Carl C. Bell, MD

In 2016, two researchers published a meta-analysis on gray matter abnormalities in youth who had conduct problems.

The study by Jack C. Rogers, PhD, and Stephane A. De Brito, PhD, found 13 well-done studies that included 394 youth with conduct problems and 390 typically developing youth. Compared with the typically developing youth, the conduct-disordered youth had decreased gray matter volume (JAMA Psychiatry. 2016 Jan;73[1]:64-72).

As I knew one of the researchers in one of the studies that made the cut, I called him up and asked whether their research had controlled for fetal alcohol exposure. They had not. I found this very curious because my experience is that youth who have been labeled with conduct disorder often have histories of prenatal fetal alcohol exposure. In addition, my understanding is that youth who have been exposed to prenatal alcohol often have symptoms of conduct disorder. Furthermore, research has shown that such youth have smaller brains (Dev Med Child Neurol. 2001 Mar;43[3]:148-54). I wondered whether the youth studied in that trial had been exposed to alcohol prenatally.

More recently, this problem has resurfaced. An article by Antonia N. Kaczkurkin, PhD, and associates about a large sample of youth was nicely done. But again, the variable of fetal alcohol exposure was not considered. The study was an elegant one that provides a strong rationale for consideration of a “psychopathology factor” in human life (Am J Psychiatry. 2019 Jun 24. doi: 10.1176/appi.ajp.2019.1807035). It shored up that argument by doing neuroimaging studies on a reasonably large sample of youth and showed that reduced cortical thickness (gray matter volume) was associated with overall psychopathology. With the exception of failing to consider the variable of fetal alcohol exposure, the study is a valuable addition to our understanding of what might be going on with psychiatric disorders.

Unfortunately – while hating to sound like a broken record – I noticed that there was no consideration of fetal alcohol exposure as a cause for the findings of the study. It does not seem like a large leap to hypothesize some of these brain imaging studies that find smaller brain components associated with psychopathology and conduct disorder to be a dynamic of fetal alcohol exposure.

It seems to me that we made a huge mistake in public health in asking women only whether they were drinking while they were pregnant because it was the wrong question. The right question is – “When did you realize you were pregnant, and were you doing any social drinking before you knew you were pregnant?”

Without understanding the etiology of the smaller brains in patients with conduct disorder or psychopathology, we are missing a golden opportunity to prevent such problems. The former editor of the American Journal of Psychiatry – Robert A. Freedman, MD – suggests that by giving phosphatidyl choline to pregnant women, such problems could be prevented.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. In 2019, he was awarded the Adolph Meyer Award by the American Psychiatric Association for lifetime achievement in psychiatric research.

In 2016, two researchers published a meta-analysis on gray matter abnormalities in youth who had conduct problems.

The study by Jack C. Rogers, PhD, and Stephane A. De Brito, PhD, found 13 well-done studies that included 394 youth with conduct problems and 390 typically developing youth. Compared with the typically developing youth, the conduct-disordered youth had decreased gray matter volume (JAMA Psychiatry. 2016 Jan;73[1]:64-72).

As I knew one of the researchers in one of the studies that made the cut, I called him up and asked whether their research had controlled for fetal alcohol exposure. They had not. I found this very curious because my experience is that youth who have been labeled with conduct disorder often have histories of prenatal fetal alcohol exposure. In addition, my understanding is that youth who have been exposed to prenatal alcohol often have symptoms of conduct disorder. Furthermore, research has shown that such youth have smaller brains (Dev Med Child Neurol. 2001 Mar;43[3]:148-54). I wondered whether the youth studied in that trial had been exposed to alcohol prenatally.

More recently, this problem has resurfaced. An article by Antonia N. Kaczkurkin, PhD, and associates about a large sample of youth was nicely done. But again, the variable of fetal alcohol exposure was not considered. The study was an elegant one that provides a strong rationale for consideration of a “psychopathology factor” in human life (Am J Psychiatry. 2019 Jun 24. doi: 10.1176/appi.ajp.2019.1807035). It shored up that argument by doing neuroimaging studies on a reasonably large sample of youth and showed that reduced cortical thickness (gray matter volume) was associated with overall psychopathology. With the exception of failing to consider the variable of fetal alcohol exposure, the study is a valuable addition to our understanding of what might be going on with psychiatric disorders.

Unfortunately – while hating to sound like a broken record – I noticed that there was no consideration of fetal alcohol exposure as a cause for the findings of the study. It does not seem like a large leap to hypothesize some of these brain imaging studies that find smaller brain components associated with psychopathology and conduct disorder to be a dynamic of fetal alcohol exposure.

It seems to me that we made a huge mistake in public health in asking women only whether they were drinking while they were pregnant because it was the wrong question. The right question is – “When did you realize you were pregnant, and were you doing any social drinking before you knew you were pregnant?”

Without understanding the etiology of the smaller brains in patients with conduct disorder or psychopathology, we are missing a golden opportunity to prevent such problems. The former editor of the American Journal of Psychiatry – Robert A. Freedman, MD – suggests that by giving phosphatidyl choline to pregnant women, such problems could be prevented.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. In 2019, he was awarded the Adolph Meyer Award by the American Psychiatric Association for lifetime achievement in psychiatric research.

In 2016, two researchers published a meta-analysis on gray matter abnormalities in youth who had conduct problems.

The study by Jack C. Rogers, PhD, and Stephane A. De Brito, PhD, found 13 well-done studies that included 394 youth with conduct problems and 390 typically developing youth. Compared with the typically developing youth, the conduct-disordered youth had decreased gray matter volume (JAMA Psychiatry. 2016 Jan;73[1]:64-72).

As I knew one of the researchers in one of the studies that made the cut, I called him up and asked whether their research had controlled for fetal alcohol exposure. They had not. I found this very curious because my experience is that youth who have been labeled with conduct disorder often have histories of prenatal fetal alcohol exposure. In addition, my understanding is that youth who have been exposed to prenatal alcohol often have symptoms of conduct disorder. Furthermore, research has shown that such youth have smaller brains (Dev Med Child Neurol. 2001 Mar;43[3]:148-54). I wondered whether the youth studied in that trial had been exposed to alcohol prenatally.

More recently, this problem has resurfaced. An article by Antonia N. Kaczkurkin, PhD, and associates about a large sample of youth was nicely done. But again, the variable of fetal alcohol exposure was not considered. The study was an elegant one that provides a strong rationale for consideration of a “psychopathology factor” in human life (Am J Psychiatry. 2019 Jun 24. doi: 10.1176/appi.ajp.2019.1807035). It shored up that argument by doing neuroimaging studies on a reasonably large sample of youth and showed that reduced cortical thickness (gray matter volume) was associated with overall psychopathology. With the exception of failing to consider the variable of fetal alcohol exposure, the study is a valuable addition to our understanding of what might be going on with psychiatric disorders.

Unfortunately – while hating to sound like a broken record – I noticed that there was no consideration of fetal alcohol exposure as a cause for the findings of the study. It does not seem like a large leap to hypothesize some of these brain imaging studies that find smaller brain components associated with psychopathology and conduct disorder to be a dynamic of fetal alcohol exposure.

It seems to me that we made a huge mistake in public health in asking women only whether they were drinking while they were pregnant because it was the wrong question. The right question is – “When did you realize you were pregnant, and were you doing any social drinking before you knew you were pregnant?”

Without understanding the etiology of the smaller brains in patients with conduct disorder or psychopathology, we are missing a golden opportunity to prevent such problems. The former editor of the American Journal of Psychiatry – Robert A. Freedman, MD – suggests that by giving phosphatidyl choline to pregnant women, such problems could be prevented.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. In 2019, he was awarded the Adolph Meyer Award by the American Psychiatric Association for lifetime achievement in psychiatric research.

The other day, I saw a patient who really brought home the importance of considering culture in psychiatry. The patient’s chief complaint was that he had been hearing the voice of an “invisible man.” I noticed he had an accent I was familiar with, and it sounded like he was from Haiti. Indeed, he was born there.

Accordingly, I asked him about voodoo. He said he is not a voodoo worshiper but he believes in voodoo – and he thought that that was what was happening to him. He reported this was the second time he heard the voices – the last time was less than a year ago. He said he came to the hospital because he was trying to wash dishes when he felt some invisible force holding him down. The patient got upset, and he broke the dishes he was washing. Of course, a big melee ensued, and the police were called. They brought the patient to my hospital.

When I spoke with him, he said he was doing pretty well with his Parkinson’s disease but he was a little stiff. The patient was on carbidopa-levodopa 25-100 mg 1.5 t.i.d. for his Parkinson’s, quetiapine 50 mg b.i.d. for his psychotic symptoms, amantadine 100 mg b.i.d. to stimulate his dopamine, ropinirole 1 mg t.i.d. for restless legs, and baclofen 10 mg t.i.d. for muscle spasms.

This is a 66-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic, and he had a wide range of affect as he was able to smile, get serious, and be sad (about his problems). His speech was relevant, linear, and goal directed. His thought processes did not show any signs of loose associations, tangentiality or circumstantiality, but he did have delusions, and current auditory and visual hallucinations. His thought content was surrounding his problems, which because of the culture he is from, were attributed by him to voodoo. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was average. Despite my explaining to him that his psychotic symptoms were caused by the medication he was taking, his judgment and insight were fair as he explained to me the things that were happening to him were so tangible they had to be real. He had no suicidal or homicidal ideation.

I decided to leave his meds as is, and I gave him 25 mg loxapine at h.s.

When I saw him a few days later, I asked him how he was doing, and he reported that the invisible man and all of his shenanigans were gone. I again explained that the medication he was taking for his Parkinson’s was causing his psychotic symptoms, and now I had proof. Had the voices been tied to voodoo, the medication would not have stopped the symptoms. He looked skeptical.

This struck me as a perfect example of the importance of culture in psychiatry, and I thought it instructive to share.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit; clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago; former president/CEO of the Community Mental Health Council; and former director of the Institute for Juvenile Research (birthplace of child psychiatry), all in Chicago. He is recipient of the American Psychiatric Association’s 2019 Adolph Meyer Award for Lifetime Achievement in Psychiatric Research. Check out Dr. Bell’s new book, Fetal Alcohol Exposure in the African-American Community, at https://thirdworldpressfoundation.org/product/pre-order-fetal-alcohol-exposure-in-the-african-american-community.

The other day, I saw a patient who really brought home the importance of considering culture in psychiatry. The patient’s chief complaint was that he had been hearing the voice of an “invisible man.” I noticed he had an accent I was familiar with, and it sounded like he was from Haiti. Indeed, he was born there.

Accordingly, I asked him about voodoo. He said he is not a voodoo worshiper but he believes in voodoo – and he thought that that was what was happening to him. He reported this was the second time he heard the voices – the last time was less than a year ago. He said he came to the hospital because he was trying to wash dishes when he felt some invisible force holding him down. The patient got upset, and he broke the dishes he was washing. Of course, a big melee ensued, and the police were called. They brought the patient to my hospital.

When I spoke with him, he said he was doing pretty well with his Parkinson’s disease but he was a little stiff. The patient was on carbidopa-levodopa 25-100 mg 1.5 t.i.d. for his Parkinson’s, quetiapine 50 mg b.i.d. for his psychotic symptoms, amantadine 100 mg b.i.d. to stimulate his dopamine, ropinirole 1 mg t.i.d. for restless legs, and baclofen 10 mg t.i.d. for muscle spasms.

This is a 66-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic, and he had a wide range of affect as he was able to smile, get serious, and be sad (about his problems). His speech was relevant, linear, and goal directed. His thought processes did not show any signs of loose associations, tangentiality or circumstantiality, but he did have delusions, and current auditory and visual hallucinations. His thought content was surrounding his problems, which because of the culture he is from, were attributed by him to voodoo. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was average. Despite my explaining to him that his psychotic symptoms were caused by the medication he was taking, his judgment and insight were fair as he explained to me the things that were happening to him were so tangible they had to be real. He had no suicidal or homicidal ideation.

I decided to leave his meds as is, and I gave him 25 mg loxapine at h.s.

When I saw him a few days later, I asked him how he was doing, and he reported that the invisible man and all of his shenanigans were gone. I again explained that the medication he was taking for his Parkinson’s was causing his psychotic symptoms, and now I had proof. Had the voices been tied to voodoo, the medication would not have stopped the symptoms. He looked skeptical.

This struck me as a perfect example of the importance of culture in psychiatry, and I thought it instructive to share.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit; clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago; former president/CEO of the Community Mental Health Council; and former director of the Institute for Juvenile Research (birthplace of child psychiatry), all in Chicago. He is recipient of the American Psychiatric Association’s 2019 Adolph Meyer Award for Lifetime Achievement in Psychiatric Research. Check out Dr. Bell’s new book, Fetal Alcohol Exposure in the African-American Community, at https://thirdworldpressfoundation.org/product/pre-order-fetal-alcohol-exposure-in-the-african-american-community.

The other day, I saw a patient who really brought home the importance of considering culture in psychiatry. The patient’s chief complaint was that he had been hearing the voice of an “invisible man.” I noticed he had an accent I was familiar with, and it sounded like he was from Haiti. Indeed, he was born there.

Accordingly, I asked him about voodoo. He said he is not a voodoo worshiper but he believes in voodoo – and he thought that that was what was happening to him. He reported this was the second time he heard the voices – the last time was less than a year ago. He said he came to the hospital because he was trying to wash dishes when he felt some invisible force holding him down. The patient got upset, and he broke the dishes he was washing. Of course, a big melee ensued, and the police were called. They brought the patient to my hospital.

When I spoke with him, he said he was doing pretty well with his Parkinson’s disease but he was a little stiff. The patient was on carbidopa-levodopa 25-100 mg 1.5 t.i.d. for his Parkinson’s, quetiapine 50 mg b.i.d. for his psychotic symptoms, amantadine 100 mg b.i.d. to stimulate his dopamine, ropinirole 1 mg t.i.d. for restless legs, and baclofen 10 mg t.i.d. for muscle spasms.

This is a 66-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic, and he had a wide range of affect as he was able to smile, get serious, and be sad (about his problems). His speech was relevant, linear, and goal directed. His thought processes did not show any signs of loose associations, tangentiality or circumstantiality, but he did have delusions, and current auditory and visual hallucinations. His thought content was surrounding his problems, which because of the culture he is from, were attributed by him to voodoo. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was average. Despite my explaining to him that his psychotic symptoms were caused by the medication he was taking, his judgment and insight were fair as he explained to me the things that were happening to him were so tangible they had to be real. He had no suicidal or homicidal ideation.

I decided to leave his meds as is, and I gave him 25 mg loxapine at h.s.

When I saw him a few days later, I asked him how he was doing, and he reported that the invisible man and all of his shenanigans were gone. I again explained that the medication he was taking for his Parkinson’s was causing his psychotic symptoms, and now I had proof. Had the voices been tied to voodoo, the medication would not have stopped the symptoms. He looked skeptical.

This struck me as a perfect example of the importance of culture in psychiatry, and I thought it instructive to share.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit; clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago; former president/CEO of the Community Mental Health Council; and former director of the Institute for Juvenile Research (birthplace of child psychiatry), all in Chicago. He is recipient of the American Psychiatric Association’s 2019 Adolph Meyer Award for Lifetime Achievement in Psychiatric Research. Check out Dr. Bell’s new book, Fetal Alcohol Exposure in the African-American Community, at https://thirdworldpressfoundation.org/product/pre-order-fetal-alcohol-exposure-in-the-african-american-community.

At the risk of too much personal self-disclosure, I feel the need to write about my having developed more empathy for women. Having been described as a “manly man,” by a woman who feels she knows me, it has always been difficult for me to understand women. Fortunately, an experience I’ve had has given me more insight into women – shallow though it may still be.

About a year ago, I had learned I had prostate carcinoma, which is now in remission – thanks to a proctectomy, radiation, and hormone therapy. The antitestosterone hormones I need to take for 2 years are turning me into an old woman, thus my newfound empathy.

After the surgery, I found myself leaking – something that I probably only experienced as a child and of which I have little memory. I now have some more empathy for the problems women have with leaking each month or in general – it is a constant preoccupation. The leuprolide shots I am taking are giving me hot flashes, causing me to be more emotional about things I really don’t understand, and apparently I am at risk for getting osteoporosis – all things that happen to women that have been mildly on my radar for years but for which I lacked direct and personal experience.

Since having my testosterone turned off by the leuprolide, my joints are more prone to aches and pains from various injuries over the years. Because I understand that “motion is lotion,” I have some control of this problem. However, the hormone therapy has greatly reduced my endurance, so my exercise tolerance is far more limited – I understand fatigue now. When I was telling another woman who feels she knows me about my experience, she told me it was hormones that made it more difficult to lose weight. And, I am gaining weight.

All in all, I believe my experience has given me more empathy for women, but I realize I still have a very long way to go. Nonetheless, I will continue in my quest to understand the opposite sex, as I am told “women hold up half the sky,” and I have always believed that to be true.

Fortunately, women are ascending in psychiatry and, with some serious dedication, the dearth of scientific understanding of women’s issues will be a thing of the past. I am hoping that women psychiatrists will answer questions that men never even thought of asking, and fill that void of knowledge that we men psychiatrists have in our testosterone-bathed brains.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.

At the risk of too much personal self-disclosure, I feel the need to write about my having developed more empathy for women. Having been described as a “manly man,” by a woman who feels she knows me, it has always been difficult for me to understand women. Fortunately, an experience I’ve had has given me more insight into women – shallow though it may still be.

About a year ago, I had learned I had prostate carcinoma, which is now in remission – thanks to a proctectomy, radiation, and hormone therapy. The antitestosterone hormones I need to take for 2 years are turning me into an old woman, thus my newfound empathy.

After the surgery, I found myself leaking – something that I probably only experienced as a child and of which I have little memory. I now have some more empathy for the problems women have with leaking each month or in general – it is a constant preoccupation. The leuprolide shots I am taking are giving me hot flashes, causing me to be more emotional about things I really don’t understand, and apparently I am at risk for getting osteoporosis – all things that happen to women that have been mildly on my radar for years but for which I lacked direct and personal experience.

Since having my testosterone turned off by the leuprolide, my joints are more prone to aches and pains from various injuries over the years. Because I understand that “motion is lotion,” I have some control of this problem. However, the hormone therapy has greatly reduced my endurance, so my exercise tolerance is far more limited – I understand fatigue now. When I was telling another woman who feels she knows me about my experience, she told me it was hormones that made it more difficult to lose weight. And, I am gaining weight.

All in all, I believe my experience has given me more empathy for women, but I realize I still have a very long way to go. Nonetheless, I will continue in my quest to understand the opposite sex, as I am told “women hold up half the sky,” and I have always believed that to be true.

Fortunately, women are ascending in psychiatry and, with some serious dedication, the dearth of scientific understanding of women’s issues will be a thing of the past. I am hoping that women psychiatrists will answer questions that men never even thought of asking, and fill that void of knowledge that we men psychiatrists have in our testosterone-bathed brains.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.

At the risk of too much personal self-disclosure, I feel the need to write about my having developed more empathy for women. Having been described as a “manly man,” by a woman who feels she knows me, it has always been difficult for me to understand women. Fortunately, an experience I’ve had has given me more insight into women – shallow though it may still be.

About a year ago, I had learned I had prostate carcinoma, which is now in remission – thanks to a proctectomy, radiation, and hormone therapy. The antitestosterone hormones I need to take for 2 years are turning me into an old woman, thus my newfound empathy.

After the surgery, I found myself leaking – something that I probably only experienced as a child and of which I have little memory. I now have some more empathy for the problems women have with leaking each month or in general – it is a constant preoccupation. The leuprolide shots I am taking are giving me hot flashes, causing me to be more emotional about things I really don’t understand, and apparently I am at risk for getting osteoporosis – all things that happen to women that have been mildly on my radar for years but for which I lacked direct and personal experience.

Since having my testosterone turned off by the leuprolide, my joints are more prone to aches and pains from various injuries over the years. Because I understand that “motion is lotion,” I have some control of this problem. However, the hormone therapy has greatly reduced my endurance, so my exercise tolerance is far more limited – I understand fatigue now. When I was telling another woman who feels she knows me about my experience, she told me it was hormones that made it more difficult to lose weight. And, I am gaining weight.

All in all, I believe my experience has given me more empathy for women, but I realize I still have a very long way to go. Nonetheless, I will continue in my quest to understand the opposite sex, as I am told “women hold up half the sky,” and I have always believed that to be true.

Fortunately, women are ascending in psychiatry and, with some serious dedication, the dearth of scientific understanding of women’s issues will be a thing of the past. I am hoping that women psychiatrists will answer questions that men never even thought of asking, and fill that void of knowledge that we men psychiatrists have in our testosterone-bathed brains.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.

I was talking to a physical therapy (PT) colleague and she was lamenting how much she hated doing documentation on patients she was treating. I suggested to her that she make her evaluations and progress notes sing. This is a concept I would sometimes use with patients who might be depressed, for example, I would ask them if anything made their heart sing to get an idea how “depressed” they might be. If they were unhappy or sad, I would advise that they engage in “heart singing” activities and behaviors, as I believe it is the “simple pleasures” in life that keep us resilient and persistent.

It is funny, when I was a resident and working in Jackson Park Hospital’s first psychiatric ward in 1972, one day in a note I wrote “I am going to give this acutely psychotic patient the big T – Thorazine to help them get some sleep at night,” I did not really think much about it until one of the nurses brought it to my attention because she thought it was unique – and a funny way of reporting plans in my progress notes.

My PT colleague told me that she remembered the first time she read one of my notes on a patient we were treating together (she needed to know the patient’s psychiatric status before she engaged them in physical therapy), and it struck her that I reported the patient was “befuddled,” and she wondered who would use befuddled in a note (lately, I have started using “flummoxed”). Another time, I was charting on a patient, and I used the word “flapdoodle” to describe the nonsense the patient was spewing (I recall this particular patient told me they graduated from grammar school at 5 years old). Another favorite word of mine that I use to describe nonsense is “claptrap.”

So, I have been making my evaluations and progress notes sing for a very long time, as doing so improves my writing skills, stimulates my thinking, turns the drudgery of charting into some fun, and creates an adventure in writing. This approach and skill has made my charting work easier for me to do – and colleagues actually read my notes.

I have also been a big user of mental status templates to cut down my time. The essential elements of a mental status are in the narrative template, and all I need to do is to edit the verbiage in the template to fit the patient’s presentation so that the mental status sings. Early on, I understood that, to be a good psychiatrist, you needed a good vocabulary so you can speak with as much precision as possible when describing a patient’s mental status.

I was seeing many Alzheimer’s patients at one point. So I developed a special mental status template for them (female and male), so all I had to do to it was cut and paste, and then edit the template to fit the patient like a glove. Template example: This is a xx-year-old female who was appropriately groomed and who was cooperative with the interview, but she could not give much information. She was not hyperactive or lethargic. Her mood was bland, and her affect was flat and bland. Her speech did not contain any relevant information. Thought processes were not evident, although she was awake. I could not get a history of delusions or current auditory or visual hallucinations. Her thought content was nondescript. She was attentive, and her recent and remote memory were poor. Clinical estimate of her intelligence could not be determined. Her judgment and insight were poor. I could not determine whether there was any suicidal or homicidal ideation.

Formulation: This is a xx-year-old female who has a major neurocognitive disorder (formerly known as dementia). She is not overtly psychotic, suicidal, homicidal, or gravely disabled, but her level of functioning leaves a lot to be desired, which is why she needs a sheltered living circumstance.

Dx: Major neurocognitive disorder (formerly known as dementia).

Here’s another example: This is a xx-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic and he had a wide range of affect as he was able to smile, get serious, and be sad (about xxx). His speech was relevant, linear, and goal directed. Thought processes did not show any signs of loose associations, tangentiality, or circumstantiality. He denies any delusions or current auditory or visual hallucinations. His thought content was surrounding xxx. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was xxx average. His judgment and insight were poor as xxx. No report of suicidal or homicidal ideation.

Formulation: xxx. He is not overtly psychotic, suicidal, homicidal, or gravely disabled so I will clear him for psychiatric discharge.

Dx: xxx.

Just me trying to make work a little easier for myself and everyone else.
 

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.

I was talking to a physical therapy (PT) colleague and she was lamenting how much she hated doing documentation on patients she was treating. I suggested to her that she make her evaluations and progress notes sing. This is a concept I would sometimes use with patients who might be depressed, for example, I would ask them if anything made their heart sing to get an idea how “depressed” they might be. If they were unhappy or sad, I would advise that they engage in “heart singing” activities and behaviors, as I believe it is the “simple pleasures” in life that keep us resilient and persistent.

It is funny, when I was a resident and working in Jackson Park Hospital’s first psychiatric ward in 1972, one day in a note I wrote “I am going to give this acutely psychotic patient the big T – Thorazine to help them get some sleep at night,” I did not really think much about it until one of the nurses brought it to my attention because she thought it was unique – and a funny way of reporting plans in my progress notes.

My PT colleague told me that she remembered the first time she read one of my notes on a patient we were treating together (she needed to know the patient’s psychiatric status before she engaged them in physical therapy), and it struck her that I reported the patient was “befuddled,” and she wondered who would use befuddled in a note (lately, I have started using “flummoxed”). Another time, I was charting on a patient, and I used the word “flapdoodle” to describe the nonsense the patient was spewing (I recall this particular patient told me they graduated from grammar school at 5 years old). Another favorite word of mine that I use to describe nonsense is “claptrap.”

So, I have been making my evaluations and progress notes sing for a very long time, as doing so improves my writing skills, stimulates my thinking, turns the drudgery of charting into some fun, and creates an adventure in writing. This approach and skill has made my charting work easier for me to do – and colleagues actually read my notes.

I have also been a big user of mental status templates to cut down my time. The essential elements of a mental status are in the narrative template, and all I need to do is to edit the verbiage in the template to fit the patient’s presentation so that the mental status sings. Early on, I understood that, to be a good psychiatrist, you needed a good vocabulary so you can speak with as much precision as possible when describing a patient’s mental status.

I was seeing many Alzheimer’s patients at one point. So I developed a special mental status template for them (female and male), so all I had to do to it was cut and paste, and then edit the template to fit the patient like a glove. Template example: This is a xx-year-old female who was appropriately groomed and who was cooperative with the interview, but she could not give much information. She was not hyperactive or lethargic. Her mood was bland, and her affect was flat and bland. Her speech did not contain any relevant information. Thought processes were not evident, although she was awake. I could not get a history of delusions or current auditory or visual hallucinations. Her thought content was nondescript. She was attentive, and her recent and remote memory were poor. Clinical estimate of her intelligence could not be determined. Her judgment and insight were poor. I could not determine whether there was any suicidal or homicidal ideation.

Formulation: This is a xx-year-old female who has a major neurocognitive disorder (formerly known as dementia). She is not overtly psychotic, suicidal, homicidal, or gravely disabled, but her level of functioning leaves a lot to be desired, which is why she needs a sheltered living circumstance.

Dx: Major neurocognitive disorder (formerly known as dementia).

Here’s another example: This is a xx-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic and he had a wide range of affect as he was able to smile, get serious, and be sad (about xxx). His speech was relevant, linear, and goal directed. Thought processes did not show any signs of loose associations, tangentiality, or circumstantiality. He denies any delusions or current auditory or visual hallucinations. His thought content was surrounding xxx. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was xxx average. His judgment and insight were poor as xxx. No report of suicidal or homicidal ideation.

Formulation: xxx. He is not overtly psychotic, suicidal, homicidal, or gravely disabled so I will clear him for psychiatric discharge.

Dx: xxx.

Just me trying to make work a little easier for myself and everyone else.
 

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.

I was talking to a physical therapy (PT) colleague and she was lamenting how much she hated doing documentation on patients she was treating. I suggested to her that she make her evaluations and progress notes sing. This is a concept I would sometimes use with patients who might be depressed, for example, I would ask them if anything made their heart sing to get an idea how “depressed” they might be. If they were unhappy or sad, I would advise that they engage in “heart singing” activities and behaviors, as I believe it is the “simple pleasures” in life that keep us resilient and persistent.

It is funny, when I was a resident and working in Jackson Park Hospital’s first psychiatric ward in 1972, one day in a note I wrote “I am going to give this acutely psychotic patient the big T – Thorazine to help them get some sleep at night,” I did not really think much about it until one of the nurses brought it to my attention because she thought it was unique – and a funny way of reporting plans in my progress notes.

My PT colleague told me that she remembered the first time she read one of my notes on a patient we were treating together (she needed to know the patient’s psychiatric status before she engaged them in physical therapy), and it struck her that I reported the patient was “befuddled,” and she wondered who would use befuddled in a note (lately, I have started using “flummoxed”). Another time, I was charting on a patient, and I used the word “flapdoodle” to describe the nonsense the patient was spewing (I recall this particular patient told me they graduated from grammar school at 5 years old). Another favorite word of mine that I use to describe nonsense is “claptrap.”

So, I have been making my evaluations and progress notes sing for a very long time, as doing so improves my writing skills, stimulates my thinking, turns the drudgery of charting into some fun, and creates an adventure in writing. This approach and skill has made my charting work easier for me to do – and colleagues actually read my notes.

I have also been a big user of mental status templates to cut down my time. The essential elements of a mental status are in the narrative template, and all I need to do is to edit the verbiage in the template to fit the patient’s presentation so that the mental status sings. Early on, I understood that, to be a good psychiatrist, you needed a good vocabulary so you can speak with as much precision as possible when describing a patient’s mental status.

I was seeing many Alzheimer’s patients at one point. So I developed a special mental status template for them (female and male), so all I had to do to it was cut and paste, and then edit the template to fit the patient like a glove. Template example: This is a xx-year-old female who was appropriately groomed and who was cooperative with the interview, but she could not give much information. She was not hyperactive or lethargic. Her mood was bland, and her affect was flat and bland. Her speech did not contain any relevant information. Thought processes were not evident, although she was awake. I could not get a history of delusions or current auditory or visual hallucinations. Her thought content was nondescript. She was attentive, and her recent and remote memory were poor. Clinical estimate of her intelligence could not be determined. Her judgment and insight were poor. I could not determine whether there was any suicidal or homicidal ideation.

Formulation: This is a xx-year-old female who has a major neurocognitive disorder (formerly known as dementia). She is not overtly psychotic, suicidal, homicidal, or gravely disabled, but her level of functioning leaves a lot to be desired, which is why she needs a sheltered living circumstance.

Dx: Major neurocognitive disorder (formerly known as dementia).

Here’s another example: This is a xx-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic and he had a wide range of affect as he was able to smile, get serious, and be sad (about xxx). His speech was relevant, linear, and goal directed. Thought processes did not show any signs of loose associations, tangentiality, or circumstantiality. He denies any delusions or current auditory or visual hallucinations. His thought content was surrounding xxx. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was xxx average. His judgment and insight were poor as xxx. No report of suicidal or homicidal ideation.

Formulation: xxx. He is not overtly psychotic, suicidal, homicidal, or gravely disabled so I will clear him for psychiatric discharge.

Dx: xxx.

Just me trying to make work a little easier for myself and everyone else.
 

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.

I have been amazed at psychiatrists who could see a patient who was obviously acutely psychotic and tell whether they had schizophrenia or bipolar disorder while the patient was acutely psychotic. I am amazed because I cannot do it, although I used to think I could.

Earlier in my career, I would see patients who were floridly psychotic who would have all the symptoms of schizophrenia, and I would think “Yep, they have schizophrenia, all right.” After all, when I was starting out in psychiatry, I thought that Schneiderian first-rank symptoms were pathognomonic of schizophrenia, but research later showed that these first-rank symptoms could also be characteristic of dissociative disorder.

I quickly learned that some of the patients I thought had schizophrenia would recover and return to their premorbid level of functioning after the psychotic episode. Accordingly, by definition – for example, there was not a deterioration of psychosocial functioning after their psychotic episode – I would have to revise their diagnosis to bipolar disorder.

Finally, I got hip and realized that I could not determine patients’ diagnoses when they were acutely psychotic, and I started diagnosing patients as having a psychosis not otherwise specified (NOS).

Of course, using the NOS designation made many of my academic colleagues scoff at my diagnostic skills, but then I read the DSM-IV Guidebook by Frances, First, and Pincus (1995), and it was explained the NOS designation was wrongly maligned. Apparently, it was learned that there was extensive comorbidity between various diagnostic categories, and, it was explicated, approximately 50% of patients could not fit neatly into any specific diagnostic category. In fact, regarding psychotic and affective disorders, depending on how good a history patients and/or their family could deliver, it would sometimes take the resolution of the patients’ psychosis before it became clear that they were or were not going to return to premorbid functioning or continue to show significant psychosocial deterioration.

Since psychiatrists do not yet have objective diagnostic tests to determine whether a psychotic patient has some form of schizophrenia or bipolar disorder, it seems to me that we should be more prudent about diagnosing a patient with either two diagnoses, because I do not think we can tell the patients’ post psychotic outcomes.

I recently had one patient who had been hospitalized for 39 days, and, who was so acutely floridly psychotic, I did not think she was going to recover. She was on antipsychotic medication at bedtime and other mood stabilizers during the day, but she had to be in soft restraints for a significant period of time and was getting several antipsychotic medication injections daily because she was extremely rambunctious and dangerously disruptive on the medical-surgical/psychiatric floor. Finally, when I reluctantly added lithium to her treatment regimen (I was unenthusiastic about putting her on lithium, which had worked for her in the past, because her kidneys were not functioning well and she had arrived at the hospital with lithium toxicity), she recovered. The transformation was remarkable.

So, it seems to me that a functional outcome assessment should determine the difference between patients who have bipolar disorder and schizophrenia as, by definition, if you do not have a deterioration in your psychosocial functioning you probably have bipolar disorder, and if you do have a deterioration in your psychosocial functioning you probably have schizophrenia. From a practical standpoint, post psychotic functioning is a major distinction between these two diagnoses by definition, and, since we don’t have objective measures to delineate bipolar disorder from schizophrenia (some studies have shown there is remarkable overlap between these two disorders), it seems to me we should give more consideration to post psychotic functioning, instead of trying to nail the patients’ diagnoses when they are acutely psychotic.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s medical/surgical-psychiatry inpatient unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Be sure to check out Dr. Bell’s new book Fetal Alcohol Exposure in the African-American Community.

I have been amazed at psychiatrists who could see a patient who was obviously acutely psychotic and tell whether they had schizophrenia or bipolar disorder while the patient was acutely psychotic. I am amazed because I cannot do it, although I used to think I could.

Earlier in my career, I would see patients who were floridly psychotic who would have all the symptoms of schizophrenia, and I would think “Yep, they have schizophrenia, all right.” After all, when I was starting out in psychiatry, I thought that Schneiderian first-rank symptoms were pathognomonic of schizophrenia, but research later showed that these first-rank symptoms could also be characteristic of dissociative disorder.

I quickly learned that some of the patients I thought had schizophrenia would recover and return to their premorbid level of functioning after the psychotic episode. Accordingly, by definition – for example, there was not a deterioration of psychosocial functioning after their psychotic episode – I would have to revise their diagnosis to bipolar disorder.

Finally, I got hip and realized that I could not determine patients’ diagnoses when they were acutely psychotic, and I started diagnosing patients as having a psychosis not otherwise specified (NOS).

Of course, using the NOS designation made many of my academic colleagues scoff at my diagnostic skills, but then I read the DSM-IV Guidebook by Frances, First, and Pincus (1995), and it was explained the NOS designation was wrongly maligned. Apparently, it was learned that there was extensive comorbidity between various diagnostic categories, and, it was explicated, approximately 50% of patients could not fit neatly into any specific diagnostic category. In fact, regarding psychotic and affective disorders, depending on how good a history patients and/or their family could deliver, it would sometimes take the resolution of the patients’ psychosis before it became clear that they were or were not going to return to premorbid functioning or continue to show significant psychosocial deterioration.

Since psychiatrists do not yet have objective diagnostic tests to determine whether a psychotic patient has some form of schizophrenia or bipolar disorder, it seems to me that we should be more prudent about diagnosing a patient with either two diagnoses, because I do not think we can tell the patients’ post psychotic outcomes.

I recently had one patient who had been hospitalized for 39 days, and, who was so acutely floridly psychotic, I did not think she was going to recover. She was on antipsychotic medication at bedtime and other mood stabilizers during the day, but she had to be in soft restraints for a significant period of time and was getting several antipsychotic medication injections daily because she was extremely rambunctious and dangerously disruptive on the medical-surgical/psychiatric floor. Finally, when I reluctantly added lithium to her treatment regimen (I was unenthusiastic about putting her on lithium, which had worked for her in the past, because her kidneys were not functioning well and she had arrived at the hospital with lithium toxicity), she recovered. The transformation was remarkable.

So, it seems to me that a functional outcome assessment should determine the difference between patients who have bipolar disorder and schizophrenia as, by definition, if you do not have a deterioration in your psychosocial functioning you probably have bipolar disorder, and if you do have a deterioration in your psychosocial functioning you probably have schizophrenia. From a practical standpoint, post psychotic functioning is a major distinction between these two diagnoses by definition, and, since we don’t have objective measures to delineate bipolar disorder from schizophrenia (some studies have shown there is remarkable overlap between these two disorders), it seems to me we should give more consideration to post psychotic functioning, instead of trying to nail the patients’ diagnoses when they are acutely psychotic.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s medical/surgical-psychiatry inpatient unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Be sure to check out Dr. Bell’s new book Fetal Alcohol Exposure in the African-American Community.

I have been amazed at psychiatrists who could see a patient who was obviously acutely psychotic and tell whether they had schizophrenia or bipolar disorder while the patient was acutely psychotic. I am amazed because I cannot do it, although I used to think I could.

Earlier in my career, I would see patients who were floridly psychotic who would have all the symptoms of schizophrenia, and I would think “Yep, they have schizophrenia, all right.” After all, when I was starting out in psychiatry, I thought that Schneiderian first-rank symptoms were pathognomonic of schizophrenia, but research later showed that these first-rank symptoms could also be characteristic of dissociative disorder.

I quickly learned that some of the patients I thought had schizophrenia would recover and return to their premorbid level of functioning after the psychotic episode. Accordingly, by definition – for example, there was not a deterioration of psychosocial functioning after their psychotic episode – I would have to revise their diagnosis to bipolar disorder.

Finally, I got hip and realized that I could not determine patients’ diagnoses when they were acutely psychotic, and I started diagnosing patients as having a psychosis not otherwise specified (NOS).

Of course, using the NOS designation made many of my academic colleagues scoff at my diagnostic skills, but then I read the DSM-IV Guidebook by Frances, First, and Pincus (1995), and it was explained the NOS designation was wrongly maligned. Apparently, it was learned that there was extensive comorbidity between various diagnostic categories, and, it was explicated, approximately 50% of patients could not fit neatly into any specific diagnostic category. In fact, regarding psychotic and affective disorders, depending on how good a history patients and/or their family could deliver, it would sometimes take the resolution of the patients’ psychosis before it became clear that they were or were not going to return to premorbid functioning or continue to show significant psychosocial deterioration.

Since psychiatrists do not yet have objective diagnostic tests to determine whether a psychotic patient has some form of schizophrenia or bipolar disorder, it seems to me that we should be more prudent about diagnosing a patient with either two diagnoses, because I do not think we can tell the patients’ post psychotic outcomes.

I recently had one patient who had been hospitalized for 39 days, and, who was so acutely floridly psychotic, I did not think she was going to recover. She was on antipsychotic medication at bedtime and other mood stabilizers during the day, but she had to be in soft restraints for a significant period of time and was getting several antipsychotic medication injections daily because she was extremely rambunctious and dangerously disruptive on the medical-surgical/psychiatric floor. Finally, when I reluctantly added lithium to her treatment regimen (I was unenthusiastic about putting her on lithium, which had worked for her in the past, because her kidneys were not functioning well and she had arrived at the hospital with lithium toxicity), she recovered. The transformation was remarkable.

So, it seems to me that a functional outcome assessment should determine the difference between patients who have bipolar disorder and schizophrenia as, by definition, if you do not have a deterioration in your psychosocial functioning you probably have bipolar disorder, and if you do have a deterioration in your psychosocial functioning you probably have schizophrenia. From a practical standpoint, post psychotic functioning is a major distinction between these two diagnoses by definition, and, since we don’t have objective measures to delineate bipolar disorder from schizophrenia (some studies have shown there is remarkable overlap between these two disorders), it seems to me we should give more consideration to post psychotic functioning, instead of trying to nail the patients’ diagnoses when they are acutely psychotic.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s medical/surgical-psychiatry inpatient unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Be sure to check out Dr. Bell’s new book Fetal Alcohol Exposure in the African-American Community.

It used to be difficult to conceive of writing about climate change in light of the illnesses we psychiatrists treat. But talking about climate change has become unavoidable. Sometimes, it seems that things weigh heavy on my heart, and I have to write about them – especially when it is serious.

David Alan Pollack, MD, has been talking about climate change for some years now, and while I understood his concern, I had yet to see the psychological effects up close and personal. After all, I live in Chicago, and we are surrounded by concrete and asphalt.

Thankfully, I also travel, and I get a chance to get into nature. While in Hawaii at the American College of Psychiatrists annual meeting in February, I went snorkeling in Hanauma Bay. I saw coral and fish. The problem is I have a very vivid memories of snorkeling in that exact same nature preserve, which also was a Marine Life Conservation District in 1972 while I was attending the American Psychiatric Association annual meeting.

The contrast between the two experiences leaves me with a glum, sad, disappointed, heart-broken feeling because it was an intimate and personal experience with climate change. In 1972, I saw every type of coral imaginable: brain coral, club finger coral, elk coral, great star coral, pillar coral, staghorn coral, table coral, and tube coral. If I remember correctly, there were corky sea fingers and sea fans, but not sea turtles. In 1972, I saw bigeyefish, damselfish, doctorfish, filefish, goatfish, gobies, hogfish, lemon butterflyfish, lizardfish, parrottfish, porcupinefish, pufferfish, queen angelfish, rock beauties, sergeant majors, soldierfish, spot-tail spot-tail butterflyfish, Spanish hogfish, squirrelfish, tangs, trunkfish, or any bluehead or yellowhead wrasses.

In 2019, I saw two pieces of coral less that 9 inches in diameter and not a single sea urchin. There were maybe three types of tropical fish that I was unfamiliar with seeing. The difference between what I saw in 1972 and what I saw in 2019 was like the difference between the rain forest in Puerto Rico and the dunes of the Sahara Desert.

Sure, I have heard David talk about the mental health effects of climate change on stress, anxiety, and depression, and I have always thought that he was right. But to see climate change up close and personal is a sobering experience. Lately, I have found myself apologizing to children I know. I apologize to them for being part of the system and process that is destroying the planet – and leaving them with a hot mess.

At this point, it seems to me that we cannot just try to save the planet by being better stewards of our garbage and pointing out measurable indicators of climate change. We need to actively rather than passively try to save the planet. Of course, the question is who will pay for the active efforts to depollute Earth. From what I saw for myself in Hanauma Bay, I don’t think we have much time. So I am hoping that more people will take the issue of climate change seriously.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Check out Dr. Bell’s new book, “Fetal Alcohol Exposure in the African-American Community,” at https://thirdworldpressfoundation.org/product/pre-order-fetal-alcohol-exposure-in-the-african-american-community/.
 

It used to be difficult to conceive of writing about climate change in light of the illnesses we psychiatrists treat. But talking about climate change has become unavoidable. Sometimes, it seems that things weigh heavy on my heart, and I have to write about them – especially when it is serious.

David Alan Pollack, MD, has been talking about climate change for some years now, and while I understood his concern, I had yet to see the psychological effects up close and personal. After all, I live in Chicago, and we are surrounded by concrete and asphalt.

Thankfully, I also travel, and I get a chance to get into nature. While in Hawaii at the American College of Psychiatrists annual meeting in February, I went snorkeling in Hanauma Bay. I saw coral and fish. The problem is I have a very vivid memories of snorkeling in that exact same nature preserve, which also was a Marine Life Conservation District in 1972 while I was attending the American Psychiatric Association annual meeting.

The contrast between the two experiences leaves me with a glum, sad, disappointed, heart-broken feeling because it was an intimate and personal experience with climate change. In 1972, I saw every type of coral imaginable: brain coral, club finger coral, elk coral, great star coral, pillar coral, staghorn coral, table coral, and tube coral. If I remember correctly, there were corky sea fingers and sea fans, but not sea turtles. In 1972, I saw bigeyefish, damselfish, doctorfish, filefish, goatfish, gobies, hogfish, lemon butterflyfish, lizardfish, parrottfish, porcupinefish, pufferfish, queen angelfish, rock beauties, sergeant majors, soldierfish, spot-tail spot-tail butterflyfish, Spanish hogfish, squirrelfish, tangs, trunkfish, or any bluehead or yellowhead wrasses.

In 2019, I saw two pieces of coral less that 9 inches in diameter and not a single sea urchin. There were maybe three types of tropical fish that I was unfamiliar with seeing. The difference between what I saw in 1972 and what I saw in 2019 was like the difference between the rain forest in Puerto Rico and the dunes of the Sahara Desert.

Sure, I have heard David talk about the mental health effects of climate change on stress, anxiety, and depression, and I have always thought that he was right. But to see climate change up close and personal is a sobering experience. Lately, I have found myself apologizing to children I know. I apologize to them for being part of the system and process that is destroying the planet – and leaving them with a hot mess.

At this point, it seems to me that we cannot just try to save the planet by being better stewards of our garbage and pointing out measurable indicators of climate change. We need to actively rather than passively try to save the planet. Of course, the question is who will pay for the active efforts to depollute Earth. From what I saw for myself in Hanauma Bay, I don’t think we have much time. So I am hoping that more people will take the issue of climate change seriously.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Check out Dr. Bell’s new book, “Fetal Alcohol Exposure in the African-American Community,” at https://thirdworldpressfoundation.org/product/pre-order-fetal-alcohol-exposure-in-the-african-american-community/.
 

It used to be difficult to conceive of writing about climate change in light of the illnesses we psychiatrists treat. But talking about climate change has become unavoidable. Sometimes, it seems that things weigh heavy on my heart, and I have to write about them – especially when it is serious.

David Alan Pollack, MD, has been talking about climate change for some years now, and while I understood his concern, I had yet to see the psychological effects up close and personal. After all, I live in Chicago, and we are surrounded by concrete and asphalt.

Thankfully, I also travel, and I get a chance to get into nature. While in Hawaii at the American College of Psychiatrists annual meeting in February, I went snorkeling in Hanauma Bay. I saw coral and fish. The problem is I have a very vivid memories of snorkeling in that exact same nature preserve, which also was a Marine Life Conservation District in 1972 while I was attending the American Psychiatric Association annual meeting.

The contrast between the two experiences leaves me with a glum, sad, disappointed, heart-broken feeling because it was an intimate and personal experience with climate change. In 1972, I saw every type of coral imaginable: brain coral, club finger coral, elk coral, great star coral, pillar coral, staghorn coral, table coral, and tube coral. If I remember correctly, there were corky sea fingers and sea fans, but not sea turtles. In 1972, I saw bigeyefish, damselfish, doctorfish, filefish, goatfish, gobies, hogfish, lemon butterflyfish, lizardfish, parrottfish, porcupinefish, pufferfish, queen angelfish, rock beauties, sergeant majors, soldierfish, spot-tail spot-tail butterflyfish, Spanish hogfish, squirrelfish, tangs, trunkfish, or any bluehead or yellowhead wrasses.

In 2019, I saw two pieces of coral less that 9 inches in diameter and not a single sea urchin. There were maybe three types of tropical fish that I was unfamiliar with seeing. The difference between what I saw in 1972 and what I saw in 2019 was like the difference between the rain forest in Puerto Rico and the dunes of the Sahara Desert.

Sure, I have heard David talk about the mental health effects of climate change on stress, anxiety, and depression, and I have always thought that he was right. But to see climate change up close and personal is a sobering experience. Lately, I have found myself apologizing to children I know. I apologize to them for being part of the system and process that is destroying the planet – and leaving them with a hot mess.

At this point, it seems to me that we cannot just try to save the planet by being better stewards of our garbage and pointing out measurable indicators of climate change. We need to actively rather than passively try to save the planet. Of course, the question is who will pay for the active efforts to depollute Earth. From what I saw for myself in Hanauma Bay, I don’t think we have much time. So I am hoping that more people will take the issue of climate change seriously.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Check out Dr. Bell’s new book, “Fetal Alcohol Exposure in the African-American Community,” at https://thirdworldpressfoundation.org/product/pre-order-fetal-alcohol-exposure-in-the-african-american-community/.
 

I have the unfortunate task of trying to teach medical students about psychiatry. I say “unfortunate,” as most of them find psychiatry a difficult art to understand, and they seem reluctant to classify psychiatry as a branch of medicine.

Wavebreakmedia/Thinkstock

In my efforts to keep things simple, I tell that them psychiatry is one of the most difficult branches of medicine as there are very few objective measures we can rely on to make sense of people’s behavior. Regrettably, the American Psychiatric Association’s Diagnostic and Statistical Manual only seems to confuse them more. So, I remind them that, in medicine, 90%-95% of diagnoses can be obtained from doing a good history, and, if we are lucky a drug level will show drugs in the system, a CT scan without contrast will show cerebral atrophy, or there will be a lab result that will be abnormal and point to a diagnosis. But mostly what they will be seeing is unusual behavior they are unable to classify.

So I try to make psychiatric diagnosis more manageable for them by telling them there are essentially five overarching categories of psychiatric illness: identifiable brain damage, psychosis, affective disorders, anxiety disorders, and personality disorders. Under the brain damage category, I include the short- and long-term effects of drugs, major neurocognitive disorders (called dementia before DSM-5), cerebrovascular infarcts, traumatic brain injury, and neurodevelopmental disorders. For their exams and, if they are interested in psychiatry, I tell them to study the DSM. I explain to them that when I was in medical school my dermatology professor told us that if we could recognize the 10 most common dermatologic disorders, we would be able to recognize 90% of the skin disorders we would see. It is similar in psychiatry – thus, my five categories.

However, because I do not want them thinking that only schizophrenia causes psychosis, I let them know that at least 40 different factors cause people to be psychotic indicated by auditory hallucinations. Those 40 factors are: 1) acute alcohol intoxication, 2) alcohol withdrawal, 3) alcoholism, 4) Alzheimer’s disease, 5) benzodiazepine withdrawal, 6) cocaine abuse and addiction, 7) chemical poisoning, 8) dehydration, 9) delirium, 10) dissociative disorders, 11) electrolyte imbalances, 12) encephalopathy of various forms, 13) ecstasy, 14) extreme fatigue, 15) falling asleep, 16) fetal alcohol exposure, 17) grief, 18) hallucinogen use, 19) heroin abuse and dependence, 20) high fever, 21) hyperglycemia, 22) hypoglycemia, 23) intellectual disability, 24) lupus, 25) major depression, 26) mania, 27) methamphetamine use, 28) Parkinson’s disease, 29) phencyclidine, 30) postictal states, 31) posttraumatic stress disorder, 32) schizoid or schizotypal personality disorder, 33) schizophrenia, 34) sleep deprivation, 35) sleep paralysis, 36) solvent abuse, 37) traumatic brain injury, 38) temporal lobe epilepsy, 39) uremia. Lastly, I ask them about No. 40 – “normal” (For example, have you ever been walking down the street and thought you heard someone calling your name, but when you turned around no one was there?). Of course, there are many more causes of psychosis, but keeping it simple makes the principle easier to remember.

Regarding affective disorders, I point out to them, as I did in a previous column, that there is a huge difference between major depressive disorders, unhappiness, or sadness, grief, and demoralization. Regarding anxiety disorders, I let the medical students know that, like personality disorders, there is a lot of comorbidity. Yet, if they can distinguish brain damage, psychosis, and affective disorders from anxiety and personality disorders, that will be good enough.

In keeping with trying to help medical students not make assumptions, I always ask them what’s wrong with people who wash their hands 30 times a day. Invariably, the answer is obsessive-compulsive disorder. So, next I ask: Isn’t it possible that the person who washes his hands 30 times a day is a surgeon – or perhaps a patient with schizophrenia who thinks that Martians are beaming germs to his hands?

I guess I raise this issue because I am concerned with the future of psychiatry, and I think that my approach to medical school education provides a framework that can help students learn how to think about and provide care for psychiatric patients.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of the Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. If you have tricks of the medical school teaching trade that you would like to share, email Dr. Bell at cpnews@mededge.com.

I have the unfortunate task of trying to teach medical students about psychiatry. I say “unfortunate,” as most of them find psychiatry a difficult art to understand, and they seem reluctant to classify psychiatry as a branch of medicine.

Wavebreakmedia/Thinkstock

In my efforts to keep things simple, I tell that them psychiatry is one of the most difficult branches of medicine as there are very few objective measures we can rely on to make sense of people’s behavior. Regrettably, the American Psychiatric Association’s Diagnostic and Statistical Manual only seems to confuse them more. So, I remind them that, in medicine, 90%-95% of diagnoses can be obtained from doing a good history, and, if we are lucky a drug level will show drugs in the system, a CT scan without contrast will show cerebral atrophy, or there will be a lab result that will be abnormal and point to a diagnosis. But mostly what they will be seeing is unusual behavior they are unable to classify.

So I try to make psychiatric diagnosis more manageable for them by telling them there are essentially five overarching categories of psychiatric illness: identifiable brain damage, psychosis, affective disorders, anxiety disorders, and personality disorders. Under the brain damage category, I include the short- and long-term effects of drugs, major neurocognitive disorders (called dementia before DSM-5), cerebrovascular infarcts, traumatic brain injury, and neurodevelopmental disorders. For their exams and, if they are interested in psychiatry, I tell them to study the DSM. I explain to them that when I was in medical school my dermatology professor told us that if we could recognize the 10 most common dermatologic disorders, we would be able to recognize 90% of the skin disorders we would see. It is similar in psychiatry – thus, my five categories.

However, because I do not want them thinking that only schizophrenia causes psychosis, I let them know that at least 40 different factors cause people to be psychotic indicated by auditory hallucinations. Those 40 factors are: 1) acute alcohol intoxication, 2) alcohol withdrawal, 3) alcoholism, 4) Alzheimer’s disease, 5) benzodiazepine withdrawal, 6) cocaine abuse and addiction, 7) chemical poisoning, 8) dehydration, 9) delirium, 10) dissociative disorders, 11) electrolyte imbalances, 12) encephalopathy of various forms, 13) ecstasy, 14) extreme fatigue, 15) falling asleep, 16) fetal alcohol exposure, 17) grief, 18) hallucinogen use, 19) heroin abuse and dependence, 20) high fever, 21) hyperglycemia, 22) hypoglycemia, 23) intellectual disability, 24) lupus, 25) major depression, 26) mania, 27) methamphetamine use, 28) Parkinson’s disease, 29) phencyclidine, 30) postictal states, 31) posttraumatic stress disorder, 32) schizoid or schizotypal personality disorder, 33) schizophrenia, 34) sleep deprivation, 35) sleep paralysis, 36) solvent abuse, 37) traumatic brain injury, 38) temporal lobe epilepsy, 39) uremia. Lastly, I ask them about No. 40 – “normal” (For example, have you ever been walking down the street and thought you heard someone calling your name, but when you turned around no one was there?). Of course, there are many more causes of psychosis, but keeping it simple makes the principle easier to remember.

Regarding affective disorders, I point out to them, as I did in a previous column, that there is a huge difference between major depressive disorders, unhappiness, or sadness, grief, and demoralization. Regarding anxiety disorders, I let the medical students know that, like personality disorders, there is a lot of comorbidity. Yet, if they can distinguish brain damage, psychosis, and affective disorders from anxiety and personality disorders, that will be good enough.

In keeping with trying to help medical students not make assumptions, I always ask them what’s wrong with people who wash their hands 30 times a day. Invariably, the answer is obsessive-compulsive disorder. So, next I ask: Isn’t it possible that the person who washes his hands 30 times a day is a surgeon – or perhaps a patient with schizophrenia who thinks that Martians are beaming germs to his hands?

I guess I raise this issue because I am concerned with the future of psychiatry, and I think that my approach to medical school education provides a framework that can help students learn how to think about and provide care for psychiatric patients.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of the Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. If you have tricks of the medical school teaching trade that you would like to share, email Dr. Bell at cpnews@mededge.com.

I have the unfortunate task of trying to teach medical students about psychiatry. I say “unfortunate,” as most of them find psychiatry a difficult art to understand, and they seem reluctant to classify psychiatry as a branch of medicine.

Wavebreakmedia/Thinkstock

In my efforts to keep things simple, I tell that them psychiatry is one of the most difficult branches of medicine as there are very few objective measures we can rely on to make sense of people’s behavior. Regrettably, the American Psychiatric Association’s Diagnostic and Statistical Manual only seems to confuse them more. So, I remind them that, in medicine, 90%-95% of diagnoses can be obtained from doing a good history, and, if we are lucky a drug level will show drugs in the system, a CT scan without contrast will show cerebral atrophy, or there will be a lab result that will be abnormal and point to a diagnosis. But mostly what they will be seeing is unusual behavior they are unable to classify.

So I try to make psychiatric diagnosis more manageable for them by telling them there are essentially five overarching categories of psychiatric illness: identifiable brain damage, psychosis, affective disorders, anxiety disorders, and personality disorders. Under the brain damage category, I include the short- and long-term effects of drugs, major neurocognitive disorders (called dementia before DSM-5), cerebrovascular infarcts, traumatic brain injury, and neurodevelopmental disorders. For their exams and, if they are interested in psychiatry, I tell them to study the DSM. I explain to them that when I was in medical school my dermatology professor told us that if we could recognize the 10 most common dermatologic disorders, we would be able to recognize 90% of the skin disorders we would see. It is similar in psychiatry – thus, my five categories.

However, because I do not want them thinking that only schizophrenia causes psychosis, I let them know that at least 40 different factors cause people to be psychotic indicated by auditory hallucinations. Those 40 factors are: 1) acute alcohol intoxication, 2) alcohol withdrawal, 3) alcoholism, 4) Alzheimer’s disease, 5) benzodiazepine withdrawal, 6) cocaine abuse and addiction, 7) chemical poisoning, 8) dehydration, 9) delirium, 10) dissociative disorders, 11) electrolyte imbalances, 12) encephalopathy of various forms, 13) ecstasy, 14) extreme fatigue, 15) falling asleep, 16) fetal alcohol exposure, 17) grief, 18) hallucinogen use, 19) heroin abuse and dependence, 20) high fever, 21) hyperglycemia, 22) hypoglycemia, 23) intellectual disability, 24) lupus, 25) major depression, 26) mania, 27) methamphetamine use, 28) Parkinson’s disease, 29) phencyclidine, 30) postictal states, 31) posttraumatic stress disorder, 32) schizoid or schizotypal personality disorder, 33) schizophrenia, 34) sleep deprivation, 35) sleep paralysis, 36) solvent abuse, 37) traumatic brain injury, 38) temporal lobe epilepsy, 39) uremia. Lastly, I ask them about No. 40 – “normal” (For example, have you ever been walking down the street and thought you heard someone calling your name, but when you turned around no one was there?). Of course, there are many more causes of psychosis, but keeping it simple makes the principle easier to remember.

Regarding affective disorders, I point out to them, as I did in a previous column, that there is a huge difference between major depressive disorders, unhappiness, or sadness, grief, and demoralization. Regarding anxiety disorders, I let the medical students know that, like personality disorders, there is a lot of comorbidity. Yet, if they can distinguish brain damage, psychosis, and affective disorders from anxiety and personality disorders, that will be good enough.

In keeping with trying to help medical students not make assumptions, I always ask them what’s wrong with people who wash their hands 30 times a day. Invariably, the answer is obsessive-compulsive disorder. So, next I ask: Isn’t it possible that the person who washes his hands 30 times a day is a surgeon – or perhaps a patient with schizophrenia who thinks that Martians are beaming germs to his hands?

I guess I raise this issue because I am concerned with the future of psychiatry, and I think that my approach to medical school education provides a framework that can help students learn how to think about and provide care for psychiatric patients.

Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of the Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. If you have tricks of the medical school teaching trade that you would like to share, email Dr. Bell at cpnews@mededge.com.

Finally, the evidence is in: Three evidence-based studies show that perinatal choline supports proper neurodevelopment in fetuses.^1,2,3

As anyone who has been following my prevention efforts knows, 4 out of 10 patients at Jackson Park Hospital on Chicago’s Southside who presented to their family medicine clinic for psychiatric care have clinical profiles that are consistent with neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE).⁴ Furthermore, since only a little can be done to ameliorate these patients’ psychopathology, I have sought out prevention interventions to stem the tide of what I have thought was a silent epidemic (“occult prenatal alcohol exposure”) for decades.

So I have been heartened that there is some sound science to suggest that perinatal choline supplementation could help. That reality, along with the American Medical Association’s resolution to support evidence-based amounts of choline in all prenatal vitamins, spurred the University of Illinois at Chicago to do something.

Thanks to the support of Enrico Benedetti, MD, professor and head of the department of surgery at the University of Illinois at Chicago, pregnant women will be offered choline supplements to support their fetuses’ neurodevelopment. In addition, there will be a video streaming in the obstetrical waiting rooms at the University of Illinois at Chicago/Mile Square clinics explaining the need for choline supplementation.

Other efforts are afoot aimed at getting this prevention intervention up and running. For example, Yavar Moghimi, MD, who is the behavioral health director for a Medicaid managed care organization in Washington, recently informed me that its clinical policy committee approved a policy highlighting the evidence behind choline supplements during pregnancy.

I am hoping the University of Illinois at Chicago initiative, entitled the “Healthy Prenatal Brain Program” will help all women by preventing the unrecognized problem I have seen among African American women who engage in social drinking before they realize that they are pregnant.⁵ After all, the problem of choline deficiency is not tied simply to prenatal alcohol exposure but also to dietary habits. For example, a study by Helen H. Jensen, PhD, and her associates found that 90% of pregnant women do not get enough choline.⁶ It is just that low-income people are the “canaries in the coal mine” when it comes to being alerted to major public health problems in America.

Another positive development is a website set up by Robert R. Freedman, MD, former chairman of the psychiatry department at the University of Colorado Denver. The site, called prenataldoctoradvice.com, provides guidance to patients about steps they can take, such as taking choline supplements during pregnancy, to improve their children's brain development and mental health.

The public health fix we are suggesting in not difficult; after all, choline is an over-the-counter nutrient, and it does not have to be prescribed by a physician. Ideally, the public health initiatives being advocated are so affordable and easy to implement that this practice will become ubiquitous, and our children will be healthier as a result. It is just a matter of taking action. Now that the evidence is finally in that perinatal choline supplements support proper neurodevelopment in fetuses, we all should move forward – and do something.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit in Chicago and chairman of the department of psychiatry at Windsor University, St. Kitts, USVI. He also is clinical professor emeritus in the department of psychiatry at the University of Illinois at Chicago; former president/CEO of Community Mental Health Council; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago.

References

1. Alcohol Clin Exp Res. 2018 Jul;42(7):1327-41.

2. Am J Psychiatry. 2016 May 1;173(5):509-16.

3. Alcohol. 2015 Nov;49(7):647-56.

4. Psychiatr Serv. 2015 May 1;66(5):539-42.

5. MDedge Psychcast. 2018 Oct 17. Fetal alcohol spectrum disorder, part II.

6. The FASEB Journal. 2007;21(6):1b21.

*This column was updated 11/30/2018.

Finally, the evidence is in: Three evidence-based studies show that perinatal choline supports proper neurodevelopment in fetuses.^1,2,3

As anyone who has been following my prevention efforts knows, 4 out of 10 patients at Jackson Park Hospital on Chicago’s Southside who presented to their family medicine clinic for psychiatric care have clinical profiles that are consistent with neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE).⁴ Furthermore, since only a little can be done to ameliorate these patients’ psychopathology, I have sought out prevention interventions to stem the tide of what I have thought was a silent epidemic (“occult prenatal alcohol exposure”) for decades.

So I have been heartened that there is some sound science to suggest that perinatal choline supplementation could help. That reality, along with the American Medical Association’s resolution to support evidence-based amounts of choline in all prenatal vitamins, spurred the University of Illinois at Chicago to do something.

Thanks to the support of Enrico Benedetti, MD, professor and head of the department of surgery at the University of Illinois at Chicago, pregnant women will be offered choline supplements to support their fetuses’ neurodevelopment. In addition, there will be a video streaming in the obstetrical waiting rooms at the University of Illinois at Chicago/Mile Square clinics explaining the need for choline supplementation.

Other efforts are afoot aimed at getting this prevention intervention up and running. For example, Yavar Moghimi, MD, who is the behavioral health director for a Medicaid managed care organization in Washington, recently informed me that its clinical policy committee approved a policy highlighting the evidence behind choline supplements during pregnancy.

I am hoping the University of Illinois at Chicago initiative, entitled the “Healthy Prenatal Brain Program” will help all women by preventing the unrecognized problem I have seen among African American women who engage in social drinking before they realize that they are pregnant.⁵ After all, the problem of choline deficiency is not tied simply to prenatal alcohol exposure but also to dietary habits. For example, a study by Helen H. Jensen, PhD, and her associates found that 90% of pregnant women do not get enough choline.⁶ It is just that low-income people are the “canaries in the coal mine” when it comes to being alerted to major public health problems in America.

Another positive development is a website set up by Robert R. Freedman, MD, former chairman of the psychiatry department at the University of Colorado Denver. The site, called prenataldoctoradvice.com, provides guidance to patients about steps they can take, such as taking choline supplements during pregnancy, to improve their children's brain development and mental health.

The public health fix we are suggesting in not difficult; after all, choline is an over-the-counter nutrient, and it does not have to be prescribed by a physician. Ideally, the public health initiatives being advocated are so affordable and easy to implement that this practice will become ubiquitous, and our children will be healthier as a result. It is just a matter of taking action. Now that the evidence is finally in that perinatal choline supplements support proper neurodevelopment in fetuses, we all should move forward – and do something.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit in Chicago and chairman of the department of psychiatry at Windsor University, St. Kitts, USVI. He also is clinical professor emeritus in the department of psychiatry at the University of Illinois at Chicago; former president/CEO of Community Mental Health Council; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago.

References

1. Alcohol Clin Exp Res. 2018 Jul;42(7):1327-41.

2. Am J Psychiatry. 2016 May 1;173(5):509-16.

3. Alcohol. 2015 Nov;49(7):647-56.

4. Psychiatr Serv. 2015 May 1;66(5):539-42.

5. MDedge Psychcast. 2018 Oct 17. Fetal alcohol spectrum disorder, part II.

6. The FASEB Journal. 2007;21(6):1b21.

*This column was updated 11/30/2018.

Finally, the evidence is in: Three evidence-based studies show that perinatal choline supports proper neurodevelopment in fetuses.^1,2,3

As anyone who has been following my prevention efforts knows, 4 out of 10 patients at Jackson Park Hospital on Chicago’s Southside who presented to their family medicine clinic for psychiatric care have clinical profiles that are consistent with neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE).⁴ Furthermore, since only a little can be done to ameliorate these patients’ psychopathology, I have sought out prevention interventions to stem the tide of what I have thought was a silent epidemic (“occult prenatal alcohol exposure”) for decades.

So I have been heartened that there is some sound science to suggest that perinatal choline supplementation could help. That reality, along with the American Medical Association’s resolution to support evidence-based amounts of choline in all prenatal vitamins, spurred the University of Illinois at Chicago to do something.

Thanks to the support of Enrico Benedetti, MD, professor and head of the department of surgery at the University of Illinois at Chicago, pregnant women will be offered choline supplements to support their fetuses’ neurodevelopment. In addition, there will be a video streaming in the obstetrical waiting rooms at the University of Illinois at Chicago/Mile Square clinics explaining the need for choline supplementation.

Other efforts are afoot aimed at getting this prevention intervention up and running. For example, Yavar Moghimi, MD, who is the behavioral health director for a Medicaid managed care organization in Washington, recently informed me that its clinical policy committee approved a policy highlighting the evidence behind choline supplements during pregnancy.

I am hoping the University of Illinois at Chicago initiative, entitled the “Healthy Prenatal Brain Program” will help all women by preventing the unrecognized problem I have seen among African American women who engage in social drinking before they realize that they are pregnant.⁵ After all, the problem of choline deficiency is not tied simply to prenatal alcohol exposure but also to dietary habits. For example, a study by Helen H. Jensen, PhD, and her associates found that 90% of pregnant women do not get enough choline.⁶ It is just that low-income people are the “canaries in the coal mine” when it comes to being alerted to major public health problems in America.

Another positive development is a website set up by Robert R. Freedman, MD, former chairman of the psychiatry department at the University of Colorado Denver. The site, called prenataldoctoradvice.com, provides guidance to patients about steps they can take, such as taking choline supplements during pregnancy, to improve their children's brain development and mental health.

The public health fix we are suggesting in not difficult; after all, choline is an over-the-counter nutrient, and it does not have to be prescribed by a physician. Ideally, the public health initiatives being advocated are so affordable and easy to implement that this practice will become ubiquitous, and our children will be healthier as a result. It is just a matter of taking action. Now that the evidence is finally in that perinatal choline supplements support proper neurodevelopment in fetuses, we all should move forward – and do something.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit in Chicago and chairman of the department of psychiatry at Windsor University, St. Kitts, USVI. He also is clinical professor emeritus in the department of psychiatry at the University of Illinois at Chicago; former president/CEO of Community Mental Health Council; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago.

References

1. Alcohol Clin Exp Res. 2018 Jul;42(7):1327-41.

2. Am J Psychiatry. 2016 May 1;173(5):509-16.

3. Alcohol. 2015 Nov;49(7):647-56.

4. Psychiatr Serv. 2015 May 1;66(5):539-42.

5. MDedge Psychcast. 2018 Oct 17. Fetal alcohol spectrum disorder, part II.

6. The FASEB Journal. 2007;21(6):1b21.

*This column was updated 11/30/2018.

I have always tried to practice common sense psychiatry, however, sometimes it seems I am alone in this pursuit. My best example is the minimal prescribing of loxapine (Adasuve) for treating the problem of psychosis, most notably schizophrenia.

Mind you, neither I nor anyone in family own stock in any pharmaceutical companies. I don’t lecture for them, so I have no conflicts in writing about this observation – which I hope will improve patient care, thereby saving lives and making a difference.

Everyone should be familiar with the evolution of atypical antipsychotics and how these medications are touted as “second-generation” classes of medication advertised as superior to the older, first-generation antipsychotics. However, as we get more experience with the second-generation atypical antipsychotics, we are learning that they have problematic side effects of their own. For example, they are associated with metabolic syndrome, so they cause weight gain, hyperglycemia, increased risk of stroke, sudden cardiac death, blood clots, and diabetes. Maybe these problems are so endemic in the low-income, African American population I treat that I am overly sensitive to trying to prevent these medical disorders while treating a patient’s mental illness. However, my public health leanings have long caused me to think that low-income African Americans are the canary in America’s health status coal mine, as it seems that what hits this group first eventually will hit the majority population. Accordingly, it seems to me that it is well advised to pay attention to this group’s well-being, physical health, and mental health challenges.

Everyone also should be aware that clozapine (Clozaril) had been dubbed the first atypical antipsychotic. But, in some regard, that designation might be given to thioridazine – although some maintain that the ratio of serotonergic to dopamine effects is not strong enough to earn that title. Unfortunately, both thioridazine and clozapine have serious side effects. Thioridazine is associated with severe cardiac arrhythmias, and clozapine has been associated with the aforementioned side effects of atypical antipsychotics but also can cause life-threatening agranulocytosis, necessitating regular white blood cell counts to monitor for this possibility.

What not everyone knows is that loxapine is a member of the dibenzoxazepine class of medication, and it is structurally related to clozapine, which belongs class of medication known as dibenzodiazepines – a class that is extraordinarily similar to dibenzoxazepine. The late William Glazer, MD, a distinguished psychopharmacologist long affiliated with Yale University, New Haven, Conn., even suggested that loxapine might behave as an atypical antipsychotic (J Clin Psychiatry. 1999;60 Suppl 10:42-6). Extensive clinical experience with loxapine suggests the same but with some key differences from the standard atypical antipsychotics regarding its side-effect profile.

First, loxapine, despite being chemically related to clozapine, does not cause agranulocytosis, so the need for white blood cell monitoring is not necessary. Second, I have not seen the problematic metabolic syndrome caused by standard atypical antipsychotic medication. It amazes me when I see patients on aripiprazole, clozapine, olanzapine, quetiapine, risperidone, or ziprasidone who also have diabetes and are on metformin – especially when the development of the patients’ diabetes can be traced back to when they were put on an atypical antipsychotic. I often find myself taking patients off their atypical antipsychotic and putting them on loxapine, resulting in gradual weight loss while maintaining the patients’ stable mental status and absence of psychotic symptoms.

It seems to me that if clozapine and loxapine are so similar (they both bind to serotonin and dopamine receptors), loxapine should be the first drug of choice for the treatment of psychotic symptoms. It acts like an atypical but without the problems of weight gain, hyperglycemia, increased risk of stroke, sudden cardiac death, blood clots, and diabetes that the atypicals may cause. Most of the hundreds of patients with psychotic symptoms I have treated over the past 40 years are on the low dose of loxapine 25 mg at bedtime (although the prescribing information on loxapine says it has to be given at least twice a day, as the half life of the medication is only 4 hours). In some rare instances, I prescribe a total of 50 mg at bedtime.

So, not prescribing loxapine does not make sense to me – other than the medication is generic and so it is not being marketed aggressively by people who make money from prescribing medication and are practicing money, not medicine. The other possibility is that most psychiatrists might not know the connection between clozapine and loxapine, so I thought I should use my influence (what little I have) to inform.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit in Chicago; and chairman of the department of psychiatry at Windsor University, St. Kitts. He also is clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; former president/CEO of Community Mental Health Council; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago.

I have always tried to practice common sense psychiatry, however, sometimes it seems I am alone in this pursuit. My best example is the minimal prescribing of loxapine (Adasuve) for treating the problem of psychosis, most notably schizophrenia.

Mind you, neither I nor anyone in family own stock in any pharmaceutical companies. I don’t lecture for them, so I have no conflicts in writing about this observation – which I hope will improve patient care, thereby saving lives and making a difference.

Everyone should be familiar with the evolution of atypical antipsychotics and how these medications are touted as “second-generation” classes of medication advertised as superior to the older, first-generation antipsychotics. However, as we get more experience with the second-generation atypical antipsychotics, we are learning that they have problematic side effects of their own. For example, they are associated with metabolic syndrome, so they cause weight gain, hyperglycemia, increased risk of stroke, sudden cardiac death, blood clots, and diabetes. Maybe these problems are so endemic in the low-income, African American population I treat that I am overly sensitive to trying to prevent these medical disorders while treating a patient’s mental illness. However, my public health leanings have long caused me to think that low-income African Americans are the canary in America’s health status coal mine, as it seems that what hits this group first eventually will hit the majority population. Accordingly, it seems to me that it is well advised to pay attention to this group’s well-being, physical health, and mental health challenges.

Everyone also should be aware that clozapine (Clozaril) had been dubbed the first atypical antipsychotic. But, in some regard, that designation might be given to thioridazine – although some maintain that the ratio of serotonergic to dopamine effects is not strong enough to earn that title. Unfortunately, both thioridazine and clozapine have serious side effects. Thioridazine is associated with severe cardiac arrhythmias, and clozapine has been associated with the aforementioned side effects of atypical antipsychotics but also can cause life-threatening agranulocytosis, necessitating regular white blood cell counts to monitor for this possibility.

What not everyone knows is that loxapine is a member of the dibenzoxazepine class of medication, and it is structurally related to clozapine, which belongs class of medication known as dibenzodiazepines – a class that is extraordinarily similar to dibenzoxazepine. The late William Glazer, MD, a distinguished psychopharmacologist long affiliated with Yale University, New Haven, Conn., even suggested that loxapine might behave as an atypical antipsychotic (J Clin Psychiatry. 1999;60 Suppl 10:42-6). Extensive clinical experience with loxapine suggests the same but with some key differences from the standard atypical antipsychotics regarding its side-effect profile.

First, loxapine, despite being chemically related to clozapine, does not cause agranulocytosis, so the need for white blood cell monitoring is not necessary. Second, I have not seen the problematic metabolic syndrome caused by standard atypical antipsychotic medication. It amazes me when I see patients on aripiprazole, clozapine, olanzapine, quetiapine, risperidone, or ziprasidone who also have diabetes and are on metformin – especially when the development of the patients’ diabetes can be traced back to when they were put on an atypical antipsychotic. I often find myself taking patients off their atypical antipsychotic and putting them on loxapine, resulting in gradual weight loss while maintaining the patients’ stable mental status and absence of psychotic symptoms.

It seems to me that if clozapine and loxapine are so similar (they both bind to serotonin and dopamine receptors), loxapine should be the first drug of choice for the treatment of psychotic symptoms. It acts like an atypical but without the problems of weight gain, hyperglycemia, increased risk of stroke, sudden cardiac death, blood clots, and diabetes that the atypicals may cause. Most of the hundreds of patients with psychotic symptoms I have treated over the past 40 years are on the low dose of loxapine 25 mg at bedtime (although the prescribing information on loxapine says it has to be given at least twice a day, as the half life of the medication is only 4 hours). In some rare instances, I prescribe a total of 50 mg at bedtime.

So, not prescribing loxapine does not make sense to me – other than the medication is generic and so it is not being marketed aggressively by people who make money from prescribing medication and are practicing money, not medicine. The other possibility is that most psychiatrists might not know the connection between clozapine and loxapine, so I thought I should use my influence (what little I have) to inform.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit in Chicago; and chairman of the department of psychiatry at Windsor University, St. Kitts. He also is clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; former president/CEO of Community Mental Health Council; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago.

I have always tried to practice common sense psychiatry, however, sometimes it seems I am alone in this pursuit. My best example is the minimal prescribing of loxapine (Adasuve) for treating the problem of psychosis, most notably schizophrenia.

Mind you, neither I nor anyone in family own stock in any pharmaceutical companies. I don’t lecture for them, so I have no conflicts in writing about this observation – which I hope will improve patient care, thereby saving lives and making a difference.

Everyone should be familiar with the evolution of atypical antipsychotics and how these medications are touted as “second-generation” classes of medication advertised as superior to the older, first-generation antipsychotics. However, as we get more experience with the second-generation atypical antipsychotics, we are learning that they have problematic side effects of their own. For example, they are associated with metabolic syndrome, so they cause weight gain, hyperglycemia, increased risk of stroke, sudden cardiac death, blood clots, and diabetes. Maybe these problems are so endemic in the low-income, African American population I treat that I am overly sensitive to trying to prevent these medical disorders while treating a patient’s mental illness. However, my public health leanings have long caused me to think that low-income African Americans are the canary in America’s health status coal mine, as it seems that what hits this group first eventually will hit the majority population. Accordingly, it seems to me that it is well advised to pay attention to this group’s well-being, physical health, and mental health challenges.

Everyone also should be aware that clozapine (Clozaril) had been dubbed the first atypical antipsychotic. But, in some regard, that designation might be given to thioridazine – although some maintain that the ratio of serotonergic to dopamine effects is not strong enough to earn that title. Unfortunately, both thioridazine and clozapine have serious side effects. Thioridazine is associated with severe cardiac arrhythmias, and clozapine has been associated with the aforementioned side effects of atypical antipsychotics but also can cause life-threatening agranulocytosis, necessitating regular white blood cell counts to monitor for this possibility.

What not everyone knows is that loxapine is a member of the dibenzoxazepine class of medication, and it is structurally related to clozapine, which belongs class of medication known as dibenzodiazepines – a class that is extraordinarily similar to dibenzoxazepine. The late William Glazer, MD, a distinguished psychopharmacologist long affiliated with Yale University, New Haven, Conn., even suggested that loxapine might behave as an atypical antipsychotic (J Clin Psychiatry. 1999;60 Suppl 10:42-6). Extensive clinical experience with loxapine suggests the same but with some key differences from the standard atypical antipsychotics regarding its side-effect profile.

First, loxapine, despite being chemically related to clozapine, does not cause agranulocytosis, so the need for white blood cell monitoring is not necessary. Second, I have not seen the problematic metabolic syndrome caused by standard atypical antipsychotic medication. It amazes me when I see patients on aripiprazole, clozapine, olanzapine, quetiapine, risperidone, or ziprasidone who also have diabetes and are on metformin – especially when the development of the patients’ diabetes can be traced back to when they were put on an atypical antipsychotic. I often find myself taking patients off their atypical antipsychotic and putting them on loxapine, resulting in gradual weight loss while maintaining the patients’ stable mental status and absence of psychotic symptoms.

It seems to me that if clozapine and loxapine are so similar (they both bind to serotonin and dopamine receptors), loxapine should be the first drug of choice for the treatment of psychotic symptoms. It acts like an atypical but without the problems of weight gain, hyperglycemia, increased risk of stroke, sudden cardiac death, blood clots, and diabetes that the atypicals may cause. Most of the hundreds of patients with psychotic symptoms I have treated over the past 40 years are on the low dose of loxapine 25 mg at bedtime (although the prescribing information on loxapine says it has to be given at least twice a day, as the half life of the medication is only 4 hours). In some rare instances, I prescribe a total of 50 mg at bedtime.

So, not prescribing loxapine does not make sense to me – other than the medication is generic and so it is not being marketed aggressively by people who make money from prescribing medication and are practicing money, not medicine. The other possibility is that most psychiatrists might not know the connection between clozapine and loxapine, so I thought I should use my influence (what little I have) to inform.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit in Chicago; and chairman of the department of psychiatry at Windsor University, St. Kitts. He also is clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; former president/CEO of Community Mental Health Council; and former director of the Institute for Juvenile Research (the birthplace of child psychiatry), all in Chicago.

Maybe it is just me. It probably is. It seems I must have taken a wrong turn in practicing psychiatry somewhere along the line.

For whatever reason, I never truly saw and appreciated the seamlessness between the psychiatric problems children, adults, and the elderly have plaguing them. Of course, I always marveled at how a child who had honest-to-goodness autism could become a full-grown adult and have an adult psychiatrist diagnose that individual as having schizophrenia; why not an adult with autism? But that was the extent of my understanding of the seamlessness between childhood and adult diagnoses. Maybe it is because I was poorly trained and never bothered to get a childhood developmental from my adult psychiatric patients. When I would present a case to supervisors as an adult psychiatric resident, I recall never presenting a child developmental history as a part of the patient’s trajectory. It was as though since there was adult psychiatry and child psychiatry, then the disorders of adults and children should be separated as well.

I know many adult psychiatrists never ask their adult patients, “How old were you when you graduated high school?” although an answer of “I never graduated,” or I graduated at 19-20” should raise questions. When I was in community psychiatry residency, I had some training at the Institute for Juvenile Research (birthplace of child psychiatry), so I understood something about children and the problems they had. Of course, back then, child psychiatric diagnoses were not that good, but with the advent of the DSM-5, children’s psychiatric diagnoses became more precise. This was probably because of research and better epidemiologic data about the prevalence of the six major neurodevelopmental disorders (intellectual disability, attention-deficit/hyperactivity disorder, speech and language disorders, autism spectrum disorders, specific learning disorders, and motor disorders). Maybe I am too old to remember, but I don’t remember anyone with a serious focus on what happens to psychiatrically ill children when they grow up to be adults or what psychiatric problems adult psychiatric patients had when they were children.

In a brilliant article in the September issue of the American Journal of Psychiatry, Avshalom Caspi, PhD, and Terrie E. Moffitt, PhD, propose that there is a single dimension of psychopathology, or “p.” This is an article that everyone should read and study (Am J Psychiatry. 2018 Sep 1;175[9]:831-44).

The authors perceptively remind us that we characterize children’s psychopathology as internalizing and externalizing disorders (with a slight nod to psychotic disorders in children), but these features do not seem prominent or ubiquitous in adult psychiatry’s thinking about adult psychiatric patients. They do a great job at pointing out there is ample evidence of a great deal of comorbidity between “discrete” children’s and adults’ psychiatric disorders. We certainly learned this from the findings of the DSM-5’s Personality and Personality Disorders Work Group.

Their p suggests a common thread between various childhood psychiatric disorders and adult psychiatric disorders. Furthermore, Dr. Caspi’s and Dr. Moffitt’s assertion that longitudinal research identifying “poor childhood self-control” (a symptom of affect dysregulation) and poor executive functioning as a salient early developmental predictor of their p sounds a lot like fetal alcohol exposure to me (Fetal Alcohol Exposure Among African Americans). So does their declaration that individuals with higher levels of p have difficulty with attention, concentration, mental control, and visual-motor problems.

Maybe I have confirmational bias, as I have seen the common thread of fetal alcohol exposure run from childhood to adults, but many of my residents and students see it as well.

Accordingly, I think we have made mistakes in psychiatry when we ask (if we ask) the mother of our patients was she drinking when she was pregnant, and “Was the patient born low-birth weight and/or premature?” We should be asking – “When did you realize you were pregnant?” “Were you doing any social drinking before you knew you were pregnant?” Thus, we miss the common thread of fetal alcohol exposure in child and adult psychopathology.

I realize that a great many competing interests are trying to get our time and attention, and there is a lot to read and figure out. In our efforts to do no harm, do psychiatrists try to take their time to fully understand things before we act? Some aspects of our understanding seem to be “no brainers,” and the continuation of child neurodevelopmental disorders morphing into adult mental disorders should be obvious. But maybe we took a wrong turn – which is why it took me 45 years to figure out that fetal alcohol exposure in utero has a significant impact on adult psychiatric disorders.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit; clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; former director of the Institute for Juvenile Research; and former president/CEO of the Community Mental Health Council, all in Chicago. He also serves as chair of psychiatry at Windsor University, St. Kitts.

Maybe it is just me. It probably is. It seems I must have taken a wrong turn in practicing psychiatry somewhere along the line.

For whatever reason, I never truly saw and appreciated the seamlessness between the psychiatric problems children, adults, and the elderly have plaguing them. Of course, I always marveled at how a child who had honest-to-goodness autism could become a full-grown adult and have an adult psychiatrist diagnose that individual as having schizophrenia; why not an adult with autism? But that was the extent of my understanding of the seamlessness between childhood and adult diagnoses. Maybe it is because I was poorly trained and never bothered to get a childhood developmental from my adult psychiatric patients. When I would present a case to supervisors as an adult psychiatric resident, I recall never presenting a child developmental history as a part of the patient’s trajectory. It was as though since there was adult psychiatry and child psychiatry, then the disorders of adults and children should be separated as well.

I know many adult psychiatrists never ask their adult patients, “How old were you when you graduated high school?” although an answer of “I never graduated,” or I graduated at 19-20” should raise questions. When I was in community psychiatry residency, I had some training at the Institute for Juvenile Research (birthplace of child psychiatry), so I understood something about children and the problems they had. Of course, back then, child psychiatric diagnoses were not that good, but with the advent of the DSM-5, children’s psychiatric diagnoses became more precise. This was probably because of research and better epidemiologic data about the prevalence of the six major neurodevelopmental disorders (intellectual disability, attention-deficit/hyperactivity disorder, speech and language disorders, autism spectrum disorders, specific learning disorders, and motor disorders). Maybe I am too old to remember, but I don’t remember anyone with a serious focus on what happens to psychiatrically ill children when they grow up to be adults or what psychiatric problems adult psychiatric patients had when they were children.

In a brilliant article in the September issue of the American Journal of Psychiatry, Avshalom Caspi, PhD, and Terrie E. Moffitt, PhD, propose that there is a single dimension of psychopathology, or “p.” This is an article that everyone should read and study (Am J Psychiatry. 2018 Sep 1;175[9]:831-44).

The authors perceptively remind us that we characterize children’s psychopathology as internalizing and externalizing disorders (with a slight nod to psychotic disorders in children), but these features do not seem prominent or ubiquitous in adult psychiatry’s thinking about adult psychiatric patients. They do a great job at pointing out there is ample evidence of a great deal of comorbidity between “discrete” children’s and adults’ psychiatric disorders. We certainly learned this from the findings of the DSM-5’s Personality and Personality Disorders Work Group.

Their p suggests a common thread between various childhood psychiatric disorders and adult psychiatric disorders. Furthermore, Dr. Caspi’s and Dr. Moffitt’s assertion that longitudinal research identifying “poor childhood self-control” (a symptom of affect dysregulation) and poor executive functioning as a salient early developmental predictor of their p sounds a lot like fetal alcohol exposure to me (Fetal Alcohol Exposure Among African Americans). So does their declaration that individuals with higher levels of p have difficulty with attention, concentration, mental control, and visual-motor problems.

Maybe I have confirmational bias, as I have seen the common thread of fetal alcohol exposure run from childhood to adults, but many of my residents and students see it as well.

Accordingly, I think we have made mistakes in psychiatry when we ask (if we ask) the mother of our patients was she drinking when she was pregnant, and “Was the patient born low-birth weight and/or premature?” We should be asking – “When did you realize you were pregnant?” “Were you doing any social drinking before you knew you were pregnant?” Thus, we miss the common thread of fetal alcohol exposure in child and adult psychopathology.

I realize that a great many competing interests are trying to get our time and attention, and there is a lot to read and figure out. In our efforts to do no harm, do psychiatrists try to take their time to fully understand things before we act? Some aspects of our understanding seem to be “no brainers,” and the continuation of child neurodevelopmental disorders morphing into adult mental disorders should be obvious. But maybe we took a wrong turn – which is why it took me 45 years to figure out that fetal alcohol exposure in utero has a significant impact on adult psychiatric disorders.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit; clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; former director of the Institute for Juvenile Research; and former president/CEO of the Community Mental Health Council, all in Chicago. He also serves as chair of psychiatry at Windsor University, St. Kitts.

Maybe it is just me. It probably is. It seems I must have taken a wrong turn in practicing psychiatry somewhere along the line.

For whatever reason, I never truly saw and appreciated the seamlessness between the psychiatric problems children, adults, and the elderly have plaguing them. Of course, I always marveled at how a child who had honest-to-goodness autism could become a full-grown adult and have an adult psychiatrist diagnose that individual as having schizophrenia; why not an adult with autism? But that was the extent of my understanding of the seamlessness between childhood and adult diagnoses. Maybe it is because I was poorly trained and never bothered to get a childhood developmental from my adult psychiatric patients. When I would present a case to supervisors as an adult psychiatric resident, I recall never presenting a child developmental history as a part of the patient’s trajectory. It was as though since there was adult psychiatry and child psychiatry, then the disorders of adults and children should be separated as well.

I know many adult psychiatrists never ask their adult patients, “How old were you when you graduated high school?” although an answer of “I never graduated,” or I graduated at 19-20” should raise questions. When I was in community psychiatry residency, I had some training at the Institute for Juvenile Research (birthplace of child psychiatry), so I understood something about children and the problems they had. Of course, back then, child psychiatric diagnoses were not that good, but with the advent of the DSM-5, children’s psychiatric diagnoses became more precise. This was probably because of research and better epidemiologic data about the prevalence of the six major neurodevelopmental disorders (intellectual disability, attention-deficit/hyperactivity disorder, speech and language disorders, autism spectrum disorders, specific learning disorders, and motor disorders). Maybe I am too old to remember, but I don’t remember anyone with a serious focus on what happens to psychiatrically ill children when they grow up to be adults or what psychiatric problems adult psychiatric patients had when they were children.

In a brilliant article in the September issue of the American Journal of Psychiatry, Avshalom Caspi, PhD, and Terrie E. Moffitt, PhD, propose that there is a single dimension of psychopathology, or “p.” This is an article that everyone should read and study (Am J Psychiatry. 2018 Sep 1;175[9]:831-44).

The authors perceptively remind us that we characterize children’s psychopathology as internalizing and externalizing disorders (with a slight nod to psychotic disorders in children), but these features do not seem prominent or ubiquitous in adult psychiatry’s thinking about adult psychiatric patients. They do a great job at pointing out there is ample evidence of a great deal of comorbidity between “discrete” children’s and adults’ psychiatric disorders. We certainly learned this from the findings of the DSM-5’s Personality and Personality Disorders Work Group.

Their p suggests a common thread between various childhood psychiatric disorders and adult psychiatric disorders. Furthermore, Dr. Caspi’s and Dr. Moffitt’s assertion that longitudinal research identifying “poor childhood self-control” (a symptom of affect dysregulation) and poor executive functioning as a salient early developmental predictor of their p sounds a lot like fetal alcohol exposure to me (Fetal Alcohol Exposure Among African Americans). So does their declaration that individuals with higher levels of p have difficulty with attention, concentration, mental control, and visual-motor problems.

Maybe I have confirmational bias, as I have seen the common thread of fetal alcohol exposure run from childhood to adults, but many of my residents and students see it as well.

Accordingly, I think we have made mistakes in psychiatry when we ask (if we ask) the mother of our patients was she drinking when she was pregnant, and “Was the patient born low-birth weight and/or premature?” We should be asking – “When did you realize you were pregnant?” “Were you doing any social drinking before you knew you were pregnant?” Thus, we miss the common thread of fetal alcohol exposure in child and adult psychopathology.

I realize that a great many competing interests are trying to get our time and attention, and there is a lot to read and figure out. In our efforts to do no harm, do psychiatrists try to take their time to fully understand things before we act? Some aspects of our understanding seem to be “no brainers,” and the continuation of child neurodevelopmental disorders morphing into adult mental disorders should be obvious. But maybe we took a wrong turn – which is why it took me 45 years to figure out that fetal alcohol exposure in utero has a significant impact on adult psychiatric disorders.

Dr. Bell is staff psychiatrist at Jackson Park Hospital’s surgical-medical/psychiatric inpatient unit; clinical professor emeritus, department of psychiatry, University of Illinois at Chicago; former director of the Institute for Juvenile Research; and former president/CEO of the Community Mental Health Council, all in Chicago. He also serves as chair of psychiatry at Windsor University, St. Kitts.