Liver cancer took nearly four times longer to progress after yttrium-90 (Y90) radioembolization than after conventional transarterial chemoembolization (cTACE), according to a single-center, randomized, phase II trial of 45 patients reported in the December issue of Gastroenterology (2016 Aug 26. doi: 10.1053/j.gastro.2016.08.029).

Median time to progression remained unreached more than 26 months after patients underwent Y90 treatment, but was only 6.8 months in the cTACE group (P = .001), Riad Salem, MD, and his associates at Northwestern University,Chicago, reported. Slow accrual limited the study size, but a post-hoc analysis showed that Y90 would have a 97% chance of significantly outperforming chemoembolization if the study had reached its enrollment target, even if the difference in time to progression was less pronounced. Furthermore, Y90 significantly outperformed chemoembolization in a competing risk analysis that accounted for liver transplantation and death, the researchers said.

Conventional transarterial chemoembolization is used in intermediate-stage liver cancer when ablation is contraindicated. However, retrospective studies have favored Y90 radioembolization, a minimally invasive procedure in which a clinician implants radioactive micron-sized particles loaded with Y90 inside blood vessels supplying a tumor. To further study this approach, the investigators randomly assigned patients with unresectable, unablatable hepatocellular carcinoma without vascular invasion, who had Child-Pugh scores of A or B, serum bilirubin levels up to 2 mg/dL, and liver enzymes up to five times the normal upper limit, to undergo selective Y90 at a dose of 120 Gy, or lipiodol-based chemoembolization at a dose of 75 mg/m^2.

Source: American Gastroenterological Association

Of 179 eligible patients, 134 (75%) declined to participate in research, opted for other trials, or chose one protocol over the other. Consequently, only 21 patients were assigned to cTACE, while 24 underwent Y90. The groups resembled each other clinically and demographically at baseline, although Y90 patients tended to have more portal hypertension and higher serum bilirubin levels. No patients died within 30 days after treatment. Each group had one case of common femoral artery pseudoaneurysm. The Y90 patients tended to have more fatigue (P = .08), and had higher rates of diarrhea (P = .03) and hypoalbuminemia (P less than .001).

Despite the small group sizes, patients were about 88% less likely to progress at a given time point after Y90, compared with cTACE (hazard ratio, 0.12; 95% confidence interval, 0.03-0.56; P = .007). To explore what might have happened had the study reached target enrollment, the researchers added another 79 hypothetical patients at the 5.1-fold higher hazard ratio (0.625) that they had used in the power calculation. The results showed that Y90 had a 97% chance of statistically outperforming cTACE under these conditions.

Inverse probability of censoring weighting, which is performed to control for dependent censoring between groups, also showed that time to progression was significantly longer with Y90 than with cTACE, the investigators said. “While the relatively low sample size is acknowledged, the seminal studies establishing cTACE as the standard of care were also limited in sample size, [were] single center, and enrolled mostly Child-Pugh A patients,” they emphasized. “Our time to progression results favoring Y90 are in line with other uncontrolled retrospective reports in patients with compromised liver function, [but] our study validates such findings with prospective randomized level I evidence.”

The National Institutes of Health and the SIR Foundation provided funding. Dr. Salem and two coinvestigators reported serving as advisors to BTG. The other coinvestigators reported having no conflicts of interest.

Liver cancer took nearly four times longer to progress after yttrium-90 (Y90) radioembolization than after conventional transarterial chemoembolization (cTACE), according to a single-center, randomized, phase II trial of 45 patients reported in the December issue of Gastroenterology (2016 Aug 26. doi: 10.1053/j.gastro.2016.08.029).

Median time to progression remained unreached more than 26 months after patients underwent Y90 treatment, but was only 6.8 months in the cTACE group (P = .001), Riad Salem, MD, and his associates at Northwestern University,Chicago, reported. Slow accrual limited the study size, but a post-hoc analysis showed that Y90 would have a 97% chance of significantly outperforming chemoembolization if the study had reached its enrollment target, even if the difference in time to progression was less pronounced. Furthermore, Y90 significantly outperformed chemoembolization in a competing risk analysis that accounted for liver transplantation and death, the researchers said.

Conventional transarterial chemoembolization is used in intermediate-stage liver cancer when ablation is contraindicated. However, retrospective studies have favored Y90 radioembolization, a minimally invasive procedure in which a clinician implants radioactive micron-sized particles loaded with Y90 inside blood vessels supplying a tumor. To further study this approach, the investigators randomly assigned patients with unresectable, unablatable hepatocellular carcinoma without vascular invasion, who had Child-Pugh scores of A or B, serum bilirubin levels up to 2 mg/dL, and liver enzymes up to five times the normal upper limit, to undergo selective Y90 at a dose of 120 Gy, or lipiodol-based chemoembolization at a dose of 75 mg/m^2.

Source: American Gastroenterological Association

Of 179 eligible patients, 134 (75%) declined to participate in research, opted for other trials, or chose one protocol over the other. Consequently, only 21 patients were assigned to cTACE, while 24 underwent Y90. The groups resembled each other clinically and demographically at baseline, although Y90 patients tended to have more portal hypertension and higher serum bilirubin levels. No patients died within 30 days after treatment. Each group had one case of common femoral artery pseudoaneurysm. The Y90 patients tended to have more fatigue (P = .08), and had higher rates of diarrhea (P = .03) and hypoalbuminemia (P less than .001).

Despite the small group sizes, patients were about 88% less likely to progress at a given time point after Y90, compared with cTACE (hazard ratio, 0.12; 95% confidence interval, 0.03-0.56; P = .007). To explore what might have happened had the study reached target enrollment, the researchers added another 79 hypothetical patients at the 5.1-fold higher hazard ratio (0.625) that they had used in the power calculation. The results showed that Y90 had a 97% chance of statistically outperforming cTACE under these conditions.

Inverse probability of censoring weighting, which is performed to control for dependent censoring between groups, also showed that time to progression was significantly longer with Y90 than with cTACE, the investigators said. “While the relatively low sample size is acknowledged, the seminal studies establishing cTACE as the standard of care were also limited in sample size, [were] single center, and enrolled mostly Child-Pugh A patients,” they emphasized. “Our time to progression results favoring Y90 are in line with other uncontrolled retrospective reports in patients with compromised liver function, [but] our study validates such findings with prospective randomized level I evidence.”

The National Institutes of Health and the SIR Foundation provided funding. Dr. Salem and two coinvestigators reported serving as advisors to BTG. The other coinvestigators reported having no conflicts of interest.

Liver cancer took nearly four times longer to progress after yttrium-90 (Y90) radioembolization than after conventional transarterial chemoembolization (cTACE), according to a single-center, randomized, phase II trial of 45 patients reported in the December issue of Gastroenterology (2016 Aug 26. doi: 10.1053/j.gastro.2016.08.029).

Median time to progression remained unreached more than 26 months after patients underwent Y90 treatment, but was only 6.8 months in the cTACE group (P = .001), Riad Salem, MD, and his associates at Northwestern University,Chicago, reported. Slow accrual limited the study size, but a post-hoc analysis showed that Y90 would have a 97% chance of significantly outperforming chemoembolization if the study had reached its enrollment target, even if the difference in time to progression was less pronounced. Furthermore, Y90 significantly outperformed chemoembolization in a competing risk analysis that accounted for liver transplantation and death, the researchers said.

Conventional transarterial chemoembolization is used in intermediate-stage liver cancer when ablation is contraindicated. However, retrospective studies have favored Y90 radioembolization, a minimally invasive procedure in which a clinician implants radioactive micron-sized particles loaded with Y90 inside blood vessels supplying a tumor. To further study this approach, the investigators randomly assigned patients with unresectable, unablatable hepatocellular carcinoma without vascular invasion, who had Child-Pugh scores of A or B, serum bilirubin levels up to 2 mg/dL, and liver enzymes up to five times the normal upper limit, to undergo selective Y90 at a dose of 120 Gy, or lipiodol-based chemoembolization at a dose of 75 mg/m^2.

Source: American Gastroenterological Association

Of 179 eligible patients, 134 (75%) declined to participate in research, opted for other trials, or chose one protocol over the other. Consequently, only 21 patients were assigned to cTACE, while 24 underwent Y90. The groups resembled each other clinically and demographically at baseline, although Y90 patients tended to have more portal hypertension and higher serum bilirubin levels. No patients died within 30 days after treatment. Each group had one case of common femoral artery pseudoaneurysm. The Y90 patients tended to have more fatigue (P = .08), and had higher rates of diarrhea (P = .03) and hypoalbuminemia (P less than .001).

Despite the small group sizes, patients were about 88% less likely to progress at a given time point after Y90, compared with cTACE (hazard ratio, 0.12; 95% confidence interval, 0.03-0.56; P = .007). To explore what might have happened had the study reached target enrollment, the researchers added another 79 hypothetical patients at the 5.1-fold higher hazard ratio (0.625) that they had used in the power calculation. The results showed that Y90 had a 97% chance of statistically outperforming cTACE under these conditions.

Inverse probability of censoring weighting, which is performed to control for dependent censoring between groups, also showed that time to progression was significantly longer with Y90 than with cTACE, the investigators said. “While the relatively low sample size is acknowledged, the seminal studies establishing cTACE as the standard of care were also limited in sample size, [were] single center, and enrolled mostly Child-Pugh A patients,” they emphasized. “Our time to progression results favoring Y90 are in line with other uncontrolled retrospective reports in patients with compromised liver function, [but] our study validates such findings with prospective randomized level I evidence.”

The National Institutes of Health and the SIR Foundation provided funding. Dr. Salem and two coinvestigators reported serving as advisors to BTG. The other coinvestigators reported having no conflicts of interest.

Mobile health indexes for remotely monitoring Crohn’s disease and ulcerative colitis accurately identified clinically active disease and changed significantly as disease activity did, researchers reported in the December issue of Clinical Gastroenterology and Hepatology.

The mobile health index for Crohn’s disease predicted clinical disease activity with an area under the receiver operating characteristic curve (AUC) of 0.90, Welmoed K. van Deen, MD, of the University of California, Los Angeles, and her associates wrote in Clinical Gastroenterology and Hepatology. The AUC for the ulcerative colitis index for ulcerative colitis was very similar, at 0.91. “The [mobile health indexes] are specifically designed for implementation on a mobile application, and are currently available to patients with IBD [inflammatory bowel disease] treated at the UCLA Center for IBD,” the researchers said. “Prospective, randomized studies need to assess the effect of remote monitoring on disease control, quality of life, patient satisfaction, and health care costs.”

Inspired by the lack of smartphone applications for remotely managing inflammatory bowel disease, the researchers administered comprehensive disease-specific questionnaires to 110 patients with Crohn’s disease and 109 patients with ulcerative colitis who visited the UCLA IBD center in 2013 and 2014. They compared patient-reported outcomes across 10 domains of disease activity with scores on a number of existing disease activity indexes, and used logistic regression to identify which self-reported outcomes best predicted disease activity in both Crohn’s disease and ulcerative colitis (Clin Gastroenterol Hepatol. 2015 Nov 18. doi: 10.1016/j.cgh.2015.10.035).

The resulting Crohn’s disease mobile health index asked how many liquid or “very soft” stools patients had per day, if they had abdominal pain, and how they would rate their well-being and level of disease control on scales ranging between 0 and 10. The ulcerative colitis mobile health index asked about number of stools the day before and had patients score abdominal pain, frequency of rectal bleeding, and level of disease control between 0 and 10. The researchers also validated each mobile health index in multicenter cohorts of 301 patients with Crohn’s disease and 265 patients with ulcerative colitis.

Each mobile health index detected clinical disease activity with about 90% accuracy, compared with standard measures, including the Crohn’s disease activity index and the Harvey Bradshaw index for Crohn’s disease, the partial Mayo score, the simple clinical colitis activity index, and the modified Truelove and Witts index for ulcerative colitis. But the mobile indexes detected endoscopic disease activity less accurately, with AUCs of 0.82 for ulcerative colitis and only 0.63 for Crohn’s disease. “As previously shown, ulcerative colitis clinical disease activity highly correlates with endoscopic disease activity, whereas correlation between Crohn’s disease symptoms and endoscopic findings is poor,” the researchers noted. However, both mobile indexes reliably detected changes in disease activity, varying significantly depending on whether patients were clinically improved, stable, or worse, regardless of whether they had Crohn’s disease (P = .003) or ulcerative colitis (P = .0025).

To explore intrapatient reliability, the researchers also compared initial and follow-up mobile health index results for subgroups of 40 Crohn’s disease patients tested a median of 21 hours apart, and 37 ulcerative colitis patients tested a median of 23 hours apart. In both cases, the intraclass correlation coefficient reached 0.94 (95% confidence interval, 0.89-0.97). “Cloud-based health technologies are predicted to revolutionize care delivery and patient engagement,” the investigators commented. “Patients can participate in their care by signaling meaningful health outcomes during year-round monitoring. Barriers for more widespread implementation of mobile health in inflammatory bowel disease care include policies affecting reimbursement and regulatory requirements, and privacy and security concerns.”

Genova Diagnostics provided stool collection kits and fecal calprotectin testing. The investigators had no disclosures.

Mobile health indexes for remotely monitoring Crohn’s disease and ulcerative colitis accurately identified clinically active disease and changed significantly as disease activity did, researchers reported in the December issue of Clinical Gastroenterology and Hepatology.

The mobile health index for Crohn’s disease predicted clinical disease activity with an area under the receiver operating characteristic curve (AUC) of 0.90, Welmoed K. van Deen, MD, of the University of California, Los Angeles, and her associates wrote in Clinical Gastroenterology and Hepatology. The AUC for the ulcerative colitis index for ulcerative colitis was very similar, at 0.91. “The [mobile health indexes] are specifically designed for implementation on a mobile application, and are currently available to patients with IBD [inflammatory bowel disease] treated at the UCLA Center for IBD,” the researchers said. “Prospective, randomized studies need to assess the effect of remote monitoring on disease control, quality of life, patient satisfaction, and health care costs.”

Inspired by the lack of smartphone applications for remotely managing inflammatory bowel disease, the researchers administered comprehensive disease-specific questionnaires to 110 patients with Crohn’s disease and 109 patients with ulcerative colitis who visited the UCLA IBD center in 2013 and 2014. They compared patient-reported outcomes across 10 domains of disease activity with scores on a number of existing disease activity indexes, and used logistic regression to identify which self-reported outcomes best predicted disease activity in both Crohn’s disease and ulcerative colitis (Clin Gastroenterol Hepatol. 2015 Nov 18. doi: 10.1016/j.cgh.2015.10.035).

The resulting Crohn’s disease mobile health index asked how many liquid or “very soft” stools patients had per day, if they had abdominal pain, and how they would rate their well-being and level of disease control on scales ranging between 0 and 10. The ulcerative colitis mobile health index asked about number of stools the day before and had patients score abdominal pain, frequency of rectal bleeding, and level of disease control between 0 and 10. The researchers also validated each mobile health index in multicenter cohorts of 301 patients with Crohn’s disease and 265 patients with ulcerative colitis.

Each mobile health index detected clinical disease activity with about 90% accuracy, compared with standard measures, including the Crohn’s disease activity index and the Harvey Bradshaw index for Crohn’s disease, the partial Mayo score, the simple clinical colitis activity index, and the modified Truelove and Witts index for ulcerative colitis. But the mobile indexes detected endoscopic disease activity less accurately, with AUCs of 0.82 for ulcerative colitis and only 0.63 for Crohn’s disease. “As previously shown, ulcerative colitis clinical disease activity highly correlates with endoscopic disease activity, whereas correlation between Crohn’s disease symptoms and endoscopic findings is poor,” the researchers noted. However, both mobile indexes reliably detected changes in disease activity, varying significantly depending on whether patients were clinically improved, stable, or worse, regardless of whether they had Crohn’s disease (P = .003) or ulcerative colitis (P = .0025).

To explore intrapatient reliability, the researchers also compared initial and follow-up mobile health index results for subgroups of 40 Crohn’s disease patients tested a median of 21 hours apart, and 37 ulcerative colitis patients tested a median of 23 hours apart. In both cases, the intraclass correlation coefficient reached 0.94 (95% confidence interval, 0.89-0.97). “Cloud-based health technologies are predicted to revolutionize care delivery and patient engagement,” the investigators commented. “Patients can participate in their care by signaling meaningful health outcomes during year-round monitoring. Barriers for more widespread implementation of mobile health in inflammatory bowel disease care include policies affecting reimbursement and regulatory requirements, and privacy and security concerns.”

Genova Diagnostics provided stool collection kits and fecal calprotectin testing. The investigators had no disclosures.

Mobile health indexes for remotely monitoring Crohn’s disease and ulcerative colitis accurately identified clinically active disease and changed significantly as disease activity did, researchers reported in the December issue of Clinical Gastroenterology and Hepatology.

The mobile health index for Crohn’s disease predicted clinical disease activity with an area under the receiver operating characteristic curve (AUC) of 0.90, Welmoed K. van Deen, MD, of the University of California, Los Angeles, and her associates wrote in Clinical Gastroenterology and Hepatology. The AUC for the ulcerative colitis index for ulcerative colitis was very similar, at 0.91. “The [mobile health indexes] are specifically designed for implementation on a mobile application, and are currently available to patients with IBD [inflammatory bowel disease] treated at the UCLA Center for IBD,” the researchers said. “Prospective, randomized studies need to assess the effect of remote monitoring on disease control, quality of life, patient satisfaction, and health care costs.”

Inspired by the lack of smartphone applications for remotely managing inflammatory bowel disease, the researchers administered comprehensive disease-specific questionnaires to 110 patients with Crohn’s disease and 109 patients with ulcerative colitis who visited the UCLA IBD center in 2013 and 2014. They compared patient-reported outcomes across 10 domains of disease activity with scores on a number of existing disease activity indexes, and used logistic regression to identify which self-reported outcomes best predicted disease activity in both Crohn’s disease and ulcerative colitis (Clin Gastroenterol Hepatol. 2015 Nov 18. doi: 10.1016/j.cgh.2015.10.035).

The resulting Crohn’s disease mobile health index asked how many liquid or “very soft” stools patients had per day, if they had abdominal pain, and how they would rate their well-being and level of disease control on scales ranging between 0 and 10. The ulcerative colitis mobile health index asked about number of stools the day before and had patients score abdominal pain, frequency of rectal bleeding, and level of disease control between 0 and 10. The researchers also validated each mobile health index in multicenter cohorts of 301 patients with Crohn’s disease and 265 patients with ulcerative colitis.

Each mobile health index detected clinical disease activity with about 90% accuracy, compared with standard measures, including the Crohn’s disease activity index and the Harvey Bradshaw index for Crohn’s disease, the partial Mayo score, the simple clinical colitis activity index, and the modified Truelove and Witts index for ulcerative colitis. But the mobile indexes detected endoscopic disease activity less accurately, with AUCs of 0.82 for ulcerative colitis and only 0.63 for Crohn’s disease. “As previously shown, ulcerative colitis clinical disease activity highly correlates with endoscopic disease activity, whereas correlation between Crohn’s disease symptoms and endoscopic findings is poor,” the researchers noted. However, both mobile indexes reliably detected changes in disease activity, varying significantly depending on whether patients were clinically improved, stable, or worse, regardless of whether they had Crohn’s disease (P = .003) or ulcerative colitis (P = .0025).

To explore intrapatient reliability, the researchers also compared initial and follow-up mobile health index results for subgroups of 40 Crohn’s disease patients tested a median of 21 hours apart, and 37 ulcerative colitis patients tested a median of 23 hours apart. In both cases, the intraclass correlation coefficient reached 0.94 (95% confidence interval, 0.89-0.97). “Cloud-based health technologies are predicted to revolutionize care delivery and patient engagement,” the investigators commented. “Patients can participate in their care by signaling meaningful health outcomes during year-round monitoring. Barriers for more widespread implementation of mobile health in inflammatory bowel disease care include policies affecting reimbursement and regulatory requirements, and privacy and security concerns.”

Genova Diagnostics provided stool collection kits and fecal calprotectin testing. The investigators had no disclosures.

Patients with diarrhea-predominant irritable bowel syndrome (IBS-D) who responded to rifaximin but relapsed after completing treatment were significantly more likely to respond to a second course of the antibiotic than to placebo, according to a report in the December issue of Gastroenterology (2016 Aug 5. doi: 10.1053/j.gastro.2016.08.003).

A total of 38% of patients who received a second course of rifaximin met the primary endpoint in the randomized double-blinded trial, compared with 31.5% of the placebo group (P = .03), Dr. Anthony Lembo of Beth Israel Deaconess Medical Center, Boston, and his associates wrote in Gastroenterology. “Although this study had a positive outcome, questions remain regarding the role of nonsystemic antibiotics in the long term, particularly when patients with IBS-D may require years of symptom management,” they added. “Further research is needed to better understand the treatment algorithm in patients who may lose responsiveness to rifaximin.”

Patients with diarrhea-predominant irritable bowel syndrome (IBS-D) who responded to rifaximin but relapsed after completing treatment were significantly more likely to respond to a second course of the antibiotic than to placebo, according to a report in the December issue of Gastroenterology (2016 Aug 5. doi: 10.1053/j.gastro.2016.08.003).

A total of 38% of patients who received a second course of rifaximin met the primary endpoint in the randomized double-blinded trial, compared with 31.5% of the placebo group (P = .03), Dr. Anthony Lembo of Beth Israel Deaconess Medical Center, Boston, and his associates wrote in Gastroenterology. “Although this study had a positive outcome, questions remain regarding the role of nonsystemic antibiotics in the long term, particularly when patients with IBS-D may require years of symptom management,” they added. “Further research is needed to better understand the treatment algorithm in patients who may lose responsiveness to rifaximin.”

Patients with diarrhea-predominant irritable bowel syndrome (IBS-D) who responded to rifaximin but relapsed after completing treatment were significantly more likely to respond to a second course of the antibiotic than to placebo, according to a report in the December issue of Gastroenterology (2016 Aug 5. doi: 10.1053/j.gastro.2016.08.003).

A total of 38% of patients who received a second course of rifaximin met the primary endpoint in the randomized double-blinded trial, compared with 31.5% of the placebo group (P = .03), Dr. Anthony Lembo of Beth Israel Deaconess Medical Center, Boston, and his associates wrote in Gastroenterology. “Although this study had a positive outcome, questions remain regarding the role of nonsystemic antibiotics in the long term, particularly when patients with IBS-D may require years of symptom management,” they added. “Further research is needed to better understand the treatment algorithm in patients who may lose responsiveness to rifaximin.”

Yoga may be a feasible and safe add-on therapy for patients with irritable bowel syndrome, based on a systematic review of six randomized controlled trials of 273 patients published in the December issue of Clinical Gastroenterology and Hepatology.

Yoga significantly outperformed no treatment and resembled pharmacologic therapies for IBS on measures of bowel symptoms, anxiety, and quality of life, said Dania Schumann of the University of Duisburg-Essen, Essen, Germany.

“Yoga also seems to be equally effective as a walking program in improving patient-reported outcomes,” she and her coinvestigators wrote. But “wide methodological heterogeneity” and a “mostly unclear risk of bias,” precluded a direct recommendation for yoga in IBS, they said. Nonetheless, “its practice need not be discouraged in this patient population, especially when [patients] believe that it benefits their health, quality of life, or IBS-related comorbidities.”

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Yoga may be a feasible and safe add-on therapy for patients with irritable bowel syndrome, based on a systematic review of six randomized controlled trials of 273 patients published in the December issue of Clinical Gastroenterology and Hepatology.

Yoga significantly outperformed no treatment and resembled pharmacologic therapies for IBS on measures of bowel symptoms, anxiety, and quality of life, said Dania Schumann of the University of Duisburg-Essen, Essen, Germany.

“Yoga also seems to be equally effective as a walking program in improving patient-reported outcomes,” she and her coinvestigators wrote. But “wide methodological heterogeneity” and a “mostly unclear risk of bias,” precluded a direct recommendation for yoga in IBS, they said. Nonetheless, “its practice need not be discouraged in this patient population, especially when [patients] believe that it benefits their health, quality of life, or IBS-related comorbidities.”

iStock

Yoga may be a feasible and safe add-on therapy for patients with irritable bowel syndrome, based on a systematic review of six randomized controlled trials of 273 patients published in the December issue of Clinical Gastroenterology and Hepatology.

Yoga significantly outperformed no treatment and resembled pharmacologic therapies for IBS on measures of bowel symptoms, anxiety, and quality of life, said Dania Schumann of the University of Duisburg-Essen, Essen, Germany.

“Yoga also seems to be equally effective as a walking program in improving patient-reported outcomes,” she and her coinvestigators wrote. But “wide methodological heterogeneity” and a “mostly unclear risk of bias,” precluded a direct recommendation for yoga in IBS, they said. Nonetheless, “its practice need not be discouraged in this patient population, especially when [patients] believe that it benefits their health, quality of life, or IBS-related comorbidities.”

iStock

Once thought to only be associated with depression, self-criticism is a transdiagnostic risk factor for diverse forms of psychopathology.^1,2 However, research has shown that self-compassion is a robust resilience factor when faced with feelings of personal inadequacy.^3,4

Self-critical individuals experience feelings of unworthiness, inferiority, failure, and guilt. They engage in constant and harsh self-scrutiny and evaluation, and fear being disapproved and criticized and losing the approval and acceptance of others.⁵ Self-compassion involves treating oneself with care and concern when confronted with personal inadequacies, mistakes, failures, and painful life situations.^6,7Although self-criticism is the aspect of perfectionism most associated with maladjustment,⁸ one can be harshly self-critical without being a perfectionist. Most studies of self-criticism have not measured shame; however, this self-conscious emotion has been implicated in diverse forms of psychopathology.⁹ In contrast to guilt, which results from acknowledging bad behavior, shame results from seeing oneself as a bad or inadequate person.

Although self-criticism is destructive across clinical disorders and interpersonal relationships, self-compassion is associated with healthy relationships, emotional well-being, and better treatment outcomes.

Recent research shows how clinicians can teach their patients how to be less self-critical and more self-compassionate. Neff^6,7 proposes that self-compassion involves treating yourself with care and concern when being confronted with personal inadequacies, mistakes, failures, and painful life situations. It consists of 3 interacting components, each of which has a positive and negative pole:

• self-kindness vs self-judgment
• a sense of common humanity vs isolation
• mindfulness vs over-identification.

Self-kindness refers to being caring and understanding with oneself rather than harshly judgmental. Instead of attacking and berating oneself for personal shortcomings, the self is offered warmth and unconditional acceptance.

Humanity involves recognizing that humans are imperfect, that all people fail, make mistakes, and have serious life challenges. By remembering that imperfection is part of life, we feel less isolated when we are in pain.

Mindfulness in the context of self-compassion involves being aware of one’s painful experiences in a balanced way that neither ignores and avoids nor exaggerates painful thoughts and emotions.

Self-compassion is more than the absence of self-judgment, although a defining feature of self-compassion is the lack of self-judgment, and self-judgment overlaps with self-criticism. Rather, self-compassion provides several access points for reducing self-criticism. For example, being kind and understanding when confronting personal inadequacies (eg, “it’s okay not to be perfect”) can counter harsh self-talk (eg, “I’m not defective”). Mindfulness of emotional pain (eg, “this is hard”) can facilitate a kind and warm response (eg, “what can I do to take care of myself right now?”) and therefore lessen self-blame (eg, “blaming myself is just causing me more suffering”). Similarly, remembering that failure is part of the human experience (eg, “it’s normal to mess up sometimes”) can lessen egocentric feelings of isolation (eg, “it’s not just me”) and over-identification (eg, “it’s not the end of the world”), resulting in lessened self-criticism (eg, “maybe it’s not just because I’m a bad person”).

Depression

Several studies have found that self-criticism predicts depression. In 3 epidemiological studies, “feeling worthless” was among the top 2 symptoms predicting a depression diagnosis and later depressive episodes.¹⁰ Self-criticism in fourth-year medical students predicted depression 2 years later, and—in males—10 years later in their medical careers better than a history of depression.¹¹ Self-critical perfectionism also is associated with suicidal ideation and lethality of suicide attempts.¹²

Self-criticism has been shown to predict depressive relapse and residual self-devaluative symptoms in recovered depressed patients.¹³ In one study, currently depressed and remitted depressed patients had higher self-criticism and lower self-compassion compared with healthy controls. Both factors were more strongly associated with depression status than higher perfectionistic beliefs and cognitions, rumination, and maladaptive emotional regulation.¹⁴

Self-criticism and response to treatment. In the National Institute of Mental Health Treatment of Depression Collaborative Research Program,¹⁵ self-critical perfectionism predicted a poorer outcome across all 4 treatments (cognitive-behavioral therapy [CBT], interpersonal psychotherapy [IPT], pharmacotherapy plus clinical management, and placebo plus clinical management). Subsequent studies found that self-criticism predicted poorer response to CBT¹⁶ and IPT.¹⁷ The authors suggest that self-criticism could interfere with treatment because self-critical patients might have difficulty developing a strong therapeutic alliance.^18,19

Anxiety disorders

Self-criticism is common across psychiatric disorders. In a study of 5,877 respondents in the National Comorbidity Survey (NCS), self-criticism was associated with social phobia, findings that were significant after controlling for current emotional distress, neuroticism, and lifetime history of mood, anxiety, and substance use disorders.²⁰ Further, in a CBT treatment study, baseline self-criticism was associated with severity of social phobia and changes in self-criticism predicted treatment outcome.²¹ Self-criticism might be an important core psychological process in the development, maintenance, and course of social phobia. Patients with social anxiety disorder have less self-compassion than healthy controls and greater fear of negative evaluation.

In the NCS, self-criticism was associated with posttraumatic stress disorder (PTSD) even after controlling for lifetime history of affective and anxiety disorders.²⁰ Self-criticism predicted greater severity of combat-related PTSD in hospitalized male veterans,²² and those with PTSD had higher scores on self-criticism scales than those with major depressive disorder.²³ In a study of Holocaust survivors, those with PTSD scored higher on self-criticism than survivors without PTSD.²⁴ Self-criticism also distinguished between female victims of domestic violence with and without PTSD.²⁵

Self-compassion could be a protective factor for posttraumatic stress.²⁶ Combat veterans with higher levels of self-compassion showed lower levels of psychopathology, better functioning in daily life, and fewer symptoms of posttraumatic stress.²⁷ In fact, self-compassion has been found to be a stronger predictor of PTSD than level of combat exposure.²⁸

In an early study, self-criticism scores were higher in patients with panic disorder than in healthy controls, but lower than in patients with depression.²⁹ In a study of a mixed sample of anxiety disorder patients, symptoms of generalized anxiety disorder were associated with shame proneness.³⁰ Consistent with these results, Hoge et al³¹ found that self-compassion was lower in generalized anxiety disorder patients compared with healthy controls with elevated stress. Low self-compassion has been associated with severity of obsessive-compulsive disorder.³²

Eating disorders

Self-criticism is correlated with eating disorder severity.³³ In a study of patients with binge eating disorder, Dunkley and Grilo³⁴ found that self-criticism was associated with the over-evaluation of shape and weight independently of self-esteem and depression. Self-criticism also is associated with body dissatisfaction, independent of self-esteem and depression. Dunkley et al³⁵ found that self-criticism, but not global self-esteem, in patients with binge eating disorder mediated the relationship between childhood abuse and body dissatisfaction and depression. Numerous studies have shown that shame is associated with more severe eating disorder pathology.³³

Self-compassion seems to buffer against body image concerns. It is associated with less body dissatisfaction, body preoccupation, and weight worries,³⁶ greater body appreciation³⁷ and less disordered eating.^37-39 Early decreases in shame during eating disorder treatment was associated with more rapid reduction in eating disorder symptoms.⁴⁰

Interpersonal relationships

Several studies have shown that self-criticism has negative effects on interpersonal relationships throughout life.^5,41,42

• Self-criticism at age 12 predicted less involvement in high school activities and, at age 31, personal and social maladjustment.⁴³
• High school students with high self-criticism reported more interpersonal problems.⁴⁴
• Self-criticism was associated with loneliness, depression, and lack of intimacy with opposite sex friends or partners during the transition to college.⁴⁵
• In a study of college roommates,⁴⁶ self-criticism was associated with increased likelihood of rejection.
• Whiffen and Aube⁴⁷ found that self-criticism was associated with marital dissatisfaction and depression.
• Self-critical mothers with postpartum depression were less satisfied with social support and were more vulnerable to depression.⁴⁸

Self-compassion appears to enhance interpersonal relationships. In a study of heterosexual couples,⁴⁹ self-compassionate individuals were described by their partners as being more emotionally connected, as well as accepting and supporting autonomy, while being less detached, controlling, and verbally or physically aggressive than those lacking self-compassion. Because self-compassionate people give themselves care and support, they seem to have more emotional resources available to give to others.

See the Box examining the evidence on the role of self-compassion in borderline personality disorder and non-suicidal self-injury.

Achieving goals

Powers et al⁵⁰ suggest that self-critics approach goals based on motivation to avoid failure and disapproval, rather than on intrinsic interest and personal meaning. In studies of college students pursuing academic, social, or weight loss goals, self-criticism was associated with less progress to that goal. Self-criticism was associated with rumination and procrastination, which the authors suggest might have focused the self-critic on potential failure, negative evaluation from others, and loss of self-esteem. Additional studies showed the deleterious effects of self-criticism on college students’ progress on obtaining academic or music performance goals and on community residents’ weight loss goals.⁵¹

Not surprisingly, self-compassion is associated with successful goal pursuit and resilience when goals are not met⁵² and less procrastination and academic worry.⁵³ Self-compassion also is associated with intrinsic motivation, goals based on mastery rather than performance, and less fear of academic failure.⁵⁴

How self-criticism and self-compassion develop

Studies have explored the impact of early relationships with parents and development of self-criticism. Parental overcontrol and restrictiveness and lack of warmth consistently have been identified as parenting styles associated with development of self-criticism in children.⁵⁵ One study found that self-criticism fully mediated the relationship between childhood verbal abuse from parents and depression and anxiety in adulthood.⁵⁶ Reports from parents on their current parenting styles are consistent with these studies.⁵⁷ Amitay et al⁵⁷ states that “[s]elf-critics’ negative childhood experiences thus seem to contribute to a pattern of entering, creating, or manipulating subsequent interpersonal environments in ways that perpetuate their negative self-image and increase vulnerability to depression.” Not surprisingly, self-criticism is associated with a fearful avoidant attachment style.⁵⁸ Review of the developmental origins of self-criticism confirms these factors and presents findings that peer relationships also are important factors in the development of self-criticism.^59,60

Early positive relationships with caregivers are associated with self-compassion. Recollections of maternal support are correlated with self-compassion and secure attachment styles in adolescents and adults.⁶¹ Pepping et al⁶² found that retrospective reports of parental rejection, overprotection, and low parental warmth was associated with low self-compassion.

Benefits of self-compassion

A growing body of research suggests that self-compassion is strongly linked to mental health. Greater self-compassion consistently has been associated with lower levels of depression and anxiety,³ with a large effect size.⁴ Of course, central to self-compassion is the lack of self-criticism, but self-compassion still protects against anxiety and depression when controlling for self-criticism and negative affect.^6,63 Self-compassion is a strong predictor of symptom severity and quality of life among individuals with anxious distress.⁶⁴

The benefits of self-compassion stem partly from a greater ability to cope with negative emotions.^6,63,65 Self-compassionate people are less likely to ruminate on their negative thoughts and emotions or suppress them,^6,66 which helps to explain why self-compassion is a negative predictor of depression.⁶⁷

Self-compassion also enhances positive mind states. A number of studies have found links between self-compassion and positive psychological qualities, such as happiness, optimism, wisdom, curiosity, and exploration, and personal initiative.^63,65,68,69 By embracing one’s suffering with compassion, negative states are ameliorated when positive emotions of kindness, connectedness, and mindful presence are generated.

Misconceptions about self-compassion

A common misconception is that abandoning self-criticism in favor of self-compassion will undermine motivation⁷⁰; however, research indicates the opposite. Although self-compassion is negatively associated with maladaptive perfectionism, it is not correlated with self-adopted performance standards.⁶ Self-compassionate people have less fear of failure⁵⁴ and, when they do fail, they are more likely to try again.⁷¹ Breines and Chen⁷² found in a series of experimental studies that engendering feelings of self-compassion for personal weaknesses, failures, and past transgressions resulted in more motivation to change, to try harder to learn, and to avoid repeating past mistakes.

Another common misunderstanding is that self-compassion is a weakness. In fact, research suggests that self-compassion is a powerful way to cope with life challenges.⁷³

Although some fear that self-compassion leads to self-indulgence, there is evidence that self-compassion promotes health-related behaviors. Self-compassionate individuals are more likely to seek medical treatment when needed,⁷⁴ exercise for intrinsic reasons,⁷⁵ and drink less alcohol.⁷⁶ Inducing self-compassion has been found to help people stick to their diets⁷⁷ and quit smoking.⁷⁸

Self-compassion interventions

Individuals can develop self-compassion. Shapira and Mongrain⁷⁹ found that adults who wrote a compassionate letter to themselves once a day for a week about the distressing events they were experiencing showed significant reductions in depression up to 3 months and significant increases in happiness up to 6 months compared with a control group who wrote about early memories. Albertson et al⁸⁰ found that, compared with a wait-list control group, 3 weeks of self-compassion meditation training improved body dissatisfaction, body shame, and body appreciation among women with body image concerns. Similarly, Smeets et al⁸¹ found that 3 weeks of self-compassion training for female college students led to significantly greater increases in mindfulness, optimism, and self-efficacy, as well as greater decreases in rumination compared with a time management control group.

The Box^6,70,82-86 describes rating scales that can measure self-compassion and self-criticism.

Mindful self-compassion (MSC), developed by Neff and Germer,⁸⁷ is an 8-week group intervention designed to teach people how to be more self-compassionate through meditation and informal practices in daily life. Results of a randomized controlled trial found that, compared with a wait-list control group, participants using MSC reported significantly greater increases in self-compassion, compassion for others, mindfulness, and life satisfaction, and greater decreases in depression, anxiety, stress, and emotional avoidance, with large effect sizes indicated. These results were maintained up to 1 year.

Compassion-focused therapy (CFT) is designed to enhance self-compassion in clinical populations.⁸⁸ The approach uses a number of imagery and experiential exercises to enhance patients’ abilities to extend feelings of reassurance, safeness, and understanding toward themselves. CFT has shown promise in treating a diverse group of clinical disorders such as depression and shame,^8,89 social anxiety and shame,⁹⁰ eating disorders,⁹¹ psychosis,⁹² and patients with acquired brain injury.⁹³ A group-based CFT intervention with a heterogeneous group of community mental health patients led to significant reductions in depression, anxiety, stress, and self-criticism.⁹⁴ See Leaviss and Utley⁹⁵ for a review of the benefits of CFT.

Fears of developing self-compassion

It is important to note that some people can access self-compassion more easily than others. Highly self-critical patients could feel anxious when learning to be compassionate to themselves, a phenomenon known as “fear of compassion”⁹⁶ or “backdraft.”⁹⁷ Backdraft occurs when a firefighter opens a door with a hot fire behind it. Oxygen rushes in, causing a burst of flame. Similarly, when the door of the heart is opened with compassion, intense pain could be released. Unconditional love reveals the conditions under which we were unloved in the past. Some individuals, especially those with a history of childhood abuse or neglect, are fearful of compassion because it activates grief associated with feelings of wanting, but not receiving, affection and care from significant others in childhood.

Clinicians should be aware that anxiety could arise and should help patients learn how to go slowly and stabilize themselves if overwhelming emotions occur as a part of self-compassion practice. Both CFT and MSC have processes to deal with fear of compassion in their protocols,^98,99 with the focus on explaining to individuals that although such fears may occur, they are a normal and necessary part of the healing process. Individuals also are taught to focus on the breath, feeling the sensations in the soles of their feet, or other mindfulness practices to ground and stabilize attention when overwhelming feelings arise.

Clinical interventions

Self-compassion interventions that I (R.W.) find most helpful, in the order I administer them, are:

• exploring perceived advantages and disadvantages of self-criticism
• presenting self-compassion as a way to get the perceived advantages of self-criticism without the disadvantages
• discussing what it means to be compassionate for someone else who is suffering, and then asking what it would be like if they treated themselves with the same compassion
• exploring patients’ misconceptions and fears of self-compassion
• directing patients to the self-compassion Web site to get an understanding of what self-compassion is and how it differs from self-esteem
• taking an example of a recent situation in which the patient was self-critical and exploring how a self-compassionate response would differ.

Asking what they would say to a friend often is an effective way to get at this. In a later therapy session, self-compassionate imagery is a useful way to get the patient to experience self-compassion on an emotional level. See Neff¹⁰⁰ and Gilbert⁹⁸ for other techniques to enhance self-compassion.

Once thought to only be associated with depression, self-criticism is a transdiagnostic risk factor for diverse forms of psychopathology.^1,2 However, research has shown that self-compassion is a robust resilience factor when faced with feelings of personal inadequacy.^3,4

Self-critical individuals experience feelings of unworthiness, inferiority, failure, and guilt. They engage in constant and harsh self-scrutiny and evaluation, and fear being disapproved and criticized and losing the approval and acceptance of others.⁵ Self-compassion involves treating oneself with care and concern when confronted with personal inadequacies, mistakes, failures, and painful life situations.^6,7Although self-criticism is the aspect of perfectionism most associated with maladjustment,⁸ one can be harshly self-critical without being a perfectionist. Most studies of self-criticism have not measured shame; however, this self-conscious emotion has been implicated in diverse forms of psychopathology.⁹ In contrast to guilt, which results from acknowledging bad behavior, shame results from seeing oneself as a bad or inadequate person.

Although self-criticism is destructive across clinical disorders and interpersonal relationships, self-compassion is associated with healthy relationships, emotional well-being, and better treatment outcomes.

Recent research shows how clinicians can teach their patients how to be less self-critical and more self-compassionate. Neff^6,7 proposes that self-compassion involves treating yourself with care and concern when being confronted with personal inadequacies, mistakes, failures, and painful life situations. It consists of 3 interacting components, each of which has a positive and negative pole:

• self-kindness vs self-judgment
• a sense of common humanity vs isolation
• mindfulness vs over-identification.

Self-kindness refers to being caring and understanding with oneself rather than harshly judgmental. Instead of attacking and berating oneself for personal shortcomings, the self is offered warmth and unconditional acceptance.

Humanity involves recognizing that humans are imperfect, that all people fail, make mistakes, and have serious life challenges. By remembering that imperfection is part of life, we feel less isolated when we are in pain.

Mindfulness in the context of self-compassion involves being aware of one’s painful experiences in a balanced way that neither ignores and avoids nor exaggerates painful thoughts and emotions.

Self-compassion is more than the absence of self-judgment, although a defining feature of self-compassion is the lack of self-judgment, and self-judgment overlaps with self-criticism. Rather, self-compassion provides several access points for reducing self-criticism. For example, being kind and understanding when confronting personal inadequacies (eg, “it’s okay not to be perfect”) can counter harsh self-talk (eg, “I’m not defective”). Mindfulness of emotional pain (eg, “this is hard”) can facilitate a kind and warm response (eg, “what can I do to take care of myself right now?”) and therefore lessen self-blame (eg, “blaming myself is just causing me more suffering”). Similarly, remembering that failure is part of the human experience (eg, “it’s normal to mess up sometimes”) can lessen egocentric feelings of isolation (eg, “it’s not just me”) and over-identification (eg, “it’s not the end of the world”), resulting in lessened self-criticism (eg, “maybe it’s not just because I’m a bad person”).

Depression

Several studies have found that self-criticism predicts depression. In 3 epidemiological studies, “feeling worthless” was among the top 2 symptoms predicting a depression diagnosis and later depressive episodes.¹⁰ Self-criticism in fourth-year medical students predicted depression 2 years later, and—in males—10 years later in their medical careers better than a history of depression.¹¹ Self-critical perfectionism also is associated with suicidal ideation and lethality of suicide attempts.¹²

Self-criticism has been shown to predict depressive relapse and residual self-devaluative symptoms in recovered depressed patients.¹³ In one study, currently depressed and remitted depressed patients had higher self-criticism and lower self-compassion compared with healthy controls. Both factors were more strongly associated with depression status than higher perfectionistic beliefs and cognitions, rumination, and maladaptive emotional regulation.¹⁴

Self-criticism and response to treatment. In the National Institute of Mental Health Treatment of Depression Collaborative Research Program,¹⁵ self-critical perfectionism predicted a poorer outcome across all 4 treatments (cognitive-behavioral therapy [CBT], interpersonal psychotherapy [IPT], pharmacotherapy plus clinical management, and placebo plus clinical management). Subsequent studies found that self-criticism predicted poorer response to CBT¹⁶ and IPT.¹⁷ The authors suggest that self-criticism could interfere with treatment because self-critical patients might have difficulty developing a strong therapeutic alliance.^18,19

Anxiety disorders

Self-criticism is common across psychiatric disorders. In a study of 5,877 respondents in the National Comorbidity Survey (NCS), self-criticism was associated with social phobia, findings that were significant after controlling for current emotional distress, neuroticism, and lifetime history of mood, anxiety, and substance use disorders.²⁰ Further, in a CBT treatment study, baseline self-criticism was associated with severity of social phobia and changes in self-criticism predicted treatment outcome.²¹ Self-criticism might be an important core psychological process in the development, maintenance, and course of social phobia. Patients with social anxiety disorder have less self-compassion than healthy controls and greater fear of negative evaluation.

In the NCS, self-criticism was associated with posttraumatic stress disorder (PTSD) even after controlling for lifetime history of affective and anxiety disorders.²⁰ Self-criticism predicted greater severity of combat-related PTSD in hospitalized male veterans,²² and those with PTSD had higher scores on self-criticism scales than those with major depressive disorder.²³ In a study of Holocaust survivors, those with PTSD scored higher on self-criticism than survivors without PTSD.²⁴ Self-criticism also distinguished between female victims of domestic violence with and without PTSD.²⁵

Self-compassion could be a protective factor for posttraumatic stress.²⁶ Combat veterans with higher levels of self-compassion showed lower levels of psychopathology, better functioning in daily life, and fewer symptoms of posttraumatic stress.²⁷ In fact, self-compassion has been found to be a stronger predictor of PTSD than level of combat exposure.²⁸

In an early study, self-criticism scores were higher in patients with panic disorder than in healthy controls, but lower than in patients with depression.²⁹ In a study of a mixed sample of anxiety disorder patients, symptoms of generalized anxiety disorder were associated with shame proneness.³⁰ Consistent with these results, Hoge et al³¹ found that self-compassion was lower in generalized anxiety disorder patients compared with healthy controls with elevated stress. Low self-compassion has been associated with severity of obsessive-compulsive disorder.³²

Eating disorders

Self-criticism is correlated with eating disorder severity.³³ In a study of patients with binge eating disorder, Dunkley and Grilo³⁴ found that self-criticism was associated with the over-evaluation of shape and weight independently of self-esteem and depression. Self-criticism also is associated with body dissatisfaction, independent of self-esteem and depression. Dunkley et al³⁵ found that self-criticism, but not global self-esteem, in patients with binge eating disorder mediated the relationship between childhood abuse and body dissatisfaction and depression. Numerous studies have shown that shame is associated with more severe eating disorder pathology.³³

Self-compassion seems to buffer against body image concerns. It is associated with less body dissatisfaction, body preoccupation, and weight worries,³⁶ greater body appreciation³⁷ and less disordered eating.^37-39 Early decreases in shame during eating disorder treatment was associated with more rapid reduction in eating disorder symptoms.⁴⁰

Interpersonal relationships

Several studies have shown that self-criticism has negative effects on interpersonal relationships throughout life.^5,41,42

• Self-criticism at age 12 predicted less involvement in high school activities and, at age 31, personal and social maladjustment.⁴³
• High school students with high self-criticism reported more interpersonal problems.⁴⁴
• Self-criticism was associated with loneliness, depression, and lack of intimacy with opposite sex friends or partners during the transition to college.⁴⁵
• In a study of college roommates,⁴⁶ self-criticism was associated with increased likelihood of rejection.
• Whiffen and Aube⁴⁷ found that self-criticism was associated with marital dissatisfaction and depression.
• Self-critical mothers with postpartum depression were less satisfied with social support and were more vulnerable to depression.⁴⁸

Self-compassion appears to enhance interpersonal relationships. In a study of heterosexual couples,⁴⁹ self-compassionate individuals were described by their partners as being more emotionally connected, as well as accepting and supporting autonomy, while being less detached, controlling, and verbally or physically aggressive than those lacking self-compassion. Because self-compassionate people give themselves care and support, they seem to have more emotional resources available to give to others.

See the Box examining the evidence on the role of self-compassion in borderline personality disorder and non-suicidal self-injury.

Achieving goals

Powers et al⁵⁰ suggest that self-critics approach goals based on motivation to avoid failure and disapproval, rather than on intrinsic interest and personal meaning. In studies of college students pursuing academic, social, or weight loss goals, self-criticism was associated with less progress to that goal. Self-criticism was associated with rumination and procrastination, which the authors suggest might have focused the self-critic on potential failure, negative evaluation from others, and loss of self-esteem. Additional studies showed the deleterious effects of self-criticism on college students’ progress on obtaining academic or music performance goals and on community residents’ weight loss goals.⁵¹

Not surprisingly, self-compassion is associated with successful goal pursuit and resilience when goals are not met⁵² and less procrastination and academic worry.⁵³ Self-compassion also is associated with intrinsic motivation, goals based on mastery rather than performance, and less fear of academic failure.⁵⁴

How self-criticism and self-compassion develop

Studies have explored the impact of early relationships with parents and development of self-criticism. Parental overcontrol and restrictiveness and lack of warmth consistently have been identified as parenting styles associated with development of self-criticism in children.⁵⁵ One study found that self-criticism fully mediated the relationship between childhood verbal abuse from parents and depression and anxiety in adulthood.⁵⁶ Reports from parents on their current parenting styles are consistent with these studies.⁵⁷ Amitay et al⁵⁷ states that “[s]elf-critics’ negative childhood experiences thus seem to contribute to a pattern of entering, creating, or manipulating subsequent interpersonal environments in ways that perpetuate their negative self-image and increase vulnerability to depression.” Not surprisingly, self-criticism is associated with a fearful avoidant attachment style.⁵⁸ Review of the developmental origins of self-criticism confirms these factors and presents findings that peer relationships also are important factors in the development of self-criticism.^59,60

Early positive relationships with caregivers are associated with self-compassion. Recollections of maternal support are correlated with self-compassion and secure attachment styles in adolescents and adults.⁶¹ Pepping et al⁶² found that retrospective reports of parental rejection, overprotection, and low parental warmth was associated with low self-compassion.

Benefits of self-compassion

A growing body of research suggests that self-compassion is strongly linked to mental health. Greater self-compassion consistently has been associated with lower levels of depression and anxiety,³ with a large effect size.⁴ Of course, central to self-compassion is the lack of self-criticism, but self-compassion still protects against anxiety and depression when controlling for self-criticism and negative affect.^6,63 Self-compassion is a strong predictor of symptom severity and quality of life among individuals with anxious distress.⁶⁴

The benefits of self-compassion stem partly from a greater ability to cope with negative emotions.^6,63,65 Self-compassionate people are less likely to ruminate on their negative thoughts and emotions or suppress them,^6,66 which helps to explain why self-compassion is a negative predictor of depression.⁶⁷

Self-compassion also enhances positive mind states. A number of studies have found links between self-compassion and positive psychological qualities, such as happiness, optimism, wisdom, curiosity, and exploration, and personal initiative.^63,65,68,69 By embracing one’s suffering with compassion, negative states are ameliorated when positive emotions of kindness, connectedness, and mindful presence are generated.

Misconceptions about self-compassion

A common misconception is that abandoning self-criticism in favor of self-compassion will undermine motivation⁷⁰; however, research indicates the opposite. Although self-compassion is negatively associated with maladaptive perfectionism, it is not correlated with self-adopted performance standards.⁶ Self-compassionate people have less fear of failure⁵⁴ and, when they do fail, they are more likely to try again.⁷¹ Breines and Chen⁷² found in a series of experimental studies that engendering feelings of self-compassion for personal weaknesses, failures, and past transgressions resulted in more motivation to change, to try harder to learn, and to avoid repeating past mistakes.

Another common misunderstanding is that self-compassion is a weakness. In fact, research suggests that self-compassion is a powerful way to cope with life challenges.⁷³

Although some fear that self-compassion leads to self-indulgence, there is evidence that self-compassion promotes health-related behaviors. Self-compassionate individuals are more likely to seek medical treatment when needed,⁷⁴ exercise for intrinsic reasons,⁷⁵ and drink less alcohol.⁷⁶ Inducing self-compassion has been found to help people stick to their diets⁷⁷ and quit smoking.⁷⁸

Self-compassion interventions

Individuals can develop self-compassion. Shapira and Mongrain⁷⁹ found that adults who wrote a compassionate letter to themselves once a day for a week about the distressing events they were experiencing showed significant reductions in depression up to 3 months and significant increases in happiness up to 6 months compared with a control group who wrote about early memories. Albertson et al⁸⁰ found that, compared with a wait-list control group, 3 weeks of self-compassion meditation training improved body dissatisfaction, body shame, and body appreciation among women with body image concerns. Similarly, Smeets et al⁸¹ found that 3 weeks of self-compassion training for female college students led to significantly greater increases in mindfulness, optimism, and self-efficacy, as well as greater decreases in rumination compared with a time management control group.

The Box^6,70,82-86 describes rating scales that can measure self-compassion and self-criticism.

Mindful self-compassion (MSC), developed by Neff and Germer,⁸⁷ is an 8-week group intervention designed to teach people how to be more self-compassionate through meditation and informal practices in daily life. Results of a randomized controlled trial found that, compared with a wait-list control group, participants using MSC reported significantly greater increases in self-compassion, compassion for others, mindfulness, and life satisfaction, and greater decreases in depression, anxiety, stress, and emotional avoidance, with large effect sizes indicated. These results were maintained up to 1 year.

Compassion-focused therapy (CFT) is designed to enhance self-compassion in clinical populations.⁸⁸ The approach uses a number of imagery and experiential exercises to enhance patients’ abilities to extend feelings of reassurance, safeness, and understanding toward themselves. CFT has shown promise in treating a diverse group of clinical disorders such as depression and shame,^8,89 social anxiety and shame,⁹⁰ eating disorders,⁹¹ psychosis,⁹² and patients with acquired brain injury.⁹³ A group-based CFT intervention with a heterogeneous group of community mental health patients led to significant reductions in depression, anxiety, stress, and self-criticism.⁹⁴ See Leaviss and Utley⁹⁵ for a review of the benefits of CFT.

Fears of developing self-compassion

It is important to note that some people can access self-compassion more easily than others. Highly self-critical patients could feel anxious when learning to be compassionate to themselves, a phenomenon known as “fear of compassion”⁹⁶ or “backdraft.”⁹⁷ Backdraft occurs when a firefighter opens a door with a hot fire behind it. Oxygen rushes in, causing a burst of flame. Similarly, when the door of the heart is opened with compassion, intense pain could be released. Unconditional love reveals the conditions under which we were unloved in the past. Some individuals, especially those with a history of childhood abuse or neglect, are fearful of compassion because it activates grief associated with feelings of wanting, but not receiving, affection and care from significant others in childhood.

Clinicians should be aware that anxiety could arise and should help patients learn how to go slowly and stabilize themselves if overwhelming emotions occur as a part of self-compassion practice. Both CFT and MSC have processes to deal with fear of compassion in their protocols,^98,99 with the focus on explaining to individuals that although such fears may occur, they are a normal and necessary part of the healing process. Individuals also are taught to focus on the breath, feeling the sensations in the soles of their feet, or other mindfulness practices to ground and stabilize attention when overwhelming feelings arise.

Clinical interventions

Self-compassion interventions that I (R.W.) find most helpful, in the order I administer them, are:

• exploring perceived advantages and disadvantages of self-criticism
• presenting self-compassion as a way to get the perceived advantages of self-criticism without the disadvantages
• discussing what it means to be compassionate for someone else who is suffering, and then asking what it would be like if they treated themselves with the same compassion
• exploring patients’ misconceptions and fears of self-compassion
• directing patients to the self-compassion Web site to get an understanding of what self-compassion is and how it differs from self-esteem
• taking an example of a recent situation in which the patient was self-critical and exploring how a self-compassionate response would differ.

Asking what they would say to a friend often is an effective way to get at this. In a later therapy session, self-compassionate imagery is a useful way to get the patient to experience self-compassion on an emotional level. See Neff¹⁰⁰ and Gilbert⁹⁸ for other techniques to enhance self-compassion.

Once thought to only be associated with depression, self-criticism is a transdiagnostic risk factor for diverse forms of psychopathology.^1,2 However, research has shown that self-compassion is a robust resilience factor when faced with feelings of personal inadequacy.^3,4

Self-critical individuals experience feelings of unworthiness, inferiority, failure, and guilt. They engage in constant and harsh self-scrutiny and evaluation, and fear being disapproved and criticized and losing the approval and acceptance of others.⁵ Self-compassion involves treating oneself with care and concern when confronted with personal inadequacies, mistakes, failures, and painful life situations.^6,7Although self-criticism is the aspect of perfectionism most associated with maladjustment,⁸ one can be harshly self-critical without being a perfectionist. Most studies of self-criticism have not measured shame; however, this self-conscious emotion has been implicated in diverse forms of psychopathology.⁹ In contrast to guilt, which results from acknowledging bad behavior, shame results from seeing oneself as a bad or inadequate person.

Although self-criticism is destructive across clinical disorders and interpersonal relationships, self-compassion is associated with healthy relationships, emotional well-being, and better treatment outcomes.

Recent research shows how clinicians can teach their patients how to be less self-critical and more self-compassionate. Neff^6,7 proposes that self-compassion involves treating yourself with care and concern when being confronted with personal inadequacies, mistakes, failures, and painful life situations. It consists of 3 interacting components, each of which has a positive and negative pole:

• self-kindness vs self-judgment
• a sense of common humanity vs isolation
• mindfulness vs over-identification.

Self-kindness refers to being caring and understanding with oneself rather than harshly judgmental. Instead of attacking and berating oneself for personal shortcomings, the self is offered warmth and unconditional acceptance.

Humanity involves recognizing that humans are imperfect, that all people fail, make mistakes, and have serious life challenges. By remembering that imperfection is part of life, we feel less isolated when we are in pain.

Mindfulness in the context of self-compassion involves being aware of one’s painful experiences in a balanced way that neither ignores and avoids nor exaggerates painful thoughts and emotions.

Self-compassion is more than the absence of self-judgment, although a defining feature of self-compassion is the lack of self-judgment, and self-judgment overlaps with self-criticism. Rather, self-compassion provides several access points for reducing self-criticism. For example, being kind and understanding when confronting personal inadequacies (eg, “it’s okay not to be perfect”) can counter harsh self-talk (eg, “I’m not defective”). Mindfulness of emotional pain (eg, “this is hard”) can facilitate a kind and warm response (eg, “what can I do to take care of myself right now?”) and therefore lessen self-blame (eg, “blaming myself is just causing me more suffering”). Similarly, remembering that failure is part of the human experience (eg, “it’s normal to mess up sometimes”) can lessen egocentric feelings of isolation (eg, “it’s not just me”) and over-identification (eg, “it’s not the end of the world”), resulting in lessened self-criticism (eg, “maybe it’s not just because I’m a bad person”).

Depression

Several studies have found that self-criticism predicts depression. In 3 epidemiological studies, “feeling worthless” was among the top 2 symptoms predicting a depression diagnosis and later depressive episodes.¹⁰ Self-criticism in fourth-year medical students predicted depression 2 years later, and—in males—10 years later in their medical careers better than a history of depression.¹¹ Self-critical perfectionism also is associated with suicidal ideation and lethality of suicide attempts.¹²

Self-criticism has been shown to predict depressive relapse and residual self-devaluative symptoms in recovered depressed patients.¹³ In one study, currently depressed and remitted depressed patients had higher self-criticism and lower self-compassion compared with healthy controls. Both factors were more strongly associated with depression status than higher perfectionistic beliefs and cognitions, rumination, and maladaptive emotional regulation.¹⁴

Self-criticism and response to treatment. In the National Institute of Mental Health Treatment of Depression Collaborative Research Program,¹⁵ self-critical perfectionism predicted a poorer outcome across all 4 treatments (cognitive-behavioral therapy [CBT], interpersonal psychotherapy [IPT], pharmacotherapy plus clinical management, and placebo plus clinical management). Subsequent studies found that self-criticism predicted poorer response to CBT¹⁶ and IPT.¹⁷ The authors suggest that self-criticism could interfere with treatment because self-critical patients might have difficulty developing a strong therapeutic alliance.^18,19

Anxiety disorders

Self-criticism is common across psychiatric disorders. In a study of 5,877 respondents in the National Comorbidity Survey (NCS), self-criticism was associated with social phobia, findings that were significant after controlling for current emotional distress, neuroticism, and lifetime history of mood, anxiety, and substance use disorders.²⁰ Further, in a CBT treatment study, baseline self-criticism was associated with severity of social phobia and changes in self-criticism predicted treatment outcome.²¹ Self-criticism might be an important core psychological process in the development, maintenance, and course of social phobia. Patients with social anxiety disorder have less self-compassion than healthy controls and greater fear of negative evaluation.

In the NCS, self-criticism was associated with posttraumatic stress disorder (PTSD) even after controlling for lifetime history of affective and anxiety disorders.²⁰ Self-criticism predicted greater severity of combat-related PTSD in hospitalized male veterans,²² and those with PTSD had higher scores on self-criticism scales than those with major depressive disorder.²³ In a study of Holocaust survivors, those with PTSD scored higher on self-criticism than survivors without PTSD.²⁴ Self-criticism also distinguished between female victims of domestic violence with and without PTSD.²⁵

Self-compassion could be a protective factor for posttraumatic stress.²⁶ Combat veterans with higher levels of self-compassion showed lower levels of psychopathology, better functioning in daily life, and fewer symptoms of posttraumatic stress.²⁷ In fact, self-compassion has been found to be a stronger predictor of PTSD than level of combat exposure.²⁸

In an early study, self-criticism scores were higher in patients with panic disorder than in healthy controls, but lower than in patients with depression.²⁹ In a study of a mixed sample of anxiety disorder patients, symptoms of generalized anxiety disorder were associated with shame proneness.³⁰ Consistent with these results, Hoge et al³¹ found that self-compassion was lower in generalized anxiety disorder patients compared with healthy controls with elevated stress. Low self-compassion has been associated with severity of obsessive-compulsive disorder.³²

Eating disorders

Self-criticism is correlated with eating disorder severity.³³ In a study of patients with binge eating disorder, Dunkley and Grilo³⁴ found that self-criticism was associated with the over-evaluation of shape and weight independently of self-esteem and depression. Self-criticism also is associated with body dissatisfaction, independent of self-esteem and depression. Dunkley et al³⁵ found that self-criticism, but not global self-esteem, in patients with binge eating disorder mediated the relationship between childhood abuse and body dissatisfaction and depression. Numerous studies have shown that shame is associated with more severe eating disorder pathology.³³

Self-compassion seems to buffer against body image concerns. It is associated with less body dissatisfaction, body preoccupation, and weight worries,³⁶ greater body appreciation³⁷ and less disordered eating.^37-39 Early decreases in shame during eating disorder treatment was associated with more rapid reduction in eating disorder symptoms.⁴⁰

Interpersonal relationships

Several studies have shown that self-criticism has negative effects on interpersonal relationships throughout life.^5,41,42

• Self-criticism at age 12 predicted less involvement in high school activities and, at age 31, personal and social maladjustment.⁴³
• High school students with high self-criticism reported more interpersonal problems.⁴⁴
• Self-criticism was associated with loneliness, depression, and lack of intimacy with opposite sex friends or partners during the transition to college.⁴⁵
• In a study of college roommates,⁴⁶ self-criticism was associated with increased likelihood of rejection.
• Whiffen and Aube⁴⁷ found that self-criticism was associated with marital dissatisfaction and depression.
• Self-critical mothers with postpartum depression were less satisfied with social support and were more vulnerable to depression.⁴⁸

Self-compassion appears to enhance interpersonal relationships. In a study of heterosexual couples,⁴⁹ self-compassionate individuals were described by their partners as being more emotionally connected, as well as accepting and supporting autonomy, while being less detached, controlling, and verbally or physically aggressive than those lacking self-compassion. Because self-compassionate people give themselves care and support, they seem to have more emotional resources available to give to others.

See the Box examining the evidence on the role of self-compassion in borderline personality disorder and non-suicidal self-injury.

Achieving goals

Powers et al⁵⁰ suggest that self-critics approach goals based on motivation to avoid failure and disapproval, rather than on intrinsic interest and personal meaning. In studies of college students pursuing academic, social, or weight loss goals, self-criticism was associated with less progress to that goal. Self-criticism was associated with rumination and procrastination, which the authors suggest might have focused the self-critic on potential failure, negative evaluation from others, and loss of self-esteem. Additional studies showed the deleterious effects of self-criticism on college students’ progress on obtaining academic or music performance goals and on community residents’ weight loss goals.⁵¹

Not surprisingly, self-compassion is associated with successful goal pursuit and resilience when goals are not met⁵² and less procrastination and academic worry.⁵³ Self-compassion also is associated with intrinsic motivation, goals based on mastery rather than performance, and less fear of academic failure.⁵⁴

How self-criticism and self-compassion develop

Studies have explored the impact of early relationships with parents and development of self-criticism. Parental overcontrol and restrictiveness and lack of warmth consistently have been identified as parenting styles associated with development of self-criticism in children.⁵⁵ One study found that self-criticism fully mediated the relationship between childhood verbal abuse from parents and depression and anxiety in adulthood.⁵⁶ Reports from parents on their current parenting styles are consistent with these studies.⁵⁷ Amitay et al⁵⁷ states that “[s]elf-critics’ negative childhood experiences thus seem to contribute to a pattern of entering, creating, or manipulating subsequent interpersonal environments in ways that perpetuate their negative self-image and increase vulnerability to depression.” Not surprisingly, self-criticism is associated with a fearful avoidant attachment style.⁵⁸ Review of the developmental origins of self-criticism confirms these factors and presents findings that peer relationships also are important factors in the development of self-criticism.^59,60

Early positive relationships with caregivers are associated with self-compassion. Recollections of maternal support are correlated with self-compassion and secure attachment styles in adolescents and adults.⁶¹ Pepping et al⁶² found that retrospective reports of parental rejection, overprotection, and low parental warmth was associated with low self-compassion.

Benefits of self-compassion

A growing body of research suggests that self-compassion is strongly linked to mental health. Greater self-compassion consistently has been associated with lower levels of depression and anxiety,³ with a large effect size.⁴ Of course, central to self-compassion is the lack of self-criticism, but self-compassion still protects against anxiety and depression when controlling for self-criticism and negative affect.^6,63 Self-compassion is a strong predictor of symptom severity and quality of life among individuals with anxious distress.⁶⁴

The benefits of self-compassion stem partly from a greater ability to cope with negative emotions.^6,63,65 Self-compassionate people are less likely to ruminate on their negative thoughts and emotions or suppress them,^6,66 which helps to explain why self-compassion is a negative predictor of depression.⁶⁷

Self-compassion also enhances positive mind states. A number of studies have found links between self-compassion and positive psychological qualities, such as happiness, optimism, wisdom, curiosity, and exploration, and personal initiative.^63,65,68,69 By embracing one’s suffering with compassion, negative states are ameliorated when positive emotions of kindness, connectedness, and mindful presence are generated.

Misconceptions about self-compassion

A common misconception is that abandoning self-criticism in favor of self-compassion will undermine motivation⁷⁰; however, research indicates the opposite. Although self-compassion is negatively associated with maladaptive perfectionism, it is not correlated with self-adopted performance standards.⁶ Self-compassionate people have less fear of failure⁵⁴ and, when they do fail, they are more likely to try again.⁷¹ Breines and Chen⁷² found in a series of experimental studies that engendering feelings of self-compassion for personal weaknesses, failures, and past transgressions resulted in more motivation to change, to try harder to learn, and to avoid repeating past mistakes.

Another common misunderstanding is that self-compassion is a weakness. In fact, research suggests that self-compassion is a powerful way to cope with life challenges.⁷³

Although some fear that self-compassion leads to self-indulgence, there is evidence that self-compassion promotes health-related behaviors. Self-compassionate individuals are more likely to seek medical treatment when needed,⁷⁴ exercise for intrinsic reasons,⁷⁵ and drink less alcohol.⁷⁶ Inducing self-compassion has been found to help people stick to their diets⁷⁷ and quit smoking.⁷⁸

Self-compassion interventions

Individuals can develop self-compassion. Shapira and Mongrain⁷⁹ found that adults who wrote a compassionate letter to themselves once a day for a week about the distressing events they were experiencing showed significant reductions in depression up to 3 months and significant increases in happiness up to 6 months compared with a control group who wrote about early memories. Albertson et al⁸⁰ found that, compared with a wait-list control group, 3 weeks of self-compassion meditation training improved body dissatisfaction, body shame, and body appreciation among women with body image concerns. Similarly, Smeets et al⁸¹ found that 3 weeks of self-compassion training for female college students led to significantly greater increases in mindfulness, optimism, and self-efficacy, as well as greater decreases in rumination compared with a time management control group.

The Box^6,70,82-86 describes rating scales that can measure self-compassion and self-criticism.

Mindful self-compassion (MSC), developed by Neff and Germer,⁸⁷ is an 8-week group intervention designed to teach people how to be more self-compassionate through meditation and informal practices in daily life. Results of a randomized controlled trial found that, compared with a wait-list control group, participants using MSC reported significantly greater increases in self-compassion, compassion for others, mindfulness, and life satisfaction, and greater decreases in depression, anxiety, stress, and emotional avoidance, with large effect sizes indicated. These results were maintained up to 1 year.

Compassion-focused therapy (CFT) is designed to enhance self-compassion in clinical populations.⁸⁸ The approach uses a number of imagery and experiential exercises to enhance patients’ abilities to extend feelings of reassurance, safeness, and understanding toward themselves. CFT has shown promise in treating a diverse group of clinical disorders such as depression and shame,^8,89 social anxiety and shame,⁹⁰ eating disorders,⁹¹ psychosis,⁹² and patients with acquired brain injury.⁹³ A group-based CFT intervention with a heterogeneous group of community mental health patients led to significant reductions in depression, anxiety, stress, and self-criticism.⁹⁴ See Leaviss and Utley⁹⁵ for a review of the benefits of CFT.

Fears of developing self-compassion

It is important to note that some people can access self-compassion more easily than others. Highly self-critical patients could feel anxious when learning to be compassionate to themselves, a phenomenon known as “fear of compassion”⁹⁶ or “backdraft.”⁹⁷ Backdraft occurs when a firefighter opens a door with a hot fire behind it. Oxygen rushes in, causing a burst of flame. Similarly, when the door of the heart is opened with compassion, intense pain could be released. Unconditional love reveals the conditions under which we were unloved in the past. Some individuals, especially those with a history of childhood abuse or neglect, are fearful of compassion because it activates grief associated with feelings of wanting, but not receiving, affection and care from significant others in childhood.

Clinicians should be aware that anxiety could arise and should help patients learn how to go slowly and stabilize themselves if overwhelming emotions occur as a part of self-compassion practice. Both CFT and MSC have processes to deal with fear of compassion in their protocols,^98,99 with the focus on explaining to individuals that although such fears may occur, they are a normal and necessary part of the healing process. Individuals also are taught to focus on the breath, feeling the sensations in the soles of their feet, or other mindfulness practices to ground and stabilize attention when overwhelming feelings arise.

Clinical interventions

Self-compassion interventions that I (R.W.) find most helpful, in the order I administer them, are:

• exploring perceived advantages and disadvantages of self-criticism
• presenting self-compassion as a way to get the perceived advantages of self-criticism without the disadvantages
• discussing what it means to be compassionate for someone else who is suffering, and then asking what it would be like if they treated themselves with the same compassion
• exploring patients’ misconceptions and fears of self-compassion
• directing patients to the self-compassion Web site to get an understanding of what self-compassion is and how it differs from self-esteem
• taking an example of a recent situation in which the patient was self-critical and exploring how a self-compassionate response would differ.

Asking what they would say to a friend often is an effective way to get at this. In a later therapy session, self-compassionate imagery is a useful way to get the patient to experience self-compassion on an emotional level. See Neff¹⁰⁰ and Gilbert⁹⁸ for other techniques to enhance self-compassion.

Alcohol withdrawal is an uncomfortable and potentially life-threatening condition that must be treated before patients can achieve sobriety. Benzodiazepines remain the first-line treatment for alcohol withdrawal; however, these agents could:

• exacerbate agitation
• interact adversely with other medications, particularly opioids
• be unsafe for outpatients at risk of drinking again.
  

Off-label use of anticonvulsants could reduce these risks. In our emergency department, we routinely use these agents as monotherapy for patients discharging to outpatient detoxification or as adjunctive treatment for patients who require admission for severe withdrawal (Table^1,2).

Gabapentin is safe for patients with liver disease and has few drug–drug interactions.¹ Dosages of at least 1,200 mg/d seems to be comparable to lorazepam for alcohol withdrawal and could help prevent relapse after the withdrawal period.¹ Many patients report that gabapentin helps them sleep. Gabapentin could cause gastrointestinal upset or slight dizziness; patients with severe renal disease might require dosage adjustments.

Carbamazepine. In a randomized double-blind trial, carbamazepine was superior to lorazepam in preventing rebound withdrawal symptoms and reducing post-treatment drinking, although both agents were effective in decreasing withdrawal symptoms.² Avoid this agent in patients with serum liver enzymes 3 times higher than normal values, renal disease, neuropathy, thrombocytopenia, or leukopenia. Drug–drug interactions typically are not of concern unless a patient takes carbamazepine for several weeks.

Divalproex with as-needed benzodiazepines reduces the duration of withdrawal and risk of medical complications.³ Avoid using divalproex in patients with thrombocytopenia, leukopenia, or severe liver disease.

Alcohol withdrawal is an uncomfortable and potentially life-threatening condition that must be treated before patients can achieve sobriety. Benzodiazepines remain the first-line treatment for alcohol withdrawal; however, these agents could:

• exacerbate agitation
• interact adversely with other medications, particularly opioids
• be unsafe for outpatients at risk of drinking again.
  

Off-label use of anticonvulsants could reduce these risks. In our emergency department, we routinely use these agents as monotherapy for patients discharging to outpatient detoxification or as adjunctive treatment for patients who require admission for severe withdrawal (Table^1,2).

Gabapentin is safe for patients with liver disease and has few drug–drug interactions.¹ Dosages of at least 1,200 mg/d seems to be comparable to lorazepam for alcohol withdrawal and could help prevent relapse after the withdrawal period.¹ Many patients report that gabapentin helps them sleep. Gabapentin could cause gastrointestinal upset or slight dizziness; patients with severe renal disease might require dosage adjustments.

Carbamazepine. In a randomized double-blind trial, carbamazepine was superior to lorazepam in preventing rebound withdrawal symptoms and reducing post-treatment drinking, although both agents were effective in decreasing withdrawal symptoms.² Avoid this agent in patients with serum liver enzymes 3 times higher than normal values, renal disease, neuropathy, thrombocytopenia, or leukopenia. Drug–drug interactions typically are not of concern unless a patient takes carbamazepine for several weeks.

Divalproex with as-needed benzodiazepines reduces the duration of withdrawal and risk of medical complications.³ Avoid using divalproex in patients with thrombocytopenia, leukopenia, or severe liver disease.

Alcohol withdrawal is an uncomfortable and potentially life-threatening condition that must be treated before patients can achieve sobriety. Benzodiazepines remain the first-line treatment for alcohol withdrawal; however, these agents could:

• exacerbate agitation
• interact adversely with other medications, particularly opioids
• be unsafe for outpatients at risk of drinking again.
  

Off-label use of anticonvulsants could reduce these risks. In our emergency department, we routinely use these agents as monotherapy for patients discharging to outpatient detoxification or as adjunctive treatment for patients who require admission for severe withdrawal (Table^1,2).

Gabapentin is safe for patients with liver disease and has few drug–drug interactions.¹ Dosages of at least 1,200 mg/d seems to be comparable to lorazepam for alcohol withdrawal and could help prevent relapse after the withdrawal period.¹ Many patients report that gabapentin helps them sleep. Gabapentin could cause gastrointestinal upset or slight dizziness; patients with severe renal disease might require dosage adjustments.

Carbamazepine. In a randomized double-blind trial, carbamazepine was superior to lorazepam in preventing rebound withdrawal symptoms and reducing post-treatment drinking, although both agents were effective in decreasing withdrawal symptoms.² Avoid this agent in patients with serum liver enzymes 3 times higher than normal values, renal disease, neuropathy, thrombocytopenia, or leukopenia. Drug–drug interactions typically are not of concern unless a patient takes carbamazepine for several weeks.

Divalproex with as-needed benzodiazepines reduces the duration of withdrawal and risk of medical complications.³ Avoid using divalproex in patients with thrombocytopenia, leukopenia, or severe liver disease.

Mr. S, age 43, has schizophrenia and been stable on clozapine for 6 years after several other antipsychotic regimens failed. Mr. S also has a history of hypertension, dyslipidemia, and gastroesophageal reflux disorder. His medication regimen includes clozapine, 400 mg/d, lisinopril, 20 mg/d, atorvastatin, 40 mg/d, omeprazole, 40 mg/d, and a multivitamin. During routine blood monitoring, Mr. S shows a significant drop in absolute neutrophil count (ANC) (750/µL) (reference range, 1,500 to 8,000 µL). Mr. S , who is African American, has no history of benign ethnic neutropenia (BEN) or ANC <1,000/µL. While reviewing his chart, clinicians note that Mr. S had an ANC of 1,350/µL3 years earlier in 2013. Because a complete workup reveals no other cause for this lab abnormality, we determine that is clozapine-induced. Mr. S’s physician asks about treatment options that would allow him to stay on clozapine.

Because of clozapine’s efficacy in treatment-resistant schizophrenia, many psychiatrists aim to

Clozapine-induced neutropenia

Clozapine was approved in 1989 for managing treatment-resistant schizophrenia after demonstrating better efficacy than chlorpromazine.¹ However, the adverse effects of neutropenia (white blood cell count [WBC] <3,000/μL) and agranulocytosis (ANC <500/μL³) leading to death were reported in later studies.^2,3 One study in the United Kingdom and Ireland reported a prevalence of 2.9% for neutropenia and 0.8% for agranulocytosis among patients taking clozapine.³ Because of this risk, the FDA mandated WBC and ANC monitoring before initiating clozapine and periodically thereafter. In October 2015, the Risk Evaluation and Mitigation Strategies program for clozapine updated recommended ANC levels and eliminated WBC monitoring. ANC monitoring frequencies are summarized in the Table.¹

The exact mechanism of clozapine-induced neutropenia is unknown, although it is possible it stems from the drug’s effect on white blood cell precursors.² Neutropenia typically appears within 3 months of clozapine initiation; however, delayed cases have been reported. Additionally, the risk is higher in certain patient populations (African heritage, Yemenite, West Indians, and Arab). Patients with a lower ANC at clozapine initiation and advanced age appear to be at higher risk.²

Filgrastim

The use of granulocyte-colony stimulating factor, such as filgrastim, often is viewed as a “rescue” treatment. Filgrastim’s mechanism of action is related to neutrophil production and proliferation. Several articles from the 1990s reported efficacy in the short-term management of low WBC or ANC. However, few articles, mainly case reports, have looked at long-term use of these agents. One article examined 3 patients, average age 45, who developed neutropenia during clozapine treatment.⁴ Filgrastim at an average dosage of 0.6 to 0.9 mg/week was used successfully. The dosage was reduced to 0.3 mg/week in 1 patient, although neutropenia returned.

Because of the lack of literature regarding long-term therapy, it is recommended to consider short-term treatment with filgrastim to normalize ANC after a severe drop in a symptomatic patient. Physicians also must consider the potential barriers to filgrastim treatment including adverse effects, such as allergic reactions, bone pain, and thrombocytopenia, and high cost.

Adjunctive lithium

Lithium could cause leukocytosis, which could balance neutropenia induced by clozapine. One of the largest studies evaluating lithium therapy with clozapine-induced neutropenia and agranulocytosis studied 25 patients taking clozapine with a previous “red result” (WBC <3,000/μL, ANC <1,500/μL, or platelets <50,000/μL).³ Lithium treatment was started before or simultaneously with the reinitiation of clozapine in most patients; the remaining patients started treatment at a later date. Only 1 of 25 patients experienced a repeat “red result.” The average lithium level was 0.54 mEq/L.

It is important to remember that initiating adjunctive lithium carries risk. Adverse effects include gastrointestinal upset, tremors, polyuria, polydipsia, and nephrotoxicity.

Additionally, there is risk that lithium simply masks the preliminary states of neutropenia leading to a more severe agranulocytosis without warning.³ Again, the mechanism of action of clozapine-induced neutropenia is thought to be related to the drug’s effect on WBC precursors. The mechanism of lithium-induced leukocytosis is unknown, therefore it’s possible that lithium will not protect a patient from clozapine-induced neutropenia or agranulocytosis, and can lead to serious adverse events.

When deciding whether to rechallenge a patient on clozapine who had a prior episode of moderate or severe neutropenia or agranulocytosis, a risk vs benefit discussion is necessary. One study found that 20 of 53 patients (38%) experienced a repeat dyscrasia when rechallenged.⁵ Of these patients, most experienced a lower ANC that presented faster and took longer to resolve.⁵ If a patient has experienced true agranulocytosis, the recommendation is to not rechallenge clozapine.

Related Resources
• Clozapine REMS Program. www.clozapinerems.com.
• Newman BM, Newman WJ. Rediscovering clozapine: adverse effects develop—what should you do now? Current Psychiatry. 2016;15(8):40-46,48,49.
• Whiskey E, Taylor D. Restarting clozapine after neutropenia: evaluating the possibilities and practicalities. CNS Drugs. 2007;21(1):25-35.

Drug Brand Names
Atorvastatin • Lipitor
Chlorpromazine • Thorazine
Clozapine • Clozaril
Fligrastim • Neupogen
Lisinopril • Prinivil
Lithium • Eskalith, Lithobid
Omeprazole • Prilosec

Mr. S, age 43, has schizophrenia and been stable on clozapine for 6 years after several other antipsychotic regimens failed. Mr. S also has a history of hypertension, dyslipidemia, and gastroesophageal reflux disorder. His medication regimen includes clozapine, 400 mg/d, lisinopril, 20 mg/d, atorvastatin, 40 mg/d, omeprazole, 40 mg/d, and a multivitamin. During routine blood monitoring, Mr. S shows a significant drop in absolute neutrophil count (ANC) (750/µL) (reference range, 1,500 to 8,000 µL). Mr. S , who is African American, has no history of benign ethnic neutropenia (BEN) or ANC <1,000/µL. While reviewing his chart, clinicians note that Mr. S had an ANC of 1,350/µL3 years earlier in 2013. Because a complete workup reveals no other cause for this lab abnormality, we determine that is clozapine-induced. Mr. S’s physician asks about treatment options that would allow him to stay on clozapine.

Because of clozapine’s efficacy in treatment-resistant schizophrenia, many psychiatrists aim to

Clozapine-induced neutropenia

Clozapine was approved in 1989 for managing treatment-resistant schizophrenia after demonstrating better efficacy than chlorpromazine.¹ However, the adverse effects of neutropenia (white blood cell count [WBC] <3,000/μL) and agranulocytosis (ANC <500/μL³) leading to death were reported in later studies.^2,3 One study in the United Kingdom and Ireland reported a prevalence of 2.9% for neutropenia and 0.8% for agranulocytosis among patients taking clozapine.³ Because of this risk, the FDA mandated WBC and ANC monitoring before initiating clozapine and periodically thereafter. In October 2015, the Risk Evaluation and Mitigation Strategies program for clozapine updated recommended ANC levels and eliminated WBC monitoring. ANC monitoring frequencies are summarized in the Table.¹

The exact mechanism of clozapine-induced neutropenia is unknown, although it is possible it stems from the drug’s effect on white blood cell precursors.² Neutropenia typically appears within 3 months of clozapine initiation; however, delayed cases have been reported. Additionally, the risk is higher in certain patient populations (African heritage, Yemenite, West Indians, and Arab). Patients with a lower ANC at clozapine initiation and advanced age appear to be at higher risk.²

Filgrastim

The use of granulocyte-colony stimulating factor, such as filgrastim, often is viewed as a “rescue” treatment. Filgrastim’s mechanism of action is related to neutrophil production and proliferation. Several articles from the 1990s reported efficacy in the short-term management of low WBC or ANC. However, few articles, mainly case reports, have looked at long-term use of these agents. One article examined 3 patients, average age 45, who developed neutropenia during clozapine treatment.⁴ Filgrastim at an average dosage of 0.6 to 0.9 mg/week was used successfully. The dosage was reduced to 0.3 mg/week in 1 patient, although neutropenia returned.

Because of the lack of literature regarding long-term therapy, it is recommended to consider short-term treatment with filgrastim to normalize ANC after a severe drop in a symptomatic patient. Physicians also must consider the potential barriers to filgrastim treatment including adverse effects, such as allergic reactions, bone pain, and thrombocytopenia, and high cost.

Adjunctive lithium

Lithium could cause leukocytosis, which could balance neutropenia induced by clozapine. One of the largest studies evaluating lithium therapy with clozapine-induced neutropenia and agranulocytosis studied 25 patients taking clozapine with a previous “red result” (WBC <3,000/μL, ANC <1,500/μL, or platelets <50,000/μL).³ Lithium treatment was started before or simultaneously with the reinitiation of clozapine in most patients; the remaining patients started treatment at a later date. Only 1 of 25 patients experienced a repeat “red result.” The average lithium level was 0.54 mEq/L.

It is important to remember that initiating adjunctive lithium carries risk. Adverse effects include gastrointestinal upset, tremors, polyuria, polydipsia, and nephrotoxicity.

Additionally, there is risk that lithium simply masks the preliminary states of neutropenia leading to a more severe agranulocytosis without warning.³ Again, the mechanism of action of clozapine-induced neutropenia is thought to be related to the drug’s effect on WBC precursors. The mechanism of lithium-induced leukocytosis is unknown, therefore it’s possible that lithium will not protect a patient from clozapine-induced neutropenia or agranulocytosis, and can lead to serious adverse events.

When deciding whether to rechallenge a patient on clozapine who had a prior episode of moderate or severe neutropenia or agranulocytosis, a risk vs benefit discussion is necessary. One study found that 20 of 53 patients (38%) experienced a repeat dyscrasia when rechallenged.⁵ Of these patients, most experienced a lower ANC that presented faster and took longer to resolve.⁵ If a patient has experienced true agranulocytosis, the recommendation is to not rechallenge clozapine.

Related Resources
• Clozapine REMS Program. www.clozapinerems.com.
• Newman BM, Newman WJ. Rediscovering clozapine: adverse effects develop—what should you do now? Current Psychiatry. 2016;15(8):40-46,48,49.
• Whiskey E, Taylor D. Restarting clozapine after neutropenia: evaluating the possibilities and practicalities. CNS Drugs. 2007;21(1):25-35.

Drug Brand Names
Atorvastatin • Lipitor
Chlorpromazine • Thorazine
Clozapine • Clozaril
Fligrastim • Neupogen
Lisinopril • Prinivil
Lithium • Eskalith, Lithobid
Omeprazole • Prilosec

Mr. S, age 43, has schizophrenia and been stable on clozapine for 6 years after several other antipsychotic regimens failed. Mr. S also has a history of hypertension, dyslipidemia, and gastroesophageal reflux disorder. His medication regimen includes clozapine, 400 mg/d, lisinopril, 20 mg/d, atorvastatin, 40 mg/d, omeprazole, 40 mg/d, and a multivitamin. During routine blood monitoring, Mr. S shows a significant drop in absolute neutrophil count (ANC) (750/µL) (reference range, 1,500 to 8,000 µL). Mr. S , who is African American, has no history of benign ethnic neutropenia (BEN) or ANC <1,000/µL. While reviewing his chart, clinicians note that Mr. S had an ANC of 1,350/µL3 years earlier in 2013. Because a complete workup reveals no other cause for this lab abnormality, we determine that is clozapine-induced. Mr. S’s physician asks about treatment options that would allow him to stay on clozapine.

Because of clozapine’s efficacy in treatment-resistant schizophrenia, many psychiatrists aim to

Clozapine-induced neutropenia

Clozapine was approved in 1989 for managing treatment-resistant schizophrenia after demonstrating better efficacy than chlorpromazine.¹ However, the adverse effects of neutropenia (white blood cell count [WBC] <3,000/μL) and agranulocytosis (ANC <500/μL³) leading to death were reported in later studies.^2,3 One study in the United Kingdom and Ireland reported a prevalence of 2.9% for neutropenia and 0.8% for agranulocytosis among patients taking clozapine.³ Because of this risk, the FDA mandated WBC and ANC monitoring before initiating clozapine and periodically thereafter. In October 2015, the Risk Evaluation and Mitigation Strategies program for clozapine updated recommended ANC levels and eliminated WBC monitoring. ANC monitoring frequencies are summarized in the Table.¹

The exact mechanism of clozapine-induced neutropenia is unknown, although it is possible it stems from the drug’s effect on white blood cell precursors.² Neutropenia typically appears within 3 months of clozapine initiation; however, delayed cases have been reported. Additionally, the risk is higher in certain patient populations (African heritage, Yemenite, West Indians, and Arab). Patients with a lower ANC at clozapine initiation and advanced age appear to be at higher risk.²

Filgrastim

The use of granulocyte-colony stimulating factor, such as filgrastim, often is viewed as a “rescue” treatment. Filgrastim’s mechanism of action is related to neutrophil production and proliferation. Several articles from the 1990s reported efficacy in the short-term management of low WBC or ANC. However, few articles, mainly case reports, have looked at long-term use of these agents. One article examined 3 patients, average age 45, who developed neutropenia during clozapine treatment.⁴ Filgrastim at an average dosage of 0.6 to 0.9 mg/week was used successfully. The dosage was reduced to 0.3 mg/week in 1 patient, although neutropenia returned.

Because of the lack of literature regarding long-term therapy, it is recommended to consider short-term treatment with filgrastim to normalize ANC after a severe drop in a symptomatic patient. Physicians also must consider the potential barriers to filgrastim treatment including adverse effects, such as allergic reactions, bone pain, and thrombocytopenia, and high cost.

Adjunctive lithium

Lithium could cause leukocytosis, which could balance neutropenia induced by clozapine. One of the largest studies evaluating lithium therapy with clozapine-induced neutropenia and agranulocytosis studied 25 patients taking clozapine with a previous “red result” (WBC <3,000/μL, ANC <1,500/μL, or platelets <50,000/μL).³ Lithium treatment was started before or simultaneously with the reinitiation of clozapine in most patients; the remaining patients started treatment at a later date. Only 1 of 25 patients experienced a repeat “red result.” The average lithium level was 0.54 mEq/L.

It is important to remember that initiating adjunctive lithium carries risk. Adverse effects include gastrointestinal upset, tremors, polyuria, polydipsia, and nephrotoxicity.

Additionally, there is risk that lithium simply masks the preliminary states of neutropenia leading to a more severe agranulocytosis without warning.³ Again, the mechanism of action of clozapine-induced neutropenia is thought to be related to the drug’s effect on WBC precursors. The mechanism of lithium-induced leukocytosis is unknown, therefore it’s possible that lithium will not protect a patient from clozapine-induced neutropenia or agranulocytosis, and can lead to serious adverse events.

When deciding whether to rechallenge a patient on clozapine who had a prior episode of moderate or severe neutropenia or agranulocytosis, a risk vs benefit discussion is necessary. One study found that 20 of 53 patients (38%) experienced a repeat dyscrasia when rechallenged.⁵ Of these patients, most experienced a lower ANC that presented faster and took longer to resolve.⁵ If a patient has experienced true agranulocytosis, the recommendation is to not rechallenge clozapine.

Related Resources
• Clozapine REMS Program. www.clozapinerems.com.
• Newman BM, Newman WJ. Rediscovering clozapine: adverse effects develop—what should you do now? Current Psychiatry. 2016;15(8):40-46,48,49.
• Whiskey E, Taylor D. Restarting clozapine after neutropenia: evaluating the possibilities and practicalities. CNS Drugs. 2007;21(1):25-35.

Drug Brand Names
Atorvastatin • Lipitor
Chlorpromazine • Thorazine
Clozapine • Clozaril
Fligrastim • Neupogen
Lisinopril • Prinivil
Lithium • Eskalith, Lithobid
Omeprazole • Prilosec

CASE Suicidal and hungry

Mr. L, age 59, attempts suicide by taking approximately 20 acetaminophen tablets of unknown dosage. He immediately comes to the emergency department where blood work reveals a 4-hour acetaminophen level of 94.8 μg/mL (therapeutic range, 10 to 30 μg/mL; toxic range, >150 μg/mL); administration of N-acetylcysteine is unnecessary. Mr. L is admitted to general medical services for monitoring and is transferred to our unit for psychiatric evaluation and management.

During our initial interview, Mr. L, who has a developmental disability, is grossly oriented and generally cooperative, reporting depressed mood with an irritable affect. He is preoccupied with having limited funds and repeatedly states he is worried that he can’t buy food, but says that the hospital could help by providing for him. Mr. L states that his depressed mood is directly related to his financial situation and, that if he had more money, he would not be suicidal. He cites worsening visual impairment that requires surgery as an additional stressor.

On several occasions, Mr. L states that the only way to help him is to give him $600 so that he can buy food and pay for medical treatment. Mr. L says he does not feel supported by his family, despite having a sister who lives nearby.

What would you include in the differential diagnosis for Mr. L?

a) major depressive disorder (MDD)
b) depression secondary to a medical condition
c) neurocognitive disorder
d) adjustment disorder with depressive features
e) factitious disorder

The authors’ observations

Our differential diagnosis included MDD, adjustment disorder, neurocognitive disorder, and factitious disorder. He did not meet criteria for MDD because he did not have excessive guilt, loss of interest, change in sleep or appetite, psychomotor dysregulation, or change in energy level. Although suicidal behavior could indicate MDD, the fact that he immediately walked to the hospital after taking an excessive amount of acetaminophen suggests that he did not want to die. Further, he attributed his suicidal thoughts to environmental stressors. Similarly, we ruled out adjustment disorder because he had no reported or observed changes in mood or anxiety. Although financial difficulties might have overwhelmed his limited coping abilities, he took too much acetaminophen to ensure that he was hospitalized. His motivation for seeking hospitalization ruled out factitious disorder. Mr. L has a developmental disability, but information obtained from collateral sources ruled out an acute change to cognitive functioning.

HISTORY Repeated admissions

Mr. L has a history of a psychiatric hospitalization 3 weeks prior to this admission. He presented to an emergency department stating that his blood glucose was low. Mr. L was noted to be confused and anxious and said he was convinced he was going to die. At that time, his thought content was hyper-religious and he claimed he could hear the devil. Mr. L was hospitalized and started on low-dosage risperidone. At discharge, he declined referral for outpatient mental health treatment because he denied having a mental illness. However, he was amenable to follow up at a wellness clinic.

Mr. L has worked at a local supermarket for 19 years and has lived independently throughout his adult life. After he returned to the community, he was repeatedly absent from work, which further exacerbated his financial strain. He attended a follow-up outpatient appointment but reported, “They didn’t help me,” although it was unclear what he meant.

Between admissions to our hospital, Mr. L had 2 visits to an emergency department, the first time saying he felt depressed and the second reporting he attempted suicide by taking 5 acetaminophen tablets. On both occasions he requested placement in a residential facility but was discharged home after an initial assessment. Emergency room records indicated that Mr. L stated, “If you cannot give me money for food, then there is no use and I would rather die.”

What is the most likely DSM-5 diagnosis for Mr. L?

a) schizophrenia
b) malingering
c) brief psychotic disorder
d) dependent personality disorder

The authors’ observations

Malingering in DSM-5 is defined as the “intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives.”¹ These external incentives include financial compensation, avoiding military duties, evading criminal charges, and avoiding work, and are collectively considered as secondary gain. Although not considered a diagnosis in the strictest sense, clinicians must differentiate malingering from other psychiatric disorders. In the literature, case reports describe patients who feigned an array of symptoms including those of posttraumatic stress disorder, paraphilias, cognitive dysfunction, depression, anxiety, and psychosis.^2-5

In Mr. L’s case, malingering presented as suicidal behavior with an inadvertently high fatality risk. Notably, Mr. L came to an emergency room a few days before this admission after swallowing 5 acetaminophen tablets in a suicide attempt, which did not lead to a medical or psychiatric hospitalization. In an attempt to ensure admission, Mr. L then took a potentially lethal dose of 20 acetaminophen tablets. In our assessment and according to his statements, the primary motivation for the suicide attempt was to obtain reliable food and housing. Mr. L’s developmental disability might have contributed to a relative lack of understanding of the consequences of his actions. In addition, poor overall communication and coping skills led to an exaggerated response to psychosocial stressors.

Malingering and suicide attempts

Few studies have investigated malingering in regards to suicide and other psychiatric emergencies. In a study of 227 consecutive psychiatric emergencies assessed for evidence of malingering, 13% were thought to be feigned or exaggerated.⁶ Interestingly, the most commonly reported secondary gain was food and shelter, similar to Mr. L. This study did not report the types of psychiatric emergencies, therefore suicidal actions associated with malingering could not be evaluated.

In another study, 40 patients hospitalized for suicidal ideation (n = 29, 72%) or suicidal gestures (n = 11, 28%) in a large, urban tertiary care center were evaluated for malingering by anonymous report of feigned or exaggerated symptoms.⁷ Most of these patients were diagnosed with a mood disorder (28%) and/or an adjustment disorder (53%). Four (10%) admitted to malingering. Among the malingerers, reasons for feigning illness included:

• wanting to be hospitalized
• wanting to make someone angry or feel sorry
• gaining access to detoxification programs
• getting treatment for emotional problems.

Interestingly, an analysis of demographic factors associated with malingering reveals an association with suicide attempts but not persistent suicidal ideations. This could be because of selection bias; patients who reported a suicide attempt might be more likely to be hospitalized.

A follow-up study⁸ evaluated 50 additional consecutive psychiatric inpatients admitted to the same tertiary care hospital for suicide risk. Unlike the previous study, a larger proportion of these patients had made a suicide attempt (n = 21, 42%) and a greater number had made a previous suicide attempt (n = 33, 66%). Primary mood disorders comprised most of the psychiatric diagnoses (n = 28, 56%). In this study, the exact nature of the suicide gestures was not documented, leaving open the question of lethality of the attempts. These studies do not suggest that those who malinger are not at risk for suicide, only that these patients tend to exaggerate the severity of their ideations or behaviors.

OUTCOME Reluctantly discharged

We contact Mr. L’s siblings, who offer to provide temporary housing and financial support and assist him with medical needs. This abated Mr. L’s suicidal ideation; however, he wishes to remain in the hospital with the goals of obtaining eyeglasses and dentures. We explain that psychiatric hospitalization is no longer indicated and he is discharged.

Which of the following is the most effective management strategy for malingering?

a) direct confrontation of the malingering patient
b) immediate discharge once malingering is identified

c) evaluation for possible comorbid psychiatric conditions

d) neuropsychiatric consultation

The authors’ observations

The challenges of treating patients who malinger include clinician uncertainty in making the diagnosis and high variability in occurrence across settings (Table 1). Current estimates indicate that 4% to 8% of medical and psychiatric cases not involved in litigation or compensation have an element of feigned symptoms.^3,9 The rate could be higher in specific circumstances such as medicolegal disputes and criminal cases.¹⁰

The societal impact of malingering is significant. Therefore, identifying these patients is an important clinical intervention that can have a wide impact.¹¹ However, it is also important to acknowledge that genuine psychiatric illness could be comorbid with malingering. Although differentiating a patient’s true from feigned symptoms can be difficult, it is critical to carefully evaluate the patient in order to provide the best treatment.

It seems that physicians can detect malingering, but documentation often is not provided. In the Rissmiller et al study,⁷ all 4 cases of malingering were identified retrospectively by study psychiatrists; however, none of their medical records included documentation of malingering, a finding also reported in the Yates et al study.⁶ Also concerning, the clinicians suspected malingering in some patients who were not feigning symptoms, suggesting that a relatively high threshold is necessary for making the diagnosis.

How to help patients who malinger

Identifying malingering in patients with obvious secondary gain is important to prevent exposure to potential adverse effects of medication and unnecessary use of medical resources. In addition, obtaining collateral information, records from previous admissions or outpatient treatment, and psychological testing adds to the body of evidence suggesting malingering. We also recommend a comprehensive psychosocial evaluation to identify the presence of secondary gain.

Management of malingering (Table 2) includes building a strong therapeutic alliance, exploring reasons for feigning symptoms, open discussion of inciting external factors such as interpersonal conflict or difficulties at work, and/or confrontation.¹⁰ In addition, supportive psychotherapy might help strengthen coping mechanisms and problem solving strategies, thereby removing the need for secondary gain.¹² Additionally, face-saving mechanisms that allow the patient to discard their feigned symptoms, or enable the person to alter his (her) history, could be to his benefit. Lastly, and importantly, clinicians should focus efforts on ruling out or effectively treating comorbid psychiatric conditions.

From a risk management standpoint, include all available data to support the malingering diagnosis in your progress notes and discharge summaries. A clinician seeking to discharge a patient suspected of malingering who is still endorsing suicidal or homicidal intent will benefit from administrative review, including legal counsel to mitigate risk, and be more confident discharging somebody assessed to be malingering.

We recognize that certain patients could trigger countertransference reactions that impel clinicians to take on a significant caretaking role. Patients skillful at deception could manifest a desire to rescue or save them. In these instances, clinicians should examine why and how these feelings have come about, particularly if there is evidence that the individual could be attempting to use the interaction to achieve secondary gain. Awareness of these feelings could help with the diagnostic formulation. Moreover, a clinician who has such strong feelings might be tempted to abet a patient in achieving the secondary gain, or protect him (her) from the natural consequences of individual’s deception (eg, not discharging a hospitalized patient). This is counter-therapeutic and reinforces maladaptive behaviors and coping processes.¹³

CASE Suicidal and hungry

Mr. L, age 59, attempts suicide by taking approximately 20 acetaminophen tablets of unknown dosage. He immediately comes to the emergency department where blood work reveals a 4-hour acetaminophen level of 94.8 μg/mL (therapeutic range, 10 to 30 μg/mL; toxic range, >150 μg/mL); administration of N-acetylcysteine is unnecessary. Mr. L is admitted to general medical services for monitoring and is transferred to our unit for psychiatric evaluation and management.

During our initial interview, Mr. L, who has a developmental disability, is grossly oriented and generally cooperative, reporting depressed mood with an irritable affect. He is preoccupied with having limited funds and repeatedly states he is worried that he can’t buy food, but says that the hospital could help by providing for him. Mr. L states that his depressed mood is directly related to his financial situation and, that if he had more money, he would not be suicidal. He cites worsening visual impairment that requires surgery as an additional stressor.

On several occasions, Mr. L states that the only way to help him is to give him $600 so that he can buy food and pay for medical treatment. Mr. L says he does not feel supported by his family, despite having a sister who lives nearby.

What would you include in the differential diagnosis for Mr. L?

a) major depressive disorder (MDD)
b) depression secondary to a medical condition
c) neurocognitive disorder
d) adjustment disorder with depressive features
e) factitious disorder

The authors’ observations

Our differential diagnosis included MDD, adjustment disorder, neurocognitive disorder, and factitious disorder. He did not meet criteria for MDD because he did not have excessive guilt, loss of interest, change in sleep or appetite, psychomotor dysregulation, or change in energy level. Although suicidal behavior could indicate MDD, the fact that he immediately walked to the hospital after taking an excessive amount of acetaminophen suggests that he did not want to die. Further, he attributed his suicidal thoughts to environmental stressors. Similarly, we ruled out adjustment disorder because he had no reported or observed changes in mood or anxiety. Although financial difficulties might have overwhelmed his limited coping abilities, he took too much acetaminophen to ensure that he was hospitalized. His motivation for seeking hospitalization ruled out factitious disorder. Mr. L has a developmental disability, but information obtained from collateral sources ruled out an acute change to cognitive functioning.

HISTORY Repeated admissions

Mr. L has a history of a psychiatric hospitalization 3 weeks prior to this admission. He presented to an emergency department stating that his blood glucose was low. Mr. L was noted to be confused and anxious and said he was convinced he was going to die. At that time, his thought content was hyper-religious and he claimed he could hear the devil. Mr. L was hospitalized and started on low-dosage risperidone. At discharge, he declined referral for outpatient mental health treatment because he denied having a mental illness. However, he was amenable to follow up at a wellness clinic.

Mr. L has worked at a local supermarket for 19 years and has lived independently throughout his adult life. After he returned to the community, he was repeatedly absent from work, which further exacerbated his financial strain. He attended a follow-up outpatient appointment but reported, “They didn’t help me,” although it was unclear what he meant.

Between admissions to our hospital, Mr. L had 2 visits to an emergency department, the first time saying he felt depressed and the second reporting he attempted suicide by taking 5 acetaminophen tablets. On both occasions he requested placement in a residential facility but was discharged home after an initial assessment. Emergency room records indicated that Mr. L stated, “If you cannot give me money for food, then there is no use and I would rather die.”

What is the most likely DSM-5 diagnosis for Mr. L?

a) schizophrenia
b) malingering
c) brief psychotic disorder
d) dependent personality disorder

The authors’ observations

Malingering in DSM-5 is defined as the “intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives.”¹ These external incentives include financial compensation, avoiding military duties, evading criminal charges, and avoiding work, and are collectively considered as secondary gain. Although not considered a diagnosis in the strictest sense, clinicians must differentiate malingering from other psychiatric disorders. In the literature, case reports describe patients who feigned an array of symptoms including those of posttraumatic stress disorder, paraphilias, cognitive dysfunction, depression, anxiety, and psychosis.^2-5

In Mr. L’s case, malingering presented as suicidal behavior with an inadvertently high fatality risk. Notably, Mr. L came to an emergency room a few days before this admission after swallowing 5 acetaminophen tablets in a suicide attempt, which did not lead to a medical or psychiatric hospitalization. In an attempt to ensure admission, Mr. L then took a potentially lethal dose of 20 acetaminophen tablets. In our assessment and according to his statements, the primary motivation for the suicide attempt was to obtain reliable food and housing. Mr. L’s developmental disability might have contributed to a relative lack of understanding of the consequences of his actions. In addition, poor overall communication and coping skills led to an exaggerated response to psychosocial stressors.

Malingering and suicide attempts

Few studies have investigated malingering in regards to suicide and other psychiatric emergencies. In a study of 227 consecutive psychiatric emergencies assessed for evidence of malingering, 13% were thought to be feigned or exaggerated.⁶ Interestingly, the most commonly reported secondary gain was food and shelter, similar to Mr. L. This study did not report the types of psychiatric emergencies, therefore suicidal actions associated with malingering could not be evaluated.

In another study, 40 patients hospitalized for suicidal ideation (n = 29, 72%) or suicidal gestures (n = 11, 28%) in a large, urban tertiary care center were evaluated for malingering by anonymous report of feigned or exaggerated symptoms.⁷ Most of these patients were diagnosed with a mood disorder (28%) and/or an adjustment disorder (53%). Four (10%) admitted to malingering. Among the malingerers, reasons for feigning illness included:

• wanting to be hospitalized
• wanting to make someone angry or feel sorry
• gaining access to detoxification programs
• getting treatment for emotional problems.

Interestingly, an analysis of demographic factors associated with malingering reveals an association with suicide attempts but not persistent suicidal ideations. This could be because of selection bias; patients who reported a suicide attempt might be more likely to be hospitalized.

A follow-up study⁸ evaluated 50 additional consecutive psychiatric inpatients admitted to the same tertiary care hospital for suicide risk. Unlike the previous study, a larger proportion of these patients had made a suicide attempt (n = 21, 42%) and a greater number had made a previous suicide attempt (n = 33, 66%). Primary mood disorders comprised most of the psychiatric diagnoses (n = 28, 56%). In this study, the exact nature of the suicide gestures was not documented, leaving open the question of lethality of the attempts. These studies do not suggest that those who malinger are not at risk for suicide, only that these patients tend to exaggerate the severity of their ideations or behaviors.

OUTCOME Reluctantly discharged

We contact Mr. L’s siblings, who offer to provide temporary housing and financial support and assist him with medical needs. This abated Mr. L’s suicidal ideation; however, he wishes to remain in the hospital with the goals of obtaining eyeglasses and dentures. We explain that psychiatric hospitalization is no longer indicated and he is discharged.

Which of the following is the most effective management strategy for malingering?

a) direct confrontation of the malingering patient
b) immediate discharge once malingering is identified

c) evaluation for possible comorbid psychiatric conditions

d) neuropsychiatric consultation

The authors’ observations

The challenges of treating patients who malinger include clinician uncertainty in making the diagnosis and high variability in occurrence across settings (Table 1). Current estimates indicate that 4% to 8% of medical and psychiatric cases not involved in litigation or compensation have an element of feigned symptoms.^3,9 The rate could be higher in specific circumstances such as medicolegal disputes and criminal cases.¹⁰

The societal impact of malingering is significant. Therefore, identifying these patients is an important clinical intervention that can have a wide impact.¹¹ However, it is also important to acknowledge that genuine psychiatric illness could be comorbid with malingering. Although differentiating a patient’s true from feigned symptoms can be difficult, it is critical to carefully evaluate the patient in order to provide the best treatment.

It seems that physicians can detect malingering, but documentation often is not provided. In the Rissmiller et al study,⁷ all 4 cases of malingering were identified retrospectively by study psychiatrists; however, none of their medical records included documentation of malingering, a finding also reported in the Yates et al study.⁶ Also concerning, the clinicians suspected malingering in some patients who were not feigning symptoms, suggesting that a relatively high threshold is necessary for making the diagnosis.

How to help patients who malinger

Identifying malingering in patients with obvious secondary gain is important to prevent exposure to potential adverse effects of medication and unnecessary use of medical resources. In addition, obtaining collateral information, records from previous admissions or outpatient treatment, and psychological testing adds to the body of evidence suggesting malingering. We also recommend a comprehensive psychosocial evaluation to identify the presence of secondary gain.

Management of malingering (Table 2) includes building a strong therapeutic alliance, exploring reasons for feigning symptoms, open discussion of inciting external factors such as interpersonal conflict or difficulties at work, and/or confrontation.¹⁰ In addition, supportive psychotherapy might help strengthen coping mechanisms and problem solving strategies, thereby removing the need for secondary gain.¹² Additionally, face-saving mechanisms that allow the patient to discard their feigned symptoms, or enable the person to alter his (her) history, could be to his benefit. Lastly, and importantly, clinicians should focus efforts on ruling out or effectively treating comorbid psychiatric conditions.

From a risk management standpoint, include all available data to support the malingering diagnosis in your progress notes and discharge summaries. A clinician seeking to discharge a patient suspected of malingering who is still endorsing suicidal or homicidal intent will benefit from administrative review, including legal counsel to mitigate risk, and be more confident discharging somebody assessed to be malingering.

We recognize that certain patients could trigger countertransference reactions that impel clinicians to take on a significant caretaking role. Patients skillful at deception could manifest a desire to rescue or save them. In these instances, clinicians should examine why and how these feelings have come about, particularly if there is evidence that the individual could be attempting to use the interaction to achieve secondary gain. Awareness of these feelings could help with the diagnostic formulation. Moreover, a clinician who has such strong feelings might be tempted to abet a patient in achieving the secondary gain, or protect him (her) from the natural consequences of individual’s deception (eg, not discharging a hospitalized patient). This is counter-therapeutic and reinforces maladaptive behaviors and coping processes.¹³

CASE Suicidal and hungry

Mr. L, age 59, attempts suicide by taking approximately 20 acetaminophen tablets of unknown dosage. He immediately comes to the emergency department where blood work reveals a 4-hour acetaminophen level of 94.8 μg/mL (therapeutic range, 10 to 30 μg/mL; toxic range, >150 μg/mL); administration of N-acetylcysteine is unnecessary. Mr. L is admitted to general medical services for monitoring and is transferred to our unit for psychiatric evaluation and management.

During our initial interview, Mr. L, who has a developmental disability, is grossly oriented and generally cooperative, reporting depressed mood with an irritable affect. He is preoccupied with having limited funds and repeatedly states he is worried that he can’t buy food, but says that the hospital could help by providing for him. Mr. L states that his depressed mood is directly related to his financial situation and, that if he had more money, he would not be suicidal. He cites worsening visual impairment that requires surgery as an additional stressor.

On several occasions, Mr. L states that the only way to help him is to give him $600 so that he can buy food and pay for medical treatment. Mr. L says he does not feel supported by his family, despite having a sister who lives nearby.

What would you include in the differential diagnosis for Mr. L?

a) major depressive disorder (MDD)
b) depression secondary to a medical condition
c) neurocognitive disorder
d) adjustment disorder with depressive features
e) factitious disorder

The authors’ observations

Our differential diagnosis included MDD, adjustment disorder, neurocognitive disorder, and factitious disorder. He did not meet criteria for MDD because he did not have excessive guilt, loss of interest, change in sleep or appetite, psychomotor dysregulation, or change in energy level. Although suicidal behavior could indicate MDD, the fact that he immediately walked to the hospital after taking an excessive amount of acetaminophen suggests that he did not want to die. Further, he attributed his suicidal thoughts to environmental stressors. Similarly, we ruled out adjustment disorder because he had no reported or observed changes in mood or anxiety. Although financial difficulties might have overwhelmed his limited coping abilities, he took too much acetaminophen to ensure that he was hospitalized. His motivation for seeking hospitalization ruled out factitious disorder. Mr. L has a developmental disability, but information obtained from collateral sources ruled out an acute change to cognitive functioning.

HISTORY Repeated admissions

Mr. L has a history of a psychiatric hospitalization 3 weeks prior to this admission. He presented to an emergency department stating that his blood glucose was low. Mr. L was noted to be confused and anxious and said he was convinced he was going to die. At that time, his thought content was hyper-religious and he claimed he could hear the devil. Mr. L was hospitalized and started on low-dosage risperidone. At discharge, he declined referral for outpatient mental health treatment because he denied having a mental illness. However, he was amenable to follow up at a wellness clinic.

Mr. L has worked at a local supermarket for 19 years and has lived independently throughout his adult life. After he returned to the community, he was repeatedly absent from work, which further exacerbated his financial strain. He attended a follow-up outpatient appointment but reported, “They didn’t help me,” although it was unclear what he meant.

Between admissions to our hospital, Mr. L had 2 visits to an emergency department, the first time saying he felt depressed and the second reporting he attempted suicide by taking 5 acetaminophen tablets. On both occasions he requested placement in a residential facility but was discharged home after an initial assessment. Emergency room records indicated that Mr. L stated, “If you cannot give me money for food, then there is no use and I would rather die.”

What is the most likely DSM-5 diagnosis for Mr. L?

a) schizophrenia
b) malingering
c) brief psychotic disorder
d) dependent personality disorder

The authors’ observations

Malingering in DSM-5 is defined as the “intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives.”¹ These external incentives include financial compensation, avoiding military duties, evading criminal charges, and avoiding work, and are collectively considered as secondary gain. Although not considered a diagnosis in the strictest sense, clinicians must differentiate malingering from other psychiatric disorders. In the literature, case reports describe patients who feigned an array of symptoms including those of posttraumatic stress disorder, paraphilias, cognitive dysfunction, depression, anxiety, and psychosis.^2-5

In Mr. L’s case, malingering presented as suicidal behavior with an inadvertently high fatality risk. Notably, Mr. L came to an emergency room a few days before this admission after swallowing 5 acetaminophen tablets in a suicide attempt, which did not lead to a medical or psychiatric hospitalization. In an attempt to ensure admission, Mr. L then took a potentially lethal dose of 20 acetaminophen tablets. In our assessment and according to his statements, the primary motivation for the suicide attempt was to obtain reliable food and housing. Mr. L’s developmental disability might have contributed to a relative lack of understanding of the consequences of his actions. In addition, poor overall communication and coping skills led to an exaggerated response to psychosocial stressors.

Malingering and suicide attempts

Few studies have investigated malingering in regards to suicide and other psychiatric emergencies. In a study of 227 consecutive psychiatric emergencies assessed for evidence of malingering, 13% were thought to be feigned or exaggerated.⁶ Interestingly, the most commonly reported secondary gain was food and shelter, similar to Mr. L. This study did not report the types of psychiatric emergencies, therefore suicidal actions associated with malingering could not be evaluated.

In another study, 40 patients hospitalized for suicidal ideation (n = 29, 72%) or suicidal gestures (n = 11, 28%) in a large, urban tertiary care center were evaluated for malingering by anonymous report of feigned or exaggerated symptoms.⁷ Most of these patients were diagnosed with a mood disorder (28%) and/or an adjustment disorder (53%). Four (10%) admitted to malingering. Among the malingerers, reasons for feigning illness included:

• wanting to be hospitalized
• wanting to make someone angry or feel sorry
• gaining access to detoxification programs
• getting treatment for emotional problems.

Interestingly, an analysis of demographic factors associated with malingering reveals an association with suicide attempts but not persistent suicidal ideations. This could be because of selection bias; patients who reported a suicide attempt might be more likely to be hospitalized.

A follow-up study⁸ evaluated 50 additional consecutive psychiatric inpatients admitted to the same tertiary care hospital for suicide risk. Unlike the previous study, a larger proportion of these patients had made a suicide attempt (n = 21, 42%) and a greater number had made a previous suicide attempt (n = 33, 66%). Primary mood disorders comprised most of the psychiatric diagnoses (n = 28, 56%). In this study, the exact nature of the suicide gestures was not documented, leaving open the question of lethality of the attempts. These studies do not suggest that those who malinger are not at risk for suicide, only that these patients tend to exaggerate the severity of their ideations or behaviors.

OUTCOME Reluctantly discharged

We contact Mr. L’s siblings, who offer to provide temporary housing and financial support and assist him with medical needs. This abated Mr. L’s suicidal ideation; however, he wishes to remain in the hospital with the goals of obtaining eyeglasses and dentures. We explain that psychiatric hospitalization is no longer indicated and he is discharged.

Which of the following is the most effective management strategy for malingering?

a) direct confrontation of the malingering patient
b) immediate discharge once malingering is identified

c) evaluation for possible comorbid psychiatric conditions

d) neuropsychiatric consultation

The authors’ observations

The challenges of treating patients who malinger include clinician uncertainty in making the diagnosis and high variability in occurrence across settings (Table 1). Current estimates indicate that 4% to 8% of medical and psychiatric cases not involved in litigation or compensation have an element of feigned symptoms.^3,9 The rate could be higher in specific circumstances such as medicolegal disputes and criminal cases.¹⁰

The societal impact of malingering is significant. Therefore, identifying these patients is an important clinical intervention that can have a wide impact.¹¹ However, it is also important to acknowledge that genuine psychiatric illness could be comorbid with malingering. Although differentiating a patient’s true from feigned symptoms can be difficult, it is critical to carefully evaluate the patient in order to provide the best treatment.

It seems that physicians can detect malingering, but documentation often is not provided. In the Rissmiller et al study,⁷ all 4 cases of malingering were identified retrospectively by study psychiatrists; however, none of their medical records included documentation of malingering, a finding also reported in the Yates et al study.⁶ Also concerning, the clinicians suspected malingering in some patients who were not feigning symptoms, suggesting that a relatively high threshold is necessary for making the diagnosis.

How to help patients who malinger

Identifying malingering in patients with obvious secondary gain is important to prevent exposure to potential adverse effects of medication and unnecessary use of medical resources. In addition, obtaining collateral information, records from previous admissions or outpatient treatment, and psychological testing adds to the body of evidence suggesting malingering. We also recommend a comprehensive psychosocial evaluation to identify the presence of secondary gain.

Management of malingering (Table 2) includes building a strong therapeutic alliance, exploring reasons for feigning symptoms, open discussion of inciting external factors such as interpersonal conflict or difficulties at work, and/or confrontation.¹⁰ In addition, supportive psychotherapy might help strengthen coping mechanisms and problem solving strategies, thereby removing the need for secondary gain.¹² Additionally, face-saving mechanisms that allow the patient to discard their feigned symptoms, or enable the person to alter his (her) history, could be to his benefit. Lastly, and importantly, clinicians should focus efforts on ruling out or effectively treating comorbid psychiatric conditions.

From a risk management standpoint, include all available data to support the malingering diagnosis in your progress notes and discharge summaries. A clinician seeking to discharge a patient suspected of malingering who is still endorsing suicidal or homicidal intent will benefit from administrative review, including legal counsel to mitigate risk, and be more confident discharging somebody assessed to be malingering.

We recognize that certain patients could trigger countertransference reactions that impel clinicians to take on a significant caretaking role. Patients skillful at deception could manifest a desire to rescue or save them. In these instances, clinicians should examine why and how these feelings have come about, particularly if there is evidence that the individual could be attempting to use the interaction to achieve secondary gain. Awareness of these feelings could help with the diagnostic formulation. Moreover, a clinician who has such strong feelings might be tempted to abet a patient in achieving the secondary gain, or protect him (her) from the natural consequences of individual’s deception (eg, not discharging a hospitalized patient). This is counter-therapeutic and reinforces maladaptive behaviors and coping processes.¹³

Dear Dr. Mossman,
Each month, I see my patient, Mr. R, for a 15-minute medication management appointment. At his latest visit, Mr. R mentioned his financial difficulties. He also observed that our office needed to have some carpentry work done—not a surprise, because he’s known in our area as one of the best carpenters around. He suggested that I hire him as payment for the next 6 appointments. What risks might I encounter if I oblige him?

Submitted by “Dr. Z”

Nearly 29 million Americans are uninsured,¹ and even more have trouble accessing mental health care.² Many psychiatrists struggle to provide affordable services while remaining financially viable.^3,4 For outpatients with limited means to pay for care, spacing appointments to fit their budgets might compromise treatment.⁵ Simply not charging patients poses its own clinical and ethical challenges.^6-8

As a result, some mental health professionals make barter arrangements to help their patients enter or continue treatment. To answer Dr. Z’s question on whether exchanging services might be a way to arrange matters with some patients, we explore:

• the idea of bartering for psychiatric treatment
• related ethical and legal considerations
• when and in what situations bartering might be appropriate.

Think of what I’m saying: Bartering for treatment

“Barter” refers to exchanging commodities, products, or services of equivalent value without using money.⁹ In 2010, Nevada Republican Senate candidate Sue Lowden encouraged barter for health care and harkened back to an earlier time where “they would bring a chicken to the doctor; they would say ‘I’ll paint your house.’”¹⁰

Such payment arrangements have been encouraged as health care has become increasingly commoditized.^11-13 This happens through both direct barter between physician and patient and barter exchanges. Barter exchange systems have been set up on Web sites (as of 2013, at least 400 such online exchanges were available¹⁴), local communities,^11,15 and social programs. For example, through the “Swapping Guns for Therapy” program, psychologists in California gave free or reduced-fee care for people who traded in their guns.¹⁶

Try to see it my way: A prevailing view of barter

Several psychiatrists recommend against bartering for treatment, for a variety of reasons.^7,8,17-19 Simon¹⁸ argues that a stable fee policy is part of a proper therapeutic framework, and money is “the only acceptable medium of exchange when receiving payment from patients.” Emotional distress and the power differential inherent in treatment might prevent a patient from making an accurate assessment of the value of the bartered goods or services,^7,8,17,18,20 which could lead to future claims of undue influence from trading goods or services below market value.¹⁷ To avoid the possibility of exploitating the patient, Simon¹⁸ recommends that the psychiatrist’s professional fee be “the only material benefit received from the patient.”

The American Psychiatric Association’s code of ethics states that “it is not ethical to switch a doctor–patient relationship to an employer–employee one … and, in most cases, such an arrangement would be unethical.”²¹ In some therapeutic settings, employing a patient risks inappropriate self-disclosure and intrusion.¹⁶

More than other physicians, psychiatrists pay special attention to professional boundaries, the technical term for the “edge of appropriate behavior,” within which safe, effective care can occur.^22,23 Although some boundary crossings can be harmless and even constructive, repeated boundary crossings are the forerunners to improper behavior, including sexual relationships with patients.^24-26

Out of concern that bartering could become the first step down a slippery ethical slope toward patient exploitation, mental health clinicians have deemed the practice “ethically troubling,”¹⁹ said it did “not usually work out well,”⁷ and declared it “so fraught with risks for both parties that it seem[ed] illogical to even consider it as an option.”²⁷

While I see it your way: What barter proponents say

Reports of bartering for chickens²⁸ and purchasing fuel from a patient in remote Alaska²⁹ show that not all physicians agree and why they feel that professional codes of ethics reflect an urban bias.^28,29 In many rural areas and small towns, access to mental health services is limited, and patients often interact with their doctors outside of clinical encounters.^23,29-31

Bartering can benefit a physician’s practice by:

• reducing the need to discount services
• eliminating bureaucratic burdens of traditional insurance arrangements
• facilitating development of a patient base
• allowing patients choice and flexibility in seeking medical care.^6,16,32

Bartering could confer certain clinical benefits, such as:

• enhancing trust and empathy³²
• encouraging patients to make their needs known constructively⁶
• modeling financial self-care⁶
• helping the doctor to feel fairly compensated for providing thoughtful care⁶
• acknowledging the patient’s cultural values^15,33
• affirming that patients and doctors both produce things of value.¹⁶

I have always thought: Other ethical models

An ethical approach to bartering that requires careful thought and respect for the patient’s needs appears consistent with a primary goal of treatment: “to increase the capacity of individuals to make more rational choices in their lives and to be relatively freer from disabling conflicts.”²⁰ Some authors criticize slippery-slope arguments and strict-rule ethical approaches as being too rigid, limiting, or risk-averse.^22,26,34 In Table 1,^{6,8,16,18,27,29-31,35-37} we list several factors that might weigh for or against a decision to enter into a barter arrangement as payment for care.

In a similar manner, Martinez^33,38 proposed a graded-risk framework that encourages examination of potential harms and benefits of a decision, potential coercive or exploitative elements, the clinician’s intentions and aspiration to professional ideals, and the context of the decision. Within this framework, some bartering arrangements might be encouraged and, perhaps, even obligatory because of the potential benefits to the patient; other arrangements (eg, trading psychotherapy for menial services) might be unjustifiable. Martinez³⁸ argues that this approach fosters mutual decision-making with patients, discourages physician paternalism, and “demands that we struggle with the particulars with each case.”

Gottlieb’s decision-making model³⁵ recognizes that trying to avoid all dual relationships is unrealistic and not all dual relationships are exploitative. Instead, a clinician must assess 3 dimensions of current and proposed relationships:

• the degree of power differential
• the duration of treatment
• the clarity of termination.

The decision-making process also requires involvement of the patient, who if “unable to recognize the dilemma or is unwilling to consider the issues before deciding, should be considered at risk, and the contemplated relationship rejected.”³⁵

So I will ask you once again: Dr. Z’s decision

In the case of Dr. Z and Mr. R, a barter arrangement might work in the sense of permitting and sustaining good care. Mr. R suggested the idea and might not be able to afford care without it. Nothing in Dr. Z’s description suggests that Mr. R has personality characteristics or other conditions that would compromise his ability to give informed consent or to understand the nuances of a barter arrangement. Dr. Z is not providing a treatment (eg, psychodynamic therapy) that a barter arrangement could contaminate. That the arrangement would be circumscribed limits the effect of a power differential, as would its brief duration and defined termination endpoint. Dr. Z’s letter to the authors also shows his willingness to seek consultation.

There’s a chance that we may fall apart: Reasons for caution

Martinez’s graded-risk approach recognizes reasons for caution:

• the risk of harm to the patient or doctor–patient relationship
• the uncertain benefit to the patient
• the blurring of Dr. Z’s self-interest and Mr. R’s needs
• some ambiguity about possible exploitation.

Dr. Z and Mr. R have not discussed the value of Mr. R’s work—which might create a rift between them—and despite Mr. R’s reputation, other carpenters are available. Future med-check appointments will give them little time to explore and discuss the meanings of the barter.

Any proposed barter arrangement creates some clinical perils that can be particularly salient in mental health treatment. Patients could view themselves as “special” or entitled to enhanced access to the doctor because of exchanged services, which could take a toll on the doctor.³⁹ The physician’s objectivity might diminish, and the business aspect of their relationship could make both parties less comfortable when discussing sensitive information relevant to treatment.^31,40 Also, the suggested barter is for services to be provided at Dr. Z’s office, where confidentiality may be breeched and transference issues could arise.

A medical malpractice claim states that a doctor has breached a duty of care to a patient such that harm (or “damages”) resulted.⁴¹ Should Dr. Z and Mr. R’s barter agreement turn sour and harm follow, Mr. R could sue for recovery of damages based of a claim of duress, undue influence, or other aspects of the doctor–patient power differential.^27,42,43 Given the published views we have described, a psychiatrist who barters also may be viewed as violating state regulations that measure the standard of care against generally accepted practice.

Only time will tell if I am right or I am wrong

If you face a situation similar to Dr. Z’s and want to consider a barter arrangement, you can take several steps to mitigate potential risk to your patient and ensure competent care (Table 2^{5,6,15,16,32,35,39,40,44-47}). One of the most important steps is to seek ongoing consultation, both before and after a decision to barter. Ideally, the consulting colleague would know you and your circumstances and would have sufficient clinical grasp of the patient to make an informed assessment of risks and benefits.³⁵ This consultation, as well as your own rationale for acting on recommendations, should be thoroughly documented in the patient’s records.^26,44,45

Certain types of barter should be off limits, including:

• trading prescription drugs for goods or services
• trading for services that tie into the success of one’s business (eg, business advising or marketing)¹⁶
• offering treatment in exchange for illegal or ethically unacceptable services.⁴⁸

Beyond ethical considerations are some practical issues. The Internal Revenue Service has specific rules regarding taxation of bartered goods and services, which must be included as taxable income.⁴⁶ If possible, an independent agent should appraise the traded goods or services before the agreement.⁶ When working in a group practice, the clinician might have to figure out how to allocate the received goods or services such as shared overhead costs.²⁸ Preferably, the patient’s goods or services should be provided before care is delivered.¹⁶ If not, the duration of services rendered should be limited, and either party should have the option to disengage from the relationship if one feels dissatisfied.¹⁶

A written contract, discussed ahead of time, can be a sound way to summarize the terms of the arrangement. Both sides also should consider what would happen if an injury occurred.¹⁶ Finally, you must adhere to any relevant state laws regarding payment for services, particularly if the patient has health insurance.³²

If the bartering arrangement does not work, you should take an open and non-defensive approach. If you believe you have made a mistake, consider apologizing.⁴⁵

Dear Dr. Mossman,
Each month, I see my patient, Mr. R, for a 15-minute medication management appointment. At his latest visit, Mr. R mentioned his financial difficulties. He also observed that our office needed to have some carpentry work done—not a surprise, because he’s known in our area as one of the best carpenters around. He suggested that I hire him as payment for the next 6 appointments. What risks might I encounter if I oblige him?

Submitted by “Dr. Z”

Nearly 29 million Americans are uninsured,¹ and even more have trouble accessing mental health care.² Many psychiatrists struggle to provide affordable services while remaining financially viable.^3,4 For outpatients with limited means to pay for care, spacing appointments to fit their budgets might compromise treatment.⁵ Simply not charging patients poses its own clinical and ethical challenges.^6-8

As a result, some mental health professionals make barter arrangements to help their patients enter or continue treatment. To answer Dr. Z’s question on whether exchanging services might be a way to arrange matters with some patients, we explore:

• the idea of bartering for psychiatric treatment
• related ethical and legal considerations
• when and in what situations bartering might be appropriate.

Think of what I’m saying: Bartering for treatment

“Barter” refers to exchanging commodities, products, or services of equivalent value without using money.⁹ In 2010, Nevada Republican Senate candidate Sue Lowden encouraged barter for health care and harkened back to an earlier time where “they would bring a chicken to the doctor; they would say ‘I’ll paint your house.’”¹⁰

Such payment arrangements have been encouraged as health care has become increasingly commoditized.^11-13 This happens through both direct barter between physician and patient and barter exchanges. Barter exchange systems have been set up on Web sites (as of 2013, at least 400 such online exchanges were available¹⁴), local communities,^11,15 and social programs. For example, through the “Swapping Guns for Therapy” program, psychologists in California gave free or reduced-fee care for people who traded in their guns.¹⁶

Try to see it my way: A prevailing view of barter

Several psychiatrists recommend against bartering for treatment, for a variety of reasons.^7,8,17-19 Simon¹⁸ argues that a stable fee policy is part of a proper therapeutic framework, and money is “the only acceptable medium of exchange when receiving payment from patients.” Emotional distress and the power differential inherent in treatment might prevent a patient from making an accurate assessment of the value of the bartered goods or services,^7,8,17,18,20 which could lead to future claims of undue influence from trading goods or services below market value.¹⁷ To avoid the possibility of exploitating the patient, Simon¹⁸ recommends that the psychiatrist’s professional fee be “the only material benefit received from the patient.”

The American Psychiatric Association’s code of ethics states that “it is not ethical to switch a doctor–patient relationship to an employer–employee one … and, in most cases, such an arrangement would be unethical.”²¹ In some therapeutic settings, employing a patient risks inappropriate self-disclosure and intrusion.¹⁶

More than other physicians, psychiatrists pay special attention to professional boundaries, the technical term for the “edge of appropriate behavior,” within which safe, effective care can occur.^22,23 Although some boundary crossings can be harmless and even constructive, repeated boundary crossings are the forerunners to improper behavior, including sexual relationships with patients.^24-26

Out of concern that bartering could become the first step down a slippery ethical slope toward patient exploitation, mental health clinicians have deemed the practice “ethically troubling,”¹⁹ said it did “not usually work out well,”⁷ and declared it “so fraught with risks for both parties that it seem[ed] illogical to even consider it as an option.”²⁷

While I see it your way: What barter proponents say

Reports of bartering for chickens²⁸ and purchasing fuel from a patient in remote Alaska²⁹ show that not all physicians agree and why they feel that professional codes of ethics reflect an urban bias.^28,29 In many rural areas and small towns, access to mental health services is limited, and patients often interact with their doctors outside of clinical encounters.^23,29-31

Bartering can benefit a physician’s practice by:

• reducing the need to discount services
• eliminating bureaucratic burdens of traditional insurance arrangements
• facilitating development of a patient base
• allowing patients choice and flexibility in seeking medical care.^6,16,32

Bartering could confer certain clinical benefits, such as:

• enhancing trust and empathy³²
• encouraging patients to make their needs known constructively⁶
• modeling financial self-care⁶
• helping the doctor to feel fairly compensated for providing thoughtful care⁶
• acknowledging the patient’s cultural values^15,33
• affirming that patients and doctors both produce things of value.¹⁶

I have always thought: Other ethical models

An ethical approach to bartering that requires careful thought and respect for the patient’s needs appears consistent with a primary goal of treatment: “to increase the capacity of individuals to make more rational choices in their lives and to be relatively freer from disabling conflicts.”²⁰ Some authors criticize slippery-slope arguments and strict-rule ethical approaches as being too rigid, limiting, or risk-averse.^22,26,34 In Table 1,^{6,8,16,18,27,29-31,35-37} we list several factors that might weigh for or against a decision to enter into a barter arrangement as payment for care.

In a similar manner, Martinez^33,38 proposed a graded-risk framework that encourages examination of potential harms and benefits of a decision, potential coercive or exploitative elements, the clinician’s intentions and aspiration to professional ideals, and the context of the decision. Within this framework, some bartering arrangements might be encouraged and, perhaps, even obligatory because of the potential benefits to the patient; other arrangements (eg, trading psychotherapy for menial services) might be unjustifiable. Martinez³⁸ argues that this approach fosters mutual decision-making with patients, discourages physician paternalism, and “demands that we struggle with the particulars with each case.”

Gottlieb’s decision-making model³⁵ recognizes that trying to avoid all dual relationships is unrealistic and not all dual relationships are exploitative. Instead, a clinician must assess 3 dimensions of current and proposed relationships:

• the degree of power differential
• the duration of treatment
• the clarity of termination.

The decision-making process also requires involvement of the patient, who if “unable to recognize the dilemma or is unwilling to consider the issues before deciding, should be considered at risk, and the contemplated relationship rejected.”³⁵

So I will ask you once again: Dr. Z’s decision

In the case of Dr. Z and Mr. R, a barter arrangement might work in the sense of permitting and sustaining good care. Mr. R suggested the idea and might not be able to afford care without it. Nothing in Dr. Z’s description suggests that Mr. R has personality characteristics or other conditions that would compromise his ability to give informed consent or to understand the nuances of a barter arrangement. Dr. Z is not providing a treatment (eg, psychodynamic therapy) that a barter arrangement could contaminate. That the arrangement would be circumscribed limits the effect of a power differential, as would its brief duration and defined termination endpoint. Dr. Z’s letter to the authors also shows his willingness to seek consultation.

There’s a chance that we may fall apart: Reasons for caution

Martinez’s graded-risk approach recognizes reasons for caution:

• the risk of harm to the patient or doctor–patient relationship
• the uncertain benefit to the patient
• the blurring of Dr. Z’s self-interest and Mr. R’s needs
• some ambiguity about possible exploitation.

Dr. Z and Mr. R have not discussed the value of Mr. R’s work—which might create a rift between them—and despite Mr. R’s reputation, other carpenters are available. Future med-check appointments will give them little time to explore and discuss the meanings of the barter.

Any proposed barter arrangement creates some clinical perils that can be particularly salient in mental health treatment. Patients could view themselves as “special” or entitled to enhanced access to the doctor because of exchanged services, which could take a toll on the doctor.³⁹ The physician’s objectivity might diminish, and the business aspect of their relationship could make both parties less comfortable when discussing sensitive information relevant to treatment.^31,40 Also, the suggested barter is for services to be provided at Dr. Z’s office, where confidentiality may be breeched and transference issues could arise.

A medical malpractice claim states that a doctor has breached a duty of care to a patient such that harm (or “damages”) resulted.⁴¹ Should Dr. Z and Mr. R’s barter agreement turn sour and harm follow, Mr. R could sue for recovery of damages based of a claim of duress, undue influence, or other aspects of the doctor–patient power differential.^27,42,43 Given the published views we have described, a psychiatrist who barters also may be viewed as violating state regulations that measure the standard of care against generally accepted practice.

Only time will tell if I am right or I am wrong

If you face a situation similar to Dr. Z’s and want to consider a barter arrangement, you can take several steps to mitigate potential risk to your patient and ensure competent care (Table 2^{5,6,15,16,32,35,39,40,44-47}). One of the most important steps is to seek ongoing consultation, both before and after a decision to barter. Ideally, the consulting colleague would know you and your circumstances and would have sufficient clinical grasp of the patient to make an informed assessment of risks and benefits.³⁵ This consultation, as well as your own rationale for acting on recommendations, should be thoroughly documented in the patient’s records.^26,44,45

Certain types of barter should be off limits, including:

• trading prescription drugs for goods or services
• trading for services that tie into the success of one’s business (eg, business advising or marketing)¹⁶
• offering treatment in exchange for illegal or ethically unacceptable services.⁴⁸

Beyond ethical considerations are some practical issues. The Internal Revenue Service has specific rules regarding taxation of bartered goods and services, which must be included as taxable income.⁴⁶ If possible, an independent agent should appraise the traded goods or services before the agreement.⁶ When working in a group practice, the clinician might have to figure out how to allocate the received goods or services such as shared overhead costs.²⁸ Preferably, the patient’s goods or services should be provided before care is delivered.¹⁶ If not, the duration of services rendered should be limited, and either party should have the option to disengage from the relationship if one feels dissatisfied.¹⁶

A written contract, discussed ahead of time, can be a sound way to summarize the terms of the arrangement. Both sides also should consider what would happen if an injury occurred.¹⁶ Finally, you must adhere to any relevant state laws regarding payment for services, particularly if the patient has health insurance.³²

If the bartering arrangement does not work, you should take an open and non-defensive approach. If you believe you have made a mistake, consider apologizing.⁴⁵

Dear Dr. Mossman,
Each month, I see my patient, Mr. R, for a 15-minute medication management appointment. At his latest visit, Mr. R mentioned his financial difficulties. He also observed that our office needed to have some carpentry work done—not a surprise, because he’s known in our area as one of the best carpenters around. He suggested that I hire him as payment for the next 6 appointments. What risks might I encounter if I oblige him?

Submitted by “Dr. Z”

Nearly 29 million Americans are uninsured,¹ and even more have trouble accessing mental health care.² Many psychiatrists struggle to provide affordable services while remaining financially viable.^3,4 For outpatients with limited means to pay for care, spacing appointments to fit their budgets might compromise treatment.⁵ Simply not charging patients poses its own clinical and ethical challenges.^6-8

As a result, some mental health professionals make barter arrangements to help their patients enter or continue treatment. To answer Dr. Z’s question on whether exchanging services might be a way to arrange matters with some patients, we explore:

• the idea of bartering for psychiatric treatment
• related ethical and legal considerations
• when and in what situations bartering might be appropriate.

Think of what I’m saying: Bartering for treatment

“Barter” refers to exchanging commodities, products, or services of equivalent value without using money.⁹ In 2010, Nevada Republican Senate candidate Sue Lowden encouraged barter for health care and harkened back to an earlier time where “they would bring a chicken to the doctor; they would say ‘I’ll paint your house.’”¹⁰

Such payment arrangements have been encouraged as health care has become increasingly commoditized.^11-13 This happens through both direct barter between physician and patient and barter exchanges. Barter exchange systems have been set up on Web sites (as of 2013, at least 400 such online exchanges were available¹⁴), local communities,^11,15 and social programs. For example, through the “Swapping Guns for Therapy” program, psychologists in California gave free or reduced-fee care for people who traded in their guns.¹⁶

Try to see it my way: A prevailing view of barter

Several psychiatrists recommend against bartering for treatment, for a variety of reasons.^7,8,17-19 Simon¹⁸ argues that a stable fee policy is part of a proper therapeutic framework, and money is “the only acceptable medium of exchange when receiving payment from patients.” Emotional distress and the power differential inherent in treatment might prevent a patient from making an accurate assessment of the value of the bartered goods or services,^7,8,17,18,20 which could lead to future claims of undue influence from trading goods or services below market value.¹⁷ To avoid the possibility of exploitating the patient, Simon¹⁸ recommends that the psychiatrist’s professional fee be “the only material benefit received from the patient.”

The American Psychiatric Association’s code of ethics states that “it is not ethical to switch a doctor–patient relationship to an employer–employee one … and, in most cases, such an arrangement would be unethical.”²¹ In some therapeutic settings, employing a patient risks inappropriate self-disclosure and intrusion.¹⁶

More than other physicians, psychiatrists pay special attention to professional boundaries, the technical term for the “edge of appropriate behavior,” within which safe, effective care can occur.^22,23 Although some boundary crossings can be harmless and even constructive, repeated boundary crossings are the forerunners to improper behavior, including sexual relationships with patients.^24-26

Out of concern that bartering could become the first step down a slippery ethical slope toward patient exploitation, mental health clinicians have deemed the practice “ethically troubling,”¹⁹ said it did “not usually work out well,”⁷ and declared it “so fraught with risks for both parties that it seem[ed] illogical to even consider it as an option.”²⁷

While I see it your way: What barter proponents say

Reports of bartering for chickens²⁸ and purchasing fuel from a patient in remote Alaska²⁹ show that not all physicians agree and why they feel that professional codes of ethics reflect an urban bias.^28,29 In many rural areas and small towns, access to mental health services is limited, and patients often interact with their doctors outside of clinical encounters.^23,29-31

Bartering can benefit a physician’s practice by:

• reducing the need to discount services
• eliminating bureaucratic burdens of traditional insurance arrangements
• facilitating development of a patient base
• allowing patients choice and flexibility in seeking medical care.^6,16,32

Bartering could confer certain clinical benefits, such as:

• enhancing trust and empathy³²
• encouraging patients to make their needs known constructively⁶
• modeling financial self-care⁶
• helping the doctor to feel fairly compensated for providing thoughtful care⁶
• acknowledging the patient’s cultural values^15,33
• affirming that patients and doctors both produce things of value.¹⁶

I have always thought: Other ethical models

An ethical approach to bartering that requires careful thought and respect for the patient’s needs appears consistent with a primary goal of treatment: “to increase the capacity of individuals to make more rational choices in their lives and to be relatively freer from disabling conflicts.”²⁰ Some authors criticize slippery-slope arguments and strict-rule ethical approaches as being too rigid, limiting, or risk-averse.^22,26,34 In Table 1,^{6,8,16,18,27,29-31,35-37} we list several factors that might weigh for or against a decision to enter into a barter arrangement as payment for care.

In a similar manner, Martinez^33,38 proposed a graded-risk framework that encourages examination of potential harms and benefits of a decision, potential coercive or exploitative elements, the clinician’s intentions and aspiration to professional ideals, and the context of the decision. Within this framework, some bartering arrangements might be encouraged and, perhaps, even obligatory because of the potential benefits to the patient; other arrangements (eg, trading psychotherapy for menial services) might be unjustifiable. Martinez³⁸ argues that this approach fosters mutual decision-making with patients, discourages physician paternalism, and “demands that we struggle with the particulars with each case.”

Gottlieb’s decision-making model³⁵ recognizes that trying to avoid all dual relationships is unrealistic and not all dual relationships are exploitative. Instead, a clinician must assess 3 dimensions of current and proposed relationships:

• the degree of power differential
• the duration of treatment
• the clarity of termination.

The decision-making process also requires involvement of the patient, who if “unable to recognize the dilemma or is unwilling to consider the issues before deciding, should be considered at risk, and the contemplated relationship rejected.”³⁵

So I will ask you once again: Dr. Z’s decision

In the case of Dr. Z and Mr. R, a barter arrangement might work in the sense of permitting and sustaining good care. Mr. R suggested the idea and might not be able to afford care without it. Nothing in Dr. Z’s description suggests that Mr. R has personality characteristics or other conditions that would compromise his ability to give informed consent or to understand the nuances of a barter arrangement. Dr. Z is not providing a treatment (eg, psychodynamic therapy) that a barter arrangement could contaminate. That the arrangement would be circumscribed limits the effect of a power differential, as would its brief duration and defined termination endpoint. Dr. Z’s letter to the authors also shows his willingness to seek consultation.

There’s a chance that we may fall apart: Reasons for caution

Martinez’s graded-risk approach recognizes reasons for caution:

• the risk of harm to the patient or doctor–patient relationship
• the uncertain benefit to the patient
• the blurring of Dr. Z’s self-interest and Mr. R’s needs
• some ambiguity about possible exploitation.

Dr. Z and Mr. R have not discussed the value of Mr. R’s work—which might create a rift between them—and despite Mr. R’s reputation, other carpenters are available. Future med-check appointments will give them little time to explore and discuss the meanings of the barter.

Any proposed barter arrangement creates some clinical perils that can be particularly salient in mental health treatment. Patients could view themselves as “special” or entitled to enhanced access to the doctor because of exchanged services, which could take a toll on the doctor.³⁹ The physician’s objectivity might diminish, and the business aspect of their relationship could make both parties less comfortable when discussing sensitive information relevant to treatment.^31,40 Also, the suggested barter is for services to be provided at Dr. Z’s office, where confidentiality may be breeched and transference issues could arise.

A medical malpractice claim states that a doctor has breached a duty of care to a patient such that harm (or “damages”) resulted.⁴¹ Should Dr. Z and Mr. R’s barter agreement turn sour and harm follow, Mr. R could sue for recovery of damages based of a claim of duress, undue influence, or other aspects of the doctor–patient power differential.^27,42,43 Given the published views we have described, a psychiatrist who barters also may be viewed as violating state regulations that measure the standard of care against generally accepted practice.

Only time will tell if I am right or I am wrong

If you face a situation similar to Dr. Z’s and want to consider a barter arrangement, you can take several steps to mitigate potential risk to your patient and ensure competent care (Table 2^{5,6,15,16,32,35,39,40,44-47}). One of the most important steps is to seek ongoing consultation, both before and after a decision to barter. Ideally, the consulting colleague would know you and your circumstances and would have sufficient clinical grasp of the patient to make an informed assessment of risks and benefits.³⁵ This consultation, as well as your own rationale for acting on recommendations, should be thoroughly documented in the patient’s records.^26,44,45

Certain types of barter should be off limits, including:

• trading prescription drugs for goods or services
• trading for services that tie into the success of one’s business (eg, business advising or marketing)¹⁶
• offering treatment in exchange for illegal or ethically unacceptable services.⁴⁸

Beyond ethical considerations are some practical issues. The Internal Revenue Service has specific rules regarding taxation of bartered goods and services, which must be included as taxable income.⁴⁶ If possible, an independent agent should appraise the traded goods or services before the agreement.⁶ When working in a group practice, the clinician might have to figure out how to allocate the received goods or services such as shared overhead costs.²⁸ Preferably, the patient’s goods or services should be provided before care is delivered.¹⁶ If not, the duration of services rendered should be limited, and either party should have the option to disengage from the relationship if one feels dissatisfied.¹⁶

A written contract, discussed ahead of time, can be a sound way to summarize the terms of the arrangement. Both sides also should consider what would happen if an injury occurred.¹⁶ Finally, you must adhere to any relevant state laws regarding payment for services, particularly if the patient has health insurance.³²

If the bartering arrangement does not work, you should take an open and non-defensive approach. If you believe you have made a mistake, consider apologizing.⁴⁵

Are you ‘neuroprotecting’ your patients?

Fortunately, many studies have demonstrated that in addition to controlling clinical symptoms, antidepressants, mood stabilizers, and atypical antipsychotics all have neuroprotective effects, including stimulating neurogenesis, preventing apoptosis, and increasing neurotrophins. However, more needs to be done to protect the brain’s gray and white matter and to prevent negative neuroplasticity and disconnectivity of brain circuits that often are documented in patients with psychotic and mood disorders.

There are, in fact, many off-label supplements with strong neuroprotective effects that psychiatrists can use as an adjunct to standard evidence-based pharmacotherapy. These agents generally are safe and well tolerated and often are sold over the counter, but are not covered by insurance. However, considering the disability that often is associated with schizophrenia, treatment-resistant depression, or psychotic mania, it is reasonable to consider using these agents, many of which are supported by studies published in peer-reviewed journals. However, because they are widely available and not proprietary and large, expensive registration trials such as the ones conducted by the pharmaceutical industry are not done, none is likely to receive FDA approval. Therefore, it is up to psychiatrists and nurse practitioners to use them judiciously in patients at risk for neurotoxicity.

Here are 10 agents with neuroprotective effects supported by published data that can be considered as add-on to the standard treatments in an effort to mitigate neurotoxicity and protect the brain from the destructive processes that accompany acute episodes of psychosis, mania, and depression.

Omega-3 fatty acids have been shown in several studies to help reduce psychopathology of psychosis, mania, or depression when used as an adjunctive agent.¹ It appears to be more effective in the early stages of psychiatric disorders than in the chronic phase. It has anti-inflammatory, anti-oxidant, and anti-apoptotic effects; activates cell-signaling pathways; and prevents synaptic loss as well as neuronal and glial death.²

N-acetylcysteine (NAC) is a powerful antioxidant that increases glutathione, which is produced in the mitochondria. Schizophrenia is associated with mitochondrial dysfunction with low levels of glutathione, which puts the brain at risk for neurodegeneration caused by high levels of free radicals produced during psychosis. Adding NAC to antipsychotics during acute psychotic episodes—especially the first episode—can significantly reduce the neurotoxic effects of reactive oxygen and nitrogen species, also known as free radicals.³ In studies of traumatic brain injury in rats, NAC reduced brain edema, neuro­inflammation, blood–brain barrier permeability, and apoptosis.⁴

Minocycline. This antibiotic has been studied extensively as an adjunctive treatment in schizophrenia and has proven to have several neuroprotective effects including anti-inflammatory, anti-oxidant, and anti-apoptotic, and reduces glutamate excitotoxicity.⁵ Several studies have documented its usefulness in acute psychotic episodes.

Vitamin D. Because of its vital role in neurodevelopment (neuronal differentiation, axonal connectivity), vitamin D deficiency has been associated with several psychiatric disorders including autism, schizophrenia, depression, and Alzheimer’s disease.⁶ Measure serum levels of vitamin D in patients with psychotic and mood disorders and implement supplementation if it is low—and it often is in these patients.

Nicotine is neuroprotective against glutamate excitotoxicity and it also inhibits apoptosis.⁷ However, it should never be administered via cigarettes, which are loaded with hundreds of toxic substances! It can be administered via patches or nicotine gum, which are usually used to help in smoking cessation. Nicotine also also can have a pro-cognitive effect.

Melatonin. Many people associate melatonin with sleep. However, it has multiple neuroprotective effects by being an antioxidant, protecting mitochondrial integrity, and modulating the immune system, as well as attenuating microglial activation, which triggers neuroinflammation and oxidative stress. It also protects against cellular senescence, which is due to inflammation and reactive oxygen species. Furthermore, melatonin is useful in ameliorating the metabolic syndrome, which is associated with neurotoxic effects on brain tissue caused by the pro-inflammatory effects of peri-omental fat in obesity.⁸ Adjunctive melatonin could be helpful in patients with schizophrenia or depression who suffer from metabolic syndrome.

Erythropoietin is a hormone produced by the kidneys to promote the formation of red blood cells. It is a potent neuroprotective cytokine that promotes neuronal survival via anti-apoptotic effects. It protects against glutamate and nitrous oxide toxicity⁹ and haloperidol-induced neuronal death.¹⁰ It is clinically used (since FDA approval in 1989) in severe anemia due to chronic kidney disease or chemotherapy, as well as in inflammatory bowel disease. It does have some “black-box” warnings so its use should be limited.

The above interventions may be helpful for some patients but not others. Practitioners should consider using 1 or more of those adjunctive neuroprotective agents in patients who are at risk for neurodegenerative changes secondary to recurrences of acute and severe psychosis or mood episodes. Although clinicians cannot monitor brain structural integrity, they can assess the rate of symptomatic improvement and degree of functional restoration in their patients. Until a cure is found, these little steps—taken cautiously and judiciously—could help alleviate our patients’ suffering and the risk of neurotoxicity associated with their serious psychiatric disorder.

Are you ‘neuroprotecting’ your patients?

Fortunately, many studies have demonstrated that in addition to controlling clinical symptoms, antidepressants, mood stabilizers, and atypical antipsychotics all have neuroprotective effects, including stimulating neurogenesis, preventing apoptosis, and increasing neurotrophins. However, more needs to be done to protect the brain’s gray and white matter and to prevent negative neuroplasticity and disconnectivity of brain circuits that often are documented in patients with psychotic and mood disorders.

There are, in fact, many off-label supplements with strong neuroprotective effects that psychiatrists can use as an adjunct to standard evidence-based pharmacotherapy. These agents generally are safe and well tolerated and often are sold over the counter, but are not covered by insurance. However, considering the disability that often is associated with schizophrenia, treatment-resistant depression, or psychotic mania, it is reasonable to consider using these agents, many of which are supported by studies published in peer-reviewed journals. However, because they are widely available and not proprietary and large, expensive registration trials such as the ones conducted by the pharmaceutical industry are not done, none is likely to receive FDA approval. Therefore, it is up to psychiatrists and nurse practitioners to use them judiciously in patients at risk for neurotoxicity.

Here are 10 agents with neuroprotective effects supported by published data that can be considered as add-on to the standard treatments in an effort to mitigate neurotoxicity and protect the brain from the destructive processes that accompany acute episodes of psychosis, mania, and depression.

Omega-3 fatty acids have been shown in several studies to help reduce psychopathology of psychosis, mania, or depression when used as an adjunctive agent.¹ It appears to be more effective in the early stages of psychiatric disorders than in the chronic phase. It has anti-inflammatory, anti-oxidant, and anti-apoptotic effects; activates cell-signaling pathways; and prevents synaptic loss as well as neuronal and glial death.²

N-acetylcysteine (NAC) is a powerful antioxidant that increases glutathione, which is produced in the mitochondria. Schizophrenia is associated with mitochondrial dysfunction with low levels of glutathione, which puts the brain at risk for neurodegeneration caused by high levels of free radicals produced during psychosis. Adding NAC to antipsychotics during acute psychotic episodes—especially the first episode—can significantly reduce the neurotoxic effects of reactive oxygen and nitrogen species, also known as free radicals.³ In studies of traumatic brain injury in rats, NAC reduced brain edema, neuro­inflammation, blood–brain barrier permeability, and apoptosis.⁴

Minocycline. This antibiotic has been studied extensively as an adjunctive treatment in schizophrenia and has proven to have several neuroprotective effects including anti-inflammatory, anti-oxidant, and anti-apoptotic, and reduces glutamate excitotoxicity.⁵ Several studies have documented its usefulness in acute psychotic episodes.

Vitamin D. Because of its vital role in neurodevelopment (neuronal differentiation, axonal connectivity), vitamin D deficiency has been associated with several psychiatric disorders including autism, schizophrenia, depression, and Alzheimer’s disease.⁶ Measure serum levels of vitamin D in patients with psychotic and mood disorders and implement supplementation if it is low—and it often is in these patients.

Nicotine is neuroprotective against glutamate excitotoxicity and it also inhibits apoptosis.⁷ However, it should never be administered via cigarettes, which are loaded with hundreds of toxic substances! It can be administered via patches or nicotine gum, which are usually used to help in smoking cessation. Nicotine also also can have a pro-cognitive effect.

Melatonin. Many people associate melatonin with sleep. However, it has multiple neuroprotective effects by being an antioxidant, protecting mitochondrial integrity, and modulating the immune system, as well as attenuating microglial activation, which triggers neuroinflammation and oxidative stress. It also protects against cellular senescence, which is due to inflammation and reactive oxygen species. Furthermore, melatonin is useful in ameliorating the metabolic syndrome, which is associated with neurotoxic effects on brain tissue caused by the pro-inflammatory effects of peri-omental fat in obesity.⁸ Adjunctive melatonin could be helpful in patients with schizophrenia or depression who suffer from metabolic syndrome.

Erythropoietin is a hormone produced by the kidneys to promote the formation of red blood cells. It is a potent neuroprotective cytokine that promotes neuronal survival via anti-apoptotic effects. It protects against glutamate and nitrous oxide toxicity⁹ and haloperidol-induced neuronal death.¹⁰ It is clinically used (since FDA approval in 1989) in severe anemia due to chronic kidney disease or chemotherapy, as well as in inflammatory bowel disease. It does have some “black-box” warnings so its use should be limited.

The above interventions may be helpful for some patients but not others. Practitioners should consider using 1 or more of those adjunctive neuroprotective agents in patients who are at risk for neurodegenerative changes secondary to recurrences of acute and severe psychosis or mood episodes. Although clinicians cannot monitor brain structural integrity, they can assess the rate of symptomatic improvement and degree of functional restoration in their patients. Until a cure is found, these little steps—taken cautiously and judiciously—could help alleviate our patients’ suffering and the risk of neurotoxicity associated with their serious psychiatric disorder.

Are you ‘neuroprotecting’ your patients?

Fortunately, many studies have demonstrated that in addition to controlling clinical symptoms, antidepressants, mood stabilizers, and atypical antipsychotics all have neuroprotective effects, including stimulating neurogenesis, preventing apoptosis, and increasing neurotrophins. However, more needs to be done to protect the brain’s gray and white matter and to prevent negative neuroplasticity and disconnectivity of brain circuits that often are documented in patients with psychotic and mood disorders.

There are, in fact, many off-label supplements with strong neuroprotective effects that psychiatrists can use as an adjunct to standard evidence-based pharmacotherapy. These agents generally are safe and well tolerated and often are sold over the counter, but are not covered by insurance. However, considering the disability that often is associated with schizophrenia, treatment-resistant depression, or psychotic mania, it is reasonable to consider using these agents, many of which are supported by studies published in peer-reviewed journals. However, because they are widely available and not proprietary and large, expensive registration trials such as the ones conducted by the pharmaceutical industry are not done, none is likely to receive FDA approval. Therefore, it is up to psychiatrists and nurse practitioners to use them judiciously in patients at risk for neurotoxicity.

Here are 10 agents with neuroprotective effects supported by published data that can be considered as add-on to the standard treatments in an effort to mitigate neurotoxicity and protect the brain from the destructive processes that accompany acute episodes of psychosis, mania, and depression.

Omega-3 fatty acids have been shown in several studies to help reduce psychopathology of psychosis, mania, or depression when used as an adjunctive agent.¹ It appears to be more effective in the early stages of psychiatric disorders than in the chronic phase. It has anti-inflammatory, anti-oxidant, and anti-apoptotic effects; activates cell-signaling pathways; and prevents synaptic loss as well as neuronal and glial death.²

N-acetylcysteine (NAC) is a powerful antioxidant that increases glutathione, which is produced in the mitochondria. Schizophrenia is associated with mitochondrial dysfunction with low levels of glutathione, which puts the brain at risk for neurodegeneration caused by high levels of free radicals produced during psychosis. Adding NAC to antipsychotics during acute psychotic episodes—especially the first episode—can significantly reduce the neurotoxic effects of reactive oxygen and nitrogen species, also known as free radicals.³ In studies of traumatic brain injury in rats, NAC reduced brain edema, neuro­inflammation, blood–brain barrier permeability, and apoptosis.⁴

Minocycline. This antibiotic has been studied extensively as an adjunctive treatment in schizophrenia and has proven to have several neuroprotective effects including anti-inflammatory, anti-oxidant, and anti-apoptotic, and reduces glutamate excitotoxicity.⁵ Several studies have documented its usefulness in acute psychotic episodes.

Vitamin D. Because of its vital role in neurodevelopment (neuronal differentiation, axonal connectivity), vitamin D deficiency has been associated with several psychiatric disorders including autism, schizophrenia, depression, and Alzheimer’s disease.⁶ Measure serum levels of vitamin D in patients with psychotic and mood disorders and implement supplementation if it is low—and it often is in these patients.

Nicotine is neuroprotective against glutamate excitotoxicity and it also inhibits apoptosis.⁷ However, it should never be administered via cigarettes, which are loaded with hundreds of toxic substances! It can be administered via patches or nicotine gum, which are usually used to help in smoking cessation. Nicotine also also can have a pro-cognitive effect.

Melatonin. Many people associate melatonin with sleep. However, it has multiple neuroprotective effects by being an antioxidant, protecting mitochondrial integrity, and modulating the immune system, as well as attenuating microglial activation, which triggers neuroinflammation and oxidative stress. It also protects against cellular senescence, which is due to inflammation and reactive oxygen species. Furthermore, melatonin is useful in ameliorating the metabolic syndrome, which is associated with neurotoxic effects on brain tissue caused by the pro-inflammatory effects of peri-omental fat in obesity.⁸ Adjunctive melatonin could be helpful in patients with schizophrenia or depression who suffer from metabolic syndrome.

Erythropoietin is a hormone produced by the kidneys to promote the formation of red blood cells. It is a potent neuroprotective cytokine that promotes neuronal survival via anti-apoptotic effects. It protects against glutamate and nitrous oxide toxicity⁹ and haloperidol-induced neuronal death.¹⁰ It is clinically used (since FDA approval in 1989) in severe anemia due to chronic kidney disease or chemotherapy, as well as in inflammatory bowel disease. It does have some “black-box” warnings so its use should be limited.

The above interventions may be helpful for some patients but not others. Practitioners should consider using 1 or more of those adjunctive neuroprotective agents in patients who are at risk for neurodegenerative changes secondary to recurrences of acute and severe psychosis or mood episodes. Although clinicians cannot monitor brain structural integrity, they can assess the rate of symptomatic improvement and degree of functional restoration in their patients. Until a cure is found, these little steps—taken cautiously and judiciously—could help alleviate our patients’ suffering and the risk of neurotoxicity associated with their serious psychiatric disorder.