Jonathan R. Scarff, MD

More on T. gondii

We reviewed the article by Dr. Torrey on Toxoplasma gondii (T. gondii) and schizophrenia (“Cats, toxoplasmosis, and psychosis: Understanding the risks,” Current Psychiatry, May 2022, p. 14-19) with interest. Understanding infections in utero, during the perinatal period, and at other critical developmental stages may offer ways to prevent neurodevelopmental disorders. There appear to be good reasons to explore infectious and immune disruption of normal brain development. In a meta-analysis of 7 studies, Nayeri et al¹ found evidence to suggest T. gondii is a risk factor for autism spectrum disorder (ASD). Given the enormous loss of human potential and suffering resulting from schizophrenia and ASD, further exploration of toxoplasmosis and other infections may be valuable as we try to reduce the severe impact of these diseases.

The natural history of toxoplasmosis is an extraordinary example of nature’s complexity. The life cycle of this parasite uses the nervous system of the mouse to increase its transmission. Behavior changes ranging from reduced cat urine avoidance and increased risk-taking are observed in mice infected with T. gondii.² Chronic toxoplasmosis may also affect human behavior.³

Cats are fascinating, complex creatures. Of note, they produce a protein structurally like the secretion of the slow loris.⁴ The loris uses this brachial gland protein secretion as part of a defense strategy.⁵ Consideration of a possible toxic, neuroimmune role of these small mammal proteins in psychiatric disorders may open other avenues to explore.⁶

Our relationship to domesticated animals has been connected to serious diseases throughout human history.⁷ Severe acute respiratory syndrome and COVID-19 appear to be linked to animal reservoirs, mammals of the small animal trade, and the fur industry.^8,9 The rapid development of vaccines for COVID-19 is commendable. In conditions with multifactorial causation, managing an infectious component is worthy of consideration.

With mounting evidence suggesting a link between T. gondii and schizophrenia, ASD, and other diseases, further epidemiological studies and pilot interventions offer value. Interventions, including encouraging keeping cats indoors only, cat immunization, and human treatment, could be implemented in high-risk families. Efficacy requires data collection. While not easy, collaborative work by psychiatrists, developmental pediatricians, veterinarians, and epidemiologists is encouraged.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Michelle Douglass, PA-S2
Duke University Physician Assistant Program
Durham, North Carolina

References

1. Nayeri T, Sarvi S, Moosazadeh M, et al. Relationship between toxoplasmosis and autism: a systematic review and meta-analysis. Microb Pathog. 2020;147:104434. doi:10.1016/j.micpath.2020.104434
2. Kochanowsky JA, Koshy AA. Toxoplasma gondii. Curr Biol. 2018;28(14):R770-R771. doi:10.1016/j.cub.2018.05.035
3. Letcher S. Parasite mind control: how a single celled parasite carried in the cat intestine may be quietly tweaking our behavior. Scientific Kenyon: The Neuroscience Edition. 2018;22(1):4-11.
4. Scheib H, Nekaris KA, Rode-Margono J, et al. The toxicological intersection between allergen and toxin: a structural comparison of the cat dander allergenic protein Fel d1 and the slow loris brachial gland secretion protein. Toxins (Basel). 2020;12(2):86. doi:10.3390/toxins12020086
5. Nekaris KA, Moore RS, Rode EJ, et al. Mad, bad and dangerous to know: the biochemistry, ecology and evolution of slow loris venom. J Venom Anim Toxins Incl Trop Dis. 2013;19(1):21. doi:10.1186/1678-9199-19-21
6. Ligabue-Braun R. Hello, kitty: could cat allergy be a form of intoxication? J Venom Anim Toxins Incl Trop Dis. 2020;26:e20200051. doi:10.1590/1678-9199-JVATITD-2020-0051
7. Pearce-Duvet JM. The origin of human pathogens: evaluating the role of agriculture and domestic animals in the evolution of human disease. Biol Rev Camb Philos Soc. 2006;81(3):369-382. doi:10.1017/S1464793106007020
8. Jo WK, de Oliveira-Filho EF, Rasche A, et al. Potential zoonotic sources of SARS-CoV-2 infections. Transbound Emerg Dis. 2021;68(4):1824-1834. doi:10.1111/tbed.13872
9. Bell D, Roberton S, Hunter PR. Animal origins of SARS coronavirus: possible links with the international trade in small carnivores. Philos Trans R Soc Lond B Biol Sci. 2004;359(1447):1107-1114. doi:10.1098/rstb.2004.1492

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

Continue to: Pramipexole for MDD

I appreciate Dr. Espejo’s recommendations for treating patients who experience limited response from initial antidepressant therapy (“Treating major depressive disorder after limited response to an initial agent,” Current Psychiatry, October 2021, p. 51-53). I would like to add that pramipexole, a dopamine receptor agonist, can also alleviate depression. A meta-analysis concluded that patients receiving monotherapy or augmentation with pramipexole (mean maximum dose 1.62 mg/d) achieved response or remission of depression.¹ In an observational study of 116 patients with unipolar or bipolar depression, nearly 75% experienced response and 66% achieved remission with pramipexole augmentation (median maximum dose 1.05 mg/d).² Pramipexole is usually well-tolerated, although patients may experience nausea, somnolence, headache, and constipation, and they should be cautioned about the risk for compulsive behaviors and psychosis.

Jonathan R. Scarff, MD
Lexington VA Health Care System
Lexington, Kentucky

References

1. Tundo A, de Filippis R, De Crescenzo F. Pramipexole in the treatment of unipolar and bipolar depression. A systematic review and meta-analysis. Acta Psychiatr Scand. 2019;140(2):116-125.
2. Tundo A, Betrò S, Iommi M, et al. Efficacy and safety of 24-week pramipexole augmentation in patients with treatment resistant depression. A retrospective cohort study. Prog Neuropsychopharmacol Biol Psychiatry. 2022;112:110425. doi:10.1016/j.pnpbp.2021.110425

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

More on T. gondii

We reviewed the article by Dr. Torrey on Toxoplasma gondii (T. gondii) and schizophrenia (“Cats, toxoplasmosis, and psychosis: Understanding the risks,” Current Psychiatry, May 2022, p. 14-19) with interest. Understanding infections in utero, during the perinatal period, and at other critical developmental stages may offer ways to prevent neurodevelopmental disorders. There appear to be good reasons to explore infectious and immune disruption of normal brain development. In a meta-analysis of 7 studies, Nayeri et al¹ found evidence to suggest T. gondii is a risk factor for autism spectrum disorder (ASD). Given the enormous loss of human potential and suffering resulting from schizophrenia and ASD, further exploration of toxoplasmosis and other infections may be valuable as we try to reduce the severe impact of these diseases.

The natural history of toxoplasmosis is an extraordinary example of nature’s complexity. The life cycle of this parasite uses the nervous system of the mouse to increase its transmission. Behavior changes ranging from reduced cat urine avoidance and increased risk-taking are observed in mice infected with T. gondii.² Chronic toxoplasmosis may also affect human behavior.³

Cats are fascinating, complex creatures. Of note, they produce a protein structurally like the secretion of the slow loris.⁴ The loris uses this brachial gland protein secretion as part of a defense strategy.⁵ Consideration of a possible toxic, neuroimmune role of these small mammal proteins in psychiatric disorders may open other avenues to explore.⁶

Our relationship to domesticated animals has been connected to serious diseases throughout human history.⁷ Severe acute respiratory syndrome and COVID-19 appear to be linked to animal reservoirs, mammals of the small animal trade, and the fur industry.^8,9 The rapid development of vaccines for COVID-19 is commendable. In conditions with multifactorial causation, managing an infectious component is worthy of consideration.

With mounting evidence suggesting a link between T. gondii and schizophrenia, ASD, and other diseases, further epidemiological studies and pilot interventions offer value. Interventions, including encouraging keeping cats indoors only, cat immunization, and human treatment, could be implemented in high-risk families. Efficacy requires data collection. While not easy, collaborative work by psychiatrists, developmental pediatricians, veterinarians, and epidemiologists is encouraged.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Michelle Douglass, PA-S2
Duke University Physician Assistant Program
Durham, North Carolina

References

1. Nayeri T, Sarvi S, Moosazadeh M, et al. Relationship between toxoplasmosis and autism: a systematic review and meta-analysis. Microb Pathog. 2020;147:104434. doi:10.1016/j.micpath.2020.104434
2. Kochanowsky JA, Koshy AA. Toxoplasma gondii. Curr Biol. 2018;28(14):R770-R771. doi:10.1016/j.cub.2018.05.035
3. Letcher S. Parasite mind control: how a single celled parasite carried in the cat intestine may be quietly tweaking our behavior. Scientific Kenyon: The Neuroscience Edition. 2018;22(1):4-11.
4. Scheib H, Nekaris KA, Rode-Margono J, et al. The toxicological intersection between allergen and toxin: a structural comparison of the cat dander allergenic protein Fel d1 and the slow loris brachial gland secretion protein. Toxins (Basel). 2020;12(2):86. doi:10.3390/toxins12020086
5. Nekaris KA, Moore RS, Rode EJ, et al. Mad, bad and dangerous to know: the biochemistry, ecology and evolution of slow loris venom. J Venom Anim Toxins Incl Trop Dis. 2013;19(1):21. doi:10.1186/1678-9199-19-21
6. Ligabue-Braun R. Hello, kitty: could cat allergy be a form of intoxication? J Venom Anim Toxins Incl Trop Dis. 2020;26:e20200051. doi:10.1590/1678-9199-JVATITD-2020-0051
7. Pearce-Duvet JM. The origin of human pathogens: evaluating the role of agriculture and domestic animals in the evolution of human disease. Biol Rev Camb Philos Soc. 2006;81(3):369-382. doi:10.1017/S1464793106007020
8. Jo WK, de Oliveira-Filho EF, Rasche A, et al. Potential zoonotic sources of SARS-CoV-2 infections. Transbound Emerg Dis. 2021;68(4):1824-1834. doi:10.1111/tbed.13872
9. Bell D, Roberton S, Hunter PR. Animal origins of SARS coronavirus: possible links with the international trade in small carnivores. Philos Trans R Soc Lond B Biol Sci. 2004;359(1447):1107-1114. doi:10.1098/rstb.2004.1492

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

Continue to: Pramipexole for MDD

I appreciate Dr. Espejo’s recommendations for treating patients who experience limited response from initial antidepressant therapy (“Treating major depressive disorder after limited response to an initial agent,” Current Psychiatry, October 2021, p. 51-53). I would like to add that pramipexole, a dopamine receptor agonist, can also alleviate depression. A meta-analysis concluded that patients receiving monotherapy or augmentation with pramipexole (mean maximum dose 1.62 mg/d) achieved response or remission of depression.¹ In an observational study of 116 patients with unipolar or bipolar depression, nearly 75% experienced response and 66% achieved remission with pramipexole augmentation (median maximum dose 1.05 mg/d).² Pramipexole is usually well-tolerated, although patients may experience nausea, somnolence, headache, and constipation, and they should be cautioned about the risk for compulsive behaviors and psychosis.

Jonathan R. Scarff, MD
Lexington VA Health Care System
Lexington, Kentucky

References

1. Tundo A, de Filippis R, De Crescenzo F. Pramipexole in the treatment of unipolar and bipolar depression. A systematic review and meta-analysis. Acta Psychiatr Scand. 2019;140(2):116-125.
2. Tundo A, Betrò S, Iommi M, et al. Efficacy and safety of 24-week pramipexole augmentation in patients with treatment resistant depression. A retrospective cohort study. Prog Neuropsychopharmacol Biol Psychiatry. 2022;112:110425. doi:10.1016/j.pnpbp.2021.110425

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

More on T. gondii

We reviewed the article by Dr. Torrey on Toxoplasma gondii (T. gondii) and schizophrenia (“Cats, toxoplasmosis, and psychosis: Understanding the risks,” Current Psychiatry, May 2022, p. 14-19) with interest. Understanding infections in utero, during the perinatal period, and at other critical developmental stages may offer ways to prevent neurodevelopmental disorders. There appear to be good reasons to explore infectious and immune disruption of normal brain development. In a meta-analysis of 7 studies, Nayeri et al¹ found evidence to suggest T. gondii is a risk factor for autism spectrum disorder (ASD). Given the enormous loss of human potential and suffering resulting from schizophrenia and ASD, further exploration of toxoplasmosis and other infections may be valuable as we try to reduce the severe impact of these diseases.

The natural history of toxoplasmosis is an extraordinary example of nature’s complexity. The life cycle of this parasite uses the nervous system of the mouse to increase its transmission. Behavior changes ranging from reduced cat urine avoidance and increased risk-taking are observed in mice infected with T. gondii.² Chronic toxoplasmosis may also affect human behavior.³

Cats are fascinating, complex creatures. Of note, they produce a protein structurally like the secretion of the slow loris.⁴ The loris uses this brachial gland protein secretion as part of a defense strategy.⁵ Consideration of a possible toxic, neuroimmune role of these small mammal proteins in psychiatric disorders may open other avenues to explore.⁶

Our relationship to domesticated animals has been connected to serious diseases throughout human history.⁷ Severe acute respiratory syndrome and COVID-19 appear to be linked to animal reservoirs, mammals of the small animal trade, and the fur industry.^8,9 The rapid development of vaccines for COVID-19 is commendable. In conditions with multifactorial causation, managing an infectious component is worthy of consideration.

With mounting evidence suggesting a link between T. gondii and schizophrenia, ASD, and other diseases, further epidemiological studies and pilot interventions offer value. Interventions, including encouraging keeping cats indoors only, cat immunization, and human treatment, could be implemented in high-risk families. Efficacy requires data collection. While not easy, collaborative work by psychiatrists, developmental pediatricians, veterinarians, and epidemiologists is encouraged.

Mark C. Chandler, MD
Triangle Neuropsychiatry
Durham, North Carolina

Michelle Douglass, PA-S2
Duke University Physician Assistant Program
Durham, North Carolina

References

1. Nayeri T, Sarvi S, Moosazadeh M, et al. Relationship between toxoplasmosis and autism: a systematic review and meta-analysis. Microb Pathog. 2020;147:104434. doi:10.1016/j.micpath.2020.104434
2. Kochanowsky JA, Koshy AA. Toxoplasma gondii. Curr Biol. 2018;28(14):R770-R771. doi:10.1016/j.cub.2018.05.035
3. Letcher S. Parasite mind control: how a single celled parasite carried in the cat intestine may be quietly tweaking our behavior. Scientific Kenyon: The Neuroscience Edition. 2018;22(1):4-11.
4. Scheib H, Nekaris KA, Rode-Margono J, et al. The toxicological intersection between allergen and toxin: a structural comparison of the cat dander allergenic protein Fel d1 and the slow loris brachial gland secretion protein. Toxins (Basel). 2020;12(2):86. doi:10.3390/toxins12020086
5. Nekaris KA, Moore RS, Rode EJ, et al. Mad, bad and dangerous to know: the biochemistry, ecology and evolution of slow loris venom. J Venom Anim Toxins Incl Trop Dis. 2013;19(1):21. doi:10.1186/1678-9199-19-21
6. Ligabue-Braun R. Hello, kitty: could cat allergy be a form of intoxication? J Venom Anim Toxins Incl Trop Dis. 2020;26:e20200051. doi:10.1590/1678-9199-JVATITD-2020-0051
7. Pearce-Duvet JM. The origin of human pathogens: evaluating the role of agriculture and domestic animals in the evolution of human disease. Biol Rev Camb Philos Soc. 2006;81(3):369-382. doi:10.1017/S1464793106007020
8. Jo WK, de Oliveira-Filho EF, Rasche A, et al. Potential zoonotic sources of SARS-CoV-2 infections. Transbound Emerg Dis. 2021;68(4):1824-1834. doi:10.1111/tbed.13872
9. Bell D, Roberton S, Hunter PR. Animal origins of SARS coronavirus: possible links with the international trade in small carnivores. Philos Trans R Soc Lond B Biol Sci. 2004;359(1447):1107-1114. doi:10.1098/rstb.2004.1492

Disclosures

The authors report no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

Continue to: Pramipexole for MDD

I appreciate Dr. Espejo’s recommendations for treating patients who experience limited response from initial antidepressant therapy (“Treating major depressive disorder after limited response to an initial agent,” Current Psychiatry, October 2021, p. 51-53). I would like to add that pramipexole, a dopamine receptor agonist, can also alleviate depression. A meta-analysis concluded that patients receiving monotherapy or augmentation with pramipexole (mean maximum dose 1.62 mg/d) achieved response or remission of depression.¹ In an observational study of 116 patients with unipolar or bipolar depression, nearly 75% experienced response and 66% achieved remission with pramipexole augmentation (median maximum dose 1.05 mg/d).² Pramipexole is usually well-tolerated, although patients may experience nausea, somnolence, headache, and constipation, and they should be cautioned about the risk for compulsive behaviors and psychosis.

Jonathan R. Scarff, MD
Lexington VA Health Care System
Lexington, Kentucky

References

1. Tundo A, de Filippis R, De Crescenzo F. Pramipexole in the treatment of unipolar and bipolar depression. A systematic review and meta-analysis. Acta Psychiatr Scand. 2019;140(2):116-125.
2. Tundo A, Betrò S, Iommi M, et al. Efficacy and safety of 24-week pramipexole augmentation in patients with treatment resistant depression. A retrospective cohort study. Prog Neuropsychopharmacol Biol Psychiatry. 2022;112:110425. doi:10.1016/j.pnpbp.2021.110425

Disclosures

The author reports no financial relationships with any companies whose products are mentioned in this letter, or with manufacturers of competing products.

I am grateful for the opportunity to clarify and correct my recent commentary.¹ I wrote that the word provider was first used to refer to health care professionals during the 1930s in Nazi Germany, when Jewish physicians were termed Behandler. The cited manuscript stated that Behandler was “freely translated” as “provider.”² However, after reading social media comments that claimed this was a mistranslation, I sought to verify the translation.

Online German-English dictionaries yielded perplexing results. The dictionary Reverso translates Behandler as “dentist,” “practitioner,” or “therapist.”³ The Past Tenses Dictionary translates Behandler as “handlers.”⁴ Although a distasteful way to refer to a clinician-patient relationship, it still doesn’t translate as “provider.” The Collins and Cambridge dictionaries do not include Behandler, and the Langenscheidt dictionary does not provide a translation, instead noting that the translation “is missing” and that they are “verifying the word in question.”^5-7 Conversely, Anbieter appears to be the commonly provided German translation for provider.

The author of the original manuscript acknowledged that although Behandler is not listed as a translation for provider, it “comes close.”² He added that Behandler is not used anymore in German medicine because of the Nazi past (Saenger P, personal communication, February 9, 2022). A native German and Professor of German Studies at the University of Kentucky shared that “My best guess is that the term Behandler was used as a short form of Krankenbehandler, the designation for Jewish doctors in Nazi Germany who were still allowed to treat Jewish patients after withdrawal of their medical license. The best translations would be (health) practitioner or health care provider.” (Hobusch H, personal communication, 2022). However, Krankenbehandler has also been translated as “practitioner of the sick.”⁸

Given this ambiguity, it is ultimately unclear whether or to what extent Behandler can be translated as provider. Despite this uncertainty, my original argument remains unchanged. It is best to refer to all health care professionals (eg, psychotherapists, physicians, nurses, phlebotomists, pharmacists, physician assistants, social workers, physical therapists, dentists, optometrists) by their credentials. Overarching terms such as clinicians, practitioners, or health care professionals also are reasonable. This ensures accurate terminology, respects individuals’ unique training and degrees, and avoids confusion within multidisciplinary health care settings.

I thank Paul Saenger, MD, and Harald Höbusch, PhD, for their helpful insights, and those individuals who raised this concern on social media.

I am grateful for the opportunity to clarify and correct my recent commentary.¹ I wrote that the word provider was first used to refer to health care professionals during the 1930s in Nazi Germany, when Jewish physicians were termed Behandler. The cited manuscript stated that Behandler was “freely translated” as “provider.”² However, after reading social media comments that claimed this was a mistranslation, I sought to verify the translation.

Online German-English dictionaries yielded perplexing results. The dictionary Reverso translates Behandler as “dentist,” “practitioner,” or “therapist.”³ The Past Tenses Dictionary translates Behandler as “handlers.”⁴ Although a distasteful way to refer to a clinician-patient relationship, it still doesn’t translate as “provider.” The Collins and Cambridge dictionaries do not include Behandler, and the Langenscheidt dictionary does not provide a translation, instead noting that the translation “is missing” and that they are “verifying the word in question.”^5-7 Conversely, Anbieter appears to be the commonly provided German translation for provider.

The author of the original manuscript acknowledged that although Behandler is not listed as a translation for provider, it “comes close.”² He added that Behandler is not used anymore in German medicine because of the Nazi past (Saenger P, personal communication, February 9, 2022). A native German and Professor of German Studies at the University of Kentucky shared that “My best guess is that the term Behandler was used as a short form of Krankenbehandler, the designation for Jewish doctors in Nazi Germany who were still allowed to treat Jewish patients after withdrawal of their medical license. The best translations would be (health) practitioner or health care provider.” (Hobusch H, personal communication, 2022). However, Krankenbehandler has also been translated as “practitioner of the sick.”⁸

Given this ambiguity, it is ultimately unclear whether or to what extent Behandler can be translated as provider. Despite this uncertainty, my original argument remains unchanged. It is best to refer to all health care professionals (eg, psychotherapists, physicians, nurses, phlebotomists, pharmacists, physician assistants, social workers, physical therapists, dentists, optometrists) by their credentials. Overarching terms such as clinicians, practitioners, or health care professionals also are reasonable. This ensures accurate terminology, respects individuals’ unique training and degrees, and avoids confusion within multidisciplinary health care settings.

I thank Paul Saenger, MD, and Harald Höbusch, PhD, for their helpful insights, and those individuals who raised this concern on social media.

I am grateful for the opportunity to clarify and correct my recent commentary.¹ I wrote that the word provider was first used to refer to health care professionals during the 1930s in Nazi Germany, when Jewish physicians were termed Behandler. The cited manuscript stated that Behandler was “freely translated” as “provider.”² However, after reading social media comments that claimed this was a mistranslation, I sought to verify the translation.

Online German-English dictionaries yielded perplexing results. The dictionary Reverso translates Behandler as “dentist,” “practitioner,” or “therapist.”³ The Past Tenses Dictionary translates Behandler as “handlers.”⁴ Although a distasteful way to refer to a clinician-patient relationship, it still doesn’t translate as “provider.” The Collins and Cambridge dictionaries do not include Behandler, and the Langenscheidt dictionary does not provide a translation, instead noting that the translation “is missing” and that they are “verifying the word in question.”^5-7 Conversely, Anbieter appears to be the commonly provided German translation for provider.

The author of the original manuscript acknowledged that although Behandler is not listed as a translation for provider, it “comes close.”² He added that Behandler is not used anymore in German medicine because of the Nazi past (Saenger P, personal communication, February 9, 2022). A native German and Professor of German Studies at the University of Kentucky shared that “My best guess is that the term Behandler was used as a short form of Krankenbehandler, the designation for Jewish doctors in Nazi Germany who were still allowed to treat Jewish patients after withdrawal of their medical license. The best translations would be (health) practitioner or health care provider.” (Hobusch H, personal communication, 2022). However, Krankenbehandler has also been translated as “practitioner of the sick.”⁸

Given this ambiguity, it is ultimately unclear whether or to what extent Behandler can be translated as provider. Despite this uncertainty, my original argument remains unchanged. It is best to refer to all health care professionals (eg, psychotherapists, physicians, nurses, phlebotomists, pharmacists, physician assistants, social workers, physical therapists, dentists, optometrists) by their credentials. Overarching terms such as clinicians, practitioners, or health care professionals also are reasonable. This ensures accurate terminology, respects individuals’ unique training and degrees, and avoids confusion within multidisciplinary health care settings.

I thank Paul Saenger, MD, and Harald Höbusch, PhD, for their helpful insights, and those individuals who raised this concern on social media.

Intermittent fasting is the purposeful, restricted intake of food (and sometimes water), usually for health or religious reasons. Common forms are alternative-day fasting or time-restricted fasting, with variable ratios of days or hours for fasting and eating/drinking.¹ For example, fasting during Ramadan, the ninth month of the Islamic calendar, occurs from dawn to sunset, for a variable duration due to latitude and seasonal shifts.² Clinicians are likely to care for a patient who occasionally fasts. While there are potential benefits of fasting, clinicians need to consider the implications for patients who fast, particularly those receiving psychotropic medications.

Potential benefits for weight loss, mood

Some research suggests fasting is popular and may have benefits for an individual’s physical and mental health. In a 2020 online poll (N = 1,241), 24% of respondents said they had tried intermittent fasting, and 87% said the practice was very effective (50%) or somewhat effective (37%) in helping them lose weight.³ While more randomized control trials are needed to examine the practice’s effectiveness in promoting and maintaining weight loss, fasting has been linked to better glucose control in both humans and animals, and patients may have better adherence with fasting compared to caloric restriction alone.¹ Improved mood, alertness, tranquility, and sometimes euphoria have been documented among individuals who fast, but these benefits may not be sustained.⁴ A prospective study of 462 participants who fasted during Ramadan found the practice reduced depression in patients with diabetes, possibly due to mindfulness, decreased inflammation from improved insulin sensitivity, and/or social cohesion.⁵

Be aware of the potential risks

Fasting may either improve or destabilize mood in people with bipolar disorder by disrupting circadian rhythm and sleep.² Fasting might exacerbate underlying eating disorders.² Increased dehydration escalates the risk for orthostatic hypotension, which might require discontinuing clozapine.⁶ Hypotension and toxicity might arise during lithium pharmacotherapy. The Table⁴ summarizes things to consider when caring for a patient who fasts while receiving pharmacotherapy.

Provide patients with guidance

Advise patients not to fast if you believe it might exacerbate their mental illness, and encourage them to discuss with their primary care physicians any potential worsening of physical illnesses.² When caring for a patient who fasts for religious reasons, consider consulting with the patient’s religious leaders.² If patients choose to fast, monitor them for mood destabilization and/or medication adverse effects. If possible, avoid altering drug treatment regimens during fasting, and carefully monitor whenever a pharmaceutical change is necessary. When appropriate, the use of long-acting injectable medications may minimize adverse effects while maintaining mood stability. Encourage patients who fast to ensure they remain hydrated and practice sleep hygiene while they fast.⁷

Intermittent fasting is the purposeful, restricted intake of food (and sometimes water), usually for health or religious reasons. Common forms are alternative-day fasting or time-restricted fasting, with variable ratios of days or hours for fasting and eating/drinking.¹ For example, fasting during Ramadan, the ninth month of the Islamic calendar, occurs from dawn to sunset, for a variable duration due to latitude and seasonal shifts.² Clinicians are likely to care for a patient who occasionally fasts. While there are potential benefits of fasting, clinicians need to consider the implications for patients who fast, particularly those receiving psychotropic medications.

Potential benefits for weight loss, mood

Some research suggests fasting is popular and may have benefits for an individual’s physical and mental health. In a 2020 online poll (N = 1,241), 24% of respondents said they had tried intermittent fasting, and 87% said the practice was very effective (50%) or somewhat effective (37%) in helping them lose weight.³ While more randomized control trials are needed to examine the practice’s effectiveness in promoting and maintaining weight loss, fasting has been linked to better glucose control in both humans and animals, and patients may have better adherence with fasting compared to caloric restriction alone.¹ Improved mood, alertness, tranquility, and sometimes euphoria have been documented among individuals who fast, but these benefits may not be sustained.⁴ A prospective study of 462 participants who fasted during Ramadan found the practice reduced depression in patients with diabetes, possibly due to mindfulness, decreased inflammation from improved insulin sensitivity, and/or social cohesion.⁵

Be aware of the potential risks

Fasting may either improve or destabilize mood in people with bipolar disorder by disrupting circadian rhythm and sleep.² Fasting might exacerbate underlying eating disorders.² Increased dehydration escalates the risk for orthostatic hypotension, which might require discontinuing clozapine.⁶ Hypotension and toxicity might arise during lithium pharmacotherapy. The Table⁴ summarizes things to consider when caring for a patient who fasts while receiving pharmacotherapy.

Provide patients with guidance

Advise patients not to fast if you believe it might exacerbate their mental illness, and encourage them to discuss with their primary care physicians any potential worsening of physical illnesses.² When caring for a patient who fasts for religious reasons, consider consulting with the patient’s religious leaders.² If patients choose to fast, monitor them for mood destabilization and/or medication adverse effects. If possible, avoid altering drug treatment regimens during fasting, and carefully monitor whenever a pharmaceutical change is necessary. When appropriate, the use of long-acting injectable medications may minimize adverse effects while maintaining mood stability. Encourage patients who fast to ensure they remain hydrated and practice sleep hygiene while they fast.⁷

Intermittent fasting is the purposeful, restricted intake of food (and sometimes water), usually for health or religious reasons. Common forms are alternative-day fasting or time-restricted fasting, with variable ratios of days or hours for fasting and eating/drinking.¹ For example, fasting during Ramadan, the ninth month of the Islamic calendar, occurs from dawn to sunset, for a variable duration due to latitude and seasonal shifts.² Clinicians are likely to care for a patient who occasionally fasts. While there are potential benefits of fasting, clinicians need to consider the implications for patients who fast, particularly those receiving psychotropic medications.

Potential benefits for weight loss, mood

Some research suggests fasting is popular and may have benefits for an individual’s physical and mental health. In a 2020 online poll (N = 1,241), 24% of respondents said they had tried intermittent fasting, and 87% said the practice was very effective (50%) or somewhat effective (37%) in helping them lose weight.³ While more randomized control trials are needed to examine the practice’s effectiveness in promoting and maintaining weight loss, fasting has been linked to better glucose control in both humans and animals, and patients may have better adherence with fasting compared to caloric restriction alone.¹ Improved mood, alertness, tranquility, and sometimes euphoria have been documented among individuals who fast, but these benefits may not be sustained.⁴ A prospective study of 462 participants who fasted during Ramadan found the practice reduced depression in patients with diabetes, possibly due to mindfulness, decreased inflammation from improved insulin sensitivity, and/or social cohesion.⁵

Be aware of the potential risks

Fasting may either improve or destabilize mood in people with bipolar disorder by disrupting circadian rhythm and sleep.² Fasting might exacerbate underlying eating disorders.² Increased dehydration escalates the risk for orthostatic hypotension, which might require discontinuing clozapine.⁶ Hypotension and toxicity might arise during lithium pharmacotherapy. The Table⁴ summarizes things to consider when caring for a patient who fasts while receiving pharmacotherapy.

Provide patients with guidance

Advise patients not to fast if you believe it might exacerbate their mental illness, and encourage them to discuss with their primary care physicians any potential worsening of physical illnesses.² When caring for a patient who fasts for religious reasons, consider consulting with the patient’s religious leaders.² If patients choose to fast, monitor them for mood destabilization and/or medication adverse effects. If possible, avoid altering drug treatment regimens during fasting, and carefully monitor whenever a pharmaceutical change is necessary. When appropriate, the use of long-acting injectable medications may minimize adverse effects while maintaining mood stability. Encourage patients who fast to ensure they remain hydrated and practice sleep hygiene while they fast.⁷

Health care has been dramatically transformed and influenced by medical and technological advances, insurance companies, state and federal legislation, and medical ethics. Amid these changes, including crises such as the ongoing coronavirus pandemic, earning the trust of patients to care for their mental and physical health remains a priority and a privilege.

It is troubling that federal health care agencies, in addition to hospitals, clinics, pharmacies, insurance companies, and administrators, often use the term provider when referring to clinicians on the multidisciplinary health care treatment team, which has become the predominant model for health care delivery. The word provider does not originate in the health care arena but from the world of commerce and contains no reference to professionalism or therapeutic relationships.¹ Therefore, it should be replaced with more appropriate terminology that acknowledges clinicians’ roles and expertise and values our unique relationship with patients.

Why Is Provider a Problem?

First, the origin of the term provider is deplorable. During its ascent to power in the 1930s, the Nazi Party promoted the devaluation and exclusion of Jews in German society, including the medical community. Due to its eugenics campaign, the Nazi Party first targeted pediatrics, a specialty in which nearly half of its practitioners were Jewish.² Beginning with female pediatricians, all Jewish physicians were redesignated as Behandler (provider) instead of Arzt (doctor).² This is the first documented demeaning of physicians as providers in modern history. Jewish doctors were soon restricted to treating only Jewish patients and were further persecuted during the Holocaust. Knowing this background, what health care organization would use a term once associated with Nazi ideology?³

Second, using provider changes the treatment relationship. The nomenclature shift in the United States also seems to have originated in political and legislative circles. Although the reasons for this shift are unclear, the terminology became more pervasive after the government first used the term provider in Title XIX of the 1965 Social Security Amendments that established Medicare and Medicaid. Paydarfar and Schwartz noted it was used “in the sense of a contractor being paid for delivering any health-related products and services.”⁴ Ironically, a 1967 medical student health organization grant proposal discussed the role of a patient advocate in facilitating communication between “health care provider and patient.”⁵ A journalist for the New York Times used the word to describe a 1970 New York Senate debate surrounding the sale of Medicaid bills to collection agencies, but it is unclear whether the senators themselves used the term.⁶ Provider was later used in the National Health Planning and Resource Development Act of 1974.⁷

Ultimately, the adaptation of this terminology led to medicine being thought of only as a business, a commoditization of care, and reinforced by referring to patients as consumers, clients, or customers.³ This terminology suggests that the clinician-patient relationship is a commercial transaction based on a market concept where patients are consumers to be serviced.^1,8 Emphasis is placed on following algorithms and treating symptoms rather than patients.⁹ Despite a goal of minimizing cost, a mismatched referral to a provider may actually compromise patient safety and cost-effectiveness due to missed diagnoses or excessive diagnostic testing.¹⁰

In addition to government, other nonclinical entities (eg, insurance companies, advocacy groups) and some clinicians may prefer the generic term provider. Besides health care commoditization, reasons may include convenience, simplifying health care nomenclature, or removing distinctions among health care professionals to reduce costs and/or increase autonomy.

However, our value as health care professionals is not simply what we can “provide.”¹¹ We seek to know patients as people, putting their needs ahead of ours.¹ We serve as confidants and advocates and not merely providers of medications, tests, or procedures.¹¹ This personalized nature of health care depends on trust and professionalism rather than dispassionate delivery of commoditized services.¹ Using traditional terminology acknowledges the true nature of the treatment relationship—one that is established not on market concepts but on medical ethics of autonomy, justice, beneficence, and nonmaleficence.

Third, provider is inaccurate and potentially disrespectful and harmful. The word doctor is derived from Latin doctus or docere, meaning to teach or instruct—a valued function in our interactions with patients, families, students, and colleagues.^12,13 In contrast, provider refers to commercial transactions or the provision of shelter, food, and love within families and communities.^1,14

Although there are no studies assessing the impact of this terminology on individual clinicians, the term provider may have a negative impact on both individual clinicians and on the health care system. Health care professionals may feel they are being disrespected by being portrayed as dispensers of services rather than as individuals.^13,15 Furthermore, provider does not acknowledge the specialized training and qualifications of multidisciplinary treatment team members. The historical and theoretical foundation, degrees awarded, and scopes of practice for physicians, physician assistants, nurse practitioners, dentists, psychologists, optometrists, physical therapists, or social workers are different yet valuable, and their expertise and accomplishment should be recognized.

The use of this term has potential for causing moral injury and reduced self-worth, sense of purpose, and meaning in our daily work; this could threaten satisfaction and commitment and lead to demoralization and burnout.^1,16 It may impair effective team dynamics, as it makes no reference to professional values and may lead patients and clinicians to place lower value on professionalism and conduct.¹⁰ It may negatively impact primary care specialties by propagating the connotation that primary care is simple care and promoting low compensation, lagging recruitment, and diminished respect.¹⁰ Finally, it is detrimental to patients by changing the nature of the relationship and failing to evoke the compassion and support that sick people (that is, patients) need and deserve.³

Last, use of this term can mislead patients. By law, a health care provider is defined as “a doctor of medicine or osteopathy who is authorized to practice medicine or surgery… or any other person determined by the Secretary [of Labor] to be capable of providing health care services,” which includes podiatrists, dentists, clinical psychologists, optometrists, chiropractors, nurse practitioners, nurse-midwives, clinical social workers, and physician assistants.¹⁷

When clinicians are categorized as providers rather than by their degrees and roles/responsibilities, patients may assume that all team members have equal training, interchangeable skills, and uniform expertise and knowledge and may conclude they can receive the same level of care from anyone.^8,10 Potential for confusion is increased by the nearly ubiquitous white laboratory coat in clinical settings and doctoral degrees attainable in different health care disciplines (eg, medicine, nursing, psychology, pharmacy, physical therapy). Patients deserve to know who does what on the team of professionals who care for them and may not be fully informed when requesting or receiving treatment if they are not provided important information, such as a clinician’s title, training, and scope of practice.^8,16

Reversing the Trend 

Increasing awareness among patients, their families, health professions students, and health care colleagues and administrators of the importance of traditional nomenclature is a first step in reversing this trend or mitigating its impact. If an overarching generic term is required, then health care professional, clinician, or practitioner are preferred.^10,12 Fifteen years ago, the Southern California Permanente Medical Group prohibited the use of the word provider to describe physicians, and its editorial style deemed it cold and institutional.¹⁶ Many, but not all, state, regional, or national medical associations and journals avoid provider in their names or titles.

I am encouraged that this journal—drawing its audience from several government health care agencies—is named Federal Practitioner rather than Federal Provider. This is reasonable and accurate, as practitioner refers to the practice of a profession, usually associated with health care.

I hope other professions can resist this trend. Lawyers are not considered legal aid providers, and teachers are not called knowledge providers.³ We do not refer to airline pilots as air transportation providers or musicians as instrument-playing melody providers. Many veterans likely would be offended if they were referred to as Constitution support and defense providers rather than by the military branch-specific titles that they earned through dedication, training, and sacrifice. The individuals in these examples demonstrate commitment to representing clients, educating students, flying passengers, playing instruments, or ensuring national defense. As health care professionals, our commitment to treating patients is equally important.⁴

Language matters when it comes to people feeling respected and achieving their full potential.¹ I encourage government health care agencies to stop referring to us as providers and resume using traditional nomenclature. This will demonstrate genuine respect for us, transparency for the patients we serve, and recognition that caring for the sick is a calling, not a commodity.

Dedication

The author dedicates this article to his father John E. Scarff, Jr, a physician and United States Army veteran.

Health care has been dramatically transformed and influenced by medical and technological advances, insurance companies, state and federal legislation, and medical ethics. Amid these changes, including crises such as the ongoing coronavirus pandemic, earning the trust of patients to care for their mental and physical health remains a priority and a privilege.

It is troubling that federal health care agencies, in addition to hospitals, clinics, pharmacies, insurance companies, and administrators, often use the term provider when referring to clinicians on the multidisciplinary health care treatment team, which has become the predominant model for health care delivery. The word provider does not originate in the health care arena but from the world of commerce and contains no reference to professionalism or therapeutic relationships.¹ Therefore, it should be replaced with more appropriate terminology that acknowledges clinicians’ roles and expertise and values our unique relationship with patients.

Why Is Provider a Problem?

First, the origin of the term provider is deplorable. During its ascent to power in the 1930s, the Nazi Party promoted the devaluation and exclusion of Jews in German society, including the medical community. Due to its eugenics campaign, the Nazi Party first targeted pediatrics, a specialty in which nearly half of its practitioners were Jewish.² Beginning with female pediatricians, all Jewish physicians were redesignated as Behandler (provider) instead of Arzt (doctor).² This is the first documented demeaning of physicians as providers in modern history. Jewish doctors were soon restricted to treating only Jewish patients and were further persecuted during the Holocaust. Knowing this background, what health care organization would use a term once associated with Nazi ideology?³

Second, using provider changes the treatment relationship. The nomenclature shift in the United States also seems to have originated in political and legislative circles. Although the reasons for this shift are unclear, the terminology became more pervasive after the government first used the term provider in Title XIX of the 1965 Social Security Amendments that established Medicare and Medicaid. Paydarfar and Schwartz noted it was used “in the sense of a contractor being paid for delivering any health-related products and services.”⁴ Ironically, a 1967 medical student health organization grant proposal discussed the role of a patient advocate in facilitating communication between “health care provider and patient.”⁵ A journalist for the New York Times used the word to describe a 1970 New York Senate debate surrounding the sale of Medicaid bills to collection agencies, but it is unclear whether the senators themselves used the term.⁶ Provider was later used in the National Health Planning and Resource Development Act of 1974.⁷

Ultimately, the adaptation of this terminology led to medicine being thought of only as a business, a commoditization of care, and reinforced by referring to patients as consumers, clients, or customers.³ This terminology suggests that the clinician-patient relationship is a commercial transaction based on a market concept where patients are consumers to be serviced.^1,8 Emphasis is placed on following algorithms and treating symptoms rather than patients.⁹ Despite a goal of minimizing cost, a mismatched referral to a provider may actually compromise patient safety and cost-effectiveness due to missed diagnoses or excessive diagnostic testing.¹⁰

In addition to government, other nonclinical entities (eg, insurance companies, advocacy groups) and some clinicians may prefer the generic term provider. Besides health care commoditization, reasons may include convenience, simplifying health care nomenclature, or removing distinctions among health care professionals to reduce costs and/or increase autonomy.

However, our value as health care professionals is not simply what we can “provide.”¹¹ We seek to know patients as people, putting their needs ahead of ours.¹ We serve as confidants and advocates and not merely providers of medications, tests, or procedures.¹¹ This personalized nature of health care depends on trust and professionalism rather than dispassionate delivery of commoditized services.¹ Using traditional terminology acknowledges the true nature of the treatment relationship—one that is established not on market concepts but on medical ethics of autonomy, justice, beneficence, and nonmaleficence.

Third, provider is inaccurate and potentially disrespectful and harmful. The word doctor is derived from Latin doctus or docere, meaning to teach or instruct—a valued function in our interactions with patients, families, students, and colleagues.^12,13 In contrast, provider refers to commercial transactions or the provision of shelter, food, and love within families and communities.^1,14

Although there are no studies assessing the impact of this terminology on individual clinicians, the term provider may have a negative impact on both individual clinicians and on the health care system. Health care professionals may feel they are being disrespected by being portrayed as dispensers of services rather than as individuals.^13,15 Furthermore, provider does not acknowledge the specialized training and qualifications of multidisciplinary treatment team members. The historical and theoretical foundation, degrees awarded, and scopes of practice for physicians, physician assistants, nurse practitioners, dentists, psychologists, optometrists, physical therapists, or social workers are different yet valuable, and their expertise and accomplishment should be recognized.

The use of this term has potential for causing moral injury and reduced self-worth, sense of purpose, and meaning in our daily work; this could threaten satisfaction and commitment and lead to demoralization and burnout.^1,16 It may impair effective team dynamics, as it makes no reference to professional values and may lead patients and clinicians to place lower value on professionalism and conduct.¹⁰ It may negatively impact primary care specialties by propagating the connotation that primary care is simple care and promoting low compensation, lagging recruitment, and diminished respect.¹⁰ Finally, it is detrimental to patients by changing the nature of the relationship and failing to evoke the compassion and support that sick people (that is, patients) need and deserve.³

Last, use of this term can mislead patients. By law, a health care provider is defined as “a doctor of medicine or osteopathy who is authorized to practice medicine or surgery… or any other person determined by the Secretary [of Labor] to be capable of providing health care services,” which includes podiatrists, dentists, clinical psychologists, optometrists, chiropractors, nurse practitioners, nurse-midwives, clinical social workers, and physician assistants.¹⁷

When clinicians are categorized as providers rather than by their degrees and roles/responsibilities, patients may assume that all team members have equal training, interchangeable skills, and uniform expertise and knowledge and may conclude they can receive the same level of care from anyone.^8,10 Potential for confusion is increased by the nearly ubiquitous white laboratory coat in clinical settings and doctoral degrees attainable in different health care disciplines (eg, medicine, nursing, psychology, pharmacy, physical therapy). Patients deserve to know who does what on the team of professionals who care for them and may not be fully informed when requesting or receiving treatment if they are not provided important information, such as a clinician’s title, training, and scope of practice.^8,16

Reversing the Trend 

Increasing awareness among patients, their families, health professions students, and health care colleagues and administrators of the importance of traditional nomenclature is a first step in reversing this trend or mitigating its impact. If an overarching generic term is required, then health care professional, clinician, or practitioner are preferred.^10,12 Fifteen years ago, the Southern California Permanente Medical Group prohibited the use of the word provider to describe physicians, and its editorial style deemed it cold and institutional.¹⁶ Many, but not all, state, regional, or national medical associations and journals avoid provider in their names or titles.

I am encouraged that this journal—drawing its audience from several government health care agencies—is named Federal Practitioner rather than Federal Provider. This is reasonable and accurate, as practitioner refers to the practice of a profession, usually associated with health care.

I hope other professions can resist this trend. Lawyers are not considered legal aid providers, and teachers are not called knowledge providers.³ We do not refer to airline pilots as air transportation providers or musicians as instrument-playing melody providers. Many veterans likely would be offended if they were referred to as Constitution support and defense providers rather than by the military branch-specific titles that they earned through dedication, training, and sacrifice. The individuals in these examples demonstrate commitment to representing clients, educating students, flying passengers, playing instruments, or ensuring national defense. As health care professionals, our commitment to treating patients is equally important.⁴

Language matters when it comes to people feeling respected and achieving their full potential.¹ I encourage government health care agencies to stop referring to us as providers and resume using traditional nomenclature. This will demonstrate genuine respect for us, transparency for the patients we serve, and recognition that caring for the sick is a calling, not a commodity.

Dedication

The author dedicates this article to his father John E. Scarff, Jr, a physician and United States Army veteran.

Health care has been dramatically transformed and influenced by medical and technological advances, insurance companies, state and federal legislation, and medical ethics. Amid these changes, including crises such as the ongoing coronavirus pandemic, earning the trust of patients to care for their mental and physical health remains a priority and a privilege.

It is troubling that federal health care agencies, in addition to hospitals, clinics, pharmacies, insurance companies, and administrators, often use the term provider when referring to clinicians on the multidisciplinary health care treatment team, which has become the predominant model for health care delivery. The word provider does not originate in the health care arena but from the world of commerce and contains no reference to professionalism or therapeutic relationships.¹ Therefore, it should be replaced with more appropriate terminology that acknowledges clinicians’ roles and expertise and values our unique relationship with patients.

Why Is Provider a Problem?

First, the origin of the term provider is deplorable. During its ascent to power in the 1930s, the Nazi Party promoted the devaluation and exclusion of Jews in German society, including the medical community. Due to its eugenics campaign, the Nazi Party first targeted pediatrics, a specialty in which nearly half of its practitioners were Jewish.² Beginning with female pediatricians, all Jewish physicians were redesignated as Behandler (provider) instead of Arzt (doctor).² This is the first documented demeaning of physicians as providers in modern history. Jewish doctors were soon restricted to treating only Jewish patients and were further persecuted during the Holocaust. Knowing this background, what health care organization would use a term once associated with Nazi ideology?³

Second, using provider changes the treatment relationship. The nomenclature shift in the United States also seems to have originated in political and legislative circles. Although the reasons for this shift are unclear, the terminology became more pervasive after the government first used the term provider in Title XIX of the 1965 Social Security Amendments that established Medicare and Medicaid. Paydarfar and Schwartz noted it was used “in the sense of a contractor being paid for delivering any health-related products and services.”⁴ Ironically, a 1967 medical student health organization grant proposal discussed the role of a patient advocate in facilitating communication between “health care provider and patient.”⁵ A journalist for the New York Times used the word to describe a 1970 New York Senate debate surrounding the sale of Medicaid bills to collection agencies, but it is unclear whether the senators themselves used the term.⁶ Provider was later used in the National Health Planning and Resource Development Act of 1974.⁷

Ultimately, the adaptation of this terminology led to medicine being thought of only as a business, a commoditization of care, and reinforced by referring to patients as consumers, clients, or customers.³ This terminology suggests that the clinician-patient relationship is a commercial transaction based on a market concept where patients are consumers to be serviced.^1,8 Emphasis is placed on following algorithms and treating symptoms rather than patients.⁹ Despite a goal of minimizing cost, a mismatched referral to a provider may actually compromise patient safety and cost-effectiveness due to missed diagnoses or excessive diagnostic testing.¹⁰

In addition to government, other nonclinical entities (eg, insurance companies, advocacy groups) and some clinicians may prefer the generic term provider. Besides health care commoditization, reasons may include convenience, simplifying health care nomenclature, or removing distinctions among health care professionals to reduce costs and/or increase autonomy.

However, our value as health care professionals is not simply what we can “provide.”¹¹ We seek to know patients as people, putting their needs ahead of ours.¹ We serve as confidants and advocates and not merely providers of medications, tests, or procedures.¹¹ This personalized nature of health care depends on trust and professionalism rather than dispassionate delivery of commoditized services.¹ Using traditional terminology acknowledges the true nature of the treatment relationship—one that is established not on market concepts but on medical ethics of autonomy, justice, beneficence, and nonmaleficence.

Third, provider is inaccurate and potentially disrespectful and harmful. The word doctor is derived from Latin doctus or docere, meaning to teach or instruct—a valued function in our interactions with patients, families, students, and colleagues.^12,13 In contrast, provider refers to commercial transactions or the provision of shelter, food, and love within families and communities.^1,14

Although there are no studies assessing the impact of this terminology on individual clinicians, the term provider may have a negative impact on both individual clinicians and on the health care system. Health care professionals may feel they are being disrespected by being portrayed as dispensers of services rather than as individuals.^13,15 Furthermore, provider does not acknowledge the specialized training and qualifications of multidisciplinary treatment team members. The historical and theoretical foundation, degrees awarded, and scopes of practice for physicians, physician assistants, nurse practitioners, dentists, psychologists, optometrists, physical therapists, or social workers are different yet valuable, and their expertise and accomplishment should be recognized.

The use of this term has potential for causing moral injury and reduced self-worth, sense of purpose, and meaning in our daily work; this could threaten satisfaction and commitment and lead to demoralization and burnout.^1,16 It may impair effective team dynamics, as it makes no reference to professional values and may lead patients and clinicians to place lower value on professionalism and conduct.¹⁰ It may negatively impact primary care specialties by propagating the connotation that primary care is simple care and promoting low compensation, lagging recruitment, and diminished respect.¹⁰ Finally, it is detrimental to patients by changing the nature of the relationship and failing to evoke the compassion and support that sick people (that is, patients) need and deserve.³

Last, use of this term can mislead patients. By law, a health care provider is defined as “a doctor of medicine or osteopathy who is authorized to practice medicine or surgery… or any other person determined by the Secretary [of Labor] to be capable of providing health care services,” which includes podiatrists, dentists, clinical psychologists, optometrists, chiropractors, nurse practitioners, nurse-midwives, clinical social workers, and physician assistants.¹⁷

When clinicians are categorized as providers rather than by their degrees and roles/responsibilities, patients may assume that all team members have equal training, interchangeable skills, and uniform expertise and knowledge and may conclude they can receive the same level of care from anyone.^8,10 Potential for confusion is increased by the nearly ubiquitous white laboratory coat in clinical settings and doctoral degrees attainable in different health care disciplines (eg, medicine, nursing, psychology, pharmacy, physical therapy). Patients deserve to know who does what on the team of professionals who care for them and may not be fully informed when requesting or receiving treatment if they are not provided important information, such as a clinician’s title, training, and scope of practice.^8,16

Reversing the Trend 

Increasing awareness among patients, their families, health professions students, and health care colleagues and administrators of the importance of traditional nomenclature is a first step in reversing this trend or mitigating its impact. If an overarching generic term is required, then health care professional, clinician, or practitioner are preferred.^10,12 Fifteen years ago, the Southern California Permanente Medical Group prohibited the use of the word provider to describe physicians, and its editorial style deemed it cold and institutional.¹⁶ Many, but not all, state, regional, or national medical associations and journals avoid provider in their names or titles.

I am encouraged that this journal—drawing its audience from several government health care agencies—is named Federal Practitioner rather than Federal Provider. This is reasonable and accurate, as practitioner refers to the practice of a profession, usually associated with health care.

I hope other professions can resist this trend. Lawyers are not considered legal aid providers, and teachers are not called knowledge providers.³ We do not refer to airline pilots as air transportation providers or musicians as instrument-playing melody providers. Many veterans likely would be offended if they were referred to as Constitution support and defense providers rather than by the military branch-specific titles that they earned through dedication, training, and sacrifice. The individuals in these examples demonstrate commitment to representing clients, educating students, flying passengers, playing instruments, or ensuring national defense. As health care professionals, our commitment to treating patients is equally important.⁴

Language matters when it comes to people feeling respected and achieving their full potential.¹ I encourage government health care agencies to stop referring to us as providers and resume using traditional nomenclature. This will demonstrate genuine respect for us, transparency for the patients we serve, and recognition that caring for the sick is a calling, not a commodity.

Dedication

The author dedicates this article to his father John E. Scarff, Jr, a physician and United States Army veteran.

Tardive dyskinesia (TD)—involuntary movement persisting for >1 month—is often caused by exposure to dopamine receptor–blocking agents such as antipsychotics.¹ The pathophysiology of TD is attributed to dopamine receptor hypersensitivity and upregulation of dopamine receptors in response to chronic receptor blockade, although striatal dysfunction, oxidative stress, and gamma-aminobutyric acid (GABA) dysfunction may play a role.¹ Because discontinuing the antipsychotic may not improve the patient’s TD symptoms and may worsen mood or psychosis, clinicians often prescribe adjunctive agents to reduce TD symptoms while continuing the antipsychotic. Clinicians can use the mnemonic ABCD to help recall 4 evidence-based treatments for TD.

Amantadine is an N-methyl-D-aspartate receptor antagonist that is postulated to improve dopaminergic signaling through increased dopamine release and inhibited postsynaptic uptake, although its exact mechanism is unclear. In a double-blind, placebo-controlled, crossover study of 22 patients with TD who were treated with amantadine, the average reduction on the Abnormal Involuntary Movement Scale (AIMS) was approximately 22%.² Adverse effects include gastrointestinal upset, mood changes, and impaired concentration.

Ginkgo Biloba contains antioxidant properties that may help reduce TD symptoms by alleviating oxidative stress. In a meta-analysis of 3 randomized controlled trials from China (N = 299), ginkgo biloba extract, 240 mg/d, significantly improved symptoms of TD compared with placebo.³ Ginkgo biloba has an antiplatelet effect and therefore should not be used in patients with an increased bleeding risk.

Clonazepam. Several small studies have examined the use of this GABA agonist for TD. In a study of 19 patients with TD, researchers found a symptom reduction of up to 35% with doses up to 4.5 mg/d.⁴ However, many studies have had small sample sizes or poor methodology. A 2018 Cochrane review recommended using other agents before considering clonazepam for TD because this medication has uncertain efficacy in treating TD, and it can cause sedation and dependence.⁵

Deutetrabenazine and valbenazine, the only FDA-approved treatments for TD, are vesicular monoamine transporter 2 (VMAT2) inhibitors, which inhibit dopamine release and decrease dopamine receptor hypersensitivity.⁶ In a 12-week, randomized, double-blind, placebo-controlled study of 117 patients with moderate-to-severe TD, those who received deutetrabenazine (up to 48 mg/d) had a significant mean reduction in AIMS score (3 points) compared with placebo.⁷ In the 1-year KINECT 3 study, 124 patients with TD who received valbenazine, 40 or 80 mg/d, had significant mean reductions in AIMS scores of 3.0 and 4.8 points, respectively.⁸ Adverse effects of these medications include somnolence, headache, akathisia, urinary tract infection, worsening mood, and suicidality. Tetrabenazine is another VMAT2 inhibitor that may be effective in doses up to 150 mg/d, but its off-label use is limited by the need for frequent dosing and a risk for suicidality.⁶

Other adjunctive treatments, such as vitamin B6, vitamin E, zonisamide, and levetiracetam, might offer some benefit in TD.⁶ However, further evidence is needed to support including these interventions in treatment guidelines.

Tardive dyskinesia (TD)—involuntary movement persisting for >1 month—is often caused by exposure to dopamine receptor–blocking agents such as antipsychotics.¹ The pathophysiology of TD is attributed to dopamine receptor hypersensitivity and upregulation of dopamine receptors in response to chronic receptor blockade, although striatal dysfunction, oxidative stress, and gamma-aminobutyric acid (GABA) dysfunction may play a role.¹ Because discontinuing the antipsychotic may not improve the patient’s TD symptoms and may worsen mood or psychosis, clinicians often prescribe adjunctive agents to reduce TD symptoms while continuing the antipsychotic. Clinicians can use the mnemonic ABCD to help recall 4 evidence-based treatments for TD.

Amantadine is an N-methyl-D-aspartate receptor antagonist that is postulated to improve dopaminergic signaling through increased dopamine release and inhibited postsynaptic uptake, although its exact mechanism is unclear. In a double-blind, placebo-controlled, crossover study of 22 patients with TD who were treated with amantadine, the average reduction on the Abnormal Involuntary Movement Scale (AIMS) was approximately 22%.² Adverse effects include gastrointestinal upset, mood changes, and impaired concentration.

Ginkgo Biloba contains antioxidant properties that may help reduce TD symptoms by alleviating oxidative stress. In a meta-analysis of 3 randomized controlled trials from China (N = 299), ginkgo biloba extract, 240 mg/d, significantly improved symptoms of TD compared with placebo.³ Ginkgo biloba has an antiplatelet effect and therefore should not be used in patients with an increased bleeding risk.

Clonazepam. Several small studies have examined the use of this GABA agonist for TD. In a study of 19 patients with TD, researchers found a symptom reduction of up to 35% with doses up to 4.5 mg/d.⁴ However, many studies have had small sample sizes or poor methodology. A 2018 Cochrane review recommended using other agents before considering clonazepam for TD because this medication has uncertain efficacy in treating TD, and it can cause sedation and dependence.⁵

Deutetrabenazine and valbenazine, the only FDA-approved treatments for TD, are vesicular monoamine transporter 2 (VMAT2) inhibitors, which inhibit dopamine release and decrease dopamine receptor hypersensitivity.⁶ In a 12-week, randomized, double-blind, placebo-controlled study of 117 patients with moderate-to-severe TD, those who received deutetrabenazine (up to 48 mg/d) had a significant mean reduction in AIMS score (3 points) compared with placebo.⁷ In the 1-year KINECT 3 study, 124 patients with TD who received valbenazine, 40 or 80 mg/d, had significant mean reductions in AIMS scores of 3.0 and 4.8 points, respectively.⁸ Adverse effects of these medications include somnolence, headache, akathisia, urinary tract infection, worsening mood, and suicidality. Tetrabenazine is another VMAT2 inhibitor that may be effective in doses up to 150 mg/d, but its off-label use is limited by the need for frequent dosing and a risk for suicidality.⁶

Other adjunctive treatments, such as vitamin B6, vitamin E, zonisamide, and levetiracetam, might offer some benefit in TD.⁶ However, further evidence is needed to support including these interventions in treatment guidelines.

Tardive dyskinesia (TD)—involuntary movement persisting for >1 month—is often caused by exposure to dopamine receptor–blocking agents such as antipsychotics.¹ The pathophysiology of TD is attributed to dopamine receptor hypersensitivity and upregulation of dopamine receptors in response to chronic receptor blockade, although striatal dysfunction, oxidative stress, and gamma-aminobutyric acid (GABA) dysfunction may play a role.¹ Because discontinuing the antipsychotic may not improve the patient’s TD symptoms and may worsen mood or psychosis, clinicians often prescribe adjunctive agents to reduce TD symptoms while continuing the antipsychotic. Clinicians can use the mnemonic ABCD to help recall 4 evidence-based treatments for TD.

Amantadine is an N-methyl-D-aspartate receptor antagonist that is postulated to improve dopaminergic signaling through increased dopamine release and inhibited postsynaptic uptake, although its exact mechanism is unclear. In a double-blind, placebo-controlled, crossover study of 22 patients with TD who were treated with amantadine, the average reduction on the Abnormal Involuntary Movement Scale (AIMS) was approximately 22%.² Adverse effects include gastrointestinal upset, mood changes, and impaired concentration.

Ginkgo Biloba contains antioxidant properties that may help reduce TD symptoms by alleviating oxidative stress. In a meta-analysis of 3 randomized controlled trials from China (N = 299), ginkgo biloba extract, 240 mg/d, significantly improved symptoms of TD compared with placebo.³ Ginkgo biloba has an antiplatelet effect and therefore should not be used in patients with an increased bleeding risk.

Clonazepam. Several small studies have examined the use of this GABA agonist for TD. In a study of 19 patients with TD, researchers found a symptom reduction of up to 35% with doses up to 4.5 mg/d.⁴ However, many studies have had small sample sizes or poor methodology. A 2018 Cochrane review recommended using other agents before considering clonazepam for TD because this medication has uncertain efficacy in treating TD, and it can cause sedation and dependence.⁵

Deutetrabenazine and valbenazine, the only FDA-approved treatments for TD, are vesicular monoamine transporter 2 (VMAT2) inhibitors, which inhibit dopamine release and decrease dopamine receptor hypersensitivity.⁶ In a 12-week, randomized, double-blind, placebo-controlled study of 117 patients with moderate-to-severe TD, those who received deutetrabenazine (up to 48 mg/d) had a significant mean reduction in AIMS score (3 points) compared with placebo.⁷ In the 1-year KINECT 3 study, 124 patients with TD who received valbenazine, 40 or 80 mg/d, had significant mean reductions in AIMS scores of 3.0 and 4.8 points, respectively.⁸ Adverse effects of these medications include somnolence, headache, akathisia, urinary tract infection, worsening mood, and suicidality. Tetrabenazine is another VMAT2 inhibitor that may be effective in doses up to 150 mg/d, but its off-label use is limited by the need for frequent dosing and a risk for suicidality.⁶

Other adjunctive treatments, such as vitamin B6, vitamin E, zonisamide, and levetiracetam, might offer some benefit in TD.⁶ However, further evidence is needed to support including these interventions in treatment guidelines.

First named by Steven Bratman in 1997, orthorexia nervosa (ON) from the Greek ortho, meaning correct, and orexi, meaning appetite, is classified as an unspecified feeding and eating disorder in the Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5).^1,2

Hypothetical Case

Mr. P is a 30-year-old male who presented to the mental health clinic with his wife. The patient recounted that he had wanted to “be healthy” since childhood and has focused on exercise and proper diet, but anxiety about diet and food intake have steadily increased. Two years ago, he adopted a vegetarian diet by progressively eliminating several foods and food groups from his diet. He now feels “proud” to eat certain organically grown fruits, vegetables, nuts, beans, and drink only fruit or vegetable juice.

His wife stated that he spent between 3 and 5 hours daily preparing food or talking to friends and family about “correct foods to eat.” He also believed that errors in dietary habits caused physical or mental illnesses. He reported significant guilt and shame whenever he “slips up” on his dietary regimen and eats anything containing seafood, beef, or pork products, which he corrects by a day of fasting. His wife was frustrated because he refused to go to restaurants and started declining offers from friends to eat dinner at their homes unless he could bring his prepared food. He describes feeling “annoyed” when he sees other people eating fast food or meat.

Mr. P reported no significant medical or surgical history. His family history was significant for anxiety in his mother. He used to drink alcohol socially but ceased a few years ago due to its carbohydrate content. He never smoked or used illicit drugs.

A mental status exam revealed a thin male who appeared his stated age. He was cooperative, casually dressed, and made fair eye contact. He spoke clearly with an anxious tone and appropriate rate and volume. His affect was congruent with stated anxious mood. He was alert, awake, and oriented to person, place, and time. He reported no paranoia, auditory or visual hallucinations, and suicidal or homicidal ideation.

A physical exam revealed a thin male in no distress who measured 5 feet 10 inches tall and weighed 145 pounds, which yielded a body mass index of 20.8. His vitals included temperature of 98° F, blood pressure 115/76, pulse 74, and oxygen saturation 98% on room air. The remaining physical examination revealed no abnormalities. A complete blood count, thyroid function, urinalysis, and urine drug screens were within normal limits. Comprehensive metabolic profile revealed decreased sodium of 130 meq/L. Electrocardiogram revealed bradycardia.

An ON diagnosis is made primarily through a clinical interview. Collateral information from individuals familiar with the patient can be helpful. Experts have proposed and recently revised criteria for ON (Table). Although the ORTO-15 assessment tool may assist with diagnosis, the tool does not substitute for the clinical interview.

Discussion

There is no reliable measure of prevalence of ON, though Varga and colleagues initially estimated ON to occur in 6.9% of the general population, and ON may occur more frequently in health care professionals and performance artists.³ However, these may be overestimates, as the assessment tool used in the study does not adequately separate people with healthy eating habits from those with ON.^4,5

Most prevalence studies were conducted in Europe and Turkey, and prevalence of ON may differ in the U.S. population. A recent assessment determined a prevalence of about 1%, similar to that of other eating disorders.⁵ No study has reported a correlation between ON and gender, but a survey of 448 college students in the U.S. (mean age 22 years) reported highest ON tendencies in Hispanic/Latino and overweight/obese students.⁶

Relationship to Other Illnesses

There is significant debate whether ON is a single syndrome, a variance of other syndromes, or a behavioral and culturally influenced attitude.^7,8 Although ON may lead to or be comorbid with anorexia nervosa (AN) or obsessive-compulsive disorder (OCD), subtle differences exist between ON and these conditions.

To meet DSM-5 diagnostic criteria for AN, patients must weigh below minimally normal weight for their height and age, have an intense fear of gaining weight or becoming fat, and have a disturbed experience of their weight or body shape or cannot recognize the severity of the low weight.² In contrast, an individual with ON may possess normal or low-normal weight. Patients with AN focus on food quantity, while patients with ON tend to focus on food quality. As summarized by Bratman, “People are ashamed of their anorexia, but they actively evangelize their orthorexia. People with anorexia skip meals; people with orthorexia do not (unless they are fasting). Those with anorexia focus only on avoiding foods, while those with orthorexia both avoid foods they think are bad and embrace foods they think are super-healthy.”⁹

Similarities between ON and OCD include anxiety, a need to exert control, and perfectionism. However, patients with OCD tend to report distress from compulsive behavior and a desire to change, thus exhibiting insight into their illness.^8,10 Similarities between obsessive-compulsive personality disorder (OCPD) and ON include perfectionism, rigid thinking, excessive devotion, hypermorality, and a preoccupation with details and perceived rules.¹¹

While no studies have yet described ON as a feature of somatoform disorders, some experts have hypothesized that preoccupation with illness in a patient with somatization disorder may engender a preoccupation with food and diet as a way to combat either real or perceived illness.¹¹ Finally, there is a report of ON associated with the prodromal phase of schizophrenia, and the development of ON may increase risk for future psychotic disorders.^11,12

Pathophysiology

The exact cause of ON is unknown, though it is likely multifactorial. Individuals with ON have neurocognitive deficits similar to those seen in patients with AN and OCD, including impairments in set-shifting (flexible problem solving), external attention, and working memory.^11,13 Given these cognitive deficits as well as similar symptomatology, there may be analogous brain dysfunction in patients with ON and AN or OCD. Neuroimaging studies of patients with AN have revealed dysregulation of dopamine transmission in the reward circuitry of the ventral striatum and the food regulatory mechanism in the hypothalamus.¹⁴

Dysmorphology of and dysfunction in neural circuitry, particularly the cortico-striato-thalamo-cortical pathway, have been implicated in OCD.¹⁵ Neuroimaging studies have revealed increased volume and activation of the orbitofrontal cortex, which may be associated with obsessions and difficulty with extinction recall.^14,15 In contrast, decreased volume and activity of the thalamus may impair its ability to inhibit the orbitofrontal cortex.^15,16 Decreased volume and activity of the cingulate gyrus may be associated with difficulty in error monitoring and fear conditioning, while overactivation of the parietal lobe and cerebellum may be associated with compulsive behaviors.^15,16

Risk Factors

Factors that contribute to the development of AN and possibly ON include development of food preferences, inherited differences in taste perception, food neophobia or pickiness, being premorbidly overweight or obese, parental feeding practices, and a history of parental eating disorders.¹⁴ One survey associated orthorexic tendencies with perfectionism, appearance orientation, overweight preoccupation, self-classified weight, and fearful and dismissing attachment styles.¹⁷ Significant predictors of ON included overweight preoccupation, appearance orientation, and a history of an eating disorder.¹⁷

Treatment

In contrast to patients with AN, patients with ON may be easily amenable to treatment, given their pursuit of and emphasis on wellness.¹⁸ Experts recommend a multidisciplinary team approach that includes physicians, psychotherapists, and dieticians.¹¹ Treatment may be undertaken in an outpatient setting, but hospitalization for refeeding is recommended in cases with significant weight loss or malnourishment.¹¹ Physical examination and laboratory studies are warranted, as excessive dietary restrictions can lead to weight loss and medical complications similar to those seen in AN, including osteopenia, anemia, hyponatremia, pancytopenia, bradycardia, and even pneumothorax and pneumomediastinum.^19-21

There are no reported studies exploring the efficacy of psychotherapy or psychotropic medications for patients with ON. However, several treatments have been proposed given the symptom overlap with AN. Serotonin reuptake inhibitors may be beneficial for anxiety and obsessive-compulsive traits.¹⁸ However, patients with ON may refuse medications as unnatural substances.¹⁸

Cognitive behavioral therapy may be beneficial to address perfectionism and cognitive distortions, and exposure and response prevention may reduce obsessive-compulsive behaviors.¹¹ Relaxation therapy may reduce mealtime anxiety. Psychoeducation may correct inaccurate beliefs about food groups, purity, and preparation, but it may induce emotional stress for the patient with ON.¹¹

Conclusion

Orthorexia nervosa is perhaps best summarized as an obsession with healthy eating with associated restrictive behaviors. However, the attempt to attain optimum health through attention to diet may lead to malnourishment, loss of relationships, and poor quality of life.¹¹ It is a little-understood disorder with uncertain etiology, imprecise assessment tools, and no formal diagnostic criteria or classification. Orthorexic characteristics vary from normal to pathologic in degree, and making a diagnosis remains a clinical judgment.²² Further research is needed to develop valid diagnostic tools and determining whether ON should be classified as a unique illness or a variation of other eating or anxiety disorders. Further research also may identify the etiology of ON, thus enabling targeted multidisciplinary treatment.

First named by Steven Bratman in 1997, orthorexia nervosa (ON) from the Greek ortho, meaning correct, and orexi, meaning appetite, is classified as an unspecified feeding and eating disorder in the Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5).^1,2

Hypothetical Case

Mr. P is a 30-year-old male who presented to the mental health clinic with his wife. The patient recounted that he had wanted to “be healthy” since childhood and has focused on exercise and proper diet, but anxiety about diet and food intake have steadily increased. Two years ago, he adopted a vegetarian diet by progressively eliminating several foods and food groups from his diet. He now feels “proud” to eat certain organically grown fruits, vegetables, nuts, beans, and drink only fruit or vegetable juice.

His wife stated that he spent between 3 and 5 hours daily preparing food or talking to friends and family about “correct foods to eat.” He also believed that errors in dietary habits caused physical or mental illnesses. He reported significant guilt and shame whenever he “slips up” on his dietary regimen and eats anything containing seafood, beef, or pork products, which he corrects by a day of fasting. His wife was frustrated because he refused to go to restaurants and started declining offers from friends to eat dinner at their homes unless he could bring his prepared food. He describes feeling “annoyed” when he sees other people eating fast food or meat.

Mr. P reported no significant medical or surgical history. His family history was significant for anxiety in his mother. He used to drink alcohol socially but ceased a few years ago due to its carbohydrate content. He never smoked or used illicit drugs.

A mental status exam revealed a thin male who appeared his stated age. He was cooperative, casually dressed, and made fair eye contact. He spoke clearly with an anxious tone and appropriate rate and volume. His affect was congruent with stated anxious mood. He was alert, awake, and oriented to person, place, and time. He reported no paranoia, auditory or visual hallucinations, and suicidal or homicidal ideation.

A physical exam revealed a thin male in no distress who measured 5 feet 10 inches tall and weighed 145 pounds, which yielded a body mass index of 20.8. His vitals included temperature of 98° F, blood pressure 115/76, pulse 74, and oxygen saturation 98% on room air. The remaining physical examination revealed no abnormalities. A complete blood count, thyroid function, urinalysis, and urine drug screens were within normal limits. Comprehensive metabolic profile revealed decreased sodium of 130 meq/L. Electrocardiogram revealed bradycardia.

An ON diagnosis is made primarily through a clinical interview. Collateral information from individuals familiar with the patient can be helpful. Experts have proposed and recently revised criteria for ON (Table). Although the ORTO-15 assessment tool may assist with diagnosis, the tool does not substitute for the clinical interview.

Discussion

There is no reliable measure of prevalence of ON, though Varga and colleagues initially estimated ON to occur in 6.9% of the general population, and ON may occur more frequently in health care professionals and performance artists.³ However, these may be overestimates, as the assessment tool used in the study does not adequately separate people with healthy eating habits from those with ON.^4,5

Most prevalence studies were conducted in Europe and Turkey, and prevalence of ON may differ in the U.S. population. A recent assessment determined a prevalence of about 1%, similar to that of other eating disorders.⁵ No study has reported a correlation between ON and gender, but a survey of 448 college students in the U.S. (mean age 22 years) reported highest ON tendencies in Hispanic/Latino and overweight/obese students.⁶

Relationship to Other Illnesses

There is significant debate whether ON is a single syndrome, a variance of other syndromes, or a behavioral and culturally influenced attitude.^7,8 Although ON may lead to or be comorbid with anorexia nervosa (AN) or obsessive-compulsive disorder (OCD), subtle differences exist between ON and these conditions.

To meet DSM-5 diagnostic criteria for AN, patients must weigh below minimally normal weight for their height and age, have an intense fear of gaining weight or becoming fat, and have a disturbed experience of their weight or body shape or cannot recognize the severity of the low weight.² In contrast, an individual with ON may possess normal or low-normal weight. Patients with AN focus on food quantity, while patients with ON tend to focus on food quality. As summarized by Bratman, “People are ashamed of their anorexia, but they actively evangelize their orthorexia. People with anorexia skip meals; people with orthorexia do not (unless they are fasting). Those with anorexia focus only on avoiding foods, while those with orthorexia both avoid foods they think are bad and embrace foods they think are super-healthy.”⁹

Similarities between ON and OCD include anxiety, a need to exert control, and perfectionism. However, patients with OCD tend to report distress from compulsive behavior and a desire to change, thus exhibiting insight into their illness.^8,10 Similarities between obsessive-compulsive personality disorder (OCPD) and ON include perfectionism, rigid thinking, excessive devotion, hypermorality, and a preoccupation with details and perceived rules.¹¹

While no studies have yet described ON as a feature of somatoform disorders, some experts have hypothesized that preoccupation with illness in a patient with somatization disorder may engender a preoccupation with food and diet as a way to combat either real or perceived illness.¹¹ Finally, there is a report of ON associated with the prodromal phase of schizophrenia, and the development of ON may increase risk for future psychotic disorders.^11,12

Pathophysiology

The exact cause of ON is unknown, though it is likely multifactorial. Individuals with ON have neurocognitive deficits similar to those seen in patients with AN and OCD, including impairments in set-shifting (flexible problem solving), external attention, and working memory.^11,13 Given these cognitive deficits as well as similar symptomatology, there may be analogous brain dysfunction in patients with ON and AN or OCD. Neuroimaging studies of patients with AN have revealed dysregulation of dopamine transmission in the reward circuitry of the ventral striatum and the food regulatory mechanism in the hypothalamus.¹⁴

Dysmorphology of and dysfunction in neural circuitry, particularly the cortico-striato-thalamo-cortical pathway, have been implicated in OCD.¹⁵ Neuroimaging studies have revealed increased volume and activation of the orbitofrontal cortex, which may be associated with obsessions and difficulty with extinction recall.^14,15 In contrast, decreased volume and activity of the thalamus may impair its ability to inhibit the orbitofrontal cortex.^15,16 Decreased volume and activity of the cingulate gyrus may be associated with difficulty in error monitoring and fear conditioning, while overactivation of the parietal lobe and cerebellum may be associated with compulsive behaviors.^15,16

Risk Factors

Factors that contribute to the development of AN and possibly ON include development of food preferences, inherited differences in taste perception, food neophobia or pickiness, being premorbidly overweight or obese, parental feeding practices, and a history of parental eating disorders.¹⁴ One survey associated orthorexic tendencies with perfectionism, appearance orientation, overweight preoccupation, self-classified weight, and fearful and dismissing attachment styles.¹⁷ Significant predictors of ON included overweight preoccupation, appearance orientation, and a history of an eating disorder.¹⁷

Treatment

In contrast to patients with AN, patients with ON may be easily amenable to treatment, given their pursuit of and emphasis on wellness.¹⁸ Experts recommend a multidisciplinary team approach that includes physicians, psychotherapists, and dieticians.¹¹ Treatment may be undertaken in an outpatient setting, but hospitalization for refeeding is recommended in cases with significant weight loss or malnourishment.¹¹ Physical examination and laboratory studies are warranted, as excessive dietary restrictions can lead to weight loss and medical complications similar to those seen in AN, including osteopenia, anemia, hyponatremia, pancytopenia, bradycardia, and even pneumothorax and pneumomediastinum.^19-21

There are no reported studies exploring the efficacy of psychotherapy or psychotropic medications for patients with ON. However, several treatments have been proposed given the symptom overlap with AN. Serotonin reuptake inhibitors may be beneficial for anxiety and obsessive-compulsive traits.¹⁸ However, patients with ON may refuse medications as unnatural substances.¹⁸

Cognitive behavioral therapy may be beneficial to address perfectionism and cognitive distortions, and exposure and response prevention may reduce obsessive-compulsive behaviors.¹¹ Relaxation therapy may reduce mealtime anxiety. Psychoeducation may correct inaccurate beliefs about food groups, purity, and preparation, but it may induce emotional stress for the patient with ON.¹¹

Conclusion

Orthorexia nervosa is perhaps best summarized as an obsession with healthy eating with associated restrictive behaviors. However, the attempt to attain optimum health through attention to diet may lead to malnourishment, loss of relationships, and poor quality of life.¹¹ It is a little-understood disorder with uncertain etiology, imprecise assessment tools, and no formal diagnostic criteria or classification. Orthorexic characteristics vary from normal to pathologic in degree, and making a diagnosis remains a clinical judgment.²² Further research is needed to develop valid diagnostic tools and determining whether ON should be classified as a unique illness or a variation of other eating or anxiety disorders. Further research also may identify the etiology of ON, thus enabling targeted multidisciplinary treatment.

First named by Steven Bratman in 1997, orthorexia nervosa (ON) from the Greek ortho, meaning correct, and orexi, meaning appetite, is classified as an unspecified feeding and eating disorder in the Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5).^1,2

Hypothetical Case

Mr. P is a 30-year-old male who presented to the mental health clinic with his wife. The patient recounted that he had wanted to “be healthy” since childhood and has focused on exercise and proper diet, but anxiety about diet and food intake have steadily increased. Two years ago, he adopted a vegetarian diet by progressively eliminating several foods and food groups from his diet. He now feels “proud” to eat certain organically grown fruits, vegetables, nuts, beans, and drink only fruit or vegetable juice.

His wife stated that he spent between 3 and 5 hours daily preparing food or talking to friends and family about “correct foods to eat.” He also believed that errors in dietary habits caused physical or mental illnesses. He reported significant guilt and shame whenever he “slips up” on his dietary regimen and eats anything containing seafood, beef, or pork products, which he corrects by a day of fasting. His wife was frustrated because he refused to go to restaurants and started declining offers from friends to eat dinner at their homes unless he could bring his prepared food. He describes feeling “annoyed” when he sees other people eating fast food or meat.

Mr. P reported no significant medical or surgical history. His family history was significant for anxiety in his mother. He used to drink alcohol socially but ceased a few years ago due to its carbohydrate content. He never smoked or used illicit drugs.

A mental status exam revealed a thin male who appeared his stated age. He was cooperative, casually dressed, and made fair eye contact. He spoke clearly with an anxious tone and appropriate rate and volume. His affect was congruent with stated anxious mood. He was alert, awake, and oriented to person, place, and time. He reported no paranoia, auditory or visual hallucinations, and suicidal or homicidal ideation.

A physical exam revealed a thin male in no distress who measured 5 feet 10 inches tall and weighed 145 pounds, which yielded a body mass index of 20.8. His vitals included temperature of 98° F, blood pressure 115/76, pulse 74, and oxygen saturation 98% on room air. The remaining physical examination revealed no abnormalities. A complete blood count, thyroid function, urinalysis, and urine drug screens were within normal limits. Comprehensive metabolic profile revealed decreased sodium of 130 meq/L. Electrocardiogram revealed bradycardia.

An ON diagnosis is made primarily through a clinical interview. Collateral information from individuals familiar with the patient can be helpful. Experts have proposed and recently revised criteria for ON (Table). Although the ORTO-15 assessment tool may assist with diagnosis, the tool does not substitute for the clinical interview.

Discussion

There is no reliable measure of prevalence of ON, though Varga and colleagues initially estimated ON to occur in 6.9% of the general population, and ON may occur more frequently in health care professionals and performance artists.³ However, these may be overestimates, as the assessment tool used in the study does not adequately separate people with healthy eating habits from those with ON.^4,5

Most prevalence studies were conducted in Europe and Turkey, and prevalence of ON may differ in the U.S. population. A recent assessment determined a prevalence of about 1%, similar to that of other eating disorders.⁵ No study has reported a correlation between ON and gender, but a survey of 448 college students in the U.S. (mean age 22 years) reported highest ON tendencies in Hispanic/Latino and overweight/obese students.⁶

Relationship to Other Illnesses

There is significant debate whether ON is a single syndrome, a variance of other syndromes, or a behavioral and culturally influenced attitude.^7,8 Although ON may lead to or be comorbid with anorexia nervosa (AN) or obsessive-compulsive disorder (OCD), subtle differences exist between ON and these conditions.

To meet DSM-5 diagnostic criteria for AN, patients must weigh below minimally normal weight for their height and age, have an intense fear of gaining weight or becoming fat, and have a disturbed experience of their weight or body shape or cannot recognize the severity of the low weight.² In contrast, an individual with ON may possess normal or low-normal weight. Patients with AN focus on food quantity, while patients with ON tend to focus on food quality. As summarized by Bratman, “People are ashamed of their anorexia, but they actively evangelize their orthorexia. People with anorexia skip meals; people with orthorexia do not (unless they are fasting). Those with anorexia focus only on avoiding foods, while those with orthorexia both avoid foods they think are bad and embrace foods they think are super-healthy.”⁹

Similarities between ON and OCD include anxiety, a need to exert control, and perfectionism. However, patients with OCD tend to report distress from compulsive behavior and a desire to change, thus exhibiting insight into their illness.^8,10 Similarities between obsessive-compulsive personality disorder (OCPD) and ON include perfectionism, rigid thinking, excessive devotion, hypermorality, and a preoccupation with details and perceived rules.¹¹

While no studies have yet described ON as a feature of somatoform disorders, some experts have hypothesized that preoccupation with illness in a patient with somatization disorder may engender a preoccupation with food and diet as a way to combat either real or perceived illness.¹¹ Finally, there is a report of ON associated with the prodromal phase of schizophrenia, and the development of ON may increase risk for future psychotic disorders.^11,12

Pathophysiology

The exact cause of ON is unknown, though it is likely multifactorial. Individuals with ON have neurocognitive deficits similar to those seen in patients with AN and OCD, including impairments in set-shifting (flexible problem solving), external attention, and working memory.^11,13 Given these cognitive deficits as well as similar symptomatology, there may be analogous brain dysfunction in patients with ON and AN or OCD. Neuroimaging studies of patients with AN have revealed dysregulation of dopamine transmission in the reward circuitry of the ventral striatum and the food regulatory mechanism in the hypothalamus.¹⁴

Dysmorphology of and dysfunction in neural circuitry, particularly the cortico-striato-thalamo-cortical pathway, have been implicated in OCD.¹⁵ Neuroimaging studies have revealed increased volume and activation of the orbitofrontal cortex, which may be associated with obsessions and difficulty with extinction recall.^14,15 In contrast, decreased volume and activity of the thalamus may impair its ability to inhibit the orbitofrontal cortex.^15,16 Decreased volume and activity of the cingulate gyrus may be associated with difficulty in error monitoring and fear conditioning, while overactivation of the parietal lobe and cerebellum may be associated with compulsive behaviors.^15,16

Risk Factors

Factors that contribute to the development of AN and possibly ON include development of food preferences, inherited differences in taste perception, food neophobia or pickiness, being premorbidly overweight or obese, parental feeding practices, and a history of parental eating disorders.¹⁴ One survey associated orthorexic tendencies with perfectionism, appearance orientation, overweight preoccupation, self-classified weight, and fearful and dismissing attachment styles.¹⁷ Significant predictors of ON included overweight preoccupation, appearance orientation, and a history of an eating disorder.¹⁷

Treatment

In contrast to patients with AN, patients with ON may be easily amenable to treatment, given their pursuit of and emphasis on wellness.¹⁸ Experts recommend a multidisciplinary team approach that includes physicians, psychotherapists, and dieticians.¹¹ Treatment may be undertaken in an outpatient setting, but hospitalization for refeeding is recommended in cases with significant weight loss or malnourishment.¹¹ Physical examination and laboratory studies are warranted, as excessive dietary restrictions can lead to weight loss and medical complications similar to those seen in AN, including osteopenia, anemia, hyponatremia, pancytopenia, bradycardia, and even pneumothorax and pneumomediastinum.^19-21

There are no reported studies exploring the efficacy of psychotherapy or psychotropic medications for patients with ON. However, several treatments have been proposed given the symptom overlap with AN. Serotonin reuptake inhibitors may be beneficial for anxiety and obsessive-compulsive traits.¹⁸ However, patients with ON may refuse medications as unnatural substances.¹⁸

Cognitive behavioral therapy may be beneficial to address perfectionism and cognitive distortions, and exposure and response prevention may reduce obsessive-compulsive behaviors.¹¹ Relaxation therapy may reduce mealtime anxiety. Psychoeducation may correct inaccurate beliefs about food groups, purity, and preparation, but it may induce emotional stress for the patient with ON.¹¹

Conclusion

Orthorexia nervosa is perhaps best summarized as an obsession with healthy eating with associated restrictive behaviors. However, the attempt to attain optimum health through attention to diet may lead to malnourishment, loss of relationships, and poor quality of life.¹¹ It is a little-understood disorder with uncertain etiology, imprecise assessment tools, and no formal diagnostic criteria or classification. Orthorexic characteristics vary from normal to pathologic in degree, and making a diagnosis remains a clinical judgment.²² Further research is needed to develop valid diagnostic tools and determining whether ON should be classified as a unique illness or a variation of other eating or anxiety disorders. Further research also may identify the etiology of ON, thus enabling targeted multidisciplinary treatment.

Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).

As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.¹ In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.

How CES works

After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.¹ The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.^1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.³

There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.¹

Evidence of efficacy

There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.

• In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.⁴
• In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.⁵ Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.⁵
• In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.⁶

Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.⁵

Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.⁷ Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.

Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).

As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.¹ In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.

How CES works

After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.¹ The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.^1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.³

There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.¹

Evidence of efficacy

There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.

• In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.⁴
• In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.⁵ Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.⁵
• In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.⁶

Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.⁵

Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.⁷ Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.

Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).

As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.¹ In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.

How CES works

After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.¹ The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.^1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.³

There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.¹

Evidence of efficacy

There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.

• In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.⁴
• In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.⁵ Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.⁵
• In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.⁶

Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.⁵

Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.⁷ Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.

Nightmares are a common feature of posttraumatic stress disorder (PTSD) that could lead to fatigue, impaired concentration, and poor work performance. The α-1 antagonist prazosin decreases noradrenergic hyperactivity and reduces nightmares; however, it can cause adverse effects, be contraindicated, or pro­vide no benefit to some patients. Consider these alternative medications to reduce nightmares in PTSD.

Alpha-2 agonists
Clonidine and guanfacine are α-2 ago­nists, used to treat attention-deficit/hyper­activity disorder and high blood pressure, that decrease noradrenergic activity, and either medication might be preferable to prazosin because they are more likely to cause sedation. A review and a case series showed that many patients—some with comorbid traumatic brain injury—reported fewer nightmares after taking 0.2 to 0.6 mg of clonidine.^1,2 Guanfacine might be more beneficial because it has a longer half-life; 2 mg of guanfacine eliminated nightmares in 1 patient.³ However, in a double-blind placebo-controlled study and an extension study, guanfacine did not reduce night­mares or other PTSD symptoms.^4,5

Initiate 0.1 mg of clonidine at bedtime, and titrate to efficacy or to 0.6 mg. Similarly, initiate guanfacine at 1 mg, and titrate to efficacy or to 4 mg. Monitor for hypoten­sion, excess sedation, dry mouth, and rebound hypertension.

Cyproheptadine
Used to treat serotonin syndrome, cypro­heptadine’s antagonism of serotonin 2A receptors has varying efficacy for reducing nightmares. Some patients have reported a decrease in nightmares at dosages rang­ing from 4 to 24 mg.^1,6 Other studies found no reduction in nightmares or diminished quality of sleep.^1,7

Initiate cyproheptadine at 4 mg/d, titrate every 2 or 3 days, and monitor for sedation, confusion, or reduced efficacy of concurrent serotonergic medications. Cyproheptadine might be preferable for its sedating effect and potential to reduce sexual adverse effects from serotonergic medications.

Topiramate
Topiramate is approved for treatment of epilepsy and migraine headache. At 75 to 100 mg/d in a clinical trial, topira­mate partially or completely suppressed nightmares.⁸ Start with 25 mg/d, titrate to efficacy, and monitor for anorexia, paresthesias, and cognitive impairment. Topiramate might be better than prazosin for patients without renal impairment who want sedation, weight loss, or reduced irritability.

Gabapentin
Gabapentin is approved to treat seizures and postherpetic neuralgia and also is used to treat neuropathic pain. When 300 to 3,600 mg/d (mean dosage, 1,300 mg/d) of gabapentin was added to medication regi­mens, most patients reported decreased fre­quency or intensity of nightmares.⁹ Monitor patients for sedation, dizziness, mood changes, and weight gain. Gabapentin might be an option for patients without renal impairment who have comorbid pain, insomnia, or anxiety.

Are these reasonable alternatives?
Despite small sample sizes in published studies and few randomized trials, cloni­dine, guanfacine, cyproheptadine, topi­ramate, and gabapentin are reasonable alternatives to prazosin for reducing night­mares in patients with PTSD.

Disclosure
The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Nightmares are a common feature of posttraumatic stress disorder (PTSD) that could lead to fatigue, impaired concentration, and poor work performance. The α-1 antagonist prazosin decreases noradrenergic hyperactivity and reduces nightmares; however, it can cause adverse effects, be contraindicated, or pro­vide no benefit to some patients. Consider these alternative medications to reduce nightmares in PTSD.

Alpha-2 agonists
Clonidine and guanfacine are α-2 ago­nists, used to treat attention-deficit/hyper­activity disorder and high blood pressure, that decrease noradrenergic activity, and either medication might be preferable to prazosin because they are more likely to cause sedation. A review and a case series showed that many patients—some with comorbid traumatic brain injury—reported fewer nightmares after taking 0.2 to 0.6 mg of clonidine.^1,2 Guanfacine might be more beneficial because it has a longer half-life; 2 mg of guanfacine eliminated nightmares in 1 patient.³ However, in a double-blind placebo-controlled study and an extension study, guanfacine did not reduce night­mares or other PTSD symptoms.^4,5

Initiate 0.1 mg of clonidine at bedtime, and titrate to efficacy or to 0.6 mg. Similarly, initiate guanfacine at 1 mg, and titrate to efficacy or to 4 mg. Monitor for hypoten­sion, excess sedation, dry mouth, and rebound hypertension.

Cyproheptadine
Used to treat serotonin syndrome, cypro­heptadine’s antagonism of serotonin 2A receptors has varying efficacy for reducing nightmares. Some patients have reported a decrease in nightmares at dosages rang­ing from 4 to 24 mg.^1,6 Other studies found no reduction in nightmares or diminished quality of sleep.^1,7

Initiate cyproheptadine at 4 mg/d, titrate every 2 or 3 days, and monitor for sedation, confusion, or reduced efficacy of concurrent serotonergic medications. Cyproheptadine might be preferable for its sedating effect and potential to reduce sexual adverse effects from serotonergic medications.

Topiramate
Topiramate is approved for treatment of epilepsy and migraine headache. At 75 to 100 mg/d in a clinical trial, topira­mate partially or completely suppressed nightmares.⁸ Start with 25 mg/d, titrate to efficacy, and monitor for anorexia, paresthesias, and cognitive impairment. Topiramate might be better than prazosin for patients without renal impairment who want sedation, weight loss, or reduced irritability.

Gabapentin
Gabapentin is approved to treat seizures and postherpetic neuralgia and also is used to treat neuropathic pain. When 300 to 3,600 mg/d (mean dosage, 1,300 mg/d) of gabapentin was added to medication regi­mens, most patients reported decreased fre­quency or intensity of nightmares.⁹ Monitor patients for sedation, dizziness, mood changes, and weight gain. Gabapentin might be an option for patients without renal impairment who have comorbid pain, insomnia, or anxiety.

Are these reasonable alternatives?
Despite small sample sizes in published studies and few randomized trials, cloni­dine, guanfacine, cyproheptadine, topi­ramate, and gabapentin are reasonable alternatives to prazosin for reducing night­mares in patients with PTSD.

Disclosure
The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Nightmares are a common feature of posttraumatic stress disorder (PTSD) that could lead to fatigue, impaired concentration, and poor work performance. The α-1 antagonist prazosin decreases noradrenergic hyperactivity and reduces nightmares; however, it can cause adverse effects, be contraindicated, or pro­vide no benefit to some patients. Consider these alternative medications to reduce nightmares in PTSD.

Alpha-2 agonists
Clonidine and guanfacine are α-2 ago­nists, used to treat attention-deficit/hyper­activity disorder and high blood pressure, that decrease noradrenergic activity, and either medication might be preferable to prazosin because they are more likely to cause sedation. A review and a case series showed that many patients—some with comorbid traumatic brain injury—reported fewer nightmares after taking 0.2 to 0.6 mg of clonidine.^1,2 Guanfacine might be more beneficial because it has a longer half-life; 2 mg of guanfacine eliminated nightmares in 1 patient.³ However, in a double-blind placebo-controlled study and an extension study, guanfacine did not reduce night­mares or other PTSD symptoms.^4,5

Initiate 0.1 mg of clonidine at bedtime, and titrate to efficacy or to 0.6 mg. Similarly, initiate guanfacine at 1 mg, and titrate to efficacy or to 4 mg. Monitor for hypoten­sion, excess sedation, dry mouth, and rebound hypertension.

Cyproheptadine
Used to treat serotonin syndrome, cypro­heptadine’s antagonism of serotonin 2A receptors has varying efficacy for reducing nightmares. Some patients have reported a decrease in nightmares at dosages rang­ing from 4 to 24 mg.^1,6 Other studies found no reduction in nightmares or diminished quality of sleep.^1,7

Initiate cyproheptadine at 4 mg/d, titrate every 2 or 3 days, and monitor for sedation, confusion, or reduced efficacy of concurrent serotonergic medications. Cyproheptadine might be preferable for its sedating effect and potential to reduce sexual adverse effects from serotonergic medications.

Topiramate
Topiramate is approved for treatment of epilepsy and migraine headache. At 75 to 100 mg/d in a clinical trial, topira­mate partially or completely suppressed nightmares.⁸ Start with 25 mg/d, titrate to efficacy, and monitor for anorexia, paresthesias, and cognitive impairment. Topiramate might be better than prazosin for patients without renal impairment who want sedation, weight loss, or reduced irritability.

Gabapentin
Gabapentin is approved to treat seizures and postherpetic neuralgia and also is used to treat neuropathic pain. When 300 to 3,600 mg/d (mean dosage, 1,300 mg/d) of gabapentin was added to medication regi­mens, most patients reported decreased fre­quency or intensity of nightmares.⁹ Monitor patients for sedation, dizziness, mood changes, and weight gain. Gabapentin might be an option for patients without renal impairment who have comorbid pain, insomnia, or anxiety.

Are these reasonable alternatives?
Despite small sample sizes in published studies and few randomized trials, cloni­dine, guanfacine, cyproheptadine, topi­ramate, and gabapentin are reasonable alternatives to prazosin for reducing night­mares in patients with PTSD.

Disclosure
The author reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.