Current Psychiatry

The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).² Among veterans, the prevalence of PTSD has been reported as:

• 31% among male Vietnam veterans (lifetime)
• 10% among Gulf War veterans
• 14% among Iraq and Afghanistan veterans.³

Why is PTSD overlooked in substance use?

Among individuals with SUD, 10% to 63% have comorbid PTSD.⁴ A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.⁵ Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.⁵ Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.

SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.⁶ Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.

Targeting mechanisms of action

Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.

Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.⁷ Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.⁸ Several studies support the efficacy of prazosin in persons suffering from PTSD.^9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)

In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.¹⁷ The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.¹⁸

Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages^8,12,13 might be needed because of the drug’s short half-life.

Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.^14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.¹⁶ The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.

Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder^19-21 and cocaine use disorder.^22,23 This “two birds with one stone” approach could become more common in clinical practice.

Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.

The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).² Among veterans, the prevalence of PTSD has been reported as:

• 31% among male Vietnam veterans (lifetime)
• 10% among Gulf War veterans
• 14% among Iraq and Afghanistan veterans.³

Why is PTSD overlooked in substance use?

Among individuals with SUD, 10% to 63% have comorbid PTSD.⁴ A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.⁵ Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.⁵ Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.

SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.⁶ Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.

Targeting mechanisms of action

Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.

Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.⁷ Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.⁸ Several studies support the efficacy of prazosin in persons suffering from PTSD.^9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)

In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.¹⁷ The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.¹⁸

Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages^8,12,13 might be needed because of the drug’s short half-life.

Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.^14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.¹⁶ The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.

Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder^19-21 and cocaine use disorder.^22,23 This “two birds with one stone” approach could become more common in clinical practice.

Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.

The primary symptoms of PTSD are recurrent and include intrusive memories and dreams of the traumatic events, flashbacks, hypervigilance, irritability, sleep disturbances, and persistent avoidance of stimuli associated with the traumatic event. According to the National Comorbidity Survey, the estimated lifetime prevalence of PTSD among adults is 6.8% and is more common in women (9.7%) than men (3.6%).² Among veterans, the prevalence of PTSD has been reported as:

• 31% among male Vietnam veterans (lifetime)
• 10% among Gulf War veterans
• 14% among Iraq and Afghanistan veterans.³

Why is PTSD overlooked in substance use?

Among individuals with SUD, 10% to 63% have comorbid PTSD.⁴ A recent report underscores the complexity and challenges of SUD–PTSD comorbidity.⁵ Most PTSD patients with comorbid SUD receive treatment only for SUD and the PTSD symptoms often are unaddressed.⁵ Those suffering from PTSD often abuse alcohol because they might consider it to be a coping strategy. Alcohol reduces hyperactivation of the dorsal anterior cingulate cortex caused by re-experiencing PTSD symptoms. Other substances of abuse, such as Cannabis, could suppress PTSD symptoms through alternate mechanisms (eg, endocannabinoid receptors). All of these could mask PTSD symptoms, which can delay diagnosis and treatment.

SUD is the tip of the “SUD-PTSD iceberg.” Some clinicians tend to focus on detoxification while completely ignoring the underlying psychopathology of SUD, which may be PTSD. Even during detoxification, PTSD should be aggressively treated.⁶ Lastly, practice guidelines for managing SUD–PTSD comorbidity are lacking.

Targeting mechanisms of action

Noradrenergic mechanisms have been strongly implicated in the pathophysiology of PTSD. However, selective serotonin reuptake inhibitors, such as sertraline and paroxetine, are the only FDA-approved pharmacotherapy options for PTSD, although their efficacy is limited, perhaps because they are serotonergic.

Prazosin, an alpha-1 (α-1) adrenergic antagonist that is FDA-approved for hypertension and benign prostatic hypertrophy, has been studied for treating nightmares in PTSD.⁷ Prazosin has shown efficacy for nightmares in PTSD and other daytime symptoms, such as flashbacks, hypervigilance, and irritability.⁸ Several studies support the efficacy of prazosin in persons suffering from PTSD.^9-11 Use of lower dosages in clinical trials might explain why prazosin did not separate from placebo in some studies. (See Table summarizing studies of prazosin dosing for PTSD.)

In a study of 12,844 veterans, the mean maximum prazosin dosage reached in the first year of treatment was 3.6 mg/d, and only 14% of patients reached the minimum Veterans Affairs recommended dosage of 6 mg/d.¹⁷ The most recent (March 2009) American Psychiatric Association practice guidelines recommend prazosin, 3 to 15 mg at bedtime.¹⁸

Prazosin has a short half-life of 2 to 3 hours and duration of action of 6 to 10 hours. Therefore, its use is limited to 2 or 3 times daily dosing. Higher (30 to 50 mg) and more frequent (2 to 3 times per day) dosages^8,12,13 might be needed because of the drug’s short half-life.

Doxazosin. Another α-1 adrenergic drug, doxazosin, 8 to 16 mg/d, has shown benefit for PTSD as well.^14,15 Doxazosin, which has a longer half-life (16 to 30 hours), requires only once-daily dosing.¹⁶ The most common side effects of prazosin and doxazosin are dizziness, headache, and drowsiness; syncope has been reported but is rare.

Prazosin and doxazosin also are used to treat substance abuse, such as alcohol use disorder^19-21 and cocaine use disorder.^22,23 This “two birds with one stone” approach could become more common in clinical practice.

Until a major breakthrough in PTSD treatment emerges, prazosin and doxazosin, although off-label, are reasonable treatment approaches.

In my first year of residency I faced a steep learning curve. I learned a lot about psychiatry, but I learned so much more about myself. If I had known then what I know now, my internship would have been smoother and more enjoyable.

Be organized. Create systems to remember your patients’ information and your to-do list. I have templates of progress notes, psychiatry assessments, mental status assessments, “rounds sheets” (a sheet listing every patient on my floor, including their diagnoses, laboratories, medications, and other notes). Although my system involves lots of paper, I like it. Make a system that works for you. Go out and have fun. I know you are tired, you haven’t slept, and your apartment is a mess, but you won’t remember that time you went home, did laundry, and went to bed early. You will remember the fun night when you and other interns went out and explored the city.

Unplug from medicine. Nothing is more boring than working for 12 hours, only to go out for drinks with coworkers and talk about work. Although you need to vent, life is more than medicine. Find time for something else. Read a book, play a video game, hang out with people who are not doctors. I started a monthly book club with other women around my age. Make some time for something other than your profession.

Reach out to your senior colleagues. I was so concerned about making a good first impression that I didn’t share my concerns with others. I kept my head low because I always blame myself first when something is wrong.

During an off-service rotation, I was unable to finish my shift because I had food poisoning. To make up for that uncompleted shift, the chief from that service gave me 2 extra night shifts. I found the measure extreme, but thought it was my fault for going home early. A few days later, the Psychiatry Chief Resident approached me, after he had seen my schedule and spoke with the other chief because he found the situation unfair. He was reaching out to me saying, “We’ve got your back.” I realized that it wasn’t always my fault, and I could speak up when there was an issue. I was fortunate to have seniors and chiefs who looked out for me. I always found support, good advice, and respect for my feelings.

If you have questions or concerns, are anxious, or feel something is wrong, approach a senior or the chief. They were in your shoes once and will give you their best advice.

Medicine is different in the United States. As an international medical graduate from Colombia, I panicked on my first day when everyone was talking in acronyms. I did not have a lot of U.S. clinical experience, and back home it’s frowned upon to write full sentences in acronyms. My students helped me get over it. I started my internship in the general medical floor and felt so embarrassed. Then I realized that it didn’t matter because it did not affect how I cared for my patients.

People understand that you are from another country. At the beginning, I used Google to search for everything, and then I realized that my 2 wonderful students didn’t think less of me because I didn’t know what BKA (below knee amputation) means. Do not be ashamed if you don’t know how things work in a different country. You will find people who are willing to help you; you will learn, and it will be a minor thing a year from now.

Keep your support system. It was 3 am in the emergency department, and on my break I went running out to the hallway feeling overwhelmed, tired, and lonely. I called my best friend across the globe.

If you moved away from home for residency, you are surrounded by new faces and far from the people you are comfortable with. Do not lose touch with them because you never know when you might need them the most. I had a hard road getting to where I am now, and many people helped me. You have to be there for them, too; a text message takes 30 seconds, and an e-mail, 1 minute.

Remember, you need to take care of yourself before taking care of others. No matter how much the MD or DO degree makes you feel like a superhero, you are still human.

In my first year of residency I faced a steep learning curve. I learned a lot about psychiatry, but I learned so much more about myself. If I had known then what I know now, my internship would have been smoother and more enjoyable.

Be organized. Create systems to remember your patients’ information and your to-do list. I have templates of progress notes, psychiatry assessments, mental status assessments, “rounds sheets” (a sheet listing every patient on my floor, including their diagnoses, laboratories, medications, and other notes). Although my system involves lots of paper, I like it. Make a system that works for you. Go out and have fun. I know you are tired, you haven’t slept, and your apartment is a mess, but you won’t remember that time you went home, did laundry, and went to bed early. You will remember the fun night when you and other interns went out and explored the city.

Unplug from medicine. Nothing is more boring than working for 12 hours, only to go out for drinks with coworkers and talk about work. Although you need to vent, life is more than medicine. Find time for something else. Read a book, play a video game, hang out with people who are not doctors. I started a monthly book club with other women around my age. Make some time for something other than your profession.

Reach out to your senior colleagues. I was so concerned about making a good first impression that I didn’t share my concerns with others. I kept my head low because I always blame myself first when something is wrong.

During an off-service rotation, I was unable to finish my shift because I had food poisoning. To make up for that uncompleted shift, the chief from that service gave me 2 extra night shifts. I found the measure extreme, but thought it was my fault for going home early. A few days later, the Psychiatry Chief Resident approached me, after he had seen my schedule and spoke with the other chief because he found the situation unfair. He was reaching out to me saying, “We’ve got your back.” I realized that it wasn’t always my fault, and I could speak up when there was an issue. I was fortunate to have seniors and chiefs who looked out for me. I always found support, good advice, and respect for my feelings.

If you have questions or concerns, are anxious, or feel something is wrong, approach a senior or the chief. They were in your shoes once and will give you their best advice.

Medicine is different in the United States. As an international medical graduate from Colombia, I panicked on my first day when everyone was talking in acronyms. I did not have a lot of U.S. clinical experience, and back home it’s frowned upon to write full sentences in acronyms. My students helped me get over it. I started my internship in the general medical floor and felt so embarrassed. Then I realized that it didn’t matter because it did not affect how I cared for my patients.

People understand that you are from another country. At the beginning, I used Google to search for everything, and then I realized that my 2 wonderful students didn’t think less of me because I didn’t know what BKA (below knee amputation) means. Do not be ashamed if you don’t know how things work in a different country. You will find people who are willing to help you; you will learn, and it will be a minor thing a year from now.

Keep your support system. It was 3 am in the emergency department, and on my break I went running out to the hallway feeling overwhelmed, tired, and lonely. I called my best friend across the globe.

If you moved away from home for residency, you are surrounded by new faces and far from the people you are comfortable with. Do not lose touch with them because you never know when you might need them the most. I had a hard road getting to where I am now, and many people helped me. You have to be there for them, too; a text message takes 30 seconds, and an e-mail, 1 minute.

Remember, you need to take care of yourself before taking care of others. No matter how much the MD or DO degree makes you feel like a superhero, you are still human.

In my first year of residency I faced a steep learning curve. I learned a lot about psychiatry, but I learned so much more about myself. If I had known then what I know now, my internship would have been smoother and more enjoyable.

Be organized. Create systems to remember your patients’ information and your to-do list. I have templates of progress notes, psychiatry assessments, mental status assessments, “rounds sheets” (a sheet listing every patient on my floor, including their diagnoses, laboratories, medications, and other notes). Although my system involves lots of paper, I like it. Make a system that works for you. Go out and have fun. I know you are tired, you haven’t slept, and your apartment is a mess, but you won’t remember that time you went home, did laundry, and went to bed early. You will remember the fun night when you and other interns went out and explored the city.

Unplug from medicine. Nothing is more boring than working for 12 hours, only to go out for drinks with coworkers and talk about work. Although you need to vent, life is more than medicine. Find time for something else. Read a book, play a video game, hang out with people who are not doctors. I started a monthly book club with other women around my age. Make some time for something other than your profession.

Reach out to your senior colleagues. I was so concerned about making a good first impression that I didn’t share my concerns with others. I kept my head low because I always blame myself first when something is wrong.

During an off-service rotation, I was unable to finish my shift because I had food poisoning. To make up for that uncompleted shift, the chief from that service gave me 2 extra night shifts. I found the measure extreme, but thought it was my fault for going home early. A few days later, the Psychiatry Chief Resident approached me, after he had seen my schedule and spoke with the other chief because he found the situation unfair. He was reaching out to me saying, “We’ve got your back.” I realized that it wasn’t always my fault, and I could speak up when there was an issue. I was fortunate to have seniors and chiefs who looked out for me. I always found support, good advice, and respect for my feelings.

If you have questions or concerns, are anxious, or feel something is wrong, approach a senior or the chief. They were in your shoes once and will give you their best advice.

Medicine is different in the United States. As an international medical graduate from Colombia, I panicked on my first day when everyone was talking in acronyms. I did not have a lot of U.S. clinical experience, and back home it’s frowned upon to write full sentences in acronyms. My students helped me get over it. I started my internship in the general medical floor and felt so embarrassed. Then I realized that it didn’t matter because it did not affect how I cared for my patients.

People understand that you are from another country. At the beginning, I used Google to search for everything, and then I realized that my 2 wonderful students didn’t think less of me because I didn’t know what BKA (below knee amputation) means. Do not be ashamed if you don’t know how things work in a different country. You will find people who are willing to help you; you will learn, and it will be a minor thing a year from now.

Keep your support system. It was 3 am in the emergency department, and on my break I went running out to the hallway feeling overwhelmed, tired, and lonely. I called my best friend across the globe.

If you moved away from home for residency, you are surrounded by new faces and far from the people you are comfortable with. Do not lose touch with them because you never know when you might need them the most. I had a hard road getting to where I am now, and many people helped me. You have to be there for them, too; a text message takes 30 seconds, and an e-mail, 1 minute.

Remember, you need to take care of yourself before taking care of others. No matter how much the MD or DO degree makes you feel like a superhero, you are still human.

Urine drug screening (UDS) is an important tool in emergency settings and substance abuse or pain management clinics. According to the 2015 National Survey on Drug Use and Health, 9.2% of individuals age ≥12 used an illicit drug other than marijuana within the previous year.¹

There are 2 types of UDS: gas chromatography–mass spectroscopy (GC-MS) and enzymatic immunoassay (EIA). A GC-MS uses a 2-step mechanisms to detect chemical compounds. First the GC separate the illicit substance into molecules, which is then introduced to the MS, which then separates compounds depending on their mass and charge using magnetic fields.^2,3 Although GC-MS is a more definitive means to confirm the presence of a specific drug, it rarely is used in clinical settings because it is expensive and time-consuming.

EIA is an anti-drug antibody added to the patient’s urine that causes a positive indicator reaction that can be measured.^2,3 It is a rapid, accurate, and cost-effective way of detecting illicit substances.⁴ However, there are limitations to EIAs used in most hospital laboratories.

Limitations of EIAs

Timing. Results of the drug screen depend on the time and frequency of drug use (Table 1).⁵

Preventing false-negatives

Substance abusing individuals could try to avoid detection of illicit drug use by using the following techniques:

• In vivo methods, such as drinking a large amount of water or using herbal products, can lead to false-negative results because of dilution.⁸
• In vitro adulterants are substances added to urine samples after urination to avoid drug detection. Active ingredients include glutaraldehyde (Clean-X), sodium or potassium nitrate (Klear, Whizzies), pyridinium chlorochromate (Urine Luck), andj (Stealth).⁹
• Other methods used to avoid drug detection include substituting a urine sample with someone else’s clean urine or adding household products, such as bleach, vinegar, or pipe cleaner.

You can spot and prevent false-negatives by:

Directly observing the patient, which helps to prevent individuals from adding foreign materials or substituting the urine sample.

Visually inspecting the urine helps identify sample tampering. Adding household adulterants can produce unusually bubbly, cloudy, clear, or dark sample.

On-site analyses and laboratory analyses of samples. Commercially sold kits can detect adulterants by on-site analysis, such as Intect 7 and AdultaCheck 4 test strips.⁹ Simple on-site methods can help discover tampering, such as measuring the urine’s temperature and using pigmented toilet water. The U.S. Substance Abuse and Mental Health Services Administration recommends validity checks during laboratory analysis for all urine samples, including temperature, creatinine, specific gravity, pH, and tests for oxidizing adulterants.¹⁰

Considerations

The results of UDS should not be interpreted as absolute. Knowing the sensitivity and specificity of the UDS that your institution uses and the patient’s current medication regimen is valuable in distinguishing between true results and false-positives. False-positives can strain the relationship between patient and provider, thus compromising care. When EIA is positive and patient denies substance use, confirming the result with GC-MS may be a good clinical practice.³ Ordering a GC-MS test can be helpful in situations requiring greater precision, such as in methadone or pain management clinics, to verify if the patient is taking a prescribed medication properly or to rule out illicit exposures with greater certainty.

Acknowledgment
The authors would like to thank Steven Lippmann, MD, for his mentorship, encouragement, and editorial support.

Urine drug screening (UDS) is an important tool in emergency settings and substance abuse or pain management clinics. According to the 2015 National Survey on Drug Use and Health, 9.2% of individuals age ≥12 used an illicit drug other than marijuana within the previous year.¹

There are 2 types of UDS: gas chromatography–mass spectroscopy (GC-MS) and enzymatic immunoassay (EIA). A GC-MS uses a 2-step mechanisms to detect chemical compounds. First the GC separate the illicit substance into molecules, which is then introduced to the MS, which then separates compounds depending on their mass and charge using magnetic fields.^2,3 Although GC-MS is a more definitive means to confirm the presence of a specific drug, it rarely is used in clinical settings because it is expensive and time-consuming.

EIA is an anti-drug antibody added to the patient’s urine that causes a positive indicator reaction that can be measured.^2,3 It is a rapid, accurate, and cost-effective way of detecting illicit substances.⁴ However, there are limitations to EIAs used in most hospital laboratories.

Limitations of EIAs

Timing. Results of the drug screen depend on the time and frequency of drug use (Table 1).⁵

Preventing false-negatives

Substance abusing individuals could try to avoid detection of illicit drug use by using the following techniques:

• In vivo methods, such as drinking a large amount of water or using herbal products, can lead to false-negative results because of dilution.⁸
• In vitro adulterants are substances added to urine samples after urination to avoid drug detection. Active ingredients include glutaraldehyde (Clean-X), sodium or potassium nitrate (Klear, Whizzies), pyridinium chlorochromate (Urine Luck), andj (Stealth).⁹
• Other methods used to avoid drug detection include substituting a urine sample with someone else’s clean urine or adding household products, such as bleach, vinegar, or pipe cleaner.

You can spot and prevent false-negatives by:

Directly observing the patient, which helps to prevent individuals from adding foreign materials or substituting the urine sample.

Visually inspecting the urine helps identify sample tampering. Adding household adulterants can produce unusually bubbly, cloudy, clear, or dark sample.

On-site analyses and laboratory analyses of samples. Commercially sold kits can detect adulterants by on-site analysis, such as Intect 7 and AdultaCheck 4 test strips.⁹ Simple on-site methods can help discover tampering, such as measuring the urine’s temperature and using pigmented toilet water. The U.S. Substance Abuse and Mental Health Services Administration recommends validity checks during laboratory analysis for all urine samples, including temperature, creatinine, specific gravity, pH, and tests for oxidizing adulterants.¹⁰

Considerations

The results of UDS should not be interpreted as absolute. Knowing the sensitivity and specificity of the UDS that your institution uses and the patient’s current medication regimen is valuable in distinguishing between true results and false-positives. False-positives can strain the relationship between patient and provider, thus compromising care. When EIA is positive and patient denies substance use, confirming the result with GC-MS may be a good clinical practice.³ Ordering a GC-MS test can be helpful in situations requiring greater precision, such as in methadone or pain management clinics, to verify if the patient is taking a prescribed medication properly or to rule out illicit exposures with greater certainty.

Acknowledgment
The authors would like to thank Steven Lippmann, MD, for his mentorship, encouragement, and editorial support.

Urine drug screening (UDS) is an important tool in emergency settings and substance abuse or pain management clinics. According to the 2015 National Survey on Drug Use and Health, 9.2% of individuals age ≥12 used an illicit drug other than marijuana within the previous year.¹

There are 2 types of UDS: gas chromatography–mass spectroscopy (GC-MS) and enzymatic immunoassay (EIA). A GC-MS uses a 2-step mechanisms to detect chemical compounds. First the GC separate the illicit substance into molecules, which is then introduced to the MS, which then separates compounds depending on their mass and charge using magnetic fields.^2,3 Although GC-MS is a more definitive means to confirm the presence of a specific drug, it rarely is used in clinical settings because it is expensive and time-consuming.

EIA is an anti-drug antibody added to the patient’s urine that causes a positive indicator reaction that can be measured.^2,3 It is a rapid, accurate, and cost-effective way of detecting illicit substances.⁴ However, there are limitations to EIAs used in most hospital laboratories.

Limitations of EIAs

Timing. Results of the drug screen depend on the time and frequency of drug use (Table 1).⁵

Preventing false-negatives

Substance abusing individuals could try to avoid detection of illicit drug use by using the following techniques:

• In vivo methods, such as drinking a large amount of water or using herbal products, can lead to false-negative results because of dilution.⁸
• In vitro adulterants are substances added to urine samples after urination to avoid drug detection. Active ingredients include glutaraldehyde (Clean-X), sodium or potassium nitrate (Klear, Whizzies), pyridinium chlorochromate (Urine Luck), andj (Stealth).⁹
• Other methods used to avoid drug detection include substituting a urine sample with someone else’s clean urine or adding household products, such as bleach, vinegar, or pipe cleaner.

You can spot and prevent false-negatives by:

Directly observing the patient, which helps to prevent individuals from adding foreign materials or substituting the urine sample.

Visually inspecting the urine helps identify sample tampering. Adding household adulterants can produce unusually bubbly, cloudy, clear, or dark sample.

On-site analyses and laboratory analyses of samples. Commercially sold kits can detect adulterants by on-site analysis, such as Intect 7 and AdultaCheck 4 test strips.⁹ Simple on-site methods can help discover tampering, such as measuring the urine’s temperature and using pigmented toilet water. The U.S. Substance Abuse and Mental Health Services Administration recommends validity checks during laboratory analysis for all urine samples, including temperature, creatinine, specific gravity, pH, and tests for oxidizing adulterants.¹⁰

Considerations

The results of UDS should not be interpreted as absolute. Knowing the sensitivity and specificity of the UDS that your institution uses and the patient’s current medication regimen is valuable in distinguishing between true results and false-positives. False-positives can strain the relationship between patient and provider, thus compromising care. When EIA is positive and patient denies substance use, confirming the result with GC-MS may be a good clinical practice.³ Ordering a GC-MS test can be helpful in situations requiring greater precision, such as in methadone or pain management clinics, to verify if the patient is taking a prescribed medication properly or to rule out illicit exposures with greater certainty.

Acknowledgment
The authors would like to thank Steven Lippmann, MD, for his mentorship, encouragement, and editorial support.

Although the meaning of these terms varied from department to department, biologically oriented programs—influenced by Eli Robins and Samuel Guze and DSM-III—were focused on descriptive psychiatry: reliable, observable, and symptom-based elements of psychiatric illness. Related and important elements were a focus on psychopharmacologic treatments, genetics, epidemiology, and putative mechanisms for both diseases and treatments. Psychodynamic programs had a primary focus on psychodynamic theory, with extensive training in long-term, depth-oriented psychotherapy. Many of these are programs employed charismatic and brilliant teachers whose supervisory and interviewing skills were legendary. And, of course, all the programs claimed they did everything and did it well.

However, none of these programs were exactly what I was looking for. Although I had a long-standing interest in psychodynamics and was fascinated by the implications of—what was then a far more nascent—neurobiology, I was looking for a program that had all of these elements, but also had a focus on, what I thought of as, “medical psychiatry.” Although this may have meant different things to others, and was known as “psychosomatic medicine” or “consultation-liaison psychiatry,” to me, it was about the psychiatric manifestations of medical and neurologic disorders.

My years training in internal medicine were full of patients with neuro­psychiatric illness due to a host of general medical and neurologic disorders. When I was an intern, the most common admitting diagnosis was what we called “Delta MS”—change in mental status. As I advanced in my residency and focused on a subspecialty of internal medicine, it became clear that whichever illnesses I studied, conditions such as anxiety disorders in Grave’s disease or the psychotic symptoms in lupus held my interest. Finally, the only specialty left was psychiatry.

The only program I found that seemed to understand medical psychiatry at the time was at Massachusetts General Hospital (MGH). MGH not only had eminent psychiatrists in every area of the field, it seemed, but also a special focus on training psychiatrists in medical settings and as medical experts. My first Chief of Psychiatry was Thomas P. Hackett, MD—a brilliant clinician, raconteur, and polymath—who had written a cri de coeur on the importance of medical skills and training in psychiatry.¹ At last, I had found a place where I could remain a physician and think and learn about every aspect of psychiatry, especially medical psychiatry.

What is medical psychiatry, and why is it relevant now?

There has been substantial and increasing interest in the integration of medical and psychiatric care. Whether it is collaborative care or co-location models, the recognition of the high rate of combined medical and psychiatric illnesses and associated increased mortality and total health care costs of these patients requires psychiatrists to be deeply familiar with the interactions among medical and psychiatric conditions.

Building on long-developed expertise in consultation-liaison psychiatry and other forms of medical psychiatric training, such as double-board medicine–psychiatry programs, medical psychiatry includes several specific areas of knowledge and skill sets, including understanding the impact that psychiatric illnesses and the medications used to treat them can have on medical illnesses and the ways in which the presence of medical disorders can change the presentation of psychiatric illnesses. Similarly, the psychiatric impact of the general medical pharmacopeia and the ways in which psychiatric illness can affect the presentation of medical illness are important for all psychiatrists to know. Most importantly, medical psychiatry should focus on the medical and neurologic causes of psychiatric illnesses. Many general medical conditions produce symptoms, which, in whole or in part, mimic psychiatric illnesses and, in some cases, could lead to psychiatric disorders, which makes identification of the underlying cause difficult.

Whether due to infectious, auto­immune, metabolic, or endocrinologic disorders, being aware of these conditions and, where clinical circumstances warrant, be able to diagnose them, with other specialists as needed, and ensure they are appropriately treated should be an essential skill for psychiatrists.

An illustrative case

I remember a case from early in my training of a woman with a late-onset mood disorder with abulia, wide-based gait, and urinary incontinence, in addition to withdrawal and loss of pleasure. Despite the skepticism of the neurology team, at autopsy she was found to have arteriosclerosis of the deep, penetrating arterioles causing white matter hyperintensities—Binswanger’s disease. There was no question that despite the neurologic cause of her symptoms treating her depression with antidepressants was needed and helpful. It also was important that her family was aware of her underlying medical condition and its implications for her care.²

Medicine is our calling

Many of these illnesses, even when identified, require expert psychiatric management of psychiatric symptoms. This should not be surprising to psychiatrists or other clinicians. No one expects a cardiologist to beg off the care of a patient with heart failure caused by alcohol abuse or a virus rather than vascular heart disease, and psychiatrists likewise need to manage psychosis due to steroid use or N-methyl-d-aspartate receptor antibodies as well as other causes. Pursuing this understanding is important from another perspective. As we consider other potential mechanisms for onset of psychiatric illness (eg, inflammation), our understanding of the mechanisms associated with general medical conditions may provide unexpected insight into the etiology of psychiatric illnesses where no general medical cause has been found. No other physician specialists are as attuned to the nuances of psychiatric illnesses, their typical and atypical presentations as psychiatrists. It is incumbent on us to pursue the medical differential of patients when we think it is needed, even if other physicians disagree.

Medical psychiatry has a broader and more inclusive perspective than what we generally mean by “biological psychiatry,” if by the latter, we mean a focus on the neurobiology and psychopharmacology of “primary” psychiatric conditions that are not secondary to other medical or neurologic disorders. As important and fundamental as deep understanding of neurobiology, genetics, and psychopharmacology are, medical psychiatry embeds our work more broadly in all of human biology and requires the full breadth of our medical training.

At a time when political battles over prescriptive privileges by non-medically trained mental health clinicians engage legislatures and professional organizations, medical psychiatry is a powerful reminder that prescribing or not prescribing medications is the final step in, what should be, an extensive, clinical evaluation including a thorough medical work up and consideration of the medical–psychiatric interactions and the differential diagnosis of these illnesses. It is, after all, what physicians do and is essential to our calling as psychiatric physicians. If psychiatrists are not at home in medicine, as Tom Hackett reminded us in 1977¹—at a time when psychiatry had temporarily eliminated the requirement for medical internships—then, indeed, psychiatry would be “homeless.”

Although the meaning of these terms varied from department to department, biologically oriented programs—influenced by Eli Robins and Samuel Guze and DSM-III—were focused on descriptive psychiatry: reliable, observable, and symptom-based elements of psychiatric illness. Related and important elements were a focus on psychopharmacologic treatments, genetics, epidemiology, and putative mechanisms for both diseases and treatments. Psychodynamic programs had a primary focus on psychodynamic theory, with extensive training in long-term, depth-oriented psychotherapy. Many of these are programs employed charismatic and brilliant teachers whose supervisory and interviewing skills were legendary. And, of course, all the programs claimed they did everything and did it well.

However, none of these programs were exactly what I was looking for. Although I had a long-standing interest in psychodynamics and was fascinated by the implications of—what was then a far more nascent—neurobiology, I was looking for a program that had all of these elements, but also had a focus on, what I thought of as, “medical psychiatry.” Although this may have meant different things to others, and was known as “psychosomatic medicine” or “consultation-liaison psychiatry,” to me, it was about the psychiatric manifestations of medical and neurologic disorders.

My years training in internal medicine were full of patients with neuro­psychiatric illness due to a host of general medical and neurologic disorders. When I was an intern, the most common admitting diagnosis was what we called “Delta MS”—change in mental status. As I advanced in my residency and focused on a subspecialty of internal medicine, it became clear that whichever illnesses I studied, conditions such as anxiety disorders in Grave’s disease or the psychotic symptoms in lupus held my interest. Finally, the only specialty left was psychiatry.

The only program I found that seemed to understand medical psychiatry at the time was at Massachusetts General Hospital (MGH). MGH not only had eminent psychiatrists in every area of the field, it seemed, but also a special focus on training psychiatrists in medical settings and as medical experts. My first Chief of Psychiatry was Thomas P. Hackett, MD—a brilliant clinician, raconteur, and polymath—who had written a cri de coeur on the importance of medical skills and training in psychiatry.¹ At last, I had found a place where I could remain a physician and think and learn about every aspect of psychiatry, especially medical psychiatry.

What is medical psychiatry, and why is it relevant now?

There has been substantial and increasing interest in the integration of medical and psychiatric care. Whether it is collaborative care or co-location models, the recognition of the high rate of combined medical and psychiatric illnesses and associated increased mortality and total health care costs of these patients requires psychiatrists to be deeply familiar with the interactions among medical and psychiatric conditions.

Building on long-developed expertise in consultation-liaison psychiatry and other forms of medical psychiatric training, such as double-board medicine–psychiatry programs, medical psychiatry includes several specific areas of knowledge and skill sets, including understanding the impact that psychiatric illnesses and the medications used to treat them can have on medical illnesses and the ways in which the presence of medical disorders can change the presentation of psychiatric illnesses. Similarly, the psychiatric impact of the general medical pharmacopeia and the ways in which psychiatric illness can affect the presentation of medical illness are important for all psychiatrists to know. Most importantly, medical psychiatry should focus on the medical and neurologic causes of psychiatric illnesses. Many general medical conditions produce symptoms, which, in whole or in part, mimic psychiatric illnesses and, in some cases, could lead to psychiatric disorders, which makes identification of the underlying cause difficult.

Whether due to infectious, auto­immune, metabolic, or endocrinologic disorders, being aware of these conditions and, where clinical circumstances warrant, be able to diagnose them, with other specialists as needed, and ensure they are appropriately treated should be an essential skill for psychiatrists.

An illustrative case

I remember a case from early in my training of a woman with a late-onset mood disorder with abulia, wide-based gait, and urinary incontinence, in addition to withdrawal and loss of pleasure. Despite the skepticism of the neurology team, at autopsy she was found to have arteriosclerosis of the deep, penetrating arterioles causing white matter hyperintensities—Binswanger’s disease. There was no question that despite the neurologic cause of her symptoms treating her depression with antidepressants was needed and helpful. It also was important that her family was aware of her underlying medical condition and its implications for her care.²

Medicine is our calling

Many of these illnesses, even when identified, require expert psychiatric management of psychiatric symptoms. This should not be surprising to psychiatrists or other clinicians. No one expects a cardiologist to beg off the care of a patient with heart failure caused by alcohol abuse or a virus rather than vascular heart disease, and psychiatrists likewise need to manage psychosis due to steroid use or N-methyl-d-aspartate receptor antibodies as well as other causes. Pursuing this understanding is important from another perspective. As we consider other potential mechanisms for onset of psychiatric illness (eg, inflammation), our understanding of the mechanisms associated with general medical conditions may provide unexpected insight into the etiology of psychiatric illnesses where no general medical cause has been found. No other physician specialists are as attuned to the nuances of psychiatric illnesses, their typical and atypical presentations as psychiatrists. It is incumbent on us to pursue the medical differential of patients when we think it is needed, even if other physicians disagree.

Medical psychiatry has a broader and more inclusive perspective than what we generally mean by “biological psychiatry,” if by the latter, we mean a focus on the neurobiology and psychopharmacology of “primary” psychiatric conditions that are not secondary to other medical or neurologic disorders. As important and fundamental as deep understanding of neurobiology, genetics, and psychopharmacology are, medical psychiatry embeds our work more broadly in all of human biology and requires the full breadth of our medical training.

At a time when political battles over prescriptive privileges by non-medically trained mental health clinicians engage legislatures and professional organizations, medical psychiatry is a powerful reminder that prescribing or not prescribing medications is the final step in, what should be, an extensive, clinical evaluation including a thorough medical work up and consideration of the medical–psychiatric interactions and the differential diagnosis of these illnesses. It is, after all, what physicians do and is essential to our calling as psychiatric physicians. If psychiatrists are not at home in medicine, as Tom Hackett reminded us in 1977¹—at a time when psychiatry had temporarily eliminated the requirement for medical internships—then, indeed, psychiatry would be “homeless.”

Although the meaning of these terms varied from department to department, biologically oriented programs—influenced by Eli Robins and Samuel Guze and DSM-III—were focused on descriptive psychiatry: reliable, observable, and symptom-based elements of psychiatric illness. Related and important elements were a focus on psychopharmacologic treatments, genetics, epidemiology, and putative mechanisms for both diseases and treatments. Psychodynamic programs had a primary focus on psychodynamic theory, with extensive training in long-term, depth-oriented psychotherapy. Many of these are programs employed charismatic and brilliant teachers whose supervisory and interviewing skills were legendary. And, of course, all the programs claimed they did everything and did it well.

However, none of these programs were exactly what I was looking for. Although I had a long-standing interest in psychodynamics and was fascinated by the implications of—what was then a far more nascent—neurobiology, I was looking for a program that had all of these elements, but also had a focus on, what I thought of as, “medical psychiatry.” Although this may have meant different things to others, and was known as “psychosomatic medicine” or “consultation-liaison psychiatry,” to me, it was about the psychiatric manifestations of medical and neurologic disorders.

My years training in internal medicine were full of patients with neuro­psychiatric illness due to a host of general medical and neurologic disorders. When I was an intern, the most common admitting diagnosis was what we called “Delta MS”—change in mental status. As I advanced in my residency and focused on a subspecialty of internal medicine, it became clear that whichever illnesses I studied, conditions such as anxiety disorders in Grave’s disease or the psychotic symptoms in lupus held my interest. Finally, the only specialty left was psychiatry.

The only program I found that seemed to understand medical psychiatry at the time was at Massachusetts General Hospital (MGH). MGH not only had eminent psychiatrists in every area of the field, it seemed, but also a special focus on training psychiatrists in medical settings and as medical experts. My first Chief of Psychiatry was Thomas P. Hackett, MD—a brilliant clinician, raconteur, and polymath—who had written a cri de coeur on the importance of medical skills and training in psychiatry.¹ At last, I had found a place where I could remain a physician and think and learn about every aspect of psychiatry, especially medical psychiatry.

What is medical psychiatry, and why is it relevant now?

There has been substantial and increasing interest in the integration of medical and psychiatric care. Whether it is collaborative care or co-location models, the recognition of the high rate of combined medical and psychiatric illnesses and associated increased mortality and total health care costs of these patients requires psychiatrists to be deeply familiar with the interactions among medical and psychiatric conditions.

Building on long-developed expertise in consultation-liaison psychiatry and other forms of medical psychiatric training, such as double-board medicine–psychiatry programs, medical psychiatry includes several specific areas of knowledge and skill sets, including understanding the impact that psychiatric illnesses and the medications used to treat them can have on medical illnesses and the ways in which the presence of medical disorders can change the presentation of psychiatric illnesses. Similarly, the psychiatric impact of the general medical pharmacopeia and the ways in which psychiatric illness can affect the presentation of medical illness are important for all psychiatrists to know. Most importantly, medical psychiatry should focus on the medical and neurologic causes of psychiatric illnesses. Many general medical conditions produce symptoms, which, in whole or in part, mimic psychiatric illnesses and, in some cases, could lead to psychiatric disorders, which makes identification of the underlying cause difficult.

Whether due to infectious, auto­immune, metabolic, or endocrinologic disorders, being aware of these conditions and, where clinical circumstances warrant, be able to diagnose them, with other specialists as needed, and ensure they are appropriately treated should be an essential skill for psychiatrists.

An illustrative case

I remember a case from early in my training of a woman with a late-onset mood disorder with abulia, wide-based gait, and urinary incontinence, in addition to withdrawal and loss of pleasure. Despite the skepticism of the neurology team, at autopsy she was found to have arteriosclerosis of the deep, penetrating arterioles causing white matter hyperintensities—Binswanger’s disease. There was no question that despite the neurologic cause of her symptoms treating her depression with antidepressants was needed and helpful. It also was important that her family was aware of her underlying medical condition and its implications for her care.²

Medicine is our calling

Many of these illnesses, even when identified, require expert psychiatric management of psychiatric symptoms. This should not be surprising to psychiatrists or other clinicians. No one expects a cardiologist to beg off the care of a patient with heart failure caused by alcohol abuse or a virus rather than vascular heart disease, and psychiatrists likewise need to manage psychosis due to steroid use or N-methyl-d-aspartate receptor antibodies as well as other causes. Pursuing this understanding is important from another perspective. As we consider other potential mechanisms for onset of psychiatric illness (eg, inflammation), our understanding of the mechanisms associated with general medical conditions may provide unexpected insight into the etiology of psychiatric illnesses where no general medical cause has been found. No other physician specialists are as attuned to the nuances of psychiatric illnesses, their typical and atypical presentations as psychiatrists. It is incumbent on us to pursue the medical differential of patients when we think it is needed, even if other physicians disagree.

Medical psychiatry has a broader and more inclusive perspective than what we generally mean by “biological psychiatry,” if by the latter, we mean a focus on the neurobiology and psychopharmacology of “primary” psychiatric conditions that are not secondary to other medical or neurologic disorders. As important and fundamental as deep understanding of neurobiology, genetics, and psychopharmacology are, medical psychiatry embeds our work more broadly in all of human biology and requires the full breadth of our medical training.

At a time when political battles over prescriptive privileges by non-medically trained mental health clinicians engage legislatures and professional organizations, medical psychiatry is a powerful reminder that prescribing or not prescribing medications is the final step in, what should be, an extensive, clinical evaluation including a thorough medical work up and consideration of the medical–psychiatric interactions and the differential diagnosis of these illnesses. It is, after all, what physicians do and is essential to our calling as psychiatric physicians. If psychiatrists are not at home in medicine, as Tom Hackett reminded us in 1977¹—at a time when psychiatry had temporarily eliminated the requirement for medical internships—then, indeed, psychiatry would be “homeless.”

There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).

Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.

Diverse presentations

Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?

Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.

As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.¹ Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.² Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.

Pharmacotherapy is underutilized

Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is under­utilized: only 3% of patients have received an FDA-approved treatment.^2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.³ Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.

Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for the most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.^4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.

Neuroscience supports the brain disease model of addiction, with neuro­plasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.⁶

Why hesitate to use pharmacotherapeutics?

There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.^4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?

Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:

• lack of familiarity with available agents
• absence of guidelines for use
• disbelief that the condition is treatable.

Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.

Therapeutic options

Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.

There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.

Psychosocial interventions

Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psycho­social therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on fellowship, accountability, monitoring, and anonymity; the forum can compete with motivational interviewing for efficacy in increasing abstinence and preventing relapse.

The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.

In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.

There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).

Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.

Diverse presentations

Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?

Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.

As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.¹ Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.² Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.

Pharmacotherapy is underutilized

Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is under­utilized: only 3% of patients have received an FDA-approved treatment.^2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.³ Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.

Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for the most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.^4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.

Neuroscience supports the brain disease model of addiction, with neuro­plasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.⁶

Why hesitate to use pharmacotherapeutics?

There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.^4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?

Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:

• lack of familiarity with available agents
• absence of guidelines for use
• disbelief that the condition is treatable.

Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.

Therapeutic options

Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.

There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.

Psychosocial interventions

Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psycho­social therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on fellowship, accountability, monitoring, and anonymity; the forum can compete with motivational interviewing for efficacy in increasing abstinence and preventing relapse.

The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.

In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.

There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).

Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.

Diverse presentations

Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?

Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.

As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.¹ Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.² Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.

Pharmacotherapy is underutilized

Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is under­utilized: only 3% of patients have received an FDA-approved treatment.^2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.³ Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.

Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for the most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.^4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.

Neuroscience supports the brain disease model of addiction, with neuro­plasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.⁶

Why hesitate to use pharmacotherapeutics?

There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.^4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?

Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:

• lack of familiarity with available agents
• absence of guidelines for use
• disbelief that the condition is treatable.

Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.

Therapeutic options

Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.

There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.

Psychosocial interventions

Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psycho­social therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on fellowship, accountability, monitoring, and anonymity; the forum can compete with motivational interviewing for efficacy in increasing abstinence and preventing relapse.

The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.

In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.

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.

In the United States, the average potency of Cannabis has increased significantly over the past few decades in response to consumer demand and policies in some states that have legalized marijuana for medicinal and recreational purposes.¹ Whereas the delta-9-tetrahydrocannabinol (THC) content of “street” marijuana was <1% in the 1970s and 4% in the 1990s, by 2012, analyses of Cannabis samples seized by law enforcement agencies documented a rise in average THC potency to >12%.^1-3

Although this increase in potency has been overstated in the media because studies did not control for the effects of changes in sampling methods on freshness, it is estimated that Cannabis potency increased 7-fold from 1970 to 2010.³ Also, Cannabis preparations such as hashish and hash oil extracts containing THC well above average—from 35% to 90% THC—are now more widely available. In states where marijuana has been legalized, high-potency Cannabis (HPC) in the form of “edibles” (eg, marijuana added to baked goods, candy, or drinks) and hash oil extracts (Table 1)^4-13 can be readily obtained from dispensaries or even at local farmers’ markets.

The potency of Cannabis, typically defined as the percentage of THC, its chief psychoactive component, varies depending on the genetic strain of the plant, cultivation techniques, and methods of processing and storage. For example, relative to “average marijuana,” hemp (Cannabis bred for industrial purposes) has very little THC, while sinsemilla (flowering buds from unpollinated female plants), hashish (Cannabis resin), and extracted hash oil contain increasing amounts of THC (Table 2).^1,2

Cannabis use disorder

Recent data indicate that the prevalence of Cannabis use disorders (eg, abuse and dependence) in the United States is approximately 3% among the general population and >30% among Cannabis users.¹⁶ The availability of increasingly potent forms of Cannabis has been cited as a possible explanation for this rise, despite no change in the prevalence of overall marijuana use between 1991 to 1992 and 2001 to 2002.¹⁷ However, while the prevalence of marijuana use disorders has continued to rise—nearly doubling from 2001 to 2002 to 2012 to 2013—this latest increase occurred with a significant increase in overall marijuana use, such that the actual rate of Cannabis use disorders among users seems to have plateaued, despite the continued rise in marijuana potency.¹⁶ This discrepancy could be explained if Cannabis users cut back past a specific threshold of increasing potency. However, 2 studies have called into question how effective such titration efforts might be in practice. In one study, Cannabis users who preferred more potent Cannabis inhaled lower volumes of smoke, but did not fully compensate for the increased potency, such that use of HPC still resulted in greater THC exposure.¹⁸ Another study found that HPC users rolled less marijuana into their joints but not enough to mitigate the impact of greater potency.¹⁹ Therefore, it appears that HPC users typically expose themselves to greater amounts of THC, which could place them at higher risk of addiction.

Although a causal association between increasing Cannabis potency and the rate of substance use disorders among users remains unclear based on epidemiologic studies from the United States, a recent study from the United Kingdom examined the impact of Cannabis potency on dependence.²⁰ This cross-sectional survey found that, although HPC was preferred by users and was rated as offering the “best high,” its use was associated with increasing severity of dependence, especially among young people. The limited available evidence supports a greater risk of Cannabis use disorders with increasing potency.

Psychosis

Based on longitudinal studies published over the past 30 years, it is clear that using Cannabis at a young age (age <15 to 18) increases the risk of developing a psychotic disorder.²¹ This association appears to be dose-dependent, with studies consistently demonstrating that psychosis risk increases with greater frequency of Cannabis use.²² The accumulated evidence to date is strong enough to view the psychotic potential of Cannabis as a significant public health concern.²¹

If risk of psychosis is proportional to the amount of Cannabis used as measured by frequency, it follows that this risk might be affected similarly by Cannabis potency. In another paper, I discussed the potential for greater risk of psychosis in the context of medical marijuana and synthetic cannabinoids.²³ My colleagues and I also have published case reports describing emerging psychosis among regular Cannabis users after escalating to higher potency medical marijuana²⁴ and a hyperconcentrated form of hash oil known as Cannabis “wax” or “dabs” that contains as much as 90% THC.⁴ Preliminary anecdotal evidence supports the plausibility of HPC being more psychotoxic than less potent forms.

Several studies from a research group in the United Kingdom, where sinsemilla has increasingly dominated the drug market, likewise have reported that the use of HPC is associated with a greater risk of psychosis. The first of these studies, published in 2009, found that adults hospitalized for first-episode psychosis were more likely to have used HPC than healthy controls.²⁵ Among Cannabis users, HPC use was associated with a 7-fold increased risk of psychosis, with daily HPC use associated with a 12-fold increased risk.

Based on a larger dataset, a second study reported that high-potency, but not low-potency, Cannabis increased the risk of first-episode psychosis with increasing frequency of use.²⁶ Daily users of HPC had a 5-fold higher risk of psychosis compared with those that had never used Cannabis. A third study reported that HPC use and daily Cannabis use were independently associated with an earlier onset of first-episode psychosis, with daily HPC users developing first-episode psychosis an average of 6 years earlier than non-Cannabis users.²⁷ Finally, a prospective study following patients with first-episode psychosis over 2 years found that the greatest risk of relapse—defined by hospital admission caused by exacerbation of psychotic symptoms—was found among self-reported daily users of HPC, while the lowest risk was among those who stopped using Cannabis after their initial psychotic episode.²⁸

The findings from these 4 studies suggest that the increased risk of psychosis with Cannabis is proportional to overall exposure, determined by both frequency of use and Cannabis potency.

Cognition

There is little doubt that using Cannabis can impair cognition acutely, “after all, this is the basic reason for its recreational use,” as one author wrote.²⁹ As with psychosis, the available evidence indicates that the degree of cognitive impairment is related to the frequency and duration of Cannabis use as well as age of onset of use.^30,31

Few studies have assessed cognitive functioning in relation to Cannabis potency with most only examining the effects of relatively low-potency Cannabis with inconsistent results. For example, 2 studies compared cognitive performance in individuals smoking Cannabis with 1.8% and 3.9% THC. One study found that using higher potency Cannabis resulted in prolonged time needed to complete certain cognitive tasks,³² whereas the other found greater impairment in performance on a decision-making task at both potencies compared with non-users but no differences between the 2 dosages.³³ Detecting significant differences may be difficult within the narrow range of low Cannabis potency studied where any findings have limited applicability in the context of today’s Cannabis with much higher THC content.

To date, only 1 study has assessed cognition at higher Cannabis potencies, comparing Cannabis with 4% THC to 13% THC.³⁴ Cognitive impairments increased with higher potency, especially in tasks that measured motor control and executive functioning. Therefore it appears that higher potency Cannabis use is associated with greater acute cognitive impairment.

The longer-term effects on cognition are less clear, with conflicting evidence about whether Cannabis use can result in residual cognitive impairment despite abstinence.^30,35 A recent review concluded that “the magnitude of neuropsychological impairment and the extent to which it persists after abstinence may depend on the frequency and the duration of Cannabis use, length of abstinence, and age at onset of use.”³¹ The effects of HPC on long-term cognitive deficits have not been studied.

Structural brain changes

A number of studies have determined an association between Cannabis use and brain changes involving structures governing memory and emotional processing, including reduced volume of the hippocampus,³⁶ temporal cortex, insula, and orbitofrontal cortex.³⁷ Although many of these changes appear to be dose-related, some morphologic changes have been reported among young recreational users without Cannabis dependence.³⁸ This has resulted in an understandable concern about the effects of Cannabis on the brains of young people with limited exposure; however, it is not yet clear to what extent detected brain changes are pathological and reflect functional deficits.

Recent research using newer neuroimaging modalities provides preliminary support of Cannabis use associated with white matter changes that, in turn, are correlated with cognitive impairment.³⁹ One study comparing low-potency Cannabis and HPC users with and without first-episode psychosis found a significant effect of Cannabis potency on disturbances in white matter microstructural organization in the corpus callosum.⁴⁰ These findings provide sufficient cause for concern that structural brain changes associated with cognitive impairment are more likely to occur with HPC use.

Recommendations for clinicians

Similar to any drug, the effects of THC and its psychiatric sequelae can be expected to increase with dosage. To date, much of the information about psychiatric risks has been based on studies of low- and moderate-potency Cannabis rather than the much higher potency Cannabis products, such as hyper-concentrated “wax dabs,” that are available today. Data from social media suggest that these products may be associated with novel patterns of use, such as with the intention of “passing out.”⁴¹ It is likely that clinicians will encounter greater psychiatric morbidity associated with HPC use.

Although clinicians may be accustomed to asking about the frequency and duration of Cannabis use, it is now prudent also to ask patients about Cannabis potency to better assess the potential risks of use. The potency of different marijuana products is openly advertised within some “medical marijuana” dispensaries, although the accuracy of information in products such as “edibles” has been called into question.⁵

Physicians are increasingly asked to provide recommendations on “medical marijuana” use. A recent paper outlined characteristics of appropriate candidates for “medical marijuana” including:

• having a debilitating condition that might benefit from Cannabis
• multiple failed trials of conventional pharmacotherapies including FDA-approved cannabinoids
• lack of substance use disorders, psychosis, or unstable mood or anxiety disorders
• residence in a state where “medical marijuana” is legal.⁴²

As part of the informed consent process, physicians providing recommendations for “medical marijuana” now must consider the effects of HPC when weighing potential risks against any benefits of Cannabis use. Those monitoring patients using Cannabis should be aware of the potential for greater psychiatric morbidity with HPC and should educate patients about that risk. Failure to adequately warn patients about such morbidity or to screen for risk factors such as psychosis could leave physicians vulnerable to malpractice litigation.

In the United States, the average potency of Cannabis has increased significantly over the past few decades in response to consumer demand and policies in some states that have legalized marijuana for medicinal and recreational purposes.¹ Whereas the delta-9-tetrahydrocannabinol (THC) content of “street” marijuana was <1% in the 1970s and 4% in the 1990s, by 2012, analyses of Cannabis samples seized by law enforcement agencies documented a rise in average THC potency to >12%.^1-3

Although this increase in potency has been overstated in the media because studies did not control for the effects of changes in sampling methods on freshness, it is estimated that Cannabis potency increased 7-fold from 1970 to 2010.³ Also, Cannabis preparations such as hashish and hash oil extracts containing THC well above average—from 35% to 90% THC—are now more widely available. In states where marijuana has been legalized, high-potency Cannabis (HPC) in the form of “edibles” (eg, marijuana added to baked goods, candy, or drinks) and hash oil extracts (Table 1)^4-13 can be readily obtained from dispensaries or even at local farmers’ markets.

The potency of Cannabis, typically defined as the percentage of THC, its chief psychoactive component, varies depending on the genetic strain of the plant, cultivation techniques, and methods of processing and storage. For example, relative to “average marijuana,” hemp (Cannabis bred for industrial purposes) has very little THC, while sinsemilla (flowering buds from unpollinated female plants), hashish (Cannabis resin), and extracted hash oil contain increasing amounts of THC (Table 2).^1,2

Cannabis use disorder

Recent data indicate that the prevalence of Cannabis use disorders (eg, abuse and dependence) in the United States is approximately 3% among the general population and >30% among Cannabis users.¹⁶ The availability of increasingly potent forms of Cannabis has been cited as a possible explanation for this rise, despite no change in the prevalence of overall marijuana use between 1991 to 1992 and 2001 to 2002.¹⁷ However, while the prevalence of marijuana use disorders has continued to rise—nearly doubling from 2001 to 2002 to 2012 to 2013—this latest increase occurred with a significant increase in overall marijuana use, such that the actual rate of Cannabis use disorders among users seems to have plateaued, despite the continued rise in marijuana potency.¹⁶ This discrepancy could be explained if Cannabis users cut back past a specific threshold of increasing potency. However, 2 studies have called into question how effective such titration efforts might be in practice. In one study, Cannabis users who preferred more potent Cannabis inhaled lower volumes of smoke, but did not fully compensate for the increased potency, such that use of HPC still resulted in greater THC exposure.¹⁸ Another study found that HPC users rolled less marijuana into their joints but not enough to mitigate the impact of greater potency.¹⁹ Therefore, it appears that HPC users typically expose themselves to greater amounts of THC, which could place them at higher risk of addiction.

Although a causal association between increasing Cannabis potency and the rate of substance use disorders among users remains unclear based on epidemiologic studies from the United States, a recent study from the United Kingdom examined the impact of Cannabis potency on dependence.²⁰ This cross-sectional survey found that, although HPC was preferred by users and was rated as offering the “best high,” its use was associated with increasing severity of dependence, especially among young people. The limited available evidence supports a greater risk of Cannabis use disorders with increasing potency.

Psychosis

Based on longitudinal studies published over the past 30 years, it is clear that using Cannabis at a young age (age <15 to 18) increases the risk of developing a psychotic disorder.²¹ This association appears to be dose-dependent, with studies consistently demonstrating that psychosis risk increases with greater frequency of Cannabis use.²² The accumulated evidence to date is strong enough to view the psychotic potential of Cannabis as a significant public health concern.²¹

If risk of psychosis is proportional to the amount of Cannabis used as measured by frequency, it follows that this risk might be affected similarly by Cannabis potency. In another paper, I discussed the potential for greater risk of psychosis in the context of medical marijuana and synthetic cannabinoids.²³ My colleagues and I also have published case reports describing emerging psychosis among regular Cannabis users after escalating to higher potency medical marijuana²⁴ and a hyperconcentrated form of hash oil known as Cannabis “wax” or “dabs” that contains as much as 90% THC.⁴ Preliminary anecdotal evidence supports the plausibility of HPC being more psychotoxic than less potent forms.

Several studies from a research group in the United Kingdom, where sinsemilla has increasingly dominated the drug market, likewise have reported that the use of HPC is associated with a greater risk of psychosis. The first of these studies, published in 2009, found that adults hospitalized for first-episode psychosis were more likely to have used HPC than healthy controls.²⁵ Among Cannabis users, HPC use was associated with a 7-fold increased risk of psychosis, with daily HPC use associated with a 12-fold increased risk.

Based on a larger dataset, a second study reported that high-potency, but not low-potency, Cannabis increased the risk of first-episode psychosis with increasing frequency of use.²⁶ Daily users of HPC had a 5-fold higher risk of psychosis compared with those that had never used Cannabis. A third study reported that HPC use and daily Cannabis use were independently associated with an earlier onset of first-episode psychosis, with daily HPC users developing first-episode psychosis an average of 6 years earlier than non-Cannabis users.²⁷ Finally, a prospective study following patients with first-episode psychosis over 2 years found that the greatest risk of relapse—defined by hospital admission caused by exacerbation of psychotic symptoms—was found among self-reported daily users of HPC, while the lowest risk was among those who stopped using Cannabis after their initial psychotic episode.²⁸

The findings from these 4 studies suggest that the increased risk of psychosis with Cannabis is proportional to overall exposure, determined by both frequency of use and Cannabis potency.

Cognition

There is little doubt that using Cannabis can impair cognition acutely, “after all, this is the basic reason for its recreational use,” as one author wrote.²⁹ As with psychosis, the available evidence indicates that the degree of cognitive impairment is related to the frequency and duration of Cannabis use as well as age of onset of use.^30,31

Few studies have assessed cognitive functioning in relation to Cannabis potency with most only examining the effects of relatively low-potency Cannabis with inconsistent results. For example, 2 studies compared cognitive performance in individuals smoking Cannabis with 1.8% and 3.9% THC. One study found that using higher potency Cannabis resulted in prolonged time needed to complete certain cognitive tasks,³² whereas the other found greater impairment in performance on a decision-making task at both potencies compared with non-users but no differences between the 2 dosages.³³ Detecting significant differences may be difficult within the narrow range of low Cannabis potency studied where any findings have limited applicability in the context of today’s Cannabis with much higher THC content.

To date, only 1 study has assessed cognition at higher Cannabis potencies, comparing Cannabis with 4% THC to 13% THC.³⁴ Cognitive impairments increased with higher potency, especially in tasks that measured motor control and executive functioning. Therefore it appears that higher potency Cannabis use is associated with greater acute cognitive impairment.

The longer-term effects on cognition are less clear, with conflicting evidence about whether Cannabis use can result in residual cognitive impairment despite abstinence.^30,35 A recent review concluded that “the magnitude of neuropsychological impairment and the extent to which it persists after abstinence may depend on the frequency and the duration of Cannabis use, length of abstinence, and age at onset of use.”³¹ The effects of HPC on long-term cognitive deficits have not been studied.

Structural brain changes

A number of studies have determined an association between Cannabis use and brain changes involving structures governing memory and emotional processing, including reduced volume of the hippocampus,³⁶ temporal cortex, insula, and orbitofrontal cortex.³⁷ Although many of these changes appear to be dose-related, some morphologic changes have been reported among young recreational users without Cannabis dependence.³⁸ This has resulted in an understandable concern about the effects of Cannabis on the brains of young people with limited exposure; however, it is not yet clear to what extent detected brain changes are pathological and reflect functional deficits.

Recent research using newer neuroimaging modalities provides preliminary support of Cannabis use associated with white matter changes that, in turn, are correlated with cognitive impairment.³⁹ One study comparing low-potency Cannabis and HPC users with and without first-episode psychosis found a significant effect of Cannabis potency on disturbances in white matter microstructural organization in the corpus callosum.⁴⁰ These findings provide sufficient cause for concern that structural brain changes associated with cognitive impairment are more likely to occur with HPC use.

Recommendations for clinicians

Similar to any drug, the effects of THC and its psychiatric sequelae can be expected to increase with dosage. To date, much of the information about psychiatric risks has been based on studies of low- and moderate-potency Cannabis rather than the much higher potency Cannabis products, such as hyper-concentrated “wax dabs,” that are available today. Data from social media suggest that these products may be associated with novel patterns of use, such as with the intention of “passing out.”⁴¹ It is likely that clinicians will encounter greater psychiatric morbidity associated with HPC use.

Although clinicians may be accustomed to asking about the frequency and duration of Cannabis use, it is now prudent also to ask patients about Cannabis potency to better assess the potential risks of use. The potency of different marijuana products is openly advertised within some “medical marijuana” dispensaries, although the accuracy of information in products such as “edibles” has been called into question.⁵

Physicians are increasingly asked to provide recommendations on “medical marijuana” use. A recent paper outlined characteristics of appropriate candidates for “medical marijuana” including:

• having a debilitating condition that might benefit from Cannabis
• multiple failed trials of conventional pharmacotherapies including FDA-approved cannabinoids
• lack of substance use disorders, psychosis, or unstable mood or anxiety disorders
• residence in a state where “medical marijuana” is legal.⁴²

As part of the informed consent process, physicians providing recommendations for “medical marijuana” now must consider the effects of HPC when weighing potential risks against any benefits of Cannabis use. Those monitoring patients using Cannabis should be aware of the potential for greater psychiatric morbidity with HPC and should educate patients about that risk. Failure to adequately warn patients about such morbidity or to screen for risk factors such as psychosis could leave physicians vulnerable to malpractice litigation.

In the United States, the average potency of Cannabis has increased significantly over the past few decades in response to consumer demand and policies in some states that have legalized marijuana for medicinal and recreational purposes.¹ Whereas the delta-9-tetrahydrocannabinol (THC) content of “street” marijuana was <1% in the 1970s and 4% in the 1990s, by 2012, analyses of Cannabis samples seized by law enforcement agencies documented a rise in average THC potency to >12%.^1-3

Although this increase in potency has been overstated in the media because studies did not control for the effects of changes in sampling methods on freshness, it is estimated that Cannabis potency increased 7-fold from 1970 to 2010.³ Also, Cannabis preparations such as hashish and hash oil extracts containing THC well above average—from 35% to 90% THC—are now more widely available. In states where marijuana has been legalized, high-potency Cannabis (HPC) in the form of “edibles” (eg, marijuana added to baked goods, candy, or drinks) and hash oil extracts (Table 1)^4-13 can be readily obtained from dispensaries or even at local farmers’ markets.

The potency of Cannabis, typically defined as the percentage of THC, its chief psychoactive component, varies depending on the genetic strain of the plant, cultivation techniques, and methods of processing and storage. For example, relative to “average marijuana,” hemp (Cannabis bred for industrial purposes) has very little THC, while sinsemilla (flowering buds from unpollinated female plants), hashish (Cannabis resin), and extracted hash oil contain increasing amounts of THC (Table 2).^1,2

Cannabis use disorder

Recent data indicate that the prevalence of Cannabis use disorders (eg, abuse and dependence) in the United States is approximately 3% among the general population and >30% among Cannabis users.¹⁶ The availability of increasingly potent forms of Cannabis has been cited as a possible explanation for this rise, despite no change in the prevalence of overall marijuana use between 1991 to 1992 and 2001 to 2002.¹⁷ However, while the prevalence of marijuana use disorders has continued to rise—nearly doubling from 2001 to 2002 to 2012 to 2013—this latest increase occurred with a significant increase in overall marijuana use, such that the actual rate of Cannabis use disorders among users seems to have plateaued, despite the continued rise in marijuana potency.¹⁶ This discrepancy could be explained if Cannabis users cut back past a specific threshold of increasing potency. However, 2 studies have called into question how effective such titration efforts might be in practice. In one study, Cannabis users who preferred more potent Cannabis inhaled lower volumes of smoke, but did not fully compensate for the increased potency, such that use of HPC still resulted in greater THC exposure.¹⁸ Another study found that HPC users rolled less marijuana into their joints but not enough to mitigate the impact of greater potency.¹⁹ Therefore, it appears that HPC users typically expose themselves to greater amounts of THC, which could place them at higher risk of addiction.

Although a causal association between increasing Cannabis potency and the rate of substance use disorders among users remains unclear based on epidemiologic studies from the United States, a recent study from the United Kingdom examined the impact of Cannabis potency on dependence.²⁰ This cross-sectional survey found that, although HPC was preferred by users and was rated as offering the “best high,” its use was associated with increasing severity of dependence, especially among young people. The limited available evidence supports a greater risk of Cannabis use disorders with increasing potency.

Psychosis

Based on longitudinal studies published over the past 30 years, it is clear that using Cannabis at a young age (age <15 to 18) increases the risk of developing a psychotic disorder.²¹ This association appears to be dose-dependent, with studies consistently demonstrating that psychosis risk increases with greater frequency of Cannabis use.²² The accumulated evidence to date is strong enough to view the psychotic potential of Cannabis as a significant public health concern.²¹

If risk of psychosis is proportional to the amount of Cannabis used as measured by frequency, it follows that this risk might be affected similarly by Cannabis potency. In another paper, I discussed the potential for greater risk of psychosis in the context of medical marijuana and synthetic cannabinoids.²³ My colleagues and I also have published case reports describing emerging psychosis among regular Cannabis users after escalating to higher potency medical marijuana²⁴ and a hyperconcentrated form of hash oil known as Cannabis “wax” or “dabs” that contains as much as 90% THC.⁴ Preliminary anecdotal evidence supports the plausibility of HPC being more psychotoxic than less potent forms.

Several studies from a research group in the United Kingdom, where sinsemilla has increasingly dominated the drug market, likewise have reported that the use of HPC is associated with a greater risk of psychosis. The first of these studies, published in 2009, found that adults hospitalized for first-episode psychosis were more likely to have used HPC than healthy controls.²⁵ Among Cannabis users, HPC use was associated with a 7-fold increased risk of psychosis, with daily HPC use associated with a 12-fold increased risk.

Based on a larger dataset, a second study reported that high-potency, but not low-potency, Cannabis increased the risk of first-episode psychosis with increasing frequency of use.²⁶ Daily users of HPC had a 5-fold higher risk of psychosis compared with those that had never used Cannabis. A third study reported that HPC use and daily Cannabis use were independently associated with an earlier onset of first-episode psychosis, with daily HPC users developing first-episode psychosis an average of 6 years earlier than non-Cannabis users.²⁷ Finally, a prospective study following patients with first-episode psychosis over 2 years found that the greatest risk of relapse—defined by hospital admission caused by exacerbation of psychotic symptoms—was found among self-reported daily users of HPC, while the lowest risk was among those who stopped using Cannabis after their initial psychotic episode.²⁸

The findings from these 4 studies suggest that the increased risk of psychosis with Cannabis is proportional to overall exposure, determined by both frequency of use and Cannabis potency.

Cognition

There is little doubt that using Cannabis can impair cognition acutely, “after all, this is the basic reason for its recreational use,” as one author wrote.²⁹ As with psychosis, the available evidence indicates that the degree of cognitive impairment is related to the frequency and duration of Cannabis use as well as age of onset of use.^30,31

Few studies have assessed cognitive functioning in relation to Cannabis potency with most only examining the effects of relatively low-potency Cannabis with inconsistent results. For example, 2 studies compared cognitive performance in individuals smoking Cannabis with 1.8% and 3.9% THC. One study found that using higher potency Cannabis resulted in prolonged time needed to complete certain cognitive tasks,³² whereas the other found greater impairment in performance on a decision-making task at both potencies compared with non-users but no differences between the 2 dosages.³³ Detecting significant differences may be difficult within the narrow range of low Cannabis potency studied where any findings have limited applicability in the context of today’s Cannabis with much higher THC content.

To date, only 1 study has assessed cognition at higher Cannabis potencies, comparing Cannabis with 4% THC to 13% THC.³⁴ Cognitive impairments increased with higher potency, especially in tasks that measured motor control and executive functioning. Therefore it appears that higher potency Cannabis use is associated with greater acute cognitive impairment.

The longer-term effects on cognition are less clear, with conflicting evidence about whether Cannabis use can result in residual cognitive impairment despite abstinence.^30,35 A recent review concluded that “the magnitude of neuropsychological impairment and the extent to which it persists after abstinence may depend on the frequency and the duration of Cannabis use, length of abstinence, and age at onset of use.”³¹ The effects of HPC on long-term cognitive deficits have not been studied.

Structural brain changes

A number of studies have determined an association between Cannabis use and brain changes involving structures governing memory and emotional processing, including reduced volume of the hippocampus,³⁶ temporal cortex, insula, and orbitofrontal cortex.³⁷ Although many of these changes appear to be dose-related, some morphologic changes have been reported among young recreational users without Cannabis dependence.³⁸ This has resulted in an understandable concern about the effects of Cannabis on the brains of young people with limited exposure; however, it is not yet clear to what extent detected brain changes are pathological and reflect functional deficits.

Recent research using newer neuroimaging modalities provides preliminary support of Cannabis use associated with white matter changes that, in turn, are correlated with cognitive impairment.³⁹ One study comparing low-potency Cannabis and HPC users with and without first-episode psychosis found a significant effect of Cannabis potency on disturbances in white matter microstructural organization in the corpus callosum.⁴⁰ These findings provide sufficient cause for concern that structural brain changes associated with cognitive impairment are more likely to occur with HPC use.

Recommendations for clinicians

Similar to any drug, the effects of THC and its psychiatric sequelae can be expected to increase with dosage. To date, much of the information about psychiatric risks has been based on studies of low- and moderate-potency Cannabis rather than the much higher potency Cannabis products, such as hyper-concentrated “wax dabs,” that are available today. Data from social media suggest that these products may be associated with novel patterns of use, such as with the intention of “passing out.”⁴¹ It is likely that clinicians will encounter greater psychiatric morbidity associated with HPC use.

Although clinicians may be accustomed to asking about the frequency and duration of Cannabis use, it is now prudent also to ask patients about Cannabis potency to better assess the potential risks of use. The potency of different marijuana products is openly advertised within some “medical marijuana” dispensaries, although the accuracy of information in products such as “edibles” has been called into question.⁵

Physicians are increasingly asked to provide recommendations on “medical marijuana” use. A recent paper outlined characteristics of appropriate candidates for “medical marijuana” including:

• having a debilitating condition that might benefit from Cannabis
• multiple failed trials of conventional pharmacotherapies including FDA-approved cannabinoids
• lack of substance use disorders, psychosis, or unstable mood or anxiety disorders
• residence in a state where “medical marijuana” is legal.⁴²

As part of the informed consent process, physicians providing recommendations for “medical marijuana” now must consider the effects of HPC when weighing potential risks against any benefits of Cannabis use. Those monitoring patients using Cannabis should be aware of the potential for greater psychiatric morbidity with HPC and should educate patients about that risk. Failure to adequately warn patients about such morbidity or to screen for risk factors such as psychosis could leave physicians vulnerable to malpractice litigation.