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Complementary treatments for anxiety: Beyond pharmacotherapy and psychotherapy
Anxiety disorders are the most common psychiatric illnesses in the United States, with a prevalence of nearly 29%.1 These disorders typically are treated with pharmacotherapy, psychotherapy, or a combination of both. Pharmacotherapy for anxiety has evolved considerably during the last 30 years, but medications are not efficacious for or tolerated by all patients. For example, selective serotonin reuptake inhibitors, which are frequently used for treating anxiety, can cause sexual dysfunction,2 weight gain,2 drug interactions,2 coagulopathies,3 and gastrointestinal disturbances.4 Psychotherapeutic techniques, such as cognitive behavioral therapy (CBT) and interpersonal therapy (IPT), are efficacious for mild to moderate anxiety.5-7
In addition to standard pharmacotherapy and psychotherapy, some evidence suggests that complementary therapies, such as yoga, massage, and relaxation techniques, may be beneficial as adjunctive treatments for anxiety. In placebo-controlled trials, several of these complementary therapies have been shown to decrease serum levels of the inflammatory biomarker cortisol. Anxiety is associated with inflammation,8 so therapies that reduce inflammation may help reduce symptoms of anxiety. Here, we describe the results of select positive randomized controlled trials (RCTs) of several complementary interventions for anxiety that might be useful as adjunctive treatments to psychotherapy or pharmacotherapy.
A look at RCTs that measured both anxiety and cortisol
We searched PubMed, Google Scholar, and Scopus to identify RCTs of complementary nonpharmacologic and nonpsychotherapeutic therapies for anxiety published from January 2010 to May 2017. We included only studies that:
- blindly assessed anxiety levels through a validated instrument (the State-Trait Anxiety Inventory [STAI])9
- measured cortisol concentrations before and after treatment.
Evaluating both STAI scores and cortisol levels is useful because doing so gives insight into both the clinical and biological efficacy of the therapies. Studies were excluded if they employed a pharmacologic agent in addition to the approach being evaluated.
We identified 26 studies, of which 14 met the inclusion/exclusion criteria. These studies found beneficial effects for yoga, massage therapy, aromatherapy massage, pet therapy, Qigong, auricular acupressure, reiki touch therapy, acupuncture, music therapy, and relaxation techniques.
Yoga
Yoga has become increasingly popular in the Western world during the last 2 decades.10 There are a variety of yoga practices; common forms include hatha yoga, power yoga, kripalu yoga, and forrest yoga.11
A study of 92 depressed pregnant women monito
Hatha yoga consists of a combination of postural exercises, breathing techniques, relaxation, and meditation. In a 12-week study of 88 postmenopausal women, those who practiced hatha yoga for 75 minutes a day had significantly lower STAI scores compared with women who exercised for 75 minutes a day and those who performed no physical activity.13
Continue to: Massage therapy
Massage therapy
Receiving as little as 15 minutes of back massage has proven to be beneficial for individuals with anxiety. In an RCT conducted in Turkey, 44 caregivers of patients with cancer were assigned to receive a back massage or to rest quietly in a room for 15 minutes once each day for 1 week.14 By the end of the week, compared with those who quietly rested, those who received the back massage had a statistically significant reduction in serum cortisol levels and STAI scores.14
Aromatherapy massage
Aromatherapy is the use of essential oils from plants through distillation.15 The scent of the oils is purported to provide medical benefits. More than 60 essential oils are used therapeutically, including rose, lavender, lemon, and orange.16 These essential oils are frequently used in combination with a massage.
In South Korea, researchers investigated the effects of aromatherapy massage on 25 women who had children diagnosed with attention-deficit/hyperactivity disorder.17 Women assigned to the treatment group received a 40-minute aromatherapy massage using mixed essential oils that contained lavender and geranium twice a week for 4 weeks. Women in the control group received no treatment. Compared with those in the control group, women who received the aromatherapy massages had a statistically significant decrease in STAI scores and salivary cortisol levels. Plasma cortisol was not significantly different between groups.17
Pet therapy
The psychological benefits of animal-assisted therapy were not evident until World War II, when dogs were used to cheer up injured soldiers.18 Today, pet therapy has been used on many inpatient units.19
In a U.S. study, 48 healthy undergraduate students were assigned to a room with a dog, a room with a friend, or a room by themselves.20 All participants were given the Trier Social Stress Test (TSST), a protocol that measures stress by having participants give a speech and perform mental arithmetic in front of an audience.The TSST is known to induce increases in cortisol levels. Although no differences in STAI scores were found among groups, students in the room with the dog had a lower spike in salivary cortisol after the TSST compared with participants who were in a room with a friend or in a room alone.20
Continue to: Qigong
Qigong
In Chinese medicine, Qi is known as a vital life force that flows through the body. The disruption of Qi is hypothesized to contribute to disease.21
Qigong is a medical therapy that focuses on uniting the body, breath, and mind to improve health.21 It consists of rhythmic, choreographed movements used to position the body into postures believed to help direct Qi to specific areas in the body. Qigong also uses sound exercises, in which an individual creates certain syllables while breathing. Six syllables are used, each of which is believed to affect a certain organ.21
Korean researchers randomly assigned 32 healthy men to a Qigong training group or a sham Qigong control group.22 Individuals in the training group performed 25 minutes of sound exercises, 20 minutes of meditation, and 15 minutes of movements. The control group learned the same movements as the experimental group, but without the conscious effort of moving Qi. After 3 sessions, those in the Qigong training group had significantly decreased STAI scores and serum cortisol levels compared with those in the sham group.22
In a different Korean study, researchers randomly assigned 50 participants with elevated distress levels to a Qigong training group or a waitlist control group in which participants called a trainer to describe stressful events.23 After 4 weeks, participants in the Qigong group had significant decreases in STAI scores compared with the control group. However, there were no changes in salivary cortisol levels.23
Auricular acupressure
Auricular acupressure involves applying pressure on certain portions of the auricle (outer ear) to alleviate pain and disease.24 Similar to Qigong, auricular acupressure focuses on reestablishing Qi in the body. Researchers randomly assigned 80 post-caesarean section women in Taiwan to 5 days of auricular acupressure or usual care.25 The women who received auricular acupressure had significantly lower STAI scores and serum cortisol levels compared with women who received routine care.25
Continue to: Reiki touch therapy
Reiki touch therapy
Reiki touch therapy originated in Japan. In this therapy, healers apply a light touch or hover their hands above an individual’s body to help direct energy.26
The effects of reiki touch therapy were recently evaluated in a U.S. study.27 Researchers randomly assigned 37 patients with human immunodeficiency virus to an experimental group that received 30 minutes of reiki touch therapy plus music therapy 6 times a week for 10 weeks, or to a music therapy–only control group. Patients who received reiki touch therapy had a significant decrease in STAI scores. Patients in this group also had a statistically significant drop in salivary cortisol levels after the first week.27
Acupuncture
Acupuncture is the application of needles to specific areas on the body. Acupuncture has been proposed to activate pain receptors, thereby producing an analgesic response.28
Researchers in Brazil randomly assigned 57 lactating women with preterm infants to an experimental group that received acupuncture or to a control group that received sham acupuncture.29 Treatment was administered at 5 points on the ear unilaterally for 5 minutes once a week for 16 months. Custom-made needles that did not actually puncture the skin were used in the sham group; a toothpick was used to create the sensation of needle perforations. STAI scores were reduced in both groups, although there was no statistically significant difference in scores between the acupuncture and sham groups.29
Music therapy
Music has been long believed to have beneficial psychological effects. In Turkey, researchers evaluated the effects of music therapy in 100 oncology patients who received port catheters.30 Patients were randomly assigned to an experimental group that received music therapy throughout the procedure or to a control group that received normal care. Patients who listened to music during port catheter placement had significantly reduced STAI scores and serum cortisol levels compared with those in the control group.30
Continue to: Relaxation techniques
Relaxation techniques
A wide range of relaxation techniques are used for therapeutic purposes. In Switzerland, researchers evaluated the anxiolytic effects of 10 minutes of progressive muscle relaxation and guided imagery in 39 pregnant women.31 Women randomly assigned to progressive muscle relaxation were instructed to systematically tense and then release muscle groups throughout their body in sequential order. Women assigned to the guided imagery intervention were told to imagine a safe place and to think of someone who could confer security and reassurance. The remainder of the women were assigned to a control group, where they sat quietly without any formal instructions. Researchers found that each group had a decrease in STAI scores and salivary cortisol levels immediately after the intervention.31
The relaxation response was first described in 1975 by Herbert Benson, MD, as a deep meditative state characterized by a decrease in tension, heart rate, and breathing rate. Several techniques can induce this state, including hypnosis, progressive muscle relaxation, yoga, and transcendental meditation.32 In a study of 15 healthy older adults (age 65 to 80), researchers randomly assigned participants to a relaxation response training group or to a control group.33 The relaxation response training included meditation, imagery, and relaxation techniques. After 5 weeks, participants who received the relaxation response training had marginally significant decreases in STAI scores compared with those in the control group.33
Consider these therapies as adjuncts
Our review of select positive RCTs (Table12-14,17,20,22,23,25,27,29-31,33) suggests that some nonpharmacologic/nonpsychotherapeutic adjunctive interventions may have beneficial effects for patients who have anxiety. Several of the controlled studies we reviewed demonstrated that these interventions are superior to placebo. The reductions in both anxiety severity as measured by the STAI and cortisol levels suggests that some of these complementary therapies deserve a second look as useful adjuncts to established anxiety treatments.
Bottom Line
A review of select randomized controlled trials suggests that some complementary therapies may be helpful as adjunctive therapy in patients with anxiety. These include yoga, massage therapy, aromatherapy massage, pet therapy, Qigong, auricular acupressure, reiki touch therapy, acupuncture, music therapy, and relaxation techniques.
Related Resources
- Bandelow B, Baldwin D, Abelli M, et al. Biological markers for anxiety disorders, OCD and PTSD: a consensus statement. Part II: neurochemistry, neurophysiology and neurocognition. World J Biol Psychiatry. 2017;18(3):162-214.
- National Institute of Mental Health. Anxiety disorders. https://www.nimh.nih.gov/health/topics/anxiety-disorders/index.shtml.
1. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62(6):593-602.
2. Masand PS, Gupta S. Long-term side effects of newer-generation antidepressants: SSRIs, venlafaxine, nefazodone, bupropion, and mirtazapine. Ann Clin Psychiatry. 2002;14(3):175-182.
3. Siddiqui R, Gawande S, Shende T, et al. SSRI-induced coagulopathy: is it reality? Therapeutic Advances in Psychopharmacology. 2011;1(6):169-174.
4. Brambilla P, Cipriani A, Hotopf M, et al. Side-effect profile of fluoxetine in comparison with other SSRIs, tricyclic and newer antidepressants: a meta-analysis of clinical trial data. Pharmacopsychiatry. 2005;38(2):69-77.
5. Slomski A. Blended CBT controls anxiety in cancer survivors. JAMA. 2017;318(4):323.
6. Forsell E, Bendix M, Holländare F, et al. Internet delivered cognitive behavior therapy for antenatal depression: a randomised controlled trial. J Affect Disord. 2017;221:56-64.
7. Lilliengren P, Johansson R, Town JM, et al. Intensive Short-Term Dynamic Psychotherapy for generalized anxiety disorder: A pilot effectiveness and process-outcome study. Clin Psychol Psychother. 2017;24(6):1313-1321.
8. Furtado M, Katzman MA. Neuroinflammatory pathways in anxiety, posttraumatic stress, and obsessive compulsive disorders. Psychiatry Res. 2015;229(1-2):37-48.
9. Spielberger CD, Gorsuch RL, Lushene R, et al. Manual for the State-Trait Anxiety Inventory. Palo Alto, CA: Consulting Psychologists Press; 1983.
10. Saper RB, Eisenberg DM, Davis RB, et al. Prevalence and patterns of adult yoga use in the United States: results of a national survey. Altern Ther Health Med. 2004;10(2):44-49.
11. Farmer J. Americanasana. Reviews in American history. 2012;40(1):145-158.
12. Field T, Diego M, Delgado J, et al. Yoga and social support reduce prenatal depression, anxiety and cortisol. J Bodyw Mov Ther: 2013;17(4):397-403.
13. Jorge MP, Santaella DF, Pontes IM, et al. Hatha Yoga practice decreases menopause symptoms and improves quality of life: a randomized controlled trial. Complement Ther Med. 2016;26:128-135.
14. Pinar R, Afsar F. Back massage to decrease state anxiety, cortisol level, blood pressure, heart rate and increase sleep quality in family caregivers of patients with cancer: a randomised controlled trial. Asian Pac J Cancer Prev. 2015;16(18):8127-8133.
15. Kuriyama H, Watanabe S, Nakaya, et al. Immunological and psychological benefits of aromatherapy massage. Evid Based Complement Alternat Med. 2005;2(2):179-184.
16. Setzer WN. Essential oils and anxiolytic aromatherapy. Nat Prod Commun. 2009;4(9):1305-1316.
17. Wu JJ, Cui Y, Yang YS, et al. Modulatory effects of aromatherapy massage intervention on electroencephalogram, psychological assessments, salivary cortisol and plasma brain-derived neurotrophic factor. Complement Ther Med. 2014;22(3):456-462.
18. Fine A. Forward. In: Fine A, ed. Handbook on animal-assisted therapy-theoretical foundations and guidelines for practice. 3rd ed. Academic Press; 2010:xvii-xviii.
19. Snipelisky D, Burton MC. Canine-assisted therapy in the inpatient setting. South Med J. 2014;107(4):265-273.
20. Polheber JP, Matchock RL. The presence of a dog attenuates cortisol and heart rate in the Trier Social Stress Test compared to human friends. J Behav Med. 2014;37(5):860-867.
21. Liu T, Qiang X, eds. Chinese medical Qigong. Philadelphia, PA: Singing Dragon; 2013:1-100,192,238,511.
22. Lee MS, Kang CW, Lim HJ, et al. Effects of Qi-training on anxiety and plasma concentrations of cortisol, ACTH, and aldosterone: a randomized placebo-controlled pilot study. Stress Health. 2004;20(5):243-248.
23. Hwang EY, Chung SY, Cho JH, et al. Effects of a brief Qigong-based stress reduction program (BQSRP) in a distressed Korean population: a randomized trial. BMC Complement Altern Med. 2013;13:113.
24. Oleson, T. Overview and history of auriculotherapy. In: Auriculotherapy manual: Chinese and Western systems of ear acupuncture. 4th ed. London: Churchill Livingstone; 2014:1.
25. Kuo SY, Tsai SH, Chen SL, et al. Auricular acupressure relieves anxiety and fatigue, and reduces cortisol levels in post-caesarean section women: a single-blind, randomised controlled study. Int J Nurs Stud. 2016;53:17-26.
26. Horan P. Introduction. In: Horan P. Empowerment through reiki: the path to personal and global transformation. 8th ed. Twin Lakes, WI: Lotus Press; 1998:13-15.
27. Bremner MN, Blake BJ, Wagner VD, et al. Effects of reiki with music compared to music only among people living with HIV. J Assoc Nurses AIDS Care. 2016;27(5):635-647.
28. Helmes JM. The basic, clinical, and speculative science of acupuncture. In: Acupuncture energetics: a clinical approach for physicians. Volume 1. Berkeley, CA: Medical Acupuncture Publishers; 1995:19-32.
29. Haddad-Rodrigues M, Spanó Nakano A, Stefanello J, et al. Acupuncture for anxiety in lactating mothers with preterm infants: a randomized controlled trial. Evid Based Complement Alternat Med. 2013;2013:169184. doi: 10.1155/2013/169184.
30. Zengin S, Kabul S, Al B, et al. Effects of music therapy on pain and anxiety in patients undergoing port catheter placement procedure. Complement Ther Med. 2013;21(6):689-696.
31. Urech C, Fink NS, Hoesli I, et al. Effects of relaxation on psychobiological wellbeing during pregnancy: a randomized controlled trial. Psychoneuroendocrinology. 2010;35(9):1348-1355.
32. Goleman D. The relaxation response. In: Mind body medicine: how to use your mind for better health. Yonkers, NY: Consumer Reports; 1993:125-149.
33. Galvin JA, Benson H, Deckro GR, et al. The relaxation response: reducing stress and improving cognition in healthy aging adults. Complement Ther Clin Pract. 2006;12(3):186-191.
Anxiety disorders are the most common psychiatric illnesses in the United States, with a prevalence of nearly 29%.1 These disorders typically are treated with pharmacotherapy, psychotherapy, or a combination of both. Pharmacotherapy for anxiety has evolved considerably during the last 30 years, but medications are not efficacious for or tolerated by all patients. For example, selective serotonin reuptake inhibitors, which are frequently used for treating anxiety, can cause sexual dysfunction,2 weight gain,2 drug interactions,2 coagulopathies,3 and gastrointestinal disturbances.4 Psychotherapeutic techniques, such as cognitive behavioral therapy (CBT) and interpersonal therapy (IPT), are efficacious for mild to moderate anxiety.5-7
In addition to standard pharmacotherapy and psychotherapy, some evidence suggests that complementary therapies, such as yoga, massage, and relaxation techniques, may be beneficial as adjunctive treatments for anxiety. In placebo-controlled trials, several of these complementary therapies have been shown to decrease serum levels of the inflammatory biomarker cortisol. Anxiety is associated with inflammation,8 so therapies that reduce inflammation may help reduce symptoms of anxiety. Here, we describe the results of select positive randomized controlled trials (RCTs) of several complementary interventions for anxiety that might be useful as adjunctive treatments to psychotherapy or pharmacotherapy.
A look at RCTs that measured both anxiety and cortisol
We searched PubMed, Google Scholar, and Scopus to identify RCTs of complementary nonpharmacologic and nonpsychotherapeutic therapies for anxiety published from January 2010 to May 2017. We included only studies that:
- blindly assessed anxiety levels through a validated instrument (the State-Trait Anxiety Inventory [STAI])9
- measured cortisol concentrations before and after treatment.
Evaluating both STAI scores and cortisol levels is useful because doing so gives insight into both the clinical and biological efficacy of the therapies. Studies were excluded if they employed a pharmacologic agent in addition to the approach being evaluated.
We identified 26 studies, of which 14 met the inclusion/exclusion criteria. These studies found beneficial effects for yoga, massage therapy, aromatherapy massage, pet therapy, Qigong, auricular acupressure, reiki touch therapy, acupuncture, music therapy, and relaxation techniques.
Yoga
Yoga has become increasingly popular in the Western world during the last 2 decades.10 There are a variety of yoga practices; common forms include hatha yoga, power yoga, kripalu yoga, and forrest yoga.11
A study of 92 depressed pregnant women monito
Hatha yoga consists of a combination of postural exercises, breathing techniques, relaxation, and meditation. In a 12-week study of 88 postmenopausal women, those who practiced hatha yoga for 75 minutes a day had significantly lower STAI scores compared with women who exercised for 75 minutes a day and those who performed no physical activity.13
Continue to: Massage therapy
Massage therapy
Receiving as little as 15 minutes of back massage has proven to be beneficial for individuals with anxiety. In an RCT conducted in Turkey, 44 caregivers of patients with cancer were assigned to receive a back massage or to rest quietly in a room for 15 minutes once each day for 1 week.14 By the end of the week, compared with those who quietly rested, those who received the back massage had a statistically significant reduction in serum cortisol levels and STAI scores.14
Aromatherapy massage
Aromatherapy is the use of essential oils from plants through distillation.15 The scent of the oils is purported to provide medical benefits. More than 60 essential oils are used therapeutically, including rose, lavender, lemon, and orange.16 These essential oils are frequently used in combination with a massage.
In South Korea, researchers investigated the effects of aromatherapy massage on 25 women who had children diagnosed with attention-deficit/hyperactivity disorder.17 Women assigned to the treatment group received a 40-minute aromatherapy massage using mixed essential oils that contained lavender and geranium twice a week for 4 weeks. Women in the control group received no treatment. Compared with those in the control group, women who received the aromatherapy massages had a statistically significant decrease in STAI scores and salivary cortisol levels. Plasma cortisol was not significantly different between groups.17
Pet therapy
The psychological benefits of animal-assisted therapy were not evident until World War II, when dogs were used to cheer up injured soldiers.18 Today, pet therapy has been used on many inpatient units.19
In a U.S. study, 48 healthy undergraduate students were assigned to a room with a dog, a room with a friend, or a room by themselves.20 All participants were given the Trier Social Stress Test (TSST), a protocol that measures stress by having participants give a speech and perform mental arithmetic in front of an audience.The TSST is known to induce increases in cortisol levels. Although no differences in STAI scores were found among groups, students in the room with the dog had a lower spike in salivary cortisol after the TSST compared with participants who were in a room with a friend or in a room alone.20
Continue to: Qigong
Qigong
In Chinese medicine, Qi is known as a vital life force that flows through the body. The disruption of Qi is hypothesized to contribute to disease.21
Qigong is a medical therapy that focuses on uniting the body, breath, and mind to improve health.21 It consists of rhythmic, choreographed movements used to position the body into postures believed to help direct Qi to specific areas in the body. Qigong also uses sound exercises, in which an individual creates certain syllables while breathing. Six syllables are used, each of which is believed to affect a certain organ.21
Korean researchers randomly assigned 32 healthy men to a Qigong training group or a sham Qigong control group.22 Individuals in the training group performed 25 minutes of sound exercises, 20 minutes of meditation, and 15 minutes of movements. The control group learned the same movements as the experimental group, but without the conscious effort of moving Qi. After 3 sessions, those in the Qigong training group had significantly decreased STAI scores and serum cortisol levels compared with those in the sham group.22
In a different Korean study, researchers randomly assigned 50 participants with elevated distress levels to a Qigong training group or a waitlist control group in which participants called a trainer to describe stressful events.23 After 4 weeks, participants in the Qigong group had significant decreases in STAI scores compared with the control group. However, there were no changes in salivary cortisol levels.23
Auricular acupressure
Auricular acupressure involves applying pressure on certain portions of the auricle (outer ear) to alleviate pain and disease.24 Similar to Qigong, auricular acupressure focuses on reestablishing Qi in the body. Researchers randomly assigned 80 post-caesarean section women in Taiwan to 5 days of auricular acupressure or usual care.25 The women who received auricular acupressure had significantly lower STAI scores and serum cortisol levels compared with women who received routine care.25
Continue to: Reiki touch therapy
Reiki touch therapy
Reiki touch therapy originated in Japan. In this therapy, healers apply a light touch or hover their hands above an individual’s body to help direct energy.26
The effects of reiki touch therapy were recently evaluated in a U.S. study.27 Researchers randomly assigned 37 patients with human immunodeficiency virus to an experimental group that received 30 minutes of reiki touch therapy plus music therapy 6 times a week for 10 weeks, or to a music therapy–only control group. Patients who received reiki touch therapy had a significant decrease in STAI scores. Patients in this group also had a statistically significant drop in salivary cortisol levels after the first week.27
Acupuncture
Acupuncture is the application of needles to specific areas on the body. Acupuncture has been proposed to activate pain receptors, thereby producing an analgesic response.28
Researchers in Brazil randomly assigned 57 lactating women with preterm infants to an experimental group that received acupuncture or to a control group that received sham acupuncture.29 Treatment was administered at 5 points on the ear unilaterally for 5 minutes once a week for 16 months. Custom-made needles that did not actually puncture the skin were used in the sham group; a toothpick was used to create the sensation of needle perforations. STAI scores were reduced in both groups, although there was no statistically significant difference in scores between the acupuncture and sham groups.29
Music therapy
Music has been long believed to have beneficial psychological effects. In Turkey, researchers evaluated the effects of music therapy in 100 oncology patients who received port catheters.30 Patients were randomly assigned to an experimental group that received music therapy throughout the procedure or to a control group that received normal care. Patients who listened to music during port catheter placement had significantly reduced STAI scores and serum cortisol levels compared with those in the control group.30
Continue to: Relaxation techniques
Relaxation techniques
A wide range of relaxation techniques are used for therapeutic purposes. In Switzerland, researchers evaluated the anxiolytic effects of 10 minutes of progressive muscle relaxation and guided imagery in 39 pregnant women.31 Women randomly assigned to progressive muscle relaxation were instructed to systematically tense and then release muscle groups throughout their body in sequential order. Women assigned to the guided imagery intervention were told to imagine a safe place and to think of someone who could confer security and reassurance. The remainder of the women were assigned to a control group, where they sat quietly without any formal instructions. Researchers found that each group had a decrease in STAI scores and salivary cortisol levels immediately after the intervention.31
The relaxation response was first described in 1975 by Herbert Benson, MD, as a deep meditative state characterized by a decrease in tension, heart rate, and breathing rate. Several techniques can induce this state, including hypnosis, progressive muscle relaxation, yoga, and transcendental meditation.32 In a study of 15 healthy older adults (age 65 to 80), researchers randomly assigned participants to a relaxation response training group or to a control group.33 The relaxation response training included meditation, imagery, and relaxation techniques. After 5 weeks, participants who received the relaxation response training had marginally significant decreases in STAI scores compared with those in the control group.33
Consider these therapies as adjuncts
Our review of select positive RCTs (Table12-14,17,20,22,23,25,27,29-31,33) suggests that some nonpharmacologic/nonpsychotherapeutic adjunctive interventions may have beneficial effects for patients who have anxiety. Several of the controlled studies we reviewed demonstrated that these interventions are superior to placebo. The reductions in both anxiety severity as measured by the STAI and cortisol levels suggests that some of these complementary therapies deserve a second look as useful adjuncts to established anxiety treatments.
Bottom Line
A review of select randomized controlled trials suggests that some complementary therapies may be helpful as adjunctive therapy in patients with anxiety. These include yoga, massage therapy, aromatherapy massage, pet therapy, Qigong, auricular acupressure, reiki touch therapy, acupuncture, music therapy, and relaxation techniques.
Related Resources
- Bandelow B, Baldwin D, Abelli M, et al. Biological markers for anxiety disorders, OCD and PTSD: a consensus statement. Part II: neurochemistry, neurophysiology and neurocognition. World J Biol Psychiatry. 2017;18(3):162-214.
- National Institute of Mental Health. Anxiety disorders. https://www.nimh.nih.gov/health/topics/anxiety-disorders/index.shtml.
Anxiety disorders are the most common psychiatric illnesses in the United States, with a prevalence of nearly 29%.1 These disorders typically are treated with pharmacotherapy, psychotherapy, or a combination of both. Pharmacotherapy for anxiety has evolved considerably during the last 30 years, but medications are not efficacious for or tolerated by all patients. For example, selective serotonin reuptake inhibitors, which are frequently used for treating anxiety, can cause sexual dysfunction,2 weight gain,2 drug interactions,2 coagulopathies,3 and gastrointestinal disturbances.4 Psychotherapeutic techniques, such as cognitive behavioral therapy (CBT) and interpersonal therapy (IPT), are efficacious for mild to moderate anxiety.5-7
In addition to standard pharmacotherapy and psychotherapy, some evidence suggests that complementary therapies, such as yoga, massage, and relaxation techniques, may be beneficial as adjunctive treatments for anxiety. In placebo-controlled trials, several of these complementary therapies have been shown to decrease serum levels of the inflammatory biomarker cortisol. Anxiety is associated with inflammation,8 so therapies that reduce inflammation may help reduce symptoms of anxiety. Here, we describe the results of select positive randomized controlled trials (RCTs) of several complementary interventions for anxiety that might be useful as adjunctive treatments to psychotherapy or pharmacotherapy.
A look at RCTs that measured both anxiety and cortisol
We searched PubMed, Google Scholar, and Scopus to identify RCTs of complementary nonpharmacologic and nonpsychotherapeutic therapies for anxiety published from January 2010 to May 2017. We included only studies that:
- blindly assessed anxiety levels through a validated instrument (the State-Trait Anxiety Inventory [STAI])9
- measured cortisol concentrations before and after treatment.
Evaluating both STAI scores and cortisol levels is useful because doing so gives insight into both the clinical and biological efficacy of the therapies. Studies were excluded if they employed a pharmacologic agent in addition to the approach being evaluated.
We identified 26 studies, of which 14 met the inclusion/exclusion criteria. These studies found beneficial effects for yoga, massage therapy, aromatherapy massage, pet therapy, Qigong, auricular acupressure, reiki touch therapy, acupuncture, music therapy, and relaxation techniques.
Yoga
Yoga has become increasingly popular in the Western world during the last 2 decades.10 There are a variety of yoga practices; common forms include hatha yoga, power yoga, kripalu yoga, and forrest yoga.11
A study of 92 depressed pregnant women monito
Hatha yoga consists of a combination of postural exercises, breathing techniques, relaxation, and meditation. In a 12-week study of 88 postmenopausal women, those who practiced hatha yoga for 75 minutes a day had significantly lower STAI scores compared with women who exercised for 75 minutes a day and those who performed no physical activity.13
Continue to: Massage therapy
Massage therapy
Receiving as little as 15 minutes of back massage has proven to be beneficial for individuals with anxiety. In an RCT conducted in Turkey, 44 caregivers of patients with cancer were assigned to receive a back massage or to rest quietly in a room for 15 minutes once each day for 1 week.14 By the end of the week, compared with those who quietly rested, those who received the back massage had a statistically significant reduction in serum cortisol levels and STAI scores.14
Aromatherapy massage
Aromatherapy is the use of essential oils from plants through distillation.15 The scent of the oils is purported to provide medical benefits. More than 60 essential oils are used therapeutically, including rose, lavender, lemon, and orange.16 These essential oils are frequently used in combination with a massage.
In South Korea, researchers investigated the effects of aromatherapy massage on 25 women who had children diagnosed with attention-deficit/hyperactivity disorder.17 Women assigned to the treatment group received a 40-minute aromatherapy massage using mixed essential oils that contained lavender and geranium twice a week for 4 weeks. Women in the control group received no treatment. Compared with those in the control group, women who received the aromatherapy massages had a statistically significant decrease in STAI scores and salivary cortisol levels. Plasma cortisol was not significantly different between groups.17
Pet therapy
The psychological benefits of animal-assisted therapy were not evident until World War II, when dogs were used to cheer up injured soldiers.18 Today, pet therapy has been used on many inpatient units.19
In a U.S. study, 48 healthy undergraduate students were assigned to a room with a dog, a room with a friend, or a room by themselves.20 All participants were given the Trier Social Stress Test (TSST), a protocol that measures stress by having participants give a speech and perform mental arithmetic in front of an audience.The TSST is known to induce increases in cortisol levels. Although no differences in STAI scores were found among groups, students in the room with the dog had a lower spike in salivary cortisol after the TSST compared with participants who were in a room with a friend or in a room alone.20
Continue to: Qigong
Qigong
In Chinese medicine, Qi is known as a vital life force that flows through the body. The disruption of Qi is hypothesized to contribute to disease.21
Qigong is a medical therapy that focuses on uniting the body, breath, and mind to improve health.21 It consists of rhythmic, choreographed movements used to position the body into postures believed to help direct Qi to specific areas in the body. Qigong also uses sound exercises, in which an individual creates certain syllables while breathing. Six syllables are used, each of which is believed to affect a certain organ.21
Korean researchers randomly assigned 32 healthy men to a Qigong training group or a sham Qigong control group.22 Individuals in the training group performed 25 minutes of sound exercises, 20 minutes of meditation, and 15 minutes of movements. The control group learned the same movements as the experimental group, but without the conscious effort of moving Qi. After 3 sessions, those in the Qigong training group had significantly decreased STAI scores and serum cortisol levels compared with those in the sham group.22
In a different Korean study, researchers randomly assigned 50 participants with elevated distress levels to a Qigong training group or a waitlist control group in which participants called a trainer to describe stressful events.23 After 4 weeks, participants in the Qigong group had significant decreases in STAI scores compared with the control group. However, there were no changes in salivary cortisol levels.23
Auricular acupressure
Auricular acupressure involves applying pressure on certain portions of the auricle (outer ear) to alleviate pain and disease.24 Similar to Qigong, auricular acupressure focuses on reestablishing Qi in the body. Researchers randomly assigned 80 post-caesarean section women in Taiwan to 5 days of auricular acupressure or usual care.25 The women who received auricular acupressure had significantly lower STAI scores and serum cortisol levels compared with women who received routine care.25
Continue to: Reiki touch therapy
Reiki touch therapy
Reiki touch therapy originated in Japan. In this therapy, healers apply a light touch or hover their hands above an individual’s body to help direct energy.26
The effects of reiki touch therapy were recently evaluated in a U.S. study.27 Researchers randomly assigned 37 patients with human immunodeficiency virus to an experimental group that received 30 minutes of reiki touch therapy plus music therapy 6 times a week for 10 weeks, or to a music therapy–only control group. Patients who received reiki touch therapy had a significant decrease in STAI scores. Patients in this group also had a statistically significant drop in salivary cortisol levels after the first week.27
Acupuncture
Acupuncture is the application of needles to specific areas on the body. Acupuncture has been proposed to activate pain receptors, thereby producing an analgesic response.28
Researchers in Brazil randomly assigned 57 lactating women with preterm infants to an experimental group that received acupuncture or to a control group that received sham acupuncture.29 Treatment was administered at 5 points on the ear unilaterally for 5 minutes once a week for 16 months. Custom-made needles that did not actually puncture the skin were used in the sham group; a toothpick was used to create the sensation of needle perforations. STAI scores were reduced in both groups, although there was no statistically significant difference in scores between the acupuncture and sham groups.29
Music therapy
Music has been long believed to have beneficial psychological effects. In Turkey, researchers evaluated the effects of music therapy in 100 oncology patients who received port catheters.30 Patients were randomly assigned to an experimental group that received music therapy throughout the procedure or to a control group that received normal care. Patients who listened to music during port catheter placement had significantly reduced STAI scores and serum cortisol levels compared with those in the control group.30
Continue to: Relaxation techniques
Relaxation techniques
A wide range of relaxation techniques are used for therapeutic purposes. In Switzerland, researchers evaluated the anxiolytic effects of 10 minutes of progressive muscle relaxation and guided imagery in 39 pregnant women.31 Women randomly assigned to progressive muscle relaxation were instructed to systematically tense and then release muscle groups throughout their body in sequential order. Women assigned to the guided imagery intervention were told to imagine a safe place and to think of someone who could confer security and reassurance. The remainder of the women were assigned to a control group, where they sat quietly without any formal instructions. Researchers found that each group had a decrease in STAI scores and salivary cortisol levels immediately after the intervention.31
The relaxation response was first described in 1975 by Herbert Benson, MD, as a deep meditative state characterized by a decrease in tension, heart rate, and breathing rate. Several techniques can induce this state, including hypnosis, progressive muscle relaxation, yoga, and transcendental meditation.32 In a study of 15 healthy older adults (age 65 to 80), researchers randomly assigned participants to a relaxation response training group or to a control group.33 The relaxation response training included meditation, imagery, and relaxation techniques. After 5 weeks, participants who received the relaxation response training had marginally significant decreases in STAI scores compared with those in the control group.33
Consider these therapies as adjuncts
Our review of select positive RCTs (Table12-14,17,20,22,23,25,27,29-31,33) suggests that some nonpharmacologic/nonpsychotherapeutic adjunctive interventions may have beneficial effects for patients who have anxiety. Several of the controlled studies we reviewed demonstrated that these interventions are superior to placebo. The reductions in both anxiety severity as measured by the STAI and cortisol levels suggests that some of these complementary therapies deserve a second look as useful adjuncts to established anxiety treatments.
Bottom Line
A review of select randomized controlled trials suggests that some complementary therapies may be helpful as adjunctive therapy in patients with anxiety. These include yoga, massage therapy, aromatherapy massage, pet therapy, Qigong, auricular acupressure, reiki touch therapy, acupuncture, music therapy, and relaxation techniques.
Related Resources
- Bandelow B, Baldwin D, Abelli M, et al. Biological markers for anxiety disorders, OCD and PTSD: a consensus statement. Part II: neurochemistry, neurophysiology and neurocognition. World J Biol Psychiatry. 2017;18(3):162-214.
- National Institute of Mental Health. Anxiety disorders. https://www.nimh.nih.gov/health/topics/anxiety-disorders/index.shtml.
1. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62(6):593-602.
2. Masand PS, Gupta S. Long-term side effects of newer-generation antidepressants: SSRIs, venlafaxine, nefazodone, bupropion, and mirtazapine. Ann Clin Psychiatry. 2002;14(3):175-182.
3. Siddiqui R, Gawande S, Shende T, et al. SSRI-induced coagulopathy: is it reality? Therapeutic Advances in Psychopharmacology. 2011;1(6):169-174.
4. Brambilla P, Cipriani A, Hotopf M, et al. Side-effect profile of fluoxetine in comparison with other SSRIs, tricyclic and newer antidepressants: a meta-analysis of clinical trial data. Pharmacopsychiatry. 2005;38(2):69-77.
5. Slomski A. Blended CBT controls anxiety in cancer survivors. JAMA. 2017;318(4):323.
6. Forsell E, Bendix M, Holländare F, et al. Internet delivered cognitive behavior therapy for antenatal depression: a randomised controlled trial. J Affect Disord. 2017;221:56-64.
7. Lilliengren P, Johansson R, Town JM, et al. Intensive Short-Term Dynamic Psychotherapy for generalized anxiety disorder: A pilot effectiveness and process-outcome study. Clin Psychol Psychother. 2017;24(6):1313-1321.
8. Furtado M, Katzman MA. Neuroinflammatory pathways in anxiety, posttraumatic stress, and obsessive compulsive disorders. Psychiatry Res. 2015;229(1-2):37-48.
9. Spielberger CD, Gorsuch RL, Lushene R, et al. Manual for the State-Trait Anxiety Inventory. Palo Alto, CA: Consulting Psychologists Press; 1983.
10. Saper RB, Eisenberg DM, Davis RB, et al. Prevalence and patterns of adult yoga use in the United States: results of a national survey. Altern Ther Health Med. 2004;10(2):44-49.
11. Farmer J. Americanasana. Reviews in American history. 2012;40(1):145-158.
12. Field T, Diego M, Delgado J, et al. Yoga and social support reduce prenatal depression, anxiety and cortisol. J Bodyw Mov Ther: 2013;17(4):397-403.
13. Jorge MP, Santaella DF, Pontes IM, et al. Hatha Yoga practice decreases menopause symptoms and improves quality of life: a randomized controlled trial. Complement Ther Med. 2016;26:128-135.
14. Pinar R, Afsar F. Back massage to decrease state anxiety, cortisol level, blood pressure, heart rate and increase sleep quality in family caregivers of patients with cancer: a randomised controlled trial. Asian Pac J Cancer Prev. 2015;16(18):8127-8133.
15. Kuriyama H, Watanabe S, Nakaya, et al. Immunological and psychological benefits of aromatherapy massage. Evid Based Complement Alternat Med. 2005;2(2):179-184.
16. Setzer WN. Essential oils and anxiolytic aromatherapy. Nat Prod Commun. 2009;4(9):1305-1316.
17. Wu JJ, Cui Y, Yang YS, et al. Modulatory effects of aromatherapy massage intervention on electroencephalogram, psychological assessments, salivary cortisol and plasma brain-derived neurotrophic factor. Complement Ther Med. 2014;22(3):456-462.
18. Fine A. Forward. In: Fine A, ed. Handbook on animal-assisted therapy-theoretical foundations and guidelines for practice. 3rd ed. Academic Press; 2010:xvii-xviii.
19. Snipelisky D, Burton MC. Canine-assisted therapy in the inpatient setting. South Med J. 2014;107(4):265-273.
20. Polheber JP, Matchock RL. The presence of a dog attenuates cortisol and heart rate in the Trier Social Stress Test compared to human friends. J Behav Med. 2014;37(5):860-867.
21. Liu T, Qiang X, eds. Chinese medical Qigong. Philadelphia, PA: Singing Dragon; 2013:1-100,192,238,511.
22. Lee MS, Kang CW, Lim HJ, et al. Effects of Qi-training on anxiety and plasma concentrations of cortisol, ACTH, and aldosterone: a randomized placebo-controlled pilot study. Stress Health. 2004;20(5):243-248.
23. Hwang EY, Chung SY, Cho JH, et al. Effects of a brief Qigong-based stress reduction program (BQSRP) in a distressed Korean population: a randomized trial. BMC Complement Altern Med. 2013;13:113.
24. Oleson, T. Overview and history of auriculotherapy. In: Auriculotherapy manual: Chinese and Western systems of ear acupuncture. 4th ed. London: Churchill Livingstone; 2014:1.
25. Kuo SY, Tsai SH, Chen SL, et al. Auricular acupressure relieves anxiety and fatigue, and reduces cortisol levels in post-caesarean section women: a single-blind, randomised controlled study. Int J Nurs Stud. 2016;53:17-26.
26. Horan P. Introduction. In: Horan P. Empowerment through reiki: the path to personal and global transformation. 8th ed. Twin Lakes, WI: Lotus Press; 1998:13-15.
27. Bremner MN, Blake BJ, Wagner VD, et al. Effects of reiki with music compared to music only among people living with HIV. J Assoc Nurses AIDS Care. 2016;27(5):635-647.
28. Helmes JM. The basic, clinical, and speculative science of acupuncture. In: Acupuncture energetics: a clinical approach for physicians. Volume 1. Berkeley, CA: Medical Acupuncture Publishers; 1995:19-32.
29. Haddad-Rodrigues M, Spanó Nakano A, Stefanello J, et al. Acupuncture for anxiety in lactating mothers with preterm infants: a randomized controlled trial. Evid Based Complement Alternat Med. 2013;2013:169184. doi: 10.1155/2013/169184.
30. Zengin S, Kabul S, Al B, et al. Effects of music therapy on pain and anxiety in patients undergoing port catheter placement procedure. Complement Ther Med. 2013;21(6):689-696.
31. Urech C, Fink NS, Hoesli I, et al. Effects of relaxation on psychobiological wellbeing during pregnancy: a randomized controlled trial. Psychoneuroendocrinology. 2010;35(9):1348-1355.
32. Goleman D. The relaxation response. In: Mind body medicine: how to use your mind for better health. Yonkers, NY: Consumer Reports; 1993:125-149.
33. Galvin JA, Benson H, Deckro GR, et al. The relaxation response: reducing stress and improving cognition in healthy aging adults. Complement Ther Clin Pract. 2006;12(3):186-191.
1. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62(6):593-602.
2. Masand PS, Gupta S. Long-term side effects of newer-generation antidepressants: SSRIs, venlafaxine, nefazodone, bupropion, and mirtazapine. Ann Clin Psychiatry. 2002;14(3):175-182.
3. Siddiqui R, Gawande S, Shende T, et al. SSRI-induced coagulopathy: is it reality? Therapeutic Advances in Psychopharmacology. 2011;1(6):169-174.
4. Brambilla P, Cipriani A, Hotopf M, et al. Side-effect profile of fluoxetine in comparison with other SSRIs, tricyclic and newer antidepressants: a meta-analysis of clinical trial data. Pharmacopsychiatry. 2005;38(2):69-77.
5. Slomski A. Blended CBT controls anxiety in cancer survivors. JAMA. 2017;318(4):323.
6. Forsell E, Bendix M, Holländare F, et al. Internet delivered cognitive behavior therapy for antenatal depression: a randomised controlled trial. J Affect Disord. 2017;221:56-64.
7. Lilliengren P, Johansson R, Town JM, et al. Intensive Short-Term Dynamic Psychotherapy for generalized anxiety disorder: A pilot effectiveness and process-outcome study. Clin Psychol Psychother. 2017;24(6):1313-1321.
8. Furtado M, Katzman MA. Neuroinflammatory pathways in anxiety, posttraumatic stress, and obsessive compulsive disorders. Psychiatry Res. 2015;229(1-2):37-48.
9. Spielberger CD, Gorsuch RL, Lushene R, et al. Manual for the State-Trait Anxiety Inventory. Palo Alto, CA: Consulting Psychologists Press; 1983.
10. Saper RB, Eisenberg DM, Davis RB, et al. Prevalence and patterns of adult yoga use in the United States: results of a national survey. Altern Ther Health Med. 2004;10(2):44-49.
11. Farmer J. Americanasana. Reviews in American history. 2012;40(1):145-158.
12. Field T, Diego M, Delgado J, et al. Yoga and social support reduce prenatal depression, anxiety and cortisol. J Bodyw Mov Ther: 2013;17(4):397-403.
13. Jorge MP, Santaella DF, Pontes IM, et al. Hatha Yoga practice decreases menopause symptoms and improves quality of life: a randomized controlled trial. Complement Ther Med. 2016;26:128-135.
14. Pinar R, Afsar F. Back massage to decrease state anxiety, cortisol level, blood pressure, heart rate and increase sleep quality in family caregivers of patients with cancer: a randomised controlled trial. Asian Pac J Cancer Prev. 2015;16(18):8127-8133.
15. Kuriyama H, Watanabe S, Nakaya, et al. Immunological and psychological benefits of aromatherapy massage. Evid Based Complement Alternat Med. 2005;2(2):179-184.
16. Setzer WN. Essential oils and anxiolytic aromatherapy. Nat Prod Commun. 2009;4(9):1305-1316.
17. Wu JJ, Cui Y, Yang YS, et al. Modulatory effects of aromatherapy massage intervention on electroencephalogram, psychological assessments, salivary cortisol and plasma brain-derived neurotrophic factor. Complement Ther Med. 2014;22(3):456-462.
18. Fine A. Forward. In: Fine A, ed. Handbook on animal-assisted therapy-theoretical foundations and guidelines for practice. 3rd ed. Academic Press; 2010:xvii-xviii.
19. Snipelisky D, Burton MC. Canine-assisted therapy in the inpatient setting. South Med J. 2014;107(4):265-273.
20. Polheber JP, Matchock RL. The presence of a dog attenuates cortisol and heart rate in the Trier Social Stress Test compared to human friends. J Behav Med. 2014;37(5):860-867.
21. Liu T, Qiang X, eds. Chinese medical Qigong. Philadelphia, PA: Singing Dragon; 2013:1-100,192,238,511.
22. Lee MS, Kang CW, Lim HJ, et al. Effects of Qi-training on anxiety and plasma concentrations of cortisol, ACTH, and aldosterone: a randomized placebo-controlled pilot study. Stress Health. 2004;20(5):243-248.
23. Hwang EY, Chung SY, Cho JH, et al. Effects of a brief Qigong-based stress reduction program (BQSRP) in a distressed Korean population: a randomized trial. BMC Complement Altern Med. 2013;13:113.
24. Oleson, T. Overview and history of auriculotherapy. In: Auriculotherapy manual: Chinese and Western systems of ear acupuncture. 4th ed. London: Churchill Livingstone; 2014:1.
25. Kuo SY, Tsai SH, Chen SL, et al. Auricular acupressure relieves anxiety and fatigue, and reduces cortisol levels in post-caesarean section women: a single-blind, randomised controlled study. Int J Nurs Stud. 2016;53:17-26.
26. Horan P. Introduction. In: Horan P. Empowerment through reiki: the path to personal and global transformation. 8th ed. Twin Lakes, WI: Lotus Press; 1998:13-15.
27. Bremner MN, Blake BJ, Wagner VD, et al. Effects of reiki with music compared to music only among people living with HIV. J Assoc Nurses AIDS Care. 2016;27(5):635-647.
28. Helmes JM. The basic, clinical, and speculative science of acupuncture. In: Acupuncture energetics: a clinical approach for physicians. Volume 1. Berkeley, CA: Medical Acupuncture Publishers; 1995:19-32.
29. Haddad-Rodrigues M, Spanó Nakano A, Stefanello J, et al. Acupuncture for anxiety in lactating mothers with preterm infants: a randomized controlled trial. Evid Based Complement Alternat Med. 2013;2013:169184. doi: 10.1155/2013/169184.
30. Zengin S, Kabul S, Al B, et al. Effects of music therapy on pain and anxiety in patients undergoing port catheter placement procedure. Complement Ther Med. 2013;21(6):689-696.
31. Urech C, Fink NS, Hoesli I, et al. Effects of relaxation on psychobiological wellbeing during pregnancy: a randomized controlled trial. Psychoneuroendocrinology. 2010;35(9):1348-1355.
32. Goleman D. The relaxation response. In: Mind body medicine: how to use your mind for better health. Yonkers, NY: Consumer Reports; 1993:125-149.
33. Galvin JA, Benson H, Deckro GR, et al. The relaxation response: reducing stress and improving cognition in healthy aging adults. Complement Ther Clin Pract. 2006;12(3):186-191.
10 Myths about ECT
As evidence supporting the use of electroconvulsive therapy (ECT) to treat patients with depression and other psychiatric illnesses continues to grow, myths about this treatment persist. In light of these myths, patients might be reluctant to receive ECT. As clinicians, we need to educate patients about the safety and effectiveness of this treatment. Here are 10 of the most commonly held myths about ECT, and why each is a misconception.
1. It is a barbaric treatment. ECT is conducted in a controlled medical environment, either during a hospitalization or as an outpatient procedure, by a team consisting of a psychiatrist, anesthesiologist, and nurse. Patients receive a short-acting intravenous anesthetic to ensure that they are unaware of the procedure, and a muscle relaxant to help prevent physical injury. Vital signs and brain waves are monitored throughout the procedure, which typically lasts 15 to 20 minutes. Patients remain relaxed, are unaware that they are having a seizure, and experience no pain. Following ECT, the patient is taken to a recovery area, where he or she is closely monitored as the medications wear off.
2. It causes brain damage. Studies using MRI to look at the brain before and after ECT have found no evidence that ECT causes negative changes in the brain’s structural anatomy.1 To the contrary, there is evidence that there is neuroplasticity in the brain in response to ECT, and the neurotrophin brain-derived neurotrophic factor also may be increased.2,3
3. It causes permanent memory loss. ECT can result in both anterograde and retrograde memory impairment; however, anterograde amnesia typically lasts only days to weeks. Retrograde amnesia is much less common, but when it occurs, it tends to be loss of memory of events that took place in the weeks leading up to and during treatment. Using an ultrabrief (as opposed to standard brief) pulse, as well as right unilateral (as opposed to bilateral) electrode placement, substantially reduces the risk of cognitive and memory adverse effects.4
4. It is a treatment of last resort. Typically, ECT is used for patients who have not responded to other interventions. However, ECT can be used as a first-line treatment for patients if a rapid or higher likelihood of response is necessary, such as when a patient is suicidal, catatonic, or malnourished as a result of severe depression.5
5. It only works for depression. Evidence shows ECT is efficacious for several psychiatric conditions, not just unipolar depressive disorder. It can effectively treat bipolar depression, mania, catatonia, and acute psychosis associated with schizophrenia and schizoaffective disorders.6 ECT also has been demonstrated to be effective in acute and maintenance treatment of Parkinson’s disease.7
6. It is not safe. Death associated with ECT is extremely rare. A recent analysis estimated that the rate of ECT-related mortality is 2.1 deaths per 100,000 treatments. In comparison, the mortality rate of general anesthesia used during surgery has been reported as 3.4 deaths per 100,000 procedures.8 Evidence also suggests ECT can be safely administered to patients who are pregnant.9
Continue to: 7. It cannot be given to patients with epilepsy
7. It cannot be given to patients with epilepsy. There are no absolute contraindications to using ECT for these patients. Most patients with epilepsy can be successfully treated with ECT without requiring an adjustment to the dose of their antiepileptic medications.10
8. It will change one’s personality. ECT has not been found to cause any alterations in personality. Patients who are treated with ECT may describe feeling more like themselves once their chronic symptoms of depression have improved. However, ECT has not been shown to effectively treat the symptoms or underlying illness of personality disorders, and it may not be an effective treatment for depression associated with borderline personality disorder.11
9. Its success rate is low. ECT has the highest response and remission rates of any form of treatment used for depression. An estimated 70% to 90% of patients with depression who are treated with ECT show improvement.12
10. It is a permanent cure. ECT is not likely a permanent solution for severe depression. The likelihood of relapse in patients with severe depression who are helped by ECT can be reduced by receiving ongoing antidepressant treatment, and some patients may require continuation or maintenance ECT.13
1. Scott AI, Turnbull LW. Do repeated courses of ECT cause brain damage detectable by MRI? Am J Psychiatry. 1990;147(3):371-372.
2. Sartorius A, Demirakca T, Böhringer A, et al. Electroconvulsive therapy increases temporal gray matter volume and cortical thickness. Eur Neuropsychopharmacol. 2016;26(3)506-517.
3. Bocchio-Chiavetto L, Zanardini R, Bortolomasi M et al. Electroconvulsive therapy (ECT) increases serum brain derived neurotrophic factor (BDNF) in drug resistant depressed patients. Eur Neuropsychopharmacol. 2006;16(8):620-624.
4. Sackeim HA, Prudic J, Nobler MS, et al. Effects of pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain Stimul. 2008;1(2):71-83.
5. American Psychiatric Association. The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging: a task force report of the American Psychiatric Association, 2nd edition. Washington, DC: American Psychiatric Association; 2001.
6. Fontenelle LF, Coutinho ES, Lins-Martins NM, et al. Electroconvulsive therapy for obsessive-compulsive disorder: a systematic review. J Clin Psychiatry. 2015;76(7):949-957.
7. Narang P, Glowacki A, Lippmann S. Electroconvulsive therapy intervention for Parkinson’s disease. Innov Clin Neurosci. 2015;12(9-10):25-28.
8. Tørring N, Sanghani SN, Petrides G, et al. The mortality rate of electroconvulsive therapy: a systematic review and pooled analysis. Acta Psychiatr Scand. 2017;135(5):388-397.
9. Sinha P, Goyal P, Andrade C. A meta-review of the safety of electroconvulsive therapy in pregnancy. J ECT. 2017;33(2):81-88.
10. Lunde ME, Lee EK, Rasmussen KG. Electroconvulsive therapy in patients with epilepsy. Epilepsy Behav. 2006;9(2):355-359.
11. Feske U, Mulsant BH, Pilkonis PA, et al. Clinical outcome of ECT in patients with major depression and comorbid borderline personality disorder. Am J Psychiatry. 2004;161(11):2073-2080.
12. Kellner CH, McClintock SM, McCall WV, et al; CORE/PRIDE Group. Brief pulse and ultrabrief pulse right unilateral electroconvulsive therapy (ECT) for major depression: efficacy, effectiveness, and cognitive effects. J Clin Psychiatry. 2014;75(7):777.
13. Jelovac A, Kolshus E, McLoughlin DM. Relapse following successful electroconvulsive therapy for major depression: a meta-analysis. Neuropsychopharmacology. 2013;38(12):2467-2474.
As evidence supporting the use of electroconvulsive therapy (ECT) to treat patients with depression and other psychiatric illnesses continues to grow, myths about this treatment persist. In light of these myths, patients might be reluctant to receive ECT. As clinicians, we need to educate patients about the safety and effectiveness of this treatment. Here are 10 of the most commonly held myths about ECT, and why each is a misconception.
1. It is a barbaric treatment. ECT is conducted in a controlled medical environment, either during a hospitalization or as an outpatient procedure, by a team consisting of a psychiatrist, anesthesiologist, and nurse. Patients receive a short-acting intravenous anesthetic to ensure that they are unaware of the procedure, and a muscle relaxant to help prevent physical injury. Vital signs and brain waves are monitored throughout the procedure, which typically lasts 15 to 20 minutes. Patients remain relaxed, are unaware that they are having a seizure, and experience no pain. Following ECT, the patient is taken to a recovery area, where he or she is closely monitored as the medications wear off.
2. It causes brain damage. Studies using MRI to look at the brain before and after ECT have found no evidence that ECT causes negative changes in the brain’s structural anatomy.1 To the contrary, there is evidence that there is neuroplasticity in the brain in response to ECT, and the neurotrophin brain-derived neurotrophic factor also may be increased.2,3
3. It causes permanent memory loss. ECT can result in both anterograde and retrograde memory impairment; however, anterograde amnesia typically lasts only days to weeks. Retrograde amnesia is much less common, but when it occurs, it tends to be loss of memory of events that took place in the weeks leading up to and during treatment. Using an ultrabrief (as opposed to standard brief) pulse, as well as right unilateral (as opposed to bilateral) electrode placement, substantially reduces the risk of cognitive and memory adverse effects.4
4. It is a treatment of last resort. Typically, ECT is used for patients who have not responded to other interventions. However, ECT can be used as a first-line treatment for patients if a rapid or higher likelihood of response is necessary, such as when a patient is suicidal, catatonic, or malnourished as a result of severe depression.5
5. It only works for depression. Evidence shows ECT is efficacious for several psychiatric conditions, not just unipolar depressive disorder. It can effectively treat bipolar depression, mania, catatonia, and acute psychosis associated with schizophrenia and schizoaffective disorders.6 ECT also has been demonstrated to be effective in acute and maintenance treatment of Parkinson’s disease.7
6. It is not safe. Death associated with ECT is extremely rare. A recent analysis estimated that the rate of ECT-related mortality is 2.1 deaths per 100,000 treatments. In comparison, the mortality rate of general anesthesia used during surgery has been reported as 3.4 deaths per 100,000 procedures.8 Evidence also suggests ECT can be safely administered to patients who are pregnant.9
Continue to: 7. It cannot be given to patients with epilepsy
7. It cannot be given to patients with epilepsy. There are no absolute contraindications to using ECT for these patients. Most patients with epilepsy can be successfully treated with ECT without requiring an adjustment to the dose of their antiepileptic medications.10
8. It will change one’s personality. ECT has not been found to cause any alterations in personality. Patients who are treated with ECT may describe feeling more like themselves once their chronic symptoms of depression have improved. However, ECT has not been shown to effectively treat the symptoms or underlying illness of personality disorders, and it may not be an effective treatment for depression associated with borderline personality disorder.11
9. Its success rate is low. ECT has the highest response and remission rates of any form of treatment used for depression. An estimated 70% to 90% of patients with depression who are treated with ECT show improvement.12
10. It is a permanent cure. ECT is not likely a permanent solution for severe depression. The likelihood of relapse in patients with severe depression who are helped by ECT can be reduced by receiving ongoing antidepressant treatment, and some patients may require continuation or maintenance ECT.13
As evidence supporting the use of electroconvulsive therapy (ECT) to treat patients with depression and other psychiatric illnesses continues to grow, myths about this treatment persist. In light of these myths, patients might be reluctant to receive ECT. As clinicians, we need to educate patients about the safety and effectiveness of this treatment. Here are 10 of the most commonly held myths about ECT, and why each is a misconception.
1. It is a barbaric treatment. ECT is conducted in a controlled medical environment, either during a hospitalization or as an outpatient procedure, by a team consisting of a psychiatrist, anesthesiologist, and nurse. Patients receive a short-acting intravenous anesthetic to ensure that they are unaware of the procedure, and a muscle relaxant to help prevent physical injury. Vital signs and brain waves are monitored throughout the procedure, which typically lasts 15 to 20 minutes. Patients remain relaxed, are unaware that they are having a seizure, and experience no pain. Following ECT, the patient is taken to a recovery area, where he or she is closely monitored as the medications wear off.
2. It causes brain damage. Studies using MRI to look at the brain before and after ECT have found no evidence that ECT causes negative changes in the brain’s structural anatomy.1 To the contrary, there is evidence that there is neuroplasticity in the brain in response to ECT, and the neurotrophin brain-derived neurotrophic factor also may be increased.2,3
3. It causes permanent memory loss. ECT can result in both anterograde and retrograde memory impairment; however, anterograde amnesia typically lasts only days to weeks. Retrograde amnesia is much less common, but when it occurs, it tends to be loss of memory of events that took place in the weeks leading up to and during treatment. Using an ultrabrief (as opposed to standard brief) pulse, as well as right unilateral (as opposed to bilateral) electrode placement, substantially reduces the risk of cognitive and memory adverse effects.4
4. It is a treatment of last resort. Typically, ECT is used for patients who have not responded to other interventions. However, ECT can be used as a first-line treatment for patients if a rapid or higher likelihood of response is necessary, such as when a patient is suicidal, catatonic, or malnourished as a result of severe depression.5
5. It only works for depression. Evidence shows ECT is efficacious for several psychiatric conditions, not just unipolar depressive disorder. It can effectively treat bipolar depression, mania, catatonia, and acute psychosis associated with schizophrenia and schizoaffective disorders.6 ECT also has been demonstrated to be effective in acute and maintenance treatment of Parkinson’s disease.7
6. It is not safe. Death associated with ECT is extremely rare. A recent analysis estimated that the rate of ECT-related mortality is 2.1 deaths per 100,000 treatments. In comparison, the mortality rate of general anesthesia used during surgery has been reported as 3.4 deaths per 100,000 procedures.8 Evidence also suggests ECT can be safely administered to patients who are pregnant.9
Continue to: 7. It cannot be given to patients with epilepsy
7. It cannot be given to patients with epilepsy. There are no absolute contraindications to using ECT for these patients. Most patients with epilepsy can be successfully treated with ECT without requiring an adjustment to the dose of their antiepileptic medications.10
8. It will change one’s personality. ECT has not been found to cause any alterations in personality. Patients who are treated with ECT may describe feeling more like themselves once their chronic symptoms of depression have improved. However, ECT has not been shown to effectively treat the symptoms or underlying illness of personality disorders, and it may not be an effective treatment for depression associated with borderline personality disorder.11
9. Its success rate is low. ECT has the highest response and remission rates of any form of treatment used for depression. An estimated 70% to 90% of patients with depression who are treated with ECT show improvement.12
10. It is a permanent cure. ECT is not likely a permanent solution for severe depression. The likelihood of relapse in patients with severe depression who are helped by ECT can be reduced by receiving ongoing antidepressant treatment, and some patients may require continuation or maintenance ECT.13
1. Scott AI, Turnbull LW. Do repeated courses of ECT cause brain damage detectable by MRI? Am J Psychiatry. 1990;147(3):371-372.
2. Sartorius A, Demirakca T, Böhringer A, et al. Electroconvulsive therapy increases temporal gray matter volume and cortical thickness. Eur Neuropsychopharmacol. 2016;26(3)506-517.
3. Bocchio-Chiavetto L, Zanardini R, Bortolomasi M et al. Electroconvulsive therapy (ECT) increases serum brain derived neurotrophic factor (BDNF) in drug resistant depressed patients. Eur Neuropsychopharmacol. 2006;16(8):620-624.
4. Sackeim HA, Prudic J, Nobler MS, et al. Effects of pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain Stimul. 2008;1(2):71-83.
5. American Psychiatric Association. The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging: a task force report of the American Psychiatric Association, 2nd edition. Washington, DC: American Psychiatric Association; 2001.
6. Fontenelle LF, Coutinho ES, Lins-Martins NM, et al. Electroconvulsive therapy for obsessive-compulsive disorder: a systematic review. J Clin Psychiatry. 2015;76(7):949-957.
7. Narang P, Glowacki A, Lippmann S. Electroconvulsive therapy intervention for Parkinson’s disease. Innov Clin Neurosci. 2015;12(9-10):25-28.
8. Tørring N, Sanghani SN, Petrides G, et al. The mortality rate of electroconvulsive therapy: a systematic review and pooled analysis. Acta Psychiatr Scand. 2017;135(5):388-397.
9. Sinha P, Goyal P, Andrade C. A meta-review of the safety of electroconvulsive therapy in pregnancy. J ECT. 2017;33(2):81-88.
10. Lunde ME, Lee EK, Rasmussen KG. Electroconvulsive therapy in patients with epilepsy. Epilepsy Behav. 2006;9(2):355-359.
11. Feske U, Mulsant BH, Pilkonis PA, et al. Clinical outcome of ECT in patients with major depression and comorbid borderline personality disorder. Am J Psychiatry. 2004;161(11):2073-2080.
12. Kellner CH, McClintock SM, McCall WV, et al; CORE/PRIDE Group. Brief pulse and ultrabrief pulse right unilateral electroconvulsive therapy (ECT) for major depression: efficacy, effectiveness, and cognitive effects. J Clin Psychiatry. 2014;75(7):777.
13. Jelovac A, Kolshus E, McLoughlin DM. Relapse following successful electroconvulsive therapy for major depression: a meta-analysis. Neuropsychopharmacology. 2013;38(12):2467-2474.
1. Scott AI, Turnbull LW. Do repeated courses of ECT cause brain damage detectable by MRI? Am J Psychiatry. 1990;147(3):371-372.
2. Sartorius A, Demirakca T, Böhringer A, et al. Electroconvulsive therapy increases temporal gray matter volume and cortical thickness. Eur Neuropsychopharmacol. 2016;26(3)506-517.
3. Bocchio-Chiavetto L, Zanardini R, Bortolomasi M et al. Electroconvulsive therapy (ECT) increases serum brain derived neurotrophic factor (BDNF) in drug resistant depressed patients. Eur Neuropsychopharmacol. 2006;16(8):620-624.
4. Sackeim HA, Prudic J, Nobler MS, et al. Effects of pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain Stimul. 2008;1(2):71-83.
5. American Psychiatric Association. The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging: a task force report of the American Psychiatric Association, 2nd edition. Washington, DC: American Psychiatric Association; 2001.
6. Fontenelle LF, Coutinho ES, Lins-Martins NM, et al. Electroconvulsive therapy for obsessive-compulsive disorder: a systematic review. J Clin Psychiatry. 2015;76(7):949-957.
7. Narang P, Glowacki A, Lippmann S. Electroconvulsive therapy intervention for Parkinson’s disease. Innov Clin Neurosci. 2015;12(9-10):25-28.
8. Tørring N, Sanghani SN, Petrides G, et al. The mortality rate of electroconvulsive therapy: a systematic review and pooled analysis. Acta Psychiatr Scand. 2017;135(5):388-397.
9. Sinha P, Goyal P, Andrade C. A meta-review of the safety of electroconvulsive therapy in pregnancy. J ECT. 2017;33(2):81-88.
10. Lunde ME, Lee EK, Rasmussen KG. Electroconvulsive therapy in patients with epilepsy. Epilepsy Behav. 2006;9(2):355-359.
11. Feske U, Mulsant BH, Pilkonis PA, et al. Clinical outcome of ECT in patients with major depression and comorbid borderline personality disorder. Am J Psychiatry. 2004;161(11):2073-2080.
12. Kellner CH, McClintock SM, McCall WV, et al; CORE/PRIDE Group. Brief pulse and ultrabrief pulse right unilateral electroconvulsive therapy (ECT) for major depression: efficacy, effectiveness, and cognitive effects. J Clin Psychiatry. 2014;75(7):777.
13. Jelovac A, Kolshus E, McLoughlin DM. Relapse following successful electroconvulsive therapy for major depression: a meta-analysis. Neuropsychopharmacology. 2013;38(12):2467-2474.
NEED HAIR: Pinpointing the cause of a patient’s hair loss
Telogen effluvium (TE)—temporary hair loss due to the shedding of telogen (resting phase of hair cycle) hair after exposure to some form of stress—is one of the most common causes of diffuse non-scarring hair loss from the scalp.1 TE is more common than anagen (growing phase of hair cycle) hair loss.2 Hair loss can be triggered by numerous factors, including certain psychotropic medications.3,4 Mood stabilizers, such as valproic acid and lithium, are most commonly implicated. Hair loss also has been associated with the use of the first-generation antipsychotics haloperidol and chlorpromazine and the second-generation antipsychotics olanzapine, quetiapine, and risperidone.5-7 We recently cared for a woman with bipolar I disorder and generalized anxiety disorder who was prescribed lurasidone and later developed TE. Her hair loss completely resolved 4 months after lurasidone was discontinued.
TE can be triggered by events that interrupt the normal hair growth cycle. Typically, it is observed approximately 3 months after a triggering event and is usually self-limiting, lasting approximately 6 months.7 Diagnostic features include a strongly positive hair-pull test, a trichogram showing >25% telogen hair, and a biopsy showing an increase in telogen follicles.8,9 To conduct the hair-pull test, grasp approximately 40 to 60 hairs between the thumb and forefinger while slightly stretching the scalp to allow your fingers to slide along the length of the hair. Usually only 2 to 3 hairs in the telogen phase can be plucked via this method; if >10% of the hairs grasped can be plucked, this indicates a pathologic process.10
Significant hair loss, particularly among women, is a distressing adverse effect that can be an important moderator of compliance, treatment adherence, and relapse. To help clinicians narrow down the wide range of potential causes of a patient’s hair loss, we created the mnemonic NEED HAIR.
Nutritional: Iron deficiency anemia, a “crash” diet, zinc deficiency, vitamin B6 or B12 deficiency, chronic starvation, diarrhea, hypoproteinemia (metabolic or dietary origin), malabsorption, or heavy metal ingestion.1
Endocrine: Thyroid disorders and the early stage of androgenic alopecia.8,11
Environmental: Stress from a severe febrile illness, emotional stress, serious injuries, major surgery, large hemorrhage, and difficult labor.12
Drugs: Oral contraceptives, antithyroid drugs, retinoids (etretinate and acitretin), anticonvulsants, antidepressants, antipsychotics, hypolipidemic drugs, anticoagulants, antihypertensives (beta blockers, angiotensin-converting enzyme inhibitors), and cytotoxic drugs.1,4-7
Continue to: Hormonal fluctuations
Hormonal fluctuations: Polycystic ovarian syndrome and postpartum hormonal changes.11
Autoimmune: Lupus erythematosus, dermatomyositis, scleroderma, Hashimoto’s thyroiditis, Sjögren’s syndrome, inflammatory bowel disease, and autoimmune atrophic gastritis.12,13
Infections and chronic illnesses: Fungal infections (eg, tinea capitis), human immunodeficiency virus, syphilis, typhoid, malaria, tuberculosis, malignancy, renal failure, hepatic failure, and other chronic illnesses.1,9
Radiation: Radiation treatment and excessive UV exposure.12,14,15
Treatment for hair loss depends on the specific caus
1. Grover C, Khurana A. Telogen effluvium. Indian J Dermatol Venerol Leprol. 2013;79(5):591-603.
2. Harrison S, Bergfeld W. Diffuse hair loss: its triggers and management. Cleve Clin J Med. 2009;76(6):361-367.
3. Gautam M. Alopecia due to psychotropic medications. Ann Pharmacother. 1999;33(5):631-637.
4. Mercke Y, Sheng H, Khan T, et al. Hair loss in psychopharmacology. Ann Clin Psychiatry. 2000;12(1):35-42.
5. Kubota T, Ishikura T, Jibiki I. Alopecia areata associated with haloperidol. Jpn J Psychiatry Neurol. 1994;48(3):579-581.
6. McLean RM, Harrison-Woolrych M. Alopecia associated with quetiapine. Int Clin Psychopharmacol 2007;22(2):117-9.
7. Kulolu M, Korkmaz S, Kilic N, et al. Olanzapine induced hair loss: a case report. Bulletin of Clinical Psychopharmacology. 2012;22(4):362-365.
8. Malkud S. Telogen effluvium: a review. J Clin Diagn Res. 2015;9(9):WE01-WE03.
9. Shrivastava SB. Diffuse hair loss in an adult female: approach to diagnosis and management. Indian J Dermatol Venerol Leprol. 2009;75(1):20-28; quiz 27-28.
10. Piérard GE, Piérard-Franchimont C, Marks R, et al; EEMCO group (European Expert Group on Efficacy Measurement of Cosmetics and Other Topical Products). EEMCO guidance for the assessment of hair shedding and alopecia. Skin Pharmacol Physiol. 2004;17(2):98-110.
11. Mirallas O, Grimalt R. The postpartum telogen effluvium fallacy. Skin Appendage Disord. 2016;1(4):198-201.
12. Rebora A. Proposing a simpler classification of telogen effluvium. Skin Appendage Disord. 2016;2(1-2):35-38.
13. Cassano N, Amerio P, D’Ovidio R, et al. Hair disorders associated with autoimmune connective tissue diseases. G Ital Dermatol Venereol. 2014;149(5):555-565.
14. Trüeb RM. Telogen effluvium: is there a need for a new classification? Skin Appendage Disord. 2016;2(1-2):39-44.
15. Ali SY, Singh G. Radiation-induced alopecia. Int J Trichology. 2010;2(2):118-119.
Telogen effluvium (TE)—temporary hair loss due to the shedding of telogen (resting phase of hair cycle) hair after exposure to some form of stress—is one of the most common causes of diffuse non-scarring hair loss from the scalp.1 TE is more common than anagen (growing phase of hair cycle) hair loss.2 Hair loss can be triggered by numerous factors, including certain psychotropic medications.3,4 Mood stabilizers, such as valproic acid and lithium, are most commonly implicated. Hair loss also has been associated with the use of the first-generation antipsychotics haloperidol and chlorpromazine and the second-generation antipsychotics olanzapine, quetiapine, and risperidone.5-7 We recently cared for a woman with bipolar I disorder and generalized anxiety disorder who was prescribed lurasidone and later developed TE. Her hair loss completely resolved 4 months after lurasidone was discontinued.
TE can be triggered by events that interrupt the normal hair growth cycle. Typically, it is observed approximately 3 months after a triggering event and is usually self-limiting, lasting approximately 6 months.7 Diagnostic features include a strongly positive hair-pull test, a trichogram showing >25% telogen hair, and a biopsy showing an increase in telogen follicles.8,9 To conduct the hair-pull test, grasp approximately 40 to 60 hairs between the thumb and forefinger while slightly stretching the scalp to allow your fingers to slide along the length of the hair. Usually only 2 to 3 hairs in the telogen phase can be plucked via this method; if >10% of the hairs grasped can be plucked, this indicates a pathologic process.10
Significant hair loss, particularly among women, is a distressing adverse effect that can be an important moderator of compliance, treatment adherence, and relapse. To help clinicians narrow down the wide range of potential causes of a patient’s hair loss, we created the mnemonic NEED HAIR.
Nutritional: Iron deficiency anemia, a “crash” diet, zinc deficiency, vitamin B6 or B12 deficiency, chronic starvation, diarrhea, hypoproteinemia (metabolic or dietary origin), malabsorption, or heavy metal ingestion.1
Endocrine: Thyroid disorders and the early stage of androgenic alopecia.8,11
Environmental: Stress from a severe febrile illness, emotional stress, serious injuries, major surgery, large hemorrhage, and difficult labor.12
Drugs: Oral contraceptives, antithyroid drugs, retinoids (etretinate and acitretin), anticonvulsants, antidepressants, antipsychotics, hypolipidemic drugs, anticoagulants, antihypertensives (beta blockers, angiotensin-converting enzyme inhibitors), and cytotoxic drugs.1,4-7
Continue to: Hormonal fluctuations
Hormonal fluctuations: Polycystic ovarian syndrome and postpartum hormonal changes.11
Autoimmune: Lupus erythematosus, dermatomyositis, scleroderma, Hashimoto’s thyroiditis, Sjögren’s syndrome, inflammatory bowel disease, and autoimmune atrophic gastritis.12,13
Infections and chronic illnesses: Fungal infections (eg, tinea capitis), human immunodeficiency virus, syphilis, typhoid, malaria, tuberculosis, malignancy, renal failure, hepatic failure, and other chronic illnesses.1,9
Radiation: Radiation treatment and excessive UV exposure.12,14,15
Treatment for hair loss depends on the specific caus
Telogen effluvium (TE)—temporary hair loss due to the shedding of telogen (resting phase of hair cycle) hair after exposure to some form of stress—is one of the most common causes of diffuse non-scarring hair loss from the scalp.1 TE is more common than anagen (growing phase of hair cycle) hair loss.2 Hair loss can be triggered by numerous factors, including certain psychotropic medications.3,4 Mood stabilizers, such as valproic acid and lithium, are most commonly implicated. Hair loss also has been associated with the use of the first-generation antipsychotics haloperidol and chlorpromazine and the second-generation antipsychotics olanzapine, quetiapine, and risperidone.5-7 We recently cared for a woman with bipolar I disorder and generalized anxiety disorder who was prescribed lurasidone and later developed TE. Her hair loss completely resolved 4 months after lurasidone was discontinued.
TE can be triggered by events that interrupt the normal hair growth cycle. Typically, it is observed approximately 3 months after a triggering event and is usually self-limiting, lasting approximately 6 months.7 Diagnostic features include a strongly positive hair-pull test, a trichogram showing >25% telogen hair, and a biopsy showing an increase in telogen follicles.8,9 To conduct the hair-pull test, grasp approximately 40 to 60 hairs between the thumb and forefinger while slightly stretching the scalp to allow your fingers to slide along the length of the hair. Usually only 2 to 3 hairs in the telogen phase can be plucked via this method; if >10% of the hairs grasped can be plucked, this indicates a pathologic process.10
Significant hair loss, particularly among women, is a distressing adverse effect that can be an important moderator of compliance, treatment adherence, and relapse. To help clinicians narrow down the wide range of potential causes of a patient’s hair loss, we created the mnemonic NEED HAIR.
Nutritional: Iron deficiency anemia, a “crash” diet, zinc deficiency, vitamin B6 or B12 deficiency, chronic starvation, diarrhea, hypoproteinemia (metabolic or dietary origin), malabsorption, or heavy metal ingestion.1
Endocrine: Thyroid disorders and the early stage of androgenic alopecia.8,11
Environmental: Stress from a severe febrile illness, emotional stress, serious injuries, major surgery, large hemorrhage, and difficult labor.12
Drugs: Oral contraceptives, antithyroid drugs, retinoids (etretinate and acitretin), anticonvulsants, antidepressants, antipsychotics, hypolipidemic drugs, anticoagulants, antihypertensives (beta blockers, angiotensin-converting enzyme inhibitors), and cytotoxic drugs.1,4-7
Continue to: Hormonal fluctuations
Hormonal fluctuations: Polycystic ovarian syndrome and postpartum hormonal changes.11
Autoimmune: Lupus erythematosus, dermatomyositis, scleroderma, Hashimoto’s thyroiditis, Sjögren’s syndrome, inflammatory bowel disease, and autoimmune atrophic gastritis.12,13
Infections and chronic illnesses: Fungal infections (eg, tinea capitis), human immunodeficiency virus, syphilis, typhoid, malaria, tuberculosis, malignancy, renal failure, hepatic failure, and other chronic illnesses.1,9
Radiation: Radiation treatment and excessive UV exposure.12,14,15
Treatment for hair loss depends on the specific caus
1. Grover C, Khurana A. Telogen effluvium. Indian J Dermatol Venerol Leprol. 2013;79(5):591-603.
2. Harrison S, Bergfeld W. Diffuse hair loss: its triggers and management. Cleve Clin J Med. 2009;76(6):361-367.
3. Gautam M. Alopecia due to psychotropic medications. Ann Pharmacother. 1999;33(5):631-637.
4. Mercke Y, Sheng H, Khan T, et al. Hair loss in psychopharmacology. Ann Clin Psychiatry. 2000;12(1):35-42.
5. Kubota T, Ishikura T, Jibiki I. Alopecia areata associated with haloperidol. Jpn J Psychiatry Neurol. 1994;48(3):579-581.
6. McLean RM, Harrison-Woolrych M. Alopecia associated with quetiapine. Int Clin Psychopharmacol 2007;22(2):117-9.
7. Kulolu M, Korkmaz S, Kilic N, et al. Olanzapine induced hair loss: a case report. Bulletin of Clinical Psychopharmacology. 2012;22(4):362-365.
8. Malkud S. Telogen effluvium: a review. J Clin Diagn Res. 2015;9(9):WE01-WE03.
9. Shrivastava SB. Diffuse hair loss in an adult female: approach to diagnosis and management. Indian J Dermatol Venerol Leprol. 2009;75(1):20-28; quiz 27-28.
10. Piérard GE, Piérard-Franchimont C, Marks R, et al; EEMCO group (European Expert Group on Efficacy Measurement of Cosmetics and Other Topical Products). EEMCO guidance for the assessment of hair shedding and alopecia. Skin Pharmacol Physiol. 2004;17(2):98-110.
11. Mirallas O, Grimalt R. The postpartum telogen effluvium fallacy. Skin Appendage Disord. 2016;1(4):198-201.
12. Rebora A. Proposing a simpler classification of telogen effluvium. Skin Appendage Disord. 2016;2(1-2):35-38.
13. Cassano N, Amerio P, D’Ovidio R, et al. Hair disorders associated with autoimmune connective tissue diseases. G Ital Dermatol Venereol. 2014;149(5):555-565.
14. Trüeb RM. Telogen effluvium: is there a need for a new classification? Skin Appendage Disord. 2016;2(1-2):39-44.
15. Ali SY, Singh G. Radiation-induced alopecia. Int J Trichology. 2010;2(2):118-119.
1. Grover C, Khurana A. Telogen effluvium. Indian J Dermatol Venerol Leprol. 2013;79(5):591-603.
2. Harrison S, Bergfeld W. Diffuse hair loss: its triggers and management. Cleve Clin J Med. 2009;76(6):361-367.
3. Gautam M. Alopecia due to psychotropic medications. Ann Pharmacother. 1999;33(5):631-637.
4. Mercke Y, Sheng H, Khan T, et al. Hair loss in psychopharmacology. Ann Clin Psychiatry. 2000;12(1):35-42.
5. Kubota T, Ishikura T, Jibiki I. Alopecia areata associated with haloperidol. Jpn J Psychiatry Neurol. 1994;48(3):579-581.
6. McLean RM, Harrison-Woolrych M. Alopecia associated with quetiapine. Int Clin Psychopharmacol 2007;22(2):117-9.
7. Kulolu M, Korkmaz S, Kilic N, et al. Olanzapine induced hair loss: a case report. Bulletin of Clinical Psychopharmacology. 2012;22(4):362-365.
8. Malkud S. Telogen effluvium: a review. J Clin Diagn Res. 2015;9(9):WE01-WE03.
9. Shrivastava SB. Diffuse hair loss in an adult female: approach to diagnosis and management. Indian J Dermatol Venerol Leprol. 2009;75(1):20-28; quiz 27-28.
10. Piérard GE, Piérard-Franchimont C, Marks R, et al; EEMCO group (European Expert Group on Efficacy Measurement of Cosmetics and Other Topical Products). EEMCO guidance for the assessment of hair shedding and alopecia. Skin Pharmacol Physiol. 2004;17(2):98-110.
11. Mirallas O, Grimalt R. The postpartum telogen effluvium fallacy. Skin Appendage Disord. 2016;1(4):198-201.
12. Rebora A. Proposing a simpler classification of telogen effluvium. Skin Appendage Disord. 2016;2(1-2):35-38.
13. Cassano N, Amerio P, D’Ovidio R, et al. Hair disorders associated with autoimmune connective tissue diseases. G Ital Dermatol Venereol. 2014;149(5):555-565.
14. Trüeb RM. Telogen effluvium: is there a need for a new classification? Skin Appendage Disord. 2016;2(1-2):39-44.
15. Ali SY, Singh G. Radiation-induced alopecia. Int J Trichology. 2010;2(2):118-119.
Cardiovascular adverse effects of psychotropics: What to look for
Most patients who take psychotropic medications are at low risk for cardiovascular adverse effects from these medications, and require only routine monitoring. However, patients with severe mental illness, those with a personal or family history of cardiovascular disease, or those receiving high doses or multiple medications are considered at high risk for morbidity and mortality from cardiovascular adverse effects. Such patients may need more careful cardiovascular monitoring.
To help identify important cardiovascular-related adverse effects of various psychotropics, we summarize these risks, and offer guidance about what you can do when your patient experiences them (Table).1
Antipsychotics and metabolic syndrome
Patients who take antipsychotics should be monitored for metabolic syndrome. The presence of 3 of the following 5 parameters is considered positive for metabolic syndrome2:
- fasting glucose ≥100 mg/dL or hemoglobin A1c ≥5.6%
- blood pressure ≥130/85 mm Hg
- triglycerides ≥150 mg/dL
- high-density lipoprotein cholesterol
- waist circumference ≥102 cm in men or ≥88 cm in women.
Stimulants and sudden cardiac death
Sudden cardiac death (SCD) in children and adolescents who take stimulants to treat attention-deficit/hyperactivity disorder is rare. For these patients, the risk of SCD is no higher than that of the general population.3 For patients who do not have any known cardiac risk factors, the American Academy of Pediatrics does not recommend performing any cardiac tests before starting stimulants.3
1. Mackin P. Cardiac side effects of psychiatric drugs. Hum Psychopharmacol. 2008;23(suppl 1):S3-S14.
2. Grundy SM, Brewer HB Jr, Cleeman JI, et al; National Heart, Lung, and Blood Institute; American Heart Association. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Arterioscler Thromb Vasc Biol. 2004;24(2):e13-e18.
3. American Academy of Pediatrics Steering Committee on Quality Improvement and Management. Classifying recommendations for clinical practice guidelines. Pediatrics. 2004;114(3):874-877.
Most patients who take psychotropic medications are at low risk for cardiovascular adverse effects from these medications, and require only routine monitoring. However, patients with severe mental illness, those with a personal or family history of cardiovascular disease, or those receiving high doses or multiple medications are considered at high risk for morbidity and mortality from cardiovascular adverse effects. Such patients may need more careful cardiovascular monitoring.
To help identify important cardiovascular-related adverse effects of various psychotropics, we summarize these risks, and offer guidance about what you can do when your patient experiences them (Table).1
Antipsychotics and metabolic syndrome
Patients who take antipsychotics should be monitored for metabolic syndrome. The presence of 3 of the following 5 parameters is considered positive for metabolic syndrome2:
- fasting glucose ≥100 mg/dL or hemoglobin A1c ≥5.6%
- blood pressure ≥130/85 mm Hg
- triglycerides ≥150 mg/dL
- high-density lipoprotein cholesterol
- waist circumference ≥102 cm in men or ≥88 cm in women.
Stimulants and sudden cardiac death
Sudden cardiac death (SCD) in children and adolescents who take stimulants to treat attention-deficit/hyperactivity disorder is rare. For these patients, the risk of SCD is no higher than that of the general population.3 For patients who do not have any known cardiac risk factors, the American Academy of Pediatrics does not recommend performing any cardiac tests before starting stimulants.3
Most patients who take psychotropic medications are at low risk for cardiovascular adverse effects from these medications, and require only routine monitoring. However, patients with severe mental illness, those with a personal or family history of cardiovascular disease, or those receiving high doses or multiple medications are considered at high risk for morbidity and mortality from cardiovascular adverse effects. Such patients may need more careful cardiovascular monitoring.
To help identify important cardiovascular-related adverse effects of various psychotropics, we summarize these risks, and offer guidance about what you can do when your patient experiences them (Table).1
Antipsychotics and metabolic syndrome
Patients who take antipsychotics should be monitored for metabolic syndrome. The presence of 3 of the following 5 parameters is considered positive for metabolic syndrome2:
- fasting glucose ≥100 mg/dL or hemoglobin A1c ≥5.6%
- blood pressure ≥130/85 mm Hg
- triglycerides ≥150 mg/dL
- high-density lipoprotein cholesterol
- waist circumference ≥102 cm in men or ≥88 cm in women.
Stimulants and sudden cardiac death
Sudden cardiac death (SCD) in children and adolescents who take stimulants to treat attention-deficit/hyperactivity disorder is rare. For these patients, the risk of SCD is no higher than that of the general population.3 For patients who do not have any known cardiac risk factors, the American Academy of Pediatrics does not recommend performing any cardiac tests before starting stimulants.3
1. Mackin P. Cardiac side effects of psychiatric drugs. Hum Psychopharmacol. 2008;23(suppl 1):S3-S14.
2. Grundy SM, Brewer HB Jr, Cleeman JI, et al; National Heart, Lung, and Blood Institute; American Heart Association. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Arterioscler Thromb Vasc Biol. 2004;24(2):e13-e18.
3. American Academy of Pediatrics Steering Committee on Quality Improvement and Management. Classifying recommendations for clinical practice guidelines. Pediatrics. 2004;114(3):874-877.
1. Mackin P. Cardiac side effects of psychiatric drugs. Hum Psychopharmacol. 2008;23(suppl 1):S3-S14.
2. Grundy SM, Brewer HB Jr, Cleeman JI, et al; National Heart, Lung, and Blood Institute; American Heart Association. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Arterioscler Thromb Vasc Biol. 2004;24(2):e13-e18.
3. American Academy of Pediatrics Steering Committee on Quality Improvement and Management. Classifying recommendations for clinical practice guidelines. Pediatrics. 2004;114(3):874-877.
Autism spectrum disorder in adults
Psychiatry’s ‘C’ words
Recently, contemporary “culture” has capriciously confounded and confused our national community with a cringeworthy “C” word. Unfortunately, this was followed by only transient public consternation, reflecting the coarsening of our social communication and discourse and the cant of many. But the ripple effects continue.
As a psychiatrist who closely observes the human condition, I contemplated the current confrontational tone in the media, and wondered how corrosive language can confuse and cloud our sensibilities.
Then it occurred to me that there are many commendable clinical “C” words that describe what we psychiatrists do in daily practice. We stay calm while facing crises, and help our patients achieve certainty when stress makes them confused. We compassionately comfort and care for our suffering patients. We strive to engender courage and confidence when fragile patients are confronted with continuous criticism by callous and condescending people. We remain composed when we counsel patients with confrontational and crabby moods and help correct their confusing conflicts. We coordinate their care with courtesy, always aspiring for a cure for their corroded emotional condition.
But then I felt compelled to go further and call on my creativity to consider “C” words that describe severe psychiatric clinical disorders. I came up with the following cogent cascade of common characteristics of serious mental disorders:
- Cerebral pathology
- Circuit disruptions of neural connections
- Chemical imbalance
- Cytokine inflammatory conflagration
- Cognitive impairment
- Chronic course
- Crippled functioning.
My compulsion continued. I decided to contemplate more “C” words that capture our therapeutic course of action to correct a patient whose cortico-limbic circuitry is being threatened with considerable, even calamitous collapse. My consideration led to clarity, and I came up with the following list of what we psychiatrists conform to in our clinical practice:
- Connect with patients
- Correct diagnosis
- Course-specific intervention
- Choose the appropriate medication
- Combine cognitive-behavioral therapy with medication
- Cognitive assessment at baseline
- Compliance/concordance with treatment
- Continuity of care
- Comorbidities, physical and psychiatric
- Collaborative care with other medical specialists
- Comprehensive treatment plan with other mental health professionals.
A book about dirty words written by a psychoanalyst called the “C” expletive the worst of all cuss words.1 Its recent emergence in the national media compromised our civility and created a cesspool of contemptible conversations. Let’s transcend the contemptible “C” word of a caustic contemporary “culture” (which had its 15 minutes of infamy), and consider the many coherent and congenial “C” words of psychiatric practice that bring peace of mind and contentment to those who suffer from psychiatric brain conditions. As for the compulsive or
Editor's note: How many C words are there in this editorial? Email answers to [email protected]
1. Arango AC. Dirty words: psychoanalytic insights. Lanham, MD: Jason Aronson, Inc.; 1989:122.
Recently, contemporary “culture” has capriciously confounded and confused our national community with a cringeworthy “C” word. Unfortunately, this was followed by only transient public consternation, reflecting the coarsening of our social communication and discourse and the cant of many. But the ripple effects continue.
As a psychiatrist who closely observes the human condition, I contemplated the current confrontational tone in the media, and wondered how corrosive language can confuse and cloud our sensibilities.
Then it occurred to me that there are many commendable clinical “C” words that describe what we psychiatrists do in daily practice. We stay calm while facing crises, and help our patients achieve certainty when stress makes them confused. We compassionately comfort and care for our suffering patients. We strive to engender courage and confidence when fragile patients are confronted with continuous criticism by callous and condescending people. We remain composed when we counsel patients with confrontational and crabby moods and help correct their confusing conflicts. We coordinate their care with courtesy, always aspiring for a cure for their corroded emotional condition.
But then I felt compelled to go further and call on my creativity to consider “C” words that describe severe psychiatric clinical disorders. I came up with the following cogent cascade of common characteristics of serious mental disorders:
- Cerebral pathology
- Circuit disruptions of neural connections
- Chemical imbalance
- Cytokine inflammatory conflagration
- Cognitive impairment
- Chronic course
- Crippled functioning.
My compulsion continued. I decided to contemplate more “C” words that capture our therapeutic course of action to correct a patient whose cortico-limbic circuitry is being threatened with considerable, even calamitous collapse. My consideration led to clarity, and I came up with the following list of what we psychiatrists conform to in our clinical practice:
- Connect with patients
- Correct diagnosis
- Course-specific intervention
- Choose the appropriate medication
- Combine cognitive-behavioral therapy with medication
- Cognitive assessment at baseline
- Compliance/concordance with treatment
- Continuity of care
- Comorbidities, physical and psychiatric
- Collaborative care with other medical specialists
- Comprehensive treatment plan with other mental health professionals.
A book about dirty words written by a psychoanalyst called the “C” expletive the worst of all cuss words.1 Its recent emergence in the national media compromised our civility and created a cesspool of contemptible conversations. Let’s transcend the contemptible “C” word of a caustic contemporary “culture” (which had its 15 minutes of infamy), and consider the many coherent and congenial “C” words of psychiatric practice that bring peace of mind and contentment to those who suffer from psychiatric brain conditions. As for the compulsive or
Editor's note: How many C words are there in this editorial? Email answers to [email protected]
Recently, contemporary “culture” has capriciously confounded and confused our national community with a cringeworthy “C” word. Unfortunately, this was followed by only transient public consternation, reflecting the coarsening of our social communication and discourse and the cant of many. But the ripple effects continue.
As a psychiatrist who closely observes the human condition, I contemplated the current confrontational tone in the media, and wondered how corrosive language can confuse and cloud our sensibilities.
Then it occurred to me that there are many commendable clinical “C” words that describe what we psychiatrists do in daily practice. We stay calm while facing crises, and help our patients achieve certainty when stress makes them confused. We compassionately comfort and care for our suffering patients. We strive to engender courage and confidence when fragile patients are confronted with continuous criticism by callous and condescending people. We remain composed when we counsel patients with confrontational and crabby moods and help correct their confusing conflicts. We coordinate their care with courtesy, always aspiring for a cure for their corroded emotional condition.
But then I felt compelled to go further and call on my creativity to consider “C” words that describe severe psychiatric clinical disorders. I came up with the following cogent cascade of common characteristics of serious mental disorders:
- Cerebral pathology
- Circuit disruptions of neural connections
- Chemical imbalance
- Cytokine inflammatory conflagration
- Cognitive impairment
- Chronic course
- Crippled functioning.
My compulsion continued. I decided to contemplate more “C” words that capture our therapeutic course of action to correct a patient whose cortico-limbic circuitry is being threatened with considerable, even calamitous collapse. My consideration led to clarity, and I came up with the following list of what we psychiatrists conform to in our clinical practice:
- Connect with patients
- Correct diagnosis
- Course-specific intervention
- Choose the appropriate medication
- Combine cognitive-behavioral therapy with medication
- Cognitive assessment at baseline
- Compliance/concordance with treatment
- Continuity of care
- Comorbidities, physical and psychiatric
- Collaborative care with other medical specialists
- Comprehensive treatment plan with other mental health professionals.
A book about dirty words written by a psychoanalyst called the “C” expletive the worst of all cuss words.1 Its recent emergence in the national media compromised our civility and created a cesspool of contemptible conversations. Let’s transcend the contemptible “C” word of a caustic contemporary “culture” (which had its 15 minutes of infamy), and consider the many coherent and congenial “C” words of psychiatric practice that bring peace of mind and contentment to those who suffer from psychiatric brain conditions. As for the compulsive or
Editor's note: How many C words are there in this editorial? Email answers to [email protected]
1. Arango AC. Dirty words: psychoanalytic insights. Lanham, MD: Jason Aronson, Inc.; 1989:122.
1. Arango AC. Dirty words: psychoanalytic insights. Lanham, MD: Jason Aronson, Inc.; 1989:122.
Was this your first one? Lessons in empathy and mourning
“Was this your first one?”
You might be asked this question in several circumstances. Was this your first 5K run? Was this your first time taking the MCAT? For me, I was asked if this was the first time a patient had died while in my care as a resident.
As it turns out, this was the first patient who died under my care. This seemed obvious to everyone around me because when I received the news, offhandedly, days after my patient’s discharge, I cried. My colleagues’ responses to my tears were kind and supportive. No one was callous or judgmental. I was given time to compose myself before continuing my rounds for the day. Yet, the most common question asked of me was, “Was this your first one?”
The implication of this question was that these situations would become easier and less emotional over time. Everyone believed my tears were a special response, privileged only to my first experience. This was conveyed to me as if it was a chance to explain my emotions. As if grieving alone was not sufficient to explain tears, I began to run through the reasons for my behavior, and my mind rapidly searched for answers. I thought:
- “I saw this patient daily for weeks, and I was close to him.”
- “There was an element of suicidality in this case, so it was different.”
- “After all, this was my first experience like this.”
In reality, these reasons were irrelevant and not needed to explain my tears. I was mourning the loss of a life—someone I had come to know well—and this was a life that ultimately could not be saved by the health care system.
These were my feelings during the July of my intern year. It is now a year later; I have since experienced an incredible number of moments that warranted mourning. There were oncology patients with advanced diseases who needed help disclosing their prognosis to family members. There were days when I was tasked with altering treatment courses from aggressive treatment to comfort measures only. There was the Christmas Eve when a pair of brothers dropped off their elderly father in the emergency department because no one was able or willing to care for him at home.
These moments can come fast, and they occur more frequently than one might imagine. Each is worthy of mourning. Each is worthy of tears, whether it is my first loss or my 50th. But the reality is that I could not function in my job and care for all my patients equally if I stopped every time to acknowledge my emotions. As much as it causes my stomach to turn, I understand the “Was this your first one?” phenomenon. To outwardly express your emotions and openly mourn in the moment, you need to have the time and allow yourself the vulnerability to do so. After your “first one,” you realize that mournful moments can occur regularly and you must choose to process emotions on your own time because you don’t have the luxury of processing a loss of life in the present moment.
Continue to: This is not to diminish...
This is not to diminish the importance of mourning or belittle the experience of processing one’s emotions. It simply highlights the importance of self-care. Emotions need to be processed outside of the hustle and bustle of the work day. There are other patients who require and deserve their clinician’s undivided attention. To truly provide patients with the highest quality of care, I find caring for myself and processing my reactions to daily events to be essential. Writing down my thoughts or talking to loved ones are ways that help me process my experiences. Taking a trip out of town, going for a hike, or watching a movie also are ways to help create balance in an emotionally charged career. I hope to use my new understanding of the “first one” phenomenon as a reminder to maintain my own well-being. In doing so, I can be attuned to my patients’ needs and provide them with empathic care. Even though my outward expression may change as I learn to process these moments differently, I want to treat each patient with the same level of empathy, value, and compassion as my first one.
“Was this your first one?”
You might be asked this question in several circumstances. Was this your first 5K run? Was this your first time taking the MCAT? For me, I was asked if this was the first time a patient had died while in my care as a resident.
As it turns out, this was the first patient who died under my care. This seemed obvious to everyone around me because when I received the news, offhandedly, days after my patient’s discharge, I cried. My colleagues’ responses to my tears were kind and supportive. No one was callous or judgmental. I was given time to compose myself before continuing my rounds for the day. Yet, the most common question asked of me was, “Was this your first one?”
The implication of this question was that these situations would become easier and less emotional over time. Everyone believed my tears were a special response, privileged only to my first experience. This was conveyed to me as if it was a chance to explain my emotions. As if grieving alone was not sufficient to explain tears, I began to run through the reasons for my behavior, and my mind rapidly searched for answers. I thought:
- “I saw this patient daily for weeks, and I was close to him.”
- “There was an element of suicidality in this case, so it was different.”
- “After all, this was my first experience like this.”
In reality, these reasons were irrelevant and not needed to explain my tears. I was mourning the loss of a life—someone I had come to know well—and this was a life that ultimately could not be saved by the health care system.
These were my feelings during the July of my intern year. It is now a year later; I have since experienced an incredible number of moments that warranted mourning. There were oncology patients with advanced diseases who needed help disclosing their prognosis to family members. There were days when I was tasked with altering treatment courses from aggressive treatment to comfort measures only. There was the Christmas Eve when a pair of brothers dropped off their elderly father in the emergency department because no one was able or willing to care for him at home.
These moments can come fast, and they occur more frequently than one might imagine. Each is worthy of mourning. Each is worthy of tears, whether it is my first loss or my 50th. But the reality is that I could not function in my job and care for all my patients equally if I stopped every time to acknowledge my emotions. As much as it causes my stomach to turn, I understand the “Was this your first one?” phenomenon. To outwardly express your emotions and openly mourn in the moment, you need to have the time and allow yourself the vulnerability to do so. After your “first one,” you realize that mournful moments can occur regularly and you must choose to process emotions on your own time because you don’t have the luxury of processing a loss of life in the present moment.
Continue to: This is not to diminish...
This is not to diminish the importance of mourning or belittle the experience of processing one’s emotions. It simply highlights the importance of self-care. Emotions need to be processed outside of the hustle and bustle of the work day. There are other patients who require and deserve their clinician’s undivided attention. To truly provide patients with the highest quality of care, I find caring for myself and processing my reactions to daily events to be essential. Writing down my thoughts or talking to loved ones are ways that help me process my experiences. Taking a trip out of town, going for a hike, or watching a movie also are ways to help create balance in an emotionally charged career. I hope to use my new understanding of the “first one” phenomenon as a reminder to maintain my own well-being. In doing so, I can be attuned to my patients’ needs and provide them with empathic care. Even though my outward expression may change as I learn to process these moments differently, I want to treat each patient with the same level of empathy, value, and compassion as my first one.
“Was this your first one?”
You might be asked this question in several circumstances. Was this your first 5K run? Was this your first time taking the MCAT? For me, I was asked if this was the first time a patient had died while in my care as a resident.
As it turns out, this was the first patient who died under my care. This seemed obvious to everyone around me because when I received the news, offhandedly, days after my patient’s discharge, I cried. My colleagues’ responses to my tears were kind and supportive. No one was callous or judgmental. I was given time to compose myself before continuing my rounds for the day. Yet, the most common question asked of me was, “Was this your first one?”
The implication of this question was that these situations would become easier and less emotional over time. Everyone believed my tears were a special response, privileged only to my first experience. This was conveyed to me as if it was a chance to explain my emotions. As if grieving alone was not sufficient to explain tears, I began to run through the reasons for my behavior, and my mind rapidly searched for answers. I thought:
- “I saw this patient daily for weeks, and I was close to him.”
- “There was an element of suicidality in this case, so it was different.”
- “After all, this was my first experience like this.”
In reality, these reasons were irrelevant and not needed to explain my tears. I was mourning the loss of a life—someone I had come to know well—and this was a life that ultimately could not be saved by the health care system.
These were my feelings during the July of my intern year. It is now a year later; I have since experienced an incredible number of moments that warranted mourning. There were oncology patients with advanced diseases who needed help disclosing their prognosis to family members. There were days when I was tasked with altering treatment courses from aggressive treatment to comfort measures only. There was the Christmas Eve when a pair of brothers dropped off their elderly father in the emergency department because no one was able or willing to care for him at home.
These moments can come fast, and they occur more frequently than one might imagine. Each is worthy of mourning. Each is worthy of tears, whether it is my first loss or my 50th. But the reality is that I could not function in my job and care for all my patients equally if I stopped every time to acknowledge my emotions. As much as it causes my stomach to turn, I understand the “Was this your first one?” phenomenon. To outwardly express your emotions and openly mourn in the moment, you need to have the time and allow yourself the vulnerability to do so. After your “first one,” you realize that mournful moments can occur regularly and you must choose to process emotions on your own time because you don’t have the luxury of processing a loss of life in the present moment.
Continue to: This is not to diminish...
This is not to diminish the importance of mourning or belittle the experience of processing one’s emotions. It simply highlights the importance of self-care. Emotions need to be processed outside of the hustle and bustle of the work day. There are other patients who require and deserve their clinician’s undivided attention. To truly provide patients with the highest quality of care, I find caring for myself and processing my reactions to daily events to be essential. Writing down my thoughts or talking to loved ones are ways that help me process my experiences. Taking a trip out of town, going for a hike, or watching a movie also are ways to help create balance in an emotionally charged career. I hope to use my new understanding of the “first one” phenomenon as a reminder to maintain my own well-being. In doing so, I can be attuned to my patients’ needs and provide them with empathic care. Even though my outward expression may change as I learn to process these moments differently, I want to treat each patient with the same level of empathy, value, and compassion as my first one.
Yoga’s lesson for a young psychiatrist
I have often turned to yoga for my own reprieve; I find the heat, breath, and movement exhilarating. Training to become a yoga teacher has taught me that medicine, not unlike yoga, requires patience and resiliency.
It is 3
4
Let me tell you, when you’re getting certified in Advanced Cardiac Life Support, you go to a class on a Saturday, there are snacks, and your instructor will probably be a paramedic who is earning side cash teaching CPR. You will watch funny videos—we even danced to the Bee Gees’ Stayin’ Alive. But this is not funny, nor is it fun. And my head is spinning so fast, the sound of the Bee Gees smears to silence.
I take off my white coat and trot to the center of the room. The lights are bright, I am hot, and people are moving really fast. I feel like I’m in a vignette. It seems like we’re in the fourth movement of a Shostakovich symphony, the attending is cueing, up and down, like Bernstein conducting the Philharmonic, her arms are flailing; this production is hers and everyone is in sync. The man’s skin is pale, almost gray, he smells like sweat and urine and vomit. His irises are blue, blue like the ocean. His beard is thick and opaque, speckled with premature dots of gray. He looks calm. Listless. Dead. He is looking at me, like the Mona Lisa, as if beckoning me to save him, to give him another chance. At life. I put my hands gently on his sternum and I start my round of chest compressions. His skin is rubbery. I feel like I’m breaking his ribs, am I? This is not like the class. The cardiac monitor flatlines. Was it like that before? I think so, I’m not really sure. The attending stops conducting and runs over. Someone taps me and says it’s time to switch. Shortly thereafter, time of death is pronounced. “Damn it,” I hear the attending exclaim quietly but deliberately. I am hot, and I have a headache. I take off my gloves. Where’s my cell phone? I’m going to check Facebook, maybe ESPN.com. I feel heavy. And then I’m sitting at the computer screen again, after the rain. The attending comes back to her seat. She has a green smoothie, she takes a sip, and is slow to return the oversized cup to the table.
This night 3 years ago remains vivid. I am looking at her now. The unabashed attending. We are all looking at her.
She pulls out a petite makeup case and opens an oval mirror. She applies 2 thin lines of lustrous lip gloss, smacks her lips, grounding herself, then places the mirror back in her bag. She takes one deep breath, pauses briefly, and, letting go, she sits up tall, her dignity restored, then looks at me and claps, “Come on, doctor, we’ve got more patients to see.”
That night in the ER, I experienced how troubling it is losing a life with the burden of responsibility, but also the beauty of Aparigraha, letting go, and moving forward. I learned this lesson, unspoken, from an admirable attending, and was reminded of it 3 years later as I pursued a deeper understanding of yoga.
I have often turned to yoga for my own reprieve; I find the heat, breath, and movement exhilarating. Training to become a yoga teacher has taught me that medicine, not unlike yoga, requires patience and resiliency.
It is 3
4
Let me tell you, when you’re getting certified in Advanced Cardiac Life Support, you go to a class on a Saturday, there are snacks, and your instructor will probably be a paramedic who is earning side cash teaching CPR. You will watch funny videos—we even danced to the Bee Gees’ Stayin’ Alive. But this is not funny, nor is it fun. And my head is spinning so fast, the sound of the Bee Gees smears to silence.
I take off my white coat and trot to the center of the room. The lights are bright, I am hot, and people are moving really fast. I feel like I’m in a vignette. It seems like we’re in the fourth movement of a Shostakovich symphony, the attending is cueing, up and down, like Bernstein conducting the Philharmonic, her arms are flailing; this production is hers and everyone is in sync. The man’s skin is pale, almost gray, he smells like sweat and urine and vomit. His irises are blue, blue like the ocean. His beard is thick and opaque, speckled with premature dots of gray. He looks calm. Listless. Dead. He is looking at me, like the Mona Lisa, as if beckoning me to save him, to give him another chance. At life. I put my hands gently on his sternum and I start my round of chest compressions. His skin is rubbery. I feel like I’m breaking his ribs, am I? This is not like the class. The cardiac monitor flatlines. Was it like that before? I think so, I’m not really sure. The attending stops conducting and runs over. Someone taps me and says it’s time to switch. Shortly thereafter, time of death is pronounced. “Damn it,” I hear the attending exclaim quietly but deliberately. I am hot, and I have a headache. I take off my gloves. Where’s my cell phone? I’m going to check Facebook, maybe ESPN.com. I feel heavy. And then I’m sitting at the computer screen again, after the rain. The attending comes back to her seat. She has a green smoothie, she takes a sip, and is slow to return the oversized cup to the table.
This night 3 years ago remains vivid. I am looking at her now. The unabashed attending. We are all looking at her.
She pulls out a petite makeup case and opens an oval mirror. She applies 2 thin lines of lustrous lip gloss, smacks her lips, grounding herself, then places the mirror back in her bag. She takes one deep breath, pauses briefly, and, letting go, she sits up tall, her dignity restored, then looks at me and claps, “Come on, doctor, we’ve got more patients to see.”
That night in the ER, I experienced how troubling it is losing a life with the burden of responsibility, but also the beauty of Aparigraha, letting go, and moving forward. I learned this lesson, unspoken, from an admirable attending, and was reminded of it 3 years later as I pursued a deeper understanding of yoga.
I have often turned to yoga for my own reprieve; I find the heat, breath, and movement exhilarating. Training to become a yoga teacher has taught me that medicine, not unlike yoga, requires patience and resiliency.
It is 3
4
Let me tell you, when you’re getting certified in Advanced Cardiac Life Support, you go to a class on a Saturday, there are snacks, and your instructor will probably be a paramedic who is earning side cash teaching CPR. You will watch funny videos—we even danced to the Bee Gees’ Stayin’ Alive. But this is not funny, nor is it fun. And my head is spinning so fast, the sound of the Bee Gees smears to silence.
I take off my white coat and trot to the center of the room. The lights are bright, I am hot, and people are moving really fast. I feel like I’m in a vignette. It seems like we’re in the fourth movement of a Shostakovich symphony, the attending is cueing, up and down, like Bernstein conducting the Philharmonic, her arms are flailing; this production is hers and everyone is in sync. The man’s skin is pale, almost gray, he smells like sweat and urine and vomit. His irises are blue, blue like the ocean. His beard is thick and opaque, speckled with premature dots of gray. He looks calm. Listless. Dead. He is looking at me, like the Mona Lisa, as if beckoning me to save him, to give him another chance. At life. I put my hands gently on his sternum and I start my round of chest compressions. His skin is rubbery. I feel like I’m breaking his ribs, am I? This is not like the class. The cardiac monitor flatlines. Was it like that before? I think so, I’m not really sure. The attending stops conducting and runs over. Someone taps me and says it’s time to switch. Shortly thereafter, time of death is pronounced. “Damn it,” I hear the attending exclaim quietly but deliberately. I am hot, and I have a headache. I take off my gloves. Where’s my cell phone? I’m going to check Facebook, maybe ESPN.com. I feel heavy. And then I’m sitting at the computer screen again, after the rain. The attending comes back to her seat. She has a green smoothie, she takes a sip, and is slow to return the oversized cup to the table.
This night 3 years ago remains vivid. I am looking at her now. The unabashed attending. We are all looking at her.
She pulls out a petite makeup case and opens an oval mirror. She applies 2 thin lines of lustrous lip gloss, smacks her lips, grounding herself, then places the mirror back in her bag. She takes one deep breath, pauses briefly, and, letting go, she sits up tall, her dignity restored, then looks at me and claps, “Come on, doctor, we’ve got more patients to see.”
That night in the ER, I experienced how troubling it is losing a life with the burden of responsibility, but also the beauty of Aparigraha, letting go, and moving forward. I learned this lesson, unspoken, from an admirable attending, and was reminded of it 3 years later as I pursued a deeper understanding of yoga.
Making sense of CYP2D6 and CYP1A2 genotype vs phenotype
The clinical response to the same dose of a drug may vary among individuals. Cytochrome P450 (CYP) 2D6 and 1A2 are enzymes that metabolize many psychotropic medications. Genetic variations in these enzymes may cause changes in their activity and result in differences in effectiveness and adverse effects. Although pharmacogenetic testing is available for CYP2D6 and CYP1A2, interpretation and clinical application of the results may not be straightforward.
Genetic variations in CYP450 enzymes determine enzymatic activity, which can have a large effect on drug levels, efficacy, and toxicity. However, there are many other important factors that clinicians should consider when trying to predict the effects of medications. While clinicians often focus on a patient’s genotype, this only provides information on a chromosomal level, and this information never changes. In contrast, a patient’s phenotype, or status of metabolism, is subject to change throughout the patient’s life.
Many circumstances influence phenotype, including the use of medications that induce or inhibit CYP450 enzymes, environmental factors, and comorbidities. Phenoconversion occurs when these factors result in a phenotype that is different from that predicted by genotype. Because of the possibility of phenoconversion, knowing a patient’s genotype may be of limited value in making clinical decisions. This article provides guidance on interpreting both the genotype and phenotype of CYP2D6 and CYP1A2. Case 1 and Case 2 illustrate these concepts.
CYP2D6
The enzyme activity of CYP2D6 varies among individuals and may include no activity, decreased activity, normal activity, or increased activity. After obtaining the genotype, the activity level of the CYP2D6 alleles may be determined. The frequency with which certain alleles occur varies with ancestry. More than 100 allelic variants and subvariants have been discovered, and new alleles are continuing to be discovered.1Table 12 lists some of the most common CYP2D6 alleles.
Based on the CYP2D6 enzyme activity determined from the alleles, 4 “traditional” phenotypes can be predicted from the genotype (Table 22). The 7-category phenotypes reported by some laboratory companies provide a more explicit method for reporting phenotypes.
Evidence suggests that, unlike most other CYP450 enzymes, CYP2D6 is not very susceptible to enzyme induction.2 Thus, genetics, rather than drug therapy, accounts for most ultra-rapid CYP2D6 metabolizers. CYP2D6 can be inhibited by the use of medications (Table 32-5) and/or substrates (Table 42,6). Similar to inhibitors, substrates may be saturating high affinity-low capacity enzymes such as CYP2D6, resulting in phenoconversion to poor metabolizers. However, this is unlikely to be the case for substrates of low affinity-high capacity enzymes such as CYP3A4.7 Ultimately, substrates and/or inhibitors of CYP2D6 may result in a phenotype that does not correspond to genotype.
Phenoconversion
Genotyping may not reflect the true prevalence of the CYP2D6 poor metabolizer phenotype when using multiple medications that are substrates and/or inhibitors of CYP2D6.8 In the presence of strong CYP2D6 inhibitors, up to 80% of individuals with a non-poor metabolizer genotype are converted to a poor metabolizer phenotype.8 While the phenotype provides a clearer representation of metabolism status than genotype, this information may not always be available.
Continue to: Determining CYP2D6 phenotype
Determining CYP2D6 phenotype
Risperidone and venlafaxine levels are useful tools for predicting CYP2D6 phenotype.3,8 When a risperidone level is ordered, the results include a risperidone level and a 9-hydroxyrisperidone level. The active metabolite of risperidone is 9-hydroxyrisperidone (
- Ultra-rapid metabolizer: 0.03 (0.02 to 0.06)
- Extensive metabolizer: 0.08 (0.04 to 0.17)
- Intermediate metabolizer: 0.56 (0.30 to 1.0)
- Poor metabolizer: 2.5 (1.8 to 4.1).
Although a R-to-9-OHR concentration ratio >1 generally indicates a poor metabolizer, it could also indicate the presence of a powerful CYP2D6 inhibitor.9
When a venlafaxine level is ordered, the results include a venlafaxine level and an O-desmethylvenlafaxine level. O-desmethylvenlafaxine (
CYP1A2
While the activity of CYP2D6 alleles is determined primarily by genetic factors and medications, the activity of CYP1A2 alleles is largely determined by environmental factors (diet, medications, disease) and genetic variability.2 Consequently, CYP1A2 genotyping may be less clinically useful than CYP2D6 genotyping. The CYP1A2 genotype–phenotype relationship incorporates the degree of allele activity (Table 52), and inducibility in the presence of environmental factors.
Continue to: CYP1A2 inhibiton
CYP1A2 inhibition
A variety of medications and environmental factors may inhibit CYP1A2.
Medications. Medications that may inhibit CYP1A2 include a
Caffeine. A significant increase in caffeine consumption can result in inhibition.3 Among non-tobacco smokers, an increase of 1 cup/d of coffee or 2 cans/d of caffeinated soda would be considered significant.3 However, tobacco smokers would require an increase of 3 cups/d of coffee or 6 cans/d of soda.
Diet. An increase in the daily dietary intake of certain vegetables for 6 days has been shown to result in inhibition.10 Apiaceous (Apiaceae or Umbelliferae) vegetables such as carrots (3/4 cup), celery (1/2 cup), dill (1 teaspoon), parsley (3 tablespoons), and parsnips (1¼ cup) can decrease CYP1A2 activity by approximately 13% to 25%. Allium (Liliaceae) vegetables, such as garlic, leeks, and onions, have no effect on CYP1A2 activity.
Infection. Pneumonia, upper respiratory infections with fever, pyelonephritis or appendicitis, or inflammation are suspected to decrease CYP1A2 activity.8
Continue to: CYP1A2 induction
CYP1A2 induction
A variety of medications and environmental factors may induce CYP1A2.
Medications. Certain medications may induce CYP1A2, including c
Cigarette smoking. A significant increase in smoking after 1 to 3 weeks may decrease drug levels, whereas a significant decrease in smoking after 1 to 3 weeks may result in elevated drug levels.3 Nicotine is not the causative agent of induction, but rather hydrocarbons found in cigarette smoke.11
Diet. An increase in daily dietary intake of certain vegetables for 6 days has been shown to result in induction.3 Brassica (Cruciferae) vegetables such as broccoli (2 cups), cauliflower (1 cup), cabbage (1 cup), and radish sprouts (1/2 cup) have been found to increase CYP1A2 activity by 18% to 37%.10 Grilled meat also plays a role in induction.10
Related Resource
- Ellingrod VL, Ward KM. Using pharmacogenetics guidelines when prescribing: What's available. Current Psychiatry. 2018;17(1):43-46.
Drug Brand Names
Amiodarone • Cordarone, Pacerone
Amitriptyline • Elavil, Endep
Aripiprazole • Abilify
Asenapine • Saphris
Atazanavir • Reyataz
Brexpiprazole • Rexulti
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Chlorpromazine • Thorazine
Chloroquine • Aralen
Cinacalcet • Sensipar
Ciprofloxacin • Cipro
Citalopram • Celexa
Clozapine • Clozaril
Desipramine • Norpramin
Desvenlafaxine • Pristiq
Diphenhydramine • Benadryl
Doxepin • Silenor
Duloxetine • Cymbalta
Escitalopram • Lexapro
Ethinyl estradiol • Estinyl
Fluoxetine • Prozac
Fluvoxamine • Luvox
Haloperidol • Haldol
Iloperidone • Fanapt
Imatinib • Gleevec
Imipramine • Tofranil
Mirtazapine • Remeron
Nortriptyline • Pamelor
Olanzapine • Zyprexa
Paliperidone • Invega
Paroxetine • Paxil
Perphenazine • Trilafon
Phenytoin • Dilantin
Pimavanserin • Nuplazid
Primidone • Mysoline
Quetiapine • Seroquel
Quinidine • Cardioquin
Rifampin • Rifadin
Risperidone • Risperdal
Sertraline • Zoloft
Terbinafine • Lamisil
Thioridazine • Mellaril
Trazodone • Desyrel, Oleptro
Venlafaxine • Effexor
Vilazodone • Viibryd
Vortioxetine • Trintellix
Ziprasidone • Geodon
1. Pharmacogene Variation Consoritum. CYP2D6 allele nomenclature. https://www.pharmvar.org/gene/CYP2D6. Updated May 22, 2018. Accessed June 11, 2018.
2. Mrazek D. Psychiatric pharmacogenomics. New York, NY: Oxford University Press; 2010:33,42,44,45,85.
3. Spina E, de Leon J. Clinical applications of CYP genotyping in psychiatry. J Neural Transm (Vienna). 2015;122(1):5-28.
4. Adedoyin A, Frye RF, Mauro K, et al. Chloroquine modulation of specific metabolizing enzymes activities: investigation with selective five drug cocktail. Br J Clin Pharmacol. 1998;46(3):215-219.
5. Filppula AM, Laitila J, Neuvonen PJ, et al. Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates. Br J Pharmacol. 2012;165(8):2787-2798.
6. U.S. National Library of Medicine. DailyMed. http://dailymed.nlm.nih.gov/dailymed/about.cfm. Accessed April 26, 2018.
7. Monte AA, Heard KJ, Campbell J, et al. The effect of CYP2D6 drug-drug interactions on hydrocodone effectiveness. Acad Emerg Med. 2014;21(8):879-885.
8. Preskorn SH, Kane CP, Lobello K, et al. Cytochrome P450 2D6 phenoconversion is common in patients being treated for depression: implications for personalized medicine. J Clin Psychiatry. 2013;74(6):614-621.
9. de Leon, J, Susce, MT, Johnson, M, et al. DNA microarray technology in the clinical environment: the AmpliChip CYP450 test for CYP2D6 and CYP2C19 genotyping. CNS Spectr. 2009;14(1):19-34.
10. Lampe JW, King IB, Li S, et al. Brassica vegetables increase and apiaceous vegetables decrease cytochrome P450 1A2 activity in humans: changes in caffeine metabolite ratios in response to controlled vegetable diets. Carcinogenesis. 2000;21(6):1157-1162.
11. Zevin S, Benowitz NL. Drug interaction with tobacco smoking. An update. Clin Pharmacokinet. 1999;36(3):425-438.
The clinical response to the same dose of a drug may vary among individuals. Cytochrome P450 (CYP) 2D6 and 1A2 are enzymes that metabolize many psychotropic medications. Genetic variations in these enzymes may cause changes in their activity and result in differences in effectiveness and adverse effects. Although pharmacogenetic testing is available for CYP2D6 and CYP1A2, interpretation and clinical application of the results may not be straightforward.
Genetic variations in CYP450 enzymes determine enzymatic activity, which can have a large effect on drug levels, efficacy, and toxicity. However, there are many other important factors that clinicians should consider when trying to predict the effects of medications. While clinicians often focus on a patient’s genotype, this only provides information on a chromosomal level, and this information never changes. In contrast, a patient’s phenotype, or status of metabolism, is subject to change throughout the patient’s life.
Many circumstances influence phenotype, including the use of medications that induce or inhibit CYP450 enzymes, environmental factors, and comorbidities. Phenoconversion occurs when these factors result in a phenotype that is different from that predicted by genotype. Because of the possibility of phenoconversion, knowing a patient’s genotype may be of limited value in making clinical decisions. This article provides guidance on interpreting both the genotype and phenotype of CYP2D6 and CYP1A2. Case 1 and Case 2 illustrate these concepts.
CYP2D6
The enzyme activity of CYP2D6 varies among individuals and may include no activity, decreased activity, normal activity, or increased activity. After obtaining the genotype, the activity level of the CYP2D6 alleles may be determined. The frequency with which certain alleles occur varies with ancestry. More than 100 allelic variants and subvariants have been discovered, and new alleles are continuing to be discovered.1Table 12 lists some of the most common CYP2D6 alleles.
Based on the CYP2D6 enzyme activity determined from the alleles, 4 “traditional” phenotypes can be predicted from the genotype (Table 22). The 7-category phenotypes reported by some laboratory companies provide a more explicit method for reporting phenotypes.
Evidence suggests that, unlike most other CYP450 enzymes, CYP2D6 is not very susceptible to enzyme induction.2 Thus, genetics, rather than drug therapy, accounts for most ultra-rapid CYP2D6 metabolizers. CYP2D6 can be inhibited by the use of medications (Table 32-5) and/or substrates (Table 42,6). Similar to inhibitors, substrates may be saturating high affinity-low capacity enzymes such as CYP2D6, resulting in phenoconversion to poor metabolizers. However, this is unlikely to be the case for substrates of low affinity-high capacity enzymes such as CYP3A4.7 Ultimately, substrates and/or inhibitors of CYP2D6 may result in a phenotype that does not correspond to genotype.
Phenoconversion
Genotyping may not reflect the true prevalence of the CYP2D6 poor metabolizer phenotype when using multiple medications that are substrates and/or inhibitors of CYP2D6.8 In the presence of strong CYP2D6 inhibitors, up to 80% of individuals with a non-poor metabolizer genotype are converted to a poor metabolizer phenotype.8 While the phenotype provides a clearer representation of metabolism status than genotype, this information may not always be available.
Continue to: Determining CYP2D6 phenotype
Determining CYP2D6 phenotype
Risperidone and venlafaxine levels are useful tools for predicting CYP2D6 phenotype.3,8 When a risperidone level is ordered, the results include a risperidone level and a 9-hydroxyrisperidone level. The active metabolite of risperidone is 9-hydroxyrisperidone (
- Ultra-rapid metabolizer: 0.03 (0.02 to 0.06)
- Extensive metabolizer: 0.08 (0.04 to 0.17)
- Intermediate metabolizer: 0.56 (0.30 to 1.0)
- Poor metabolizer: 2.5 (1.8 to 4.1).
Although a R-to-9-OHR concentration ratio >1 generally indicates a poor metabolizer, it could also indicate the presence of a powerful CYP2D6 inhibitor.9
When a venlafaxine level is ordered, the results include a venlafaxine level and an O-desmethylvenlafaxine level. O-desmethylvenlafaxine (
CYP1A2
While the activity of CYP2D6 alleles is determined primarily by genetic factors and medications, the activity of CYP1A2 alleles is largely determined by environmental factors (diet, medications, disease) and genetic variability.2 Consequently, CYP1A2 genotyping may be less clinically useful than CYP2D6 genotyping. The CYP1A2 genotype–phenotype relationship incorporates the degree of allele activity (Table 52), and inducibility in the presence of environmental factors.
Continue to: CYP1A2 inhibiton
CYP1A2 inhibition
A variety of medications and environmental factors may inhibit CYP1A2.
Medications. Medications that may inhibit CYP1A2 include a
Caffeine. A significant increase in caffeine consumption can result in inhibition.3 Among non-tobacco smokers, an increase of 1 cup/d of coffee or 2 cans/d of caffeinated soda would be considered significant.3 However, tobacco smokers would require an increase of 3 cups/d of coffee or 6 cans/d of soda.
Diet. An increase in the daily dietary intake of certain vegetables for 6 days has been shown to result in inhibition.10 Apiaceous (Apiaceae or Umbelliferae) vegetables such as carrots (3/4 cup), celery (1/2 cup), dill (1 teaspoon), parsley (3 tablespoons), and parsnips (1¼ cup) can decrease CYP1A2 activity by approximately 13% to 25%. Allium (Liliaceae) vegetables, such as garlic, leeks, and onions, have no effect on CYP1A2 activity.
Infection. Pneumonia, upper respiratory infections with fever, pyelonephritis or appendicitis, or inflammation are suspected to decrease CYP1A2 activity.8
Continue to: CYP1A2 induction
CYP1A2 induction
A variety of medications and environmental factors may induce CYP1A2.
Medications. Certain medications may induce CYP1A2, including c
Cigarette smoking. A significant increase in smoking after 1 to 3 weeks may decrease drug levels, whereas a significant decrease in smoking after 1 to 3 weeks may result in elevated drug levels.3 Nicotine is not the causative agent of induction, but rather hydrocarbons found in cigarette smoke.11
Diet. An increase in daily dietary intake of certain vegetables for 6 days has been shown to result in induction.3 Brassica (Cruciferae) vegetables such as broccoli (2 cups), cauliflower (1 cup), cabbage (1 cup), and radish sprouts (1/2 cup) have been found to increase CYP1A2 activity by 18% to 37%.10 Grilled meat also plays a role in induction.10
Related Resource
- Ellingrod VL, Ward KM. Using pharmacogenetics guidelines when prescribing: What's available. Current Psychiatry. 2018;17(1):43-46.
Drug Brand Names
Amiodarone • Cordarone, Pacerone
Amitriptyline • Elavil, Endep
Aripiprazole • Abilify
Asenapine • Saphris
Atazanavir • Reyataz
Brexpiprazole • Rexulti
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Chlorpromazine • Thorazine
Chloroquine • Aralen
Cinacalcet • Sensipar
Ciprofloxacin • Cipro
Citalopram • Celexa
Clozapine • Clozaril
Desipramine • Norpramin
Desvenlafaxine • Pristiq
Diphenhydramine • Benadryl
Doxepin • Silenor
Duloxetine • Cymbalta
Escitalopram • Lexapro
Ethinyl estradiol • Estinyl
Fluoxetine • Prozac
Fluvoxamine • Luvox
Haloperidol • Haldol
Iloperidone • Fanapt
Imatinib • Gleevec
Imipramine • Tofranil
Mirtazapine • Remeron
Nortriptyline • Pamelor
Olanzapine • Zyprexa
Paliperidone • Invega
Paroxetine • Paxil
Perphenazine • Trilafon
Phenytoin • Dilantin
Pimavanserin • Nuplazid
Primidone • Mysoline
Quetiapine • Seroquel
Quinidine • Cardioquin
Rifampin • Rifadin
Risperidone • Risperdal
Sertraline • Zoloft
Terbinafine • Lamisil
Thioridazine • Mellaril
Trazodone • Desyrel, Oleptro
Venlafaxine • Effexor
Vilazodone • Viibryd
Vortioxetine • Trintellix
Ziprasidone • Geodon
The clinical response to the same dose of a drug may vary among individuals. Cytochrome P450 (CYP) 2D6 and 1A2 are enzymes that metabolize many psychotropic medications. Genetic variations in these enzymes may cause changes in their activity and result in differences in effectiveness and adverse effects. Although pharmacogenetic testing is available for CYP2D6 and CYP1A2, interpretation and clinical application of the results may not be straightforward.
Genetic variations in CYP450 enzymes determine enzymatic activity, which can have a large effect on drug levels, efficacy, and toxicity. However, there are many other important factors that clinicians should consider when trying to predict the effects of medications. While clinicians often focus on a patient’s genotype, this only provides information on a chromosomal level, and this information never changes. In contrast, a patient’s phenotype, or status of metabolism, is subject to change throughout the patient’s life.
Many circumstances influence phenotype, including the use of medications that induce or inhibit CYP450 enzymes, environmental factors, and comorbidities. Phenoconversion occurs when these factors result in a phenotype that is different from that predicted by genotype. Because of the possibility of phenoconversion, knowing a patient’s genotype may be of limited value in making clinical decisions. This article provides guidance on interpreting both the genotype and phenotype of CYP2D6 and CYP1A2. Case 1 and Case 2 illustrate these concepts.
CYP2D6
The enzyme activity of CYP2D6 varies among individuals and may include no activity, decreased activity, normal activity, or increased activity. After obtaining the genotype, the activity level of the CYP2D6 alleles may be determined. The frequency with which certain alleles occur varies with ancestry. More than 100 allelic variants and subvariants have been discovered, and new alleles are continuing to be discovered.1Table 12 lists some of the most common CYP2D6 alleles.
Based on the CYP2D6 enzyme activity determined from the alleles, 4 “traditional” phenotypes can be predicted from the genotype (Table 22). The 7-category phenotypes reported by some laboratory companies provide a more explicit method for reporting phenotypes.
Evidence suggests that, unlike most other CYP450 enzymes, CYP2D6 is not very susceptible to enzyme induction.2 Thus, genetics, rather than drug therapy, accounts for most ultra-rapid CYP2D6 metabolizers. CYP2D6 can be inhibited by the use of medications (Table 32-5) and/or substrates (Table 42,6). Similar to inhibitors, substrates may be saturating high affinity-low capacity enzymes such as CYP2D6, resulting in phenoconversion to poor metabolizers. However, this is unlikely to be the case for substrates of low affinity-high capacity enzymes such as CYP3A4.7 Ultimately, substrates and/or inhibitors of CYP2D6 may result in a phenotype that does not correspond to genotype.
Phenoconversion
Genotyping may not reflect the true prevalence of the CYP2D6 poor metabolizer phenotype when using multiple medications that are substrates and/or inhibitors of CYP2D6.8 In the presence of strong CYP2D6 inhibitors, up to 80% of individuals with a non-poor metabolizer genotype are converted to a poor metabolizer phenotype.8 While the phenotype provides a clearer representation of metabolism status than genotype, this information may not always be available.
Continue to: Determining CYP2D6 phenotype
Determining CYP2D6 phenotype
Risperidone and venlafaxine levels are useful tools for predicting CYP2D6 phenotype.3,8 When a risperidone level is ordered, the results include a risperidone level and a 9-hydroxyrisperidone level. The active metabolite of risperidone is 9-hydroxyrisperidone (
- Ultra-rapid metabolizer: 0.03 (0.02 to 0.06)
- Extensive metabolizer: 0.08 (0.04 to 0.17)
- Intermediate metabolizer: 0.56 (0.30 to 1.0)
- Poor metabolizer: 2.5 (1.8 to 4.1).
Although a R-to-9-OHR concentration ratio >1 generally indicates a poor metabolizer, it could also indicate the presence of a powerful CYP2D6 inhibitor.9
When a venlafaxine level is ordered, the results include a venlafaxine level and an O-desmethylvenlafaxine level. O-desmethylvenlafaxine (
CYP1A2
While the activity of CYP2D6 alleles is determined primarily by genetic factors and medications, the activity of CYP1A2 alleles is largely determined by environmental factors (diet, medications, disease) and genetic variability.2 Consequently, CYP1A2 genotyping may be less clinically useful than CYP2D6 genotyping. The CYP1A2 genotype–phenotype relationship incorporates the degree of allele activity (Table 52), and inducibility in the presence of environmental factors.
Continue to: CYP1A2 inhibiton
CYP1A2 inhibition
A variety of medications and environmental factors may inhibit CYP1A2.
Medications. Medications that may inhibit CYP1A2 include a
Caffeine. A significant increase in caffeine consumption can result in inhibition.3 Among non-tobacco smokers, an increase of 1 cup/d of coffee or 2 cans/d of caffeinated soda would be considered significant.3 However, tobacco smokers would require an increase of 3 cups/d of coffee or 6 cans/d of soda.
Diet. An increase in the daily dietary intake of certain vegetables for 6 days has been shown to result in inhibition.10 Apiaceous (Apiaceae or Umbelliferae) vegetables such as carrots (3/4 cup), celery (1/2 cup), dill (1 teaspoon), parsley (3 tablespoons), and parsnips (1¼ cup) can decrease CYP1A2 activity by approximately 13% to 25%. Allium (Liliaceae) vegetables, such as garlic, leeks, and onions, have no effect on CYP1A2 activity.
Infection. Pneumonia, upper respiratory infections with fever, pyelonephritis or appendicitis, or inflammation are suspected to decrease CYP1A2 activity.8
Continue to: CYP1A2 induction
CYP1A2 induction
A variety of medications and environmental factors may induce CYP1A2.
Medications. Certain medications may induce CYP1A2, including c
Cigarette smoking. A significant increase in smoking after 1 to 3 weeks may decrease drug levels, whereas a significant decrease in smoking after 1 to 3 weeks may result in elevated drug levels.3 Nicotine is not the causative agent of induction, but rather hydrocarbons found in cigarette smoke.11
Diet. An increase in daily dietary intake of certain vegetables for 6 days has been shown to result in induction.3 Brassica (Cruciferae) vegetables such as broccoli (2 cups), cauliflower (1 cup), cabbage (1 cup), and radish sprouts (1/2 cup) have been found to increase CYP1A2 activity by 18% to 37%.10 Grilled meat also plays a role in induction.10
Related Resource
- Ellingrod VL, Ward KM. Using pharmacogenetics guidelines when prescribing: What's available. Current Psychiatry. 2018;17(1):43-46.
Drug Brand Names
Amiodarone • Cordarone, Pacerone
Amitriptyline • Elavil, Endep
Aripiprazole • Abilify
Asenapine • Saphris
Atazanavir • Reyataz
Brexpiprazole • Rexulti
Bupropion • Wellbutrin, Zyban
Carbamazepine • Carbatrol, Tegretol
Chlorpromazine • Thorazine
Chloroquine • Aralen
Cinacalcet • Sensipar
Ciprofloxacin • Cipro
Citalopram • Celexa
Clozapine • Clozaril
Desipramine • Norpramin
Desvenlafaxine • Pristiq
Diphenhydramine • Benadryl
Doxepin • Silenor
Duloxetine • Cymbalta
Escitalopram • Lexapro
Ethinyl estradiol • Estinyl
Fluoxetine • Prozac
Fluvoxamine • Luvox
Haloperidol • Haldol
Iloperidone • Fanapt
Imatinib • Gleevec
Imipramine • Tofranil
Mirtazapine • Remeron
Nortriptyline • Pamelor
Olanzapine • Zyprexa
Paliperidone • Invega
Paroxetine • Paxil
Perphenazine • Trilafon
Phenytoin • Dilantin
Pimavanserin • Nuplazid
Primidone • Mysoline
Quetiapine • Seroquel
Quinidine • Cardioquin
Rifampin • Rifadin
Risperidone • Risperdal
Sertraline • Zoloft
Terbinafine • Lamisil
Thioridazine • Mellaril
Trazodone • Desyrel, Oleptro
Venlafaxine • Effexor
Vilazodone • Viibryd
Vortioxetine • Trintellix
Ziprasidone • Geodon
1. Pharmacogene Variation Consoritum. CYP2D6 allele nomenclature. https://www.pharmvar.org/gene/CYP2D6. Updated May 22, 2018. Accessed June 11, 2018.
2. Mrazek D. Psychiatric pharmacogenomics. New York, NY: Oxford University Press; 2010:33,42,44,45,85.
3. Spina E, de Leon J. Clinical applications of CYP genotyping in psychiatry. J Neural Transm (Vienna). 2015;122(1):5-28.
4. Adedoyin A, Frye RF, Mauro K, et al. Chloroquine modulation of specific metabolizing enzymes activities: investigation with selective five drug cocktail. Br J Clin Pharmacol. 1998;46(3):215-219.
5. Filppula AM, Laitila J, Neuvonen PJ, et al. Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates. Br J Pharmacol. 2012;165(8):2787-2798.
6. U.S. National Library of Medicine. DailyMed. http://dailymed.nlm.nih.gov/dailymed/about.cfm. Accessed April 26, 2018.
7. Monte AA, Heard KJ, Campbell J, et al. The effect of CYP2D6 drug-drug interactions on hydrocodone effectiveness. Acad Emerg Med. 2014;21(8):879-885.
8. Preskorn SH, Kane CP, Lobello K, et al. Cytochrome P450 2D6 phenoconversion is common in patients being treated for depression: implications for personalized medicine. J Clin Psychiatry. 2013;74(6):614-621.
9. de Leon, J, Susce, MT, Johnson, M, et al. DNA microarray technology in the clinical environment: the AmpliChip CYP450 test for CYP2D6 and CYP2C19 genotyping. CNS Spectr. 2009;14(1):19-34.
10. Lampe JW, King IB, Li S, et al. Brassica vegetables increase and apiaceous vegetables decrease cytochrome P450 1A2 activity in humans: changes in caffeine metabolite ratios in response to controlled vegetable diets. Carcinogenesis. 2000;21(6):1157-1162.
11. Zevin S, Benowitz NL. Drug interaction with tobacco smoking. An update. Clin Pharmacokinet. 1999;36(3):425-438.
1. Pharmacogene Variation Consoritum. CYP2D6 allele nomenclature. https://www.pharmvar.org/gene/CYP2D6. Updated May 22, 2018. Accessed June 11, 2018.
2. Mrazek D. Psychiatric pharmacogenomics. New York, NY: Oxford University Press; 2010:33,42,44,45,85.
3. Spina E, de Leon J. Clinical applications of CYP genotyping in psychiatry. J Neural Transm (Vienna). 2015;122(1):5-28.
4. Adedoyin A, Frye RF, Mauro K, et al. Chloroquine modulation of specific metabolizing enzymes activities: investigation with selective five drug cocktail. Br J Clin Pharmacol. 1998;46(3):215-219.
5. Filppula AM, Laitila J, Neuvonen PJ, et al. Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates. Br J Pharmacol. 2012;165(8):2787-2798.
6. U.S. National Library of Medicine. DailyMed. http://dailymed.nlm.nih.gov/dailymed/about.cfm. Accessed April 26, 2018.
7. Monte AA, Heard KJ, Campbell J, et al. The effect of CYP2D6 drug-drug interactions on hydrocodone effectiveness. Acad Emerg Med. 2014;21(8):879-885.
8. Preskorn SH, Kane CP, Lobello K, et al. Cytochrome P450 2D6 phenoconversion is common in patients being treated for depression: implications for personalized medicine. J Clin Psychiatry. 2013;74(6):614-621.
9. de Leon, J, Susce, MT, Johnson, M, et al. DNA microarray technology in the clinical environment: the AmpliChip CYP450 test for CYP2D6 and CYP2C19 genotyping. CNS Spectr. 2009;14(1):19-34.
10. Lampe JW, King IB, Li S, et al. Brassica vegetables increase and apiaceous vegetables decrease cytochrome P450 1A2 activity in humans: changes in caffeine metabolite ratios in response to controlled vegetable diets. Carcinogenesis. 2000;21(6):1157-1162.
11. Zevin S, Benowitz NL. Drug interaction with tobacco smoking. An update. Clin Pharmacokinet. 1999;36(3):425-438.
Is this adolescent suicidal? Challenges in pediatric inpatient consultation-liaison
CASE Attempted suicide?
Ms. S, a 16-year-old Yemeni-American girl, is brought to the emergency department (ED) by her mother and brother after ingesting an overdose of painkillers and fainting. During the initial evaluation, Ms. S says she had in the past attempted suicide by knife. The medical team suspects that the current overdose is a suicide attempt, and they call the consultation-liaison (C-L) psychiatry/psychology team. Ms. S’s brother strongly denies that his sister had previously attempted suicide, stating, “She’s from a good family, and she is smart. She cannot feel that way.” He also requests the name of the clinician who documented this information in the medical record.
During the consultation, Ms. S reports that the previous morning, she developed strong abdominal pain and discovered that she was menstruating for the first time. She explains that she did not understand what was happening to her and that no one had discussed menstruation with her before. Ms. S took her mother’s opioid pain medication. Ms. S reports she took one pill, but when it did not immediately alleviate her pain, she ingested several more. After this, Ms. S says she went to play with her siblings, but gradually became dizzy and confused, and informed her sister and mother of this. The family was fasting in observance of Ramadan, and as they walked toward the mosque, Ms. S fainted, which prompted her family to bring her to the ED.
During the C-L consultation, Ms. S’s brother, who speaks English, is present, as is her mother, who speaks only Arabic and thus needs a phone interpreter. As the C-L team asks Ms. S a question, it is translated to her mother, and then Ms. S’s response is also translated, and then finally, the mother shares her own response. At times, her brother provides translation. Ms. S speaks in English, but often asks for the translation of words or questions.
Ms. S reports that she and her family emigrated from Yemen to the United States 9 months ago. Ms. S says that she enjoys school and is doing well academically. She denies experiencing any anxiety, worry, or stress related to her life in Yemen, her move to a new country, her parents’ health, school, or other domains. Ms. S also denies any history of depressive episodes or previous suicidal ideation, intention, or attempt, which contradicts her endorsement of a previous suicide attempt to one clinician when she was initially evaluated.
[polldaddy:10040204]
Continue to: The authors' observation
The authors’ observation
The C-L team determined that Ms. S did not meet criteria for major depressive disorder. She did not endorse current feelings of depression and denied anhedonia and other associated symptoms included in DSM-5 criteria for major depressive disorder or adjustment disorder with depressed mood (Table 11).
Although Ms. S and her family recently emigrated from Yemen, she did not report any symptoms consistent with an adjustment disorder with depression. Further,
Accurate case conceptualization and diagnosis is particularly crucial in C-L services, where there is an urgency for clinical decision-making after an initial evaluation without the luxury of amending conceptualization in follow-up sessions. Providing a diagnosis for which a patient does not fully or accurately meet the criteria can have deleterious effects. An inaccurate diagnosis for Ms. S would have unnecessarily added the perceived stigma of a mental disorder to her medical record. Additionally, misdiagnosing or pathologizing a natural process of acculturation could have led to inappropriate or even harmful treatment.
The C-L team evaluated alternative explanations for Ms. S’s statements that suggested she was suicidal. First, they considered her mental status at the time she presented to the ED. An overdose of opioids alters mental status. Complicating reversal of opioid overdose is that some opioids have longer half-lives than naloxone, an opioid antagonist, so the individual can become reintoxicated. Similarly, some opioids are more potent and difficult to reverse.2 An altered mental status may have limited Ms. S’s ability to comprehend and answer questions accurately when she first presented to the ED.
Continue to: Cultural factors and the clinical evaluation
Cultural factors and the clinical evaluation
Next, the C-L team considered Ms. S’s clinical picture as it related to her cultural background. Cultural factors interact with the clinical evaluation in a complex manner, influencing the way patients approach the encounter, the symptoms they report, and the language they use to describe their experiences. While these variables are thoroughly evaluated during comprehensive psychological assessments, within the inpatient consultation service, the goal for pediatric C-L clinicians is to conduct a focused assessment to answer specific and critically important questions about a youth’s psychological functioning. Thus, the fundamental challenge of inpatient consultation is to answer the referral question in a brief period and in a culturally informed manner, to appraise the referring medical team about the relevant clinical and cultural issues, with the goal of ethical and clinically sound decision-making.
The C-L team considered key cultural factors in its assessment of Ms. S (Table 31). Several issues were of concern. First, language is often cited as the top barrier to health care access by Arab Americans, even by those with competency in English.3
Experts in culture argue that even with access to interpreters, many words and phrases lack direct translation, and their implicit meaning may be difficult to reveal. Additionally, at times more significance is placed on nonverbal cues and unspoken expectations.4 This can create barriers to communication with clinicians, especially in the context of an inpatient psychiatric consultation, when thorough understanding of an adolescent and family often needs to occur in a single encounter, and clinicians may not appreciate the subtle nuances of nonverbal communication.
The language barrier also may have influenced Ms. S’s initial endorsement of a previous suicide attempt by knife because the medical staff first interviewed Ms. S without an interpreter. For instance, many medical and psychosocial providers probe patients regarding suicidality with questions such as “Have you ever hurt yourself?” or “Have you ever tried to hurt yourself?” It is possible that in another language, an individual might interpret that question as, “Have you ever gotten hurt?” This interpretation completely alters the meaning of the question and eliminates intention or motivation to harm oneself. Language ambiguity and lack of shared cultural understanding may have influenced Ms. S’s interpretation of and response to such questions. Ms. S and her family were perplexed by the C-L team’s reference to the knife and continued to deny the incident.
Continue to: Cultural attitudes to puberty
Cultural attitudes to puberty
Cultures vary with respect to education of sensitive topics such as puberty. The medical providers assumed that Ms. S was informed about the onset of menses. Therefore, they could not consider the strong impact of such an event on an unsuspecting adolescent. Many adolescent girls in Yemen have poor health and lack menstruation-related knowledge, and many are “prescribed” medications by their mothers without contacting a physician.5 Ms. S reported to the C-L team that no one from her family had discussed menstruation with her. She reported that since arriving at the hospital, nurses had educated her about menstruation, and that she was no longer afraid. She also noted that if she experienced such pain again, she would go to the hospital or “just deal with it.”
Family identification and attitudes toward mental health
Ms. S’s strong identification with her family and attitudes toward mental health may have limited what she chose to disclose regarding her experiences of loss related to leaving her country of origin, adjustment, and acculturation to the new environment, as well as feelings of sadness. Family has a central and critical role in Arab cultures. Commitment to a family’s well-being and enhancement of honor and status is highly valued and encouraged.4 Conversely, being concerned with individual needs may be a source of guilt and feelings of betraying the family.6 Arab Americans tend not to discuss personal problems with people outside their extended family, including counselors and therapists, partly because of cultural stigma against mental illness7,8 and partly because revealing family problems to strangers (ie, clinicians) may be considered a cultural taboo9 and a threat to family honor.10 Although Ms. S was interviewed privately when she first came to the ED and also during the psychiatric consultation, the stigma of psychiatric problems11 and possible concerns about protecting her family’s name may have influenced her readiness to reveal intimate information to “strangers.”
Additionally, family statements that appeared to imply negative beliefs about mental health would have strongly deterred Ms. S from expressing any psychological concerns. For example, Ms. S’s brother took offense when the C-L team said it was evaluating his sister because she had said she had previously attempted suicide.
The tenets of Islam may have provided a framework through which Ms. S interprets emotional concerns and may have defined her explanatory models of psychological stress. For instance, it is not uncommon among American Muslims to view mental health problems as rising from “loss of faith in God,”9 and suicidal ideation may not be disclosed because suicide is forbidden in Islam.12 Therefore, it might be particularly difficult to assess suicidal ideation in a patient who is Muslim, especially those who are less acculturated to Western culture.13
Continue to: Directly asking Ms. S...
Directly asking Ms. S if she had thoughts of harming herself may have been too frightening or guilt-provoking for an adolescent with her background. Asking about passive expression of suicidal ideation would have been more culturally appropriate. For example, asking, “Do you wish that God would let you die?”12 may have elicited more meaningful clinical information about Ms. S’s emotional state and possibly suicide risk.
Furthermore, Ms. S’s identification of coping strategies (ie, “just deal with it”) may have sounded limited to a Western clinician, but this may have been consistent with cultural norms of emotional expression of limiting complaints.4 Also, among Arab Americans, psychiatric symptoms often are expressed through somatization.7,14 Expressing psychological pain through physical symptoms appears protective against public stigma. Public image and opinion is important, and behaviors that would reflect well to others are dictated by the family. These attitudes, beliefs, and values likely impact how Ms. S presented her psychological concerns.
[polldaddy:10040206]
The authors’ observations
Although inpatient hospitalization was initially considered, it was not pursued due to denial of past and current suicidal ideation or suicide attempts, the lack of comorbidity, age-appropriate functioning, and a supportive family environment. Similarly, due to the absence of acute psychiatric symptoms, partial hospitalization was not pursued. The C-L team evaluated treatment options with extreme caution and sensitivity because recommending the wrong treatment option could have deleterious effects on Ms. S and her family’s life. If inpatient hospitalization had been pursued, it could have likely caused the family unnecessary suffering and could have negatively affected familial relationships. Strong feelings of shame, betrayal, and guilt would be intensified, impairing the family’s cohesion, removing environmental and family supports, and putting Ms. S at further risk of developing more severe symptoms of low mood.
Although there were significant concerns about making the wrong recommendation to the family, the C-L team’s highest priority was Ms. S’s safety. Despite cultural concerns, the team would have recommended hospitalization if Ms. S’s clinical picture had warranted this decision.
Continue to: OUTCOME Culturally-appropriate outpatient therapy
OUTCOME Culturally-appropriate outpatient therapy
Due to the lack of substantial evidence of apparent risk for self-harm, the presence of a supportive family, and Ms. S’s high academic performance and future orientation, the C-L team concludes that Ms. S’s concerns were most likely the result of the challenges of acculturation related to the language barrier and a lack of health knowledge. However, the C-L team remains cautious that Ms. S may have minimized or denied her mental health concerns due to various cultural factors. The team recommends that Ms. S seek outpatient psychotherapy from a clinician who specializes in working with Arab American individuals and families in their native language. The C-L team communicates these conclusions to the medical team verbally and in writing.
The authors’ observations
Cultural issues experienced during this consultation may not generalize to other Arab American adolescents and their families because there is diversity even within groups that share common cultural characteristics. Nevertheless, this case underscores the challenge of accurately assessing suicide risk, and making a differential diagnosis in the presence of complex cultural data and the dilemmas clinicians may encounter when attempting to answer important referral questions such as, “Is this adolescent suicidal and in need of psychiatric hospitalization?”
Bottom Line
Cultural factors and attitudes toward mental health and language barriers may play a large role in how patients answer clinical questions. Cultural issues may add a level of intricacy not easily resolved within the restrictions of an inpatient setting, and this complexity may influence clinical judgment, recommendations, and possibly health outcomes. Culturally appropriate psychotherapy is key for patients experiencing difficulty with acculturation.
Related Resources
- Adam B. Caring for Muslim patients: Understanding cultural and religious factors. Current Psychiatry. 2017;16(12):56-57.
- Nassar-McMillan SC, Hakim-Larson J. Counseling considerations among Arab Americans. Journal of Counseling & Development. 2003;81(2):150-159.
- Sue DW. Multidimensional facets of cultural competence. The Counseling Psychologist. 2001;29(6):790-821.
Drug Brand Name
Naloxone • Narcan
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Meehan TJ, Bryant SM, Aks SE. Drugs of abuse: the highs and lows of altered mental states in the emergency department. Emerg Med Clin North Am. 2010;28(3):663-682.
3. Shah SM, Ayash C, Pharaon NA, et al. Arab American immigrants in New York: health care and cancer knowledge, attitudes, and beliefs. J Immigr Minor Health. 2008;10(5):429-436.
4. Budman CL, Lipson JG, Meleis AI. The cultural consultant in mental health care: the case of an Arab adolescent. Am J Orthopsychiatry. 1992; 62(3):359-370.
5. Mohamed EM, Mohamed AG, Al-Ajeal Ly. Knowledge, beliefs and practices regarding menstruation among adolescent schoolgirls in Seiyun City, Yemen. Al-Azhar Assiut Medical Journal. 2011;9(3):67-86.
6. Gorkin M, Masalha S, Yatziv G. Psychotherapy of Israeli-Arab patients: some cultural considerations. Journal of Psychoanalytic Anthropology. 1985;8(4);215-230.
7. Gearing RE, MacKenzie MJ, Ibrahim RW, et al. Stigma and mental health treatment of adolescents with depression in Jordan. Community Ment Health J. 2015;51(1):111-117.
8. Timimi SB. Adolescence in immigrant Arab families. Psychotherapy: theory, research, practice, training. 1995;32(1):141-149.
9. Ahmed S and Reddy LA. Understanding the mental health needs of American Muslims: recommendations and considerations for practice. Journal of Multicultural Counseling and Development. 2007;35(4):207-218.
10. Abudabbeh N, Nydell MK. Transcultural counseling and Arab Americans. In: McFadden J, ed. Transcultural counseling: bilateral and international perspectives. Alexandria, VA. American Counseling Association. 1993:261-284.
11. Erickson CD, al-Timimi NR. Providing mental health services to Arab Americans: recommendations and considerations. Cultur Divers Ethnic Minor Psychol. 2001;7(4):308-327.
12. Ali SR, Liu WM, Humedian M. Islam 101: understanding the religion and therapy implications. Prof Psychol Res Pr. 2004;35(6):635-642.
13. Hedayat-Diba Z. Psychotherapy with Muslims. In: Richards PS, Bergin AE, eds. Handbook of psychotherapy and religious diversity, 2nd ed. Washington, DC: Amercian Psychological Association. 2000:289-314.
14. Al-Krenawi A. Mental health practice in Arab countries. Curr Opin in Psychiatry. 2005;18(5):560-564.
CASE Attempted suicide?
Ms. S, a 16-year-old Yemeni-American girl, is brought to the emergency department (ED) by her mother and brother after ingesting an overdose of painkillers and fainting. During the initial evaluation, Ms. S says she had in the past attempted suicide by knife. The medical team suspects that the current overdose is a suicide attempt, and they call the consultation-liaison (C-L) psychiatry/psychology team. Ms. S’s brother strongly denies that his sister had previously attempted suicide, stating, “She’s from a good family, and she is smart. She cannot feel that way.” He also requests the name of the clinician who documented this information in the medical record.
During the consultation, Ms. S reports that the previous morning, she developed strong abdominal pain and discovered that she was menstruating for the first time. She explains that she did not understand what was happening to her and that no one had discussed menstruation with her before. Ms. S took her mother’s opioid pain medication. Ms. S reports she took one pill, but when it did not immediately alleviate her pain, she ingested several more. After this, Ms. S says she went to play with her siblings, but gradually became dizzy and confused, and informed her sister and mother of this. The family was fasting in observance of Ramadan, and as they walked toward the mosque, Ms. S fainted, which prompted her family to bring her to the ED.
During the C-L consultation, Ms. S’s brother, who speaks English, is present, as is her mother, who speaks only Arabic and thus needs a phone interpreter. As the C-L team asks Ms. S a question, it is translated to her mother, and then Ms. S’s response is also translated, and then finally, the mother shares her own response. At times, her brother provides translation. Ms. S speaks in English, but often asks for the translation of words or questions.
Ms. S reports that she and her family emigrated from Yemen to the United States 9 months ago. Ms. S says that she enjoys school and is doing well academically. She denies experiencing any anxiety, worry, or stress related to her life in Yemen, her move to a new country, her parents’ health, school, or other domains. Ms. S also denies any history of depressive episodes or previous suicidal ideation, intention, or attempt, which contradicts her endorsement of a previous suicide attempt to one clinician when she was initially evaluated.
[polldaddy:10040204]
Continue to: The authors' observation
The authors’ observation
The C-L team determined that Ms. S did not meet criteria for major depressive disorder. She did not endorse current feelings of depression and denied anhedonia and other associated symptoms included in DSM-5 criteria for major depressive disorder or adjustment disorder with depressed mood (Table 11).
Although Ms. S and her family recently emigrated from Yemen, she did not report any symptoms consistent with an adjustment disorder with depression. Further,
Accurate case conceptualization and diagnosis is particularly crucial in C-L services, where there is an urgency for clinical decision-making after an initial evaluation without the luxury of amending conceptualization in follow-up sessions. Providing a diagnosis for which a patient does not fully or accurately meet the criteria can have deleterious effects. An inaccurate diagnosis for Ms. S would have unnecessarily added the perceived stigma of a mental disorder to her medical record. Additionally, misdiagnosing or pathologizing a natural process of acculturation could have led to inappropriate or even harmful treatment.
The C-L team evaluated alternative explanations for Ms. S’s statements that suggested she was suicidal. First, they considered her mental status at the time she presented to the ED. An overdose of opioids alters mental status. Complicating reversal of opioid overdose is that some opioids have longer half-lives than naloxone, an opioid antagonist, so the individual can become reintoxicated. Similarly, some opioids are more potent and difficult to reverse.2 An altered mental status may have limited Ms. S’s ability to comprehend and answer questions accurately when she first presented to the ED.
Continue to: Cultural factors and the clinical evaluation
Cultural factors and the clinical evaluation
Next, the C-L team considered Ms. S’s clinical picture as it related to her cultural background. Cultural factors interact with the clinical evaluation in a complex manner, influencing the way patients approach the encounter, the symptoms they report, and the language they use to describe their experiences. While these variables are thoroughly evaluated during comprehensive psychological assessments, within the inpatient consultation service, the goal for pediatric C-L clinicians is to conduct a focused assessment to answer specific and critically important questions about a youth’s psychological functioning. Thus, the fundamental challenge of inpatient consultation is to answer the referral question in a brief period and in a culturally informed manner, to appraise the referring medical team about the relevant clinical and cultural issues, with the goal of ethical and clinically sound decision-making.
The C-L team considered key cultural factors in its assessment of Ms. S (Table 31). Several issues were of concern. First, language is often cited as the top barrier to health care access by Arab Americans, even by those with competency in English.3
Experts in culture argue that even with access to interpreters, many words and phrases lack direct translation, and their implicit meaning may be difficult to reveal. Additionally, at times more significance is placed on nonverbal cues and unspoken expectations.4 This can create barriers to communication with clinicians, especially in the context of an inpatient psychiatric consultation, when thorough understanding of an adolescent and family often needs to occur in a single encounter, and clinicians may not appreciate the subtle nuances of nonverbal communication.
The language barrier also may have influenced Ms. S’s initial endorsement of a previous suicide attempt by knife because the medical staff first interviewed Ms. S without an interpreter. For instance, many medical and psychosocial providers probe patients regarding suicidality with questions such as “Have you ever hurt yourself?” or “Have you ever tried to hurt yourself?” It is possible that in another language, an individual might interpret that question as, “Have you ever gotten hurt?” This interpretation completely alters the meaning of the question and eliminates intention or motivation to harm oneself. Language ambiguity and lack of shared cultural understanding may have influenced Ms. S’s interpretation of and response to such questions. Ms. S and her family were perplexed by the C-L team’s reference to the knife and continued to deny the incident.
Continue to: Cultural attitudes to puberty
Cultural attitudes to puberty
Cultures vary with respect to education of sensitive topics such as puberty. The medical providers assumed that Ms. S was informed about the onset of menses. Therefore, they could not consider the strong impact of such an event on an unsuspecting adolescent. Many adolescent girls in Yemen have poor health and lack menstruation-related knowledge, and many are “prescribed” medications by their mothers without contacting a physician.5 Ms. S reported to the C-L team that no one from her family had discussed menstruation with her. She reported that since arriving at the hospital, nurses had educated her about menstruation, and that she was no longer afraid. She also noted that if she experienced such pain again, she would go to the hospital or “just deal with it.”
Family identification and attitudes toward mental health
Ms. S’s strong identification with her family and attitudes toward mental health may have limited what she chose to disclose regarding her experiences of loss related to leaving her country of origin, adjustment, and acculturation to the new environment, as well as feelings of sadness. Family has a central and critical role in Arab cultures. Commitment to a family’s well-being and enhancement of honor and status is highly valued and encouraged.4 Conversely, being concerned with individual needs may be a source of guilt and feelings of betraying the family.6 Arab Americans tend not to discuss personal problems with people outside their extended family, including counselors and therapists, partly because of cultural stigma against mental illness7,8 and partly because revealing family problems to strangers (ie, clinicians) may be considered a cultural taboo9 and a threat to family honor.10 Although Ms. S was interviewed privately when she first came to the ED and also during the psychiatric consultation, the stigma of psychiatric problems11 and possible concerns about protecting her family’s name may have influenced her readiness to reveal intimate information to “strangers.”
Additionally, family statements that appeared to imply negative beliefs about mental health would have strongly deterred Ms. S from expressing any psychological concerns. For example, Ms. S’s brother took offense when the C-L team said it was evaluating his sister because she had said she had previously attempted suicide.
The tenets of Islam may have provided a framework through which Ms. S interprets emotional concerns and may have defined her explanatory models of psychological stress. For instance, it is not uncommon among American Muslims to view mental health problems as rising from “loss of faith in God,”9 and suicidal ideation may not be disclosed because suicide is forbidden in Islam.12 Therefore, it might be particularly difficult to assess suicidal ideation in a patient who is Muslim, especially those who are less acculturated to Western culture.13
Continue to: Directly asking Ms. S...
Directly asking Ms. S if she had thoughts of harming herself may have been too frightening or guilt-provoking for an adolescent with her background. Asking about passive expression of suicidal ideation would have been more culturally appropriate. For example, asking, “Do you wish that God would let you die?”12 may have elicited more meaningful clinical information about Ms. S’s emotional state and possibly suicide risk.
Furthermore, Ms. S’s identification of coping strategies (ie, “just deal with it”) may have sounded limited to a Western clinician, but this may have been consistent with cultural norms of emotional expression of limiting complaints.4 Also, among Arab Americans, psychiatric symptoms often are expressed through somatization.7,14 Expressing psychological pain through physical symptoms appears protective against public stigma. Public image and opinion is important, and behaviors that would reflect well to others are dictated by the family. These attitudes, beliefs, and values likely impact how Ms. S presented her psychological concerns.
[polldaddy:10040206]
The authors’ observations
Although inpatient hospitalization was initially considered, it was not pursued due to denial of past and current suicidal ideation or suicide attempts, the lack of comorbidity, age-appropriate functioning, and a supportive family environment. Similarly, due to the absence of acute psychiatric symptoms, partial hospitalization was not pursued. The C-L team evaluated treatment options with extreme caution and sensitivity because recommending the wrong treatment option could have deleterious effects on Ms. S and her family’s life. If inpatient hospitalization had been pursued, it could have likely caused the family unnecessary suffering and could have negatively affected familial relationships. Strong feelings of shame, betrayal, and guilt would be intensified, impairing the family’s cohesion, removing environmental and family supports, and putting Ms. S at further risk of developing more severe symptoms of low mood.
Although there were significant concerns about making the wrong recommendation to the family, the C-L team’s highest priority was Ms. S’s safety. Despite cultural concerns, the team would have recommended hospitalization if Ms. S’s clinical picture had warranted this decision.
Continue to: OUTCOME Culturally-appropriate outpatient therapy
OUTCOME Culturally-appropriate outpatient therapy
Due to the lack of substantial evidence of apparent risk for self-harm, the presence of a supportive family, and Ms. S’s high academic performance and future orientation, the C-L team concludes that Ms. S’s concerns were most likely the result of the challenges of acculturation related to the language barrier and a lack of health knowledge. However, the C-L team remains cautious that Ms. S may have minimized or denied her mental health concerns due to various cultural factors. The team recommends that Ms. S seek outpatient psychotherapy from a clinician who specializes in working with Arab American individuals and families in their native language. The C-L team communicates these conclusions to the medical team verbally and in writing.
The authors’ observations
Cultural issues experienced during this consultation may not generalize to other Arab American adolescents and their families because there is diversity even within groups that share common cultural characteristics. Nevertheless, this case underscores the challenge of accurately assessing suicide risk, and making a differential diagnosis in the presence of complex cultural data and the dilemmas clinicians may encounter when attempting to answer important referral questions such as, “Is this adolescent suicidal and in need of psychiatric hospitalization?”
Bottom Line
Cultural factors and attitudes toward mental health and language barriers may play a large role in how patients answer clinical questions. Cultural issues may add a level of intricacy not easily resolved within the restrictions of an inpatient setting, and this complexity may influence clinical judgment, recommendations, and possibly health outcomes. Culturally appropriate psychotherapy is key for patients experiencing difficulty with acculturation.
Related Resources
- Adam B. Caring for Muslim patients: Understanding cultural and religious factors. Current Psychiatry. 2017;16(12):56-57.
- Nassar-McMillan SC, Hakim-Larson J. Counseling considerations among Arab Americans. Journal of Counseling & Development. 2003;81(2):150-159.
- Sue DW. Multidimensional facets of cultural competence. The Counseling Psychologist. 2001;29(6):790-821.
Drug Brand Name
Naloxone • Narcan
CASE Attempted suicide?
Ms. S, a 16-year-old Yemeni-American girl, is brought to the emergency department (ED) by her mother and brother after ingesting an overdose of painkillers and fainting. During the initial evaluation, Ms. S says she had in the past attempted suicide by knife. The medical team suspects that the current overdose is a suicide attempt, and they call the consultation-liaison (C-L) psychiatry/psychology team. Ms. S’s brother strongly denies that his sister had previously attempted suicide, stating, “She’s from a good family, and she is smart. She cannot feel that way.” He also requests the name of the clinician who documented this information in the medical record.
During the consultation, Ms. S reports that the previous morning, she developed strong abdominal pain and discovered that she was menstruating for the first time. She explains that she did not understand what was happening to her and that no one had discussed menstruation with her before. Ms. S took her mother’s opioid pain medication. Ms. S reports she took one pill, but when it did not immediately alleviate her pain, she ingested several more. After this, Ms. S says she went to play with her siblings, but gradually became dizzy and confused, and informed her sister and mother of this. The family was fasting in observance of Ramadan, and as they walked toward the mosque, Ms. S fainted, which prompted her family to bring her to the ED.
During the C-L consultation, Ms. S’s brother, who speaks English, is present, as is her mother, who speaks only Arabic and thus needs a phone interpreter. As the C-L team asks Ms. S a question, it is translated to her mother, and then Ms. S’s response is also translated, and then finally, the mother shares her own response. At times, her brother provides translation. Ms. S speaks in English, but often asks for the translation of words or questions.
Ms. S reports that she and her family emigrated from Yemen to the United States 9 months ago. Ms. S says that she enjoys school and is doing well academically. She denies experiencing any anxiety, worry, or stress related to her life in Yemen, her move to a new country, her parents’ health, school, or other domains. Ms. S also denies any history of depressive episodes or previous suicidal ideation, intention, or attempt, which contradicts her endorsement of a previous suicide attempt to one clinician when she was initially evaluated.
[polldaddy:10040204]
Continue to: The authors' observation
The authors’ observation
The C-L team determined that Ms. S did not meet criteria for major depressive disorder. She did not endorse current feelings of depression and denied anhedonia and other associated symptoms included in DSM-5 criteria for major depressive disorder or adjustment disorder with depressed mood (Table 11).
Although Ms. S and her family recently emigrated from Yemen, she did not report any symptoms consistent with an adjustment disorder with depression. Further,
Accurate case conceptualization and diagnosis is particularly crucial in C-L services, where there is an urgency for clinical decision-making after an initial evaluation without the luxury of amending conceptualization in follow-up sessions. Providing a diagnosis for which a patient does not fully or accurately meet the criteria can have deleterious effects. An inaccurate diagnosis for Ms. S would have unnecessarily added the perceived stigma of a mental disorder to her medical record. Additionally, misdiagnosing or pathologizing a natural process of acculturation could have led to inappropriate or even harmful treatment.
The C-L team evaluated alternative explanations for Ms. S’s statements that suggested she was suicidal. First, they considered her mental status at the time she presented to the ED. An overdose of opioids alters mental status. Complicating reversal of opioid overdose is that some opioids have longer half-lives than naloxone, an opioid antagonist, so the individual can become reintoxicated. Similarly, some opioids are more potent and difficult to reverse.2 An altered mental status may have limited Ms. S’s ability to comprehend and answer questions accurately when she first presented to the ED.
Continue to: Cultural factors and the clinical evaluation
Cultural factors and the clinical evaluation
Next, the C-L team considered Ms. S’s clinical picture as it related to her cultural background. Cultural factors interact with the clinical evaluation in a complex manner, influencing the way patients approach the encounter, the symptoms they report, and the language they use to describe their experiences. While these variables are thoroughly evaluated during comprehensive psychological assessments, within the inpatient consultation service, the goal for pediatric C-L clinicians is to conduct a focused assessment to answer specific and critically important questions about a youth’s psychological functioning. Thus, the fundamental challenge of inpatient consultation is to answer the referral question in a brief period and in a culturally informed manner, to appraise the referring medical team about the relevant clinical and cultural issues, with the goal of ethical and clinically sound decision-making.
The C-L team considered key cultural factors in its assessment of Ms. S (Table 31). Several issues were of concern. First, language is often cited as the top barrier to health care access by Arab Americans, even by those with competency in English.3
Experts in culture argue that even with access to interpreters, many words and phrases lack direct translation, and their implicit meaning may be difficult to reveal. Additionally, at times more significance is placed on nonverbal cues and unspoken expectations.4 This can create barriers to communication with clinicians, especially in the context of an inpatient psychiatric consultation, when thorough understanding of an adolescent and family often needs to occur in a single encounter, and clinicians may not appreciate the subtle nuances of nonverbal communication.
The language barrier also may have influenced Ms. S’s initial endorsement of a previous suicide attempt by knife because the medical staff first interviewed Ms. S without an interpreter. For instance, many medical and psychosocial providers probe patients regarding suicidality with questions such as “Have you ever hurt yourself?” or “Have you ever tried to hurt yourself?” It is possible that in another language, an individual might interpret that question as, “Have you ever gotten hurt?” This interpretation completely alters the meaning of the question and eliminates intention or motivation to harm oneself. Language ambiguity and lack of shared cultural understanding may have influenced Ms. S’s interpretation of and response to such questions. Ms. S and her family were perplexed by the C-L team’s reference to the knife and continued to deny the incident.
Continue to: Cultural attitudes to puberty
Cultural attitudes to puberty
Cultures vary with respect to education of sensitive topics such as puberty. The medical providers assumed that Ms. S was informed about the onset of menses. Therefore, they could not consider the strong impact of such an event on an unsuspecting adolescent. Many adolescent girls in Yemen have poor health and lack menstruation-related knowledge, and many are “prescribed” medications by their mothers without contacting a physician.5 Ms. S reported to the C-L team that no one from her family had discussed menstruation with her. She reported that since arriving at the hospital, nurses had educated her about menstruation, and that she was no longer afraid. She also noted that if she experienced such pain again, she would go to the hospital or “just deal with it.”
Family identification and attitudes toward mental health
Ms. S’s strong identification with her family and attitudes toward mental health may have limited what she chose to disclose regarding her experiences of loss related to leaving her country of origin, adjustment, and acculturation to the new environment, as well as feelings of sadness. Family has a central and critical role in Arab cultures. Commitment to a family’s well-being and enhancement of honor and status is highly valued and encouraged.4 Conversely, being concerned with individual needs may be a source of guilt and feelings of betraying the family.6 Arab Americans tend not to discuss personal problems with people outside their extended family, including counselors and therapists, partly because of cultural stigma against mental illness7,8 and partly because revealing family problems to strangers (ie, clinicians) may be considered a cultural taboo9 and a threat to family honor.10 Although Ms. S was interviewed privately when she first came to the ED and also during the psychiatric consultation, the stigma of psychiatric problems11 and possible concerns about protecting her family’s name may have influenced her readiness to reveal intimate information to “strangers.”
Additionally, family statements that appeared to imply negative beliefs about mental health would have strongly deterred Ms. S from expressing any psychological concerns. For example, Ms. S’s brother took offense when the C-L team said it was evaluating his sister because she had said she had previously attempted suicide.
The tenets of Islam may have provided a framework through which Ms. S interprets emotional concerns and may have defined her explanatory models of psychological stress. For instance, it is not uncommon among American Muslims to view mental health problems as rising from “loss of faith in God,”9 and suicidal ideation may not be disclosed because suicide is forbidden in Islam.12 Therefore, it might be particularly difficult to assess suicidal ideation in a patient who is Muslim, especially those who are less acculturated to Western culture.13
Continue to: Directly asking Ms. S...
Directly asking Ms. S if she had thoughts of harming herself may have been too frightening or guilt-provoking for an adolescent with her background. Asking about passive expression of suicidal ideation would have been more culturally appropriate. For example, asking, “Do you wish that God would let you die?”12 may have elicited more meaningful clinical information about Ms. S’s emotional state and possibly suicide risk.
Furthermore, Ms. S’s identification of coping strategies (ie, “just deal with it”) may have sounded limited to a Western clinician, but this may have been consistent with cultural norms of emotional expression of limiting complaints.4 Also, among Arab Americans, psychiatric symptoms often are expressed through somatization.7,14 Expressing psychological pain through physical symptoms appears protective against public stigma. Public image and opinion is important, and behaviors that would reflect well to others are dictated by the family. These attitudes, beliefs, and values likely impact how Ms. S presented her psychological concerns.
[polldaddy:10040206]
The authors’ observations
Although inpatient hospitalization was initially considered, it was not pursued due to denial of past and current suicidal ideation or suicide attempts, the lack of comorbidity, age-appropriate functioning, and a supportive family environment. Similarly, due to the absence of acute psychiatric symptoms, partial hospitalization was not pursued. The C-L team evaluated treatment options with extreme caution and sensitivity because recommending the wrong treatment option could have deleterious effects on Ms. S and her family’s life. If inpatient hospitalization had been pursued, it could have likely caused the family unnecessary suffering and could have negatively affected familial relationships. Strong feelings of shame, betrayal, and guilt would be intensified, impairing the family’s cohesion, removing environmental and family supports, and putting Ms. S at further risk of developing more severe symptoms of low mood.
Although there were significant concerns about making the wrong recommendation to the family, the C-L team’s highest priority was Ms. S’s safety. Despite cultural concerns, the team would have recommended hospitalization if Ms. S’s clinical picture had warranted this decision.
Continue to: OUTCOME Culturally-appropriate outpatient therapy
OUTCOME Culturally-appropriate outpatient therapy
Due to the lack of substantial evidence of apparent risk for self-harm, the presence of a supportive family, and Ms. S’s high academic performance and future orientation, the C-L team concludes that Ms. S’s concerns were most likely the result of the challenges of acculturation related to the language barrier and a lack of health knowledge. However, the C-L team remains cautious that Ms. S may have minimized or denied her mental health concerns due to various cultural factors. The team recommends that Ms. S seek outpatient psychotherapy from a clinician who specializes in working with Arab American individuals and families in their native language. The C-L team communicates these conclusions to the medical team verbally and in writing.
The authors’ observations
Cultural issues experienced during this consultation may not generalize to other Arab American adolescents and their families because there is diversity even within groups that share common cultural characteristics. Nevertheless, this case underscores the challenge of accurately assessing suicide risk, and making a differential diagnosis in the presence of complex cultural data and the dilemmas clinicians may encounter when attempting to answer important referral questions such as, “Is this adolescent suicidal and in need of psychiatric hospitalization?”
Bottom Line
Cultural factors and attitudes toward mental health and language barriers may play a large role in how patients answer clinical questions. Cultural issues may add a level of intricacy not easily resolved within the restrictions of an inpatient setting, and this complexity may influence clinical judgment, recommendations, and possibly health outcomes. Culturally appropriate psychotherapy is key for patients experiencing difficulty with acculturation.
Related Resources
- Adam B. Caring for Muslim patients: Understanding cultural and religious factors. Current Psychiatry. 2017;16(12):56-57.
- Nassar-McMillan SC, Hakim-Larson J. Counseling considerations among Arab Americans. Journal of Counseling & Development. 2003;81(2):150-159.
- Sue DW. Multidimensional facets of cultural competence. The Counseling Psychologist. 2001;29(6):790-821.
Drug Brand Name
Naloxone • Narcan
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Meehan TJ, Bryant SM, Aks SE. Drugs of abuse: the highs and lows of altered mental states in the emergency department. Emerg Med Clin North Am. 2010;28(3):663-682.
3. Shah SM, Ayash C, Pharaon NA, et al. Arab American immigrants in New York: health care and cancer knowledge, attitudes, and beliefs. J Immigr Minor Health. 2008;10(5):429-436.
4. Budman CL, Lipson JG, Meleis AI. The cultural consultant in mental health care: the case of an Arab adolescent. Am J Orthopsychiatry. 1992; 62(3):359-370.
5. Mohamed EM, Mohamed AG, Al-Ajeal Ly. Knowledge, beliefs and practices regarding menstruation among adolescent schoolgirls in Seiyun City, Yemen. Al-Azhar Assiut Medical Journal. 2011;9(3):67-86.
6. Gorkin M, Masalha S, Yatziv G. Psychotherapy of Israeli-Arab patients: some cultural considerations. Journal of Psychoanalytic Anthropology. 1985;8(4);215-230.
7. Gearing RE, MacKenzie MJ, Ibrahim RW, et al. Stigma and mental health treatment of adolescents with depression in Jordan. Community Ment Health J. 2015;51(1):111-117.
8. Timimi SB. Adolescence in immigrant Arab families. Psychotherapy: theory, research, practice, training. 1995;32(1):141-149.
9. Ahmed S and Reddy LA. Understanding the mental health needs of American Muslims: recommendations and considerations for practice. Journal of Multicultural Counseling and Development. 2007;35(4):207-218.
10. Abudabbeh N, Nydell MK. Transcultural counseling and Arab Americans. In: McFadden J, ed. Transcultural counseling: bilateral and international perspectives. Alexandria, VA. American Counseling Association. 1993:261-284.
11. Erickson CD, al-Timimi NR. Providing mental health services to Arab Americans: recommendations and considerations. Cultur Divers Ethnic Minor Psychol. 2001;7(4):308-327.
12. Ali SR, Liu WM, Humedian M. Islam 101: understanding the religion and therapy implications. Prof Psychol Res Pr. 2004;35(6):635-642.
13. Hedayat-Diba Z. Psychotherapy with Muslims. In: Richards PS, Bergin AE, eds. Handbook of psychotherapy and religious diversity, 2nd ed. Washington, DC: Amercian Psychological Association. 2000:289-314.
14. Al-Krenawi A. Mental health practice in Arab countries. Curr Opin in Psychiatry. 2005;18(5):560-564.
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Meehan TJ, Bryant SM, Aks SE. Drugs of abuse: the highs and lows of altered mental states in the emergency department. Emerg Med Clin North Am. 2010;28(3):663-682.
3. Shah SM, Ayash C, Pharaon NA, et al. Arab American immigrants in New York: health care and cancer knowledge, attitudes, and beliefs. J Immigr Minor Health. 2008;10(5):429-436.
4. Budman CL, Lipson JG, Meleis AI. The cultural consultant in mental health care: the case of an Arab adolescent. Am J Orthopsychiatry. 1992; 62(3):359-370.
5. Mohamed EM, Mohamed AG, Al-Ajeal Ly. Knowledge, beliefs and practices regarding menstruation among adolescent schoolgirls in Seiyun City, Yemen. Al-Azhar Assiut Medical Journal. 2011;9(3):67-86.
6. Gorkin M, Masalha S, Yatziv G. Psychotherapy of Israeli-Arab patients: some cultural considerations. Journal of Psychoanalytic Anthropology. 1985;8(4);215-230.
7. Gearing RE, MacKenzie MJ, Ibrahim RW, et al. Stigma and mental health treatment of adolescents with depression in Jordan. Community Ment Health J. 2015;51(1):111-117.
8. Timimi SB. Adolescence in immigrant Arab families. Psychotherapy: theory, research, practice, training. 1995;32(1):141-149.
9. Ahmed S and Reddy LA. Understanding the mental health needs of American Muslims: recommendations and considerations for practice. Journal of Multicultural Counseling and Development. 2007;35(4):207-218.
10. Abudabbeh N, Nydell MK. Transcultural counseling and Arab Americans. In: McFadden J, ed. Transcultural counseling: bilateral and international perspectives. Alexandria, VA. American Counseling Association. 1993:261-284.
11. Erickson CD, al-Timimi NR. Providing mental health services to Arab Americans: recommendations and considerations. Cultur Divers Ethnic Minor Psychol. 2001;7(4):308-327.
12. Ali SR, Liu WM, Humedian M. Islam 101: understanding the religion and therapy implications. Prof Psychol Res Pr. 2004;35(6):635-642.
13. Hedayat-Diba Z. Psychotherapy with Muslims. In: Richards PS, Bergin AE, eds. Handbook of psychotherapy and religious diversity, 2nd ed. Washington, DC: Amercian Psychological Association. 2000:289-314.
14. Al-Krenawi A. Mental health practice in Arab countries. Curr Opin in Psychiatry. 2005;18(5):560-564.
