handling mortgages, planning for vacations).

I’d like to have a forum to discuss the business of medicine with colleagues and share what works and what doesn't.

To address one issue I raised above, I have not gone to an all-cash basis in my practice but certainly have considered it. Dealing with the various health insurance plans is generally an onerous task. Some years back, an employee of mine who had worked for one of the insurance industry leaders shared that her instructions there were to take a certain percentage of daily claims and shred them. The object, of course, was to delay payment as long as possible and keep the money in the insurer's accounts. Prior to electronic billing, I received claim forms that had been rejected because I had not kept my signature within the lines or didn't sign the form with the signature that the insurer thought was right. With electronic billing, those wily contortions to avoid payment have not really gone away. Now, some insurers simply forget to pay or dance around and say certain things aren't covered.

Dealing with insurance companies requires a lot of personnel time and adds much overhead cost. Hence, some of my colleagues have gone to cash-only practices and believe that the patients they lost are made up for by the new patients who are willing to pay in full. A compromise is to accept patients who have insurance but, instead of dealing with insurers yourself, give patients a superbill so that they submit the claims.

My feeling is that physicians have become servants of the insurance companies—passively accepting the limitations decreed and the payments accorded per the insurers' dictation—all under the guise of cost effectiveness, but medical costs are going out of control.

I have a fantasy that if a vast number of doctors refuse to recognize health insurance, then insurers would disappear since we really control their existence. What do you think?

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

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