Commentary

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact [email protected].

Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common.

One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.

What smoking does for patients with schizophrenia

The high prevalence of smoking among patients with schizophrenia (50% to 88%) greatly exceeds the rates of smoking among patients with other psychiatric illnesses.^1,2 The role of smoking in relation to schizophrenia and other psychoses is multidimensional, and evidence implicates smoking as a risk factor for schizophrenia.^3,4

Two mechanisms may help explain tobacco use in patients with schizophrenia: reducing the adverse effects of antipsychotic medications and promoting neural transmission of dopamine. Second-generation antipsychotics (SGAs) are a first-line treatment, but they can produce EPS, metabolic dysregulation, and blood disorders such as hyponatremia and (rarely) agranulocytosis (1% with clozapine).⁵ Compared to those who are nonsmokers, patients with schizophrenia who smoke are more likely to experience more severe symptoms (eg, hallucinations and delusions) and less severe EPS.^5,6 Research suggests that exposure to polycyclic aromatic hydrocarbons released during smoking induces cytochrome P450 1A2, an enzyme that metabolizes antipsychotic medications such as haloperidol, clozapine, and olanzapine. Increased metabolism results in lower serum concentrations of antipsychotics, lower efficacy, and more severe positive symptoms.^5,6

Additionally, tobacco is an activator of nicotinic acetylcholine receptors (nAChR).⁶ When these receptors become activated, dopamine is released. Dopamine serves as a mediator of reward for nicotine use. In the context of schizophrenia, tobacco use opposes the mechanism of action of SGAs, which is to block neural transmission of dopamine.⁶ The etiology of EPS is related to the blockade of postsynaptic dopamine release in the striatum.⁶ By activating nAChR, smoking induces a downstream release of dopamine that can alleviate iatrogenic EPS by restoring neural transmission of dopamine.⁶ Nicotine may also modulate alpha-7 nicotinic receptor dysfunction, and improve the ability to filter out irrelevant environmental stimuli (impaired sensory gating), which can be overwhelming for patients with schizophrenia. It also can improve cognitive dysfunction and attention by inducing the release of dopamine in mesocortical pathways.⁷ The implications of this neural pathway are significant because smoking is significantly greater in tobacco users who are diagnosed with schizophrenia compared to tobacco users who lack a psychiatric diagnosis.^6,7 Smoking may enhance dopaminergic neural transmission to a far greater extent in tobacco users with schizophrenia compared to tobacco users who do not develop schizophrenia, which suggests intrinsic differences at the neuronal level. Neural differences between tobacco users with or without schizophrenia may synergize with smoking in clinically and biologically meaningful ways. These pathways require further research to support or disprove these hypotheses.

Aside from the dopaminergic system, mechanisms influencing tobacco use among patients with schizophrenia may also be related to nicotine’s mild antidepressant effects. Evidence suggests a clinically meaningful association between nicotine dependence and mood disorders, and this association may be due to the antidepressant effects of nicotine.^8-13 Patients with schizophrenia may experience respite from depressive symptoms through their tobacco use, eventually leading to nicotine dependence.

Continue to: Treatment of schizophrenia...

Treatment of schizophrenia involves multimodal management of a patient’s life, including reducing maladaptive habits that are harmful to health. Chronic smoking in patients with schizophrenia is associated not only with atherosclerosis and cardiovascular disease, but also with poor neurologic functioning, such as significant impairment in attention, working memory, learning, executive function, reasoning, problem-solving and speed of processing.¹⁴ One study found that in patients with schizophrenia, smoking increased the 20-year cardiovascular mortality risk by 86%.¹⁵

Despite challenges to abstinence, smoking cessation should be discussed with these patients, especially given the high prevalence of smoking among this vulnerable population. Bupropion and varenicline have been studied in the context of smoking cessation among patients with schizophrenia. Data on varenicline are mixed. Smokers with schizophrenia who received bupropion showed higher rates of abstinence from smoking compared to those who received placebo.¹⁶

As part of the biopsychosocial model of clinical care, sociodemographic factors must be considered in assessing the relationship between tobacco use and schizophrenia, because a large proportion of patients diagnosed with schizophrenia are members of underrepresented minority groups.¹⁷ A PubMed database search using keywords “African American” or “Black,” “tobacco,” and “schizophrenia” located only 12 studies, most of which lacked relevance to this question. Han et al¹⁸ is 1 of the few studies to investigate sociodemographic factors as they relate to tobacco use among adults with psychoses. Social determinants of health and other confounding variables also need defining to truly distinguish causation from correlation, especially regarding tobacco use and its association with other health risk behaviors.¹⁹

Without the street medicine component of the medical school training I received, the pattern of smoking among patients with schizophrenia may have remained invisible or insignificant to me, as tobacco use is not permitted in the inpatient and outpatient academic settings. This experience not only raised insightful questions, but also emphasized the clinical value of seeing patients within their living environment.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact [email protected].

Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common.

One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.

What smoking does for patients with schizophrenia

The high prevalence of smoking among patients with schizophrenia (50% to 88%) greatly exceeds the rates of smoking among patients with other psychiatric illnesses.^1,2 The role of smoking in relation to schizophrenia and other psychoses is multidimensional, and evidence implicates smoking as a risk factor for schizophrenia.^3,4

Two mechanisms may help explain tobacco use in patients with schizophrenia: reducing the adverse effects of antipsychotic medications and promoting neural transmission of dopamine. Second-generation antipsychotics (SGAs) are a first-line treatment, but they can produce EPS, metabolic dysregulation, and blood disorders such as hyponatremia and (rarely) agranulocytosis (1% with clozapine).⁵ Compared to those who are nonsmokers, patients with schizophrenia who smoke are more likely to experience more severe symptoms (eg, hallucinations and delusions) and less severe EPS.^5,6 Research suggests that exposure to polycyclic aromatic hydrocarbons released during smoking induces cytochrome P450 1A2, an enzyme that metabolizes antipsychotic medications such as haloperidol, clozapine, and olanzapine. Increased metabolism results in lower serum concentrations of antipsychotics, lower efficacy, and more severe positive symptoms.^5,6

Additionally, tobacco is an activator of nicotinic acetylcholine receptors (nAChR).⁶ When these receptors become activated, dopamine is released. Dopamine serves as a mediator of reward for nicotine use. In the context of schizophrenia, tobacco use opposes the mechanism of action of SGAs, which is to block neural transmission of dopamine.⁶ The etiology of EPS is related to the blockade of postsynaptic dopamine release in the striatum.⁶ By activating nAChR, smoking induces a downstream release of dopamine that can alleviate iatrogenic EPS by restoring neural transmission of dopamine.⁶ Nicotine may also modulate alpha-7 nicotinic receptor dysfunction, and improve the ability to filter out irrelevant environmental stimuli (impaired sensory gating), which can be overwhelming for patients with schizophrenia. It also can improve cognitive dysfunction and attention by inducing the release of dopamine in mesocortical pathways.⁷ The implications of this neural pathway are significant because smoking is significantly greater in tobacco users who are diagnosed with schizophrenia compared to tobacco users who lack a psychiatric diagnosis.^6,7 Smoking may enhance dopaminergic neural transmission to a far greater extent in tobacco users with schizophrenia compared to tobacco users who do not develop schizophrenia, which suggests intrinsic differences at the neuronal level. Neural differences between tobacco users with or without schizophrenia may synergize with smoking in clinically and biologically meaningful ways. These pathways require further research to support or disprove these hypotheses.

Aside from the dopaminergic system, mechanisms influencing tobacco use among patients with schizophrenia may also be related to nicotine’s mild antidepressant effects. Evidence suggests a clinically meaningful association between nicotine dependence and mood disorders, and this association may be due to the antidepressant effects of nicotine.^8-13 Patients with schizophrenia may experience respite from depressive symptoms through their tobacco use, eventually leading to nicotine dependence.

Continue to: Treatment of schizophrenia...

Treatment of schizophrenia involves multimodal management of a patient’s life, including reducing maladaptive habits that are harmful to health. Chronic smoking in patients with schizophrenia is associated not only with atherosclerosis and cardiovascular disease, but also with poor neurologic functioning, such as significant impairment in attention, working memory, learning, executive function, reasoning, problem-solving and speed of processing.¹⁴ One study found that in patients with schizophrenia, smoking increased the 20-year cardiovascular mortality risk by 86%.¹⁵

Despite challenges to abstinence, smoking cessation should be discussed with these patients, especially given the high prevalence of smoking among this vulnerable population. Bupropion and varenicline have been studied in the context of smoking cessation among patients with schizophrenia. Data on varenicline are mixed. Smokers with schizophrenia who received bupropion showed higher rates of abstinence from smoking compared to those who received placebo.¹⁶

As part of the biopsychosocial model of clinical care, sociodemographic factors must be considered in assessing the relationship between tobacco use and schizophrenia, because a large proportion of patients diagnosed with schizophrenia are members of underrepresented minority groups.¹⁷ A PubMed database search using keywords “African American” or “Black,” “tobacco,” and “schizophrenia” located only 12 studies, most of which lacked relevance to this question. Han et al¹⁸ is 1 of the few studies to investigate sociodemographic factors as they relate to tobacco use among adults with psychoses. Social determinants of health and other confounding variables also need defining to truly distinguish causation from correlation, especially regarding tobacco use and its association with other health risk behaviors.¹⁹

Without the street medicine component of the medical school training I received, the pattern of smoking among patients with schizophrenia may have remained invisible or insignificant to me, as tobacco use is not permitted in the inpatient and outpatient academic settings. This experience not only raised insightful questions, but also emphasized the clinical value of seeing patients within their living environment.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact [email protected].

Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common.

One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.

What smoking does for patients with schizophrenia

The high prevalence of smoking among patients with schizophrenia (50% to 88%) greatly exceeds the rates of smoking among patients with other psychiatric illnesses.^1,2 The role of smoking in relation to schizophrenia and other psychoses is multidimensional, and evidence implicates smoking as a risk factor for schizophrenia.^3,4

Two mechanisms may help explain tobacco use in patients with schizophrenia: reducing the adverse effects of antipsychotic medications and promoting neural transmission of dopamine. Second-generation antipsychotics (SGAs) are a first-line treatment, but they can produce EPS, metabolic dysregulation, and blood disorders such as hyponatremia and (rarely) agranulocytosis (1% with clozapine).⁵ Compared to those who are nonsmokers, patients with schizophrenia who smoke are more likely to experience more severe symptoms (eg, hallucinations and delusions) and less severe EPS.^5,6 Research suggests that exposure to polycyclic aromatic hydrocarbons released during smoking induces cytochrome P450 1A2, an enzyme that metabolizes antipsychotic medications such as haloperidol, clozapine, and olanzapine. Increased metabolism results in lower serum concentrations of antipsychotics, lower efficacy, and more severe positive symptoms.^5,6

Additionally, tobacco is an activator of nicotinic acetylcholine receptors (nAChR).⁶ When these receptors become activated, dopamine is released. Dopamine serves as a mediator of reward for nicotine use. In the context of schizophrenia, tobacco use opposes the mechanism of action of SGAs, which is to block neural transmission of dopamine.⁶ The etiology of EPS is related to the blockade of postsynaptic dopamine release in the striatum.⁶ By activating nAChR, smoking induces a downstream release of dopamine that can alleviate iatrogenic EPS by restoring neural transmission of dopamine.⁶ Nicotine may also modulate alpha-7 nicotinic receptor dysfunction, and improve the ability to filter out irrelevant environmental stimuli (impaired sensory gating), which can be overwhelming for patients with schizophrenia. It also can improve cognitive dysfunction and attention by inducing the release of dopamine in mesocortical pathways.⁷ The implications of this neural pathway are significant because smoking is significantly greater in tobacco users who are diagnosed with schizophrenia compared to tobacco users who lack a psychiatric diagnosis.^6,7 Smoking may enhance dopaminergic neural transmission to a far greater extent in tobacco users with schizophrenia compared to tobacco users who do not develop schizophrenia, which suggests intrinsic differences at the neuronal level. Neural differences between tobacco users with or without schizophrenia may synergize with smoking in clinically and biologically meaningful ways. These pathways require further research to support or disprove these hypotheses.

Aside from the dopaminergic system, mechanisms influencing tobacco use among patients with schizophrenia may also be related to nicotine’s mild antidepressant effects. Evidence suggests a clinically meaningful association between nicotine dependence and mood disorders, and this association may be due to the antidepressant effects of nicotine.^8-13 Patients with schizophrenia may experience respite from depressive symptoms through their tobacco use, eventually leading to nicotine dependence.

Continue to: Treatment of schizophrenia...

Treatment of schizophrenia involves multimodal management of a patient’s life, including reducing maladaptive habits that are harmful to health. Chronic smoking in patients with schizophrenia is associated not only with atherosclerosis and cardiovascular disease, but also with poor neurologic functioning, such as significant impairment in attention, working memory, learning, executive function, reasoning, problem-solving and speed of processing.¹⁴ One study found that in patients with schizophrenia, smoking increased the 20-year cardiovascular mortality risk by 86%.¹⁵

Despite challenges to abstinence, smoking cessation should be discussed with these patients, especially given the high prevalence of smoking among this vulnerable population. Bupropion and varenicline have been studied in the context of smoking cessation among patients with schizophrenia. Data on varenicline are mixed. Smokers with schizophrenia who received bupropion showed higher rates of abstinence from smoking compared to those who received placebo.¹⁶

As part of the biopsychosocial model of clinical care, sociodemographic factors must be considered in assessing the relationship between tobacco use and schizophrenia, because a large proportion of patients diagnosed with schizophrenia are members of underrepresented minority groups.¹⁷ A PubMed database search using keywords “African American” or “Black,” “tobacco,” and “schizophrenia” located only 12 studies, most of which lacked relevance to this question. Han et al¹⁸ is 1 of the few studies to investigate sociodemographic factors as they relate to tobacco use among adults with psychoses. Social determinants of health and other confounding variables also need defining to truly distinguish causation from correlation, especially regarding tobacco use and its association with other health risk behaviors.¹⁹

Without the street medicine component of the medical school training I received, the pattern of smoking among patients with schizophrenia may have remained invisible or insignificant to me, as tobacco use is not permitted in the inpatient and outpatient academic settings. This experience not only raised insightful questions, but also emphasized the clinical value of seeing patients within their living environment.

Thank you very much to Drs. Vincent, Good, and El-Mallakh for their guest editorial on interventional psychiatry (“Interventional psychiatry: What are the next steps?” Current Psychiatry, July 2023, p. 7-9, doi:10.12788/cp.0378). Your addressing the “gap in training” regarding “evidence the growth of interventional psychiatry has exceeded the capacity of the current training infrastructure to provide trainees with adequate exposure to these procedures” is right on the mark, as is the observation that the Accreditation Council for Graduate Medical Education (ACGME) Psychiatry Milestones “do not indicate how competency in these therapies can be achieved.”

The Clinical Transcranial Magnetic Stimulation Society (CTMSS) is well aware of these issues and is actively addressing them:

1. We have increased the number of PULSES courses—designed to serve as intensive, introductory courses on TMS—we provide, and increased the number of members on our PULSES team to address this. We have also increased the number of PULSES scholarships for psychiatry residents that cover the costs of the conference and materials.

2. We created a standing Resident Subcommittee of our Education Committee that is focused on psychiatry resident training. We realize not all psychiatric residency programs have active TMS programs or attendings who are trained in TMS. Last year we presented lectures aimed at introducing TMS to PGY-1 and PGY-2 psychiatry residents. These were recorded and are available for free on the CTMSS website (www.clinicaltmssociety.org).

3. The Resident Subcommittee presented the American Association of Directors of Psychiatric Residency Training with a curriculum submission that was accepted and will be available to all psychiatric residents across the country free of charge. (Current Psychiatry Associate Editor Phillip G. Janicak, MD was very helpful to our subcommittee with this project.)

4. The topic of resident/fellow training in all forms of neuromodulation was discussed during our monthly Grand Rounds webinar and at our annual meeting.

5. The issue of having a broader base of knowledge and training in neuromodulation was a topic at a recent Education Committee meeting, and this year we are adding lectures on electroconvulsive therapy and esketamine to our Grand Rounds webinars. Many CTMSS members are trained and knowledgeable in multiple neuromodulation modalities.

Continue to: 6. Many CTMSS members...

6. Many CTMSS members are involved in academic programs or are invited to training programs to teach psychiatric residents as guest lecturers.

7. The UK's Royal College of Psychiatrists has requested access to our prerecorded lectures, and CTMSS members are working on translating our lectures into Spanish.

Resident education is a key component of the main goals of the CTMSS. Our Board of Directors is fully committed to resident education and has directed the Education Committee to address it. We look forward to moving forward on educating psychiatric residents, with the hope of eventually engaging the ACGME to acknowledge TMS by name in the ACGME guidelines, provide residents with at least basic information on TMS, and clarify how competency in these therapies can be achieved.

Thank you very much to Drs. Vincent, Good, and El-Mallakh for their guest editorial on interventional psychiatry (“Interventional psychiatry: What are the next steps?” Current Psychiatry, July 2023, p. 7-9, doi:10.12788/cp.0378). Your addressing the “gap in training” regarding “evidence the growth of interventional psychiatry has exceeded the capacity of the current training infrastructure to provide trainees with adequate exposure to these procedures” is right on the mark, as is the observation that the Accreditation Council for Graduate Medical Education (ACGME) Psychiatry Milestones “do not indicate how competency in these therapies can be achieved.”

The Clinical Transcranial Magnetic Stimulation Society (CTMSS) is well aware of these issues and is actively addressing them:

1. We have increased the number of PULSES courses—designed to serve as intensive, introductory courses on TMS—we provide, and increased the number of members on our PULSES team to address this. We have also increased the number of PULSES scholarships for psychiatry residents that cover the costs of the conference and materials.

2. We created a standing Resident Subcommittee of our Education Committee that is focused on psychiatry resident training. We realize not all psychiatric residency programs have active TMS programs or attendings who are trained in TMS. Last year we presented lectures aimed at introducing TMS to PGY-1 and PGY-2 psychiatry residents. These were recorded and are available for free on the CTMSS website (www.clinicaltmssociety.org).

3. The Resident Subcommittee presented the American Association of Directors of Psychiatric Residency Training with a curriculum submission that was accepted and will be available to all psychiatric residents across the country free of charge. (Current Psychiatry Associate Editor Phillip G. Janicak, MD was very helpful to our subcommittee with this project.)

4. The topic of resident/fellow training in all forms of neuromodulation was discussed during our monthly Grand Rounds webinar and at our annual meeting.

5. The issue of having a broader base of knowledge and training in neuromodulation was a topic at a recent Education Committee meeting, and this year we are adding lectures on electroconvulsive therapy and esketamine to our Grand Rounds webinars. Many CTMSS members are trained and knowledgeable in multiple neuromodulation modalities.

Continue to: 6. Many CTMSS members...

6. Many CTMSS members are involved in academic programs or are invited to training programs to teach psychiatric residents as guest lecturers.

7. The UK's Royal College of Psychiatrists has requested access to our prerecorded lectures, and CTMSS members are working on translating our lectures into Spanish.

Resident education is a key component of the main goals of the CTMSS. Our Board of Directors is fully committed to resident education and has directed the Education Committee to address it. We look forward to moving forward on educating psychiatric residents, with the hope of eventually engaging the ACGME to acknowledge TMS by name in the ACGME guidelines, provide residents with at least basic information on TMS, and clarify how competency in these therapies can be achieved.

Thank you very much to Drs. Vincent, Good, and El-Mallakh for their guest editorial on interventional psychiatry (“Interventional psychiatry: What are the next steps?” Current Psychiatry, July 2023, p. 7-9, doi:10.12788/cp.0378). Your addressing the “gap in training” regarding “evidence the growth of interventional psychiatry has exceeded the capacity of the current training infrastructure to provide trainees with adequate exposure to these procedures” is right on the mark, as is the observation that the Accreditation Council for Graduate Medical Education (ACGME) Psychiatry Milestones “do not indicate how competency in these therapies can be achieved.”

The Clinical Transcranial Magnetic Stimulation Society (CTMSS) is well aware of these issues and is actively addressing them:

1. We have increased the number of PULSES courses—designed to serve as intensive, introductory courses on TMS—we provide, and increased the number of members on our PULSES team to address this. We have also increased the number of PULSES scholarships for psychiatry residents that cover the costs of the conference and materials.

2. We created a standing Resident Subcommittee of our Education Committee that is focused on psychiatry resident training. We realize not all psychiatric residency programs have active TMS programs or attendings who are trained in TMS. Last year we presented lectures aimed at introducing TMS to PGY-1 and PGY-2 psychiatry residents. These were recorded and are available for free on the CTMSS website (www.clinicaltmssociety.org).

3. The Resident Subcommittee presented the American Association of Directors of Psychiatric Residency Training with a curriculum submission that was accepted and will be available to all psychiatric residents across the country free of charge. (Current Psychiatry Associate Editor Phillip G. Janicak, MD was very helpful to our subcommittee with this project.)

4. The topic of resident/fellow training in all forms of neuromodulation was discussed during our monthly Grand Rounds webinar and at our annual meeting.

5. The issue of having a broader base of knowledge and training in neuromodulation was a topic at a recent Education Committee meeting, and this year we are adding lectures on electroconvulsive therapy and esketamine to our Grand Rounds webinars. Many CTMSS members are trained and knowledgeable in multiple neuromodulation modalities.

Continue to: 6. Many CTMSS members...

6. Many CTMSS members are involved in academic programs or are invited to training programs to teach psychiatric residents as guest lecturers.

7. The UK's Royal College of Psychiatrists has requested access to our prerecorded lectures, and CTMSS members are working on translating our lectures into Spanish.

Resident education is a key component of the main goals of the CTMSS. Our Board of Directors is fully committed to resident education and has directed the Education Committee to address it. We look forward to moving forward on educating psychiatric residents, with the hope of eventually engaging the ACGME to acknowledge TMS by name in the ACGME guidelines, provide residents with at least basic information on TMS, and clarify how competency in these therapies can be achieved.

AGA has long been a powerful voice in advocating locally and nationally for issues of critical importance to our profession and patients.

While AGA’s advocacy efforts related to access to colorectal cancer screening are frequently highlighted, this is one aspect of a larger advocacy agenda.

This month, I wish to highlight AGA’s extensive advocacy efforts focused on expanding access to obesity treatment. More than 2 in 5 adults in the U.S. have obesity, and weight management has been shown to be beneficial in patients with comorbid gastrointestinal diseases, such as metabolic dysfunction–associated steatotic liver disease, gastroesophageal reflux disease, gallbladder disease, pancreatitis, and GI malignancy.

In 2022, Inside Scope, a podcast by AGA, featured a 6-part seriescalled “Obesity in GI.” In July, Drs. Octavia Pickett-Blakely and Naresh Gunaratnam moderated a Gastro Bites lunch-and-learn session on “Obesity in GI Care – Embracing and Putting It into Practice” in which they discussed models of care delivery supporting obesity management in GI practice.

In November 2022, AGA released “AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity,” (https://shorturl.at/bDNOV) to aid clinicians in appropriately prescribing obesity pharmacotherapy on the front lines of care.

On the policy front, in June, AGA held a Capitol Hill briefing in support of H.R.1577 - Treat and Reduce Obesity Act of 2021 (TROA), a bipartisan bill that would improve access to obesity treatment and care by expanding coverage under Medicare Part D for FDA-approved obesity pharmacotherapy, as well as related services such as behavioral, nutrition, and other counseling. Please check out our new obesity advocacy toolkit for more information.

This month we update you on important multi-society guidance regarding peri-endoscopic management of GLP-1 receptor agonists. We highlight new AGA Clinical Practice Updates on ostomy management and use of gastric POEM for treatment of gastroparesis, as well as a randomized controlled trial from Gastroenterology showing the effectiveness of hemostatic powder in the management of malignant GI bleeding as compared with standard care.

In our Member Spotlight, we feature gastroenterologist Sameer Berry, MD, MBA, who discusses his role as a physician-entrepreneur seeking to transform GI care delivery through his AGA GI Opportunity Fund–supported company, Oshi Health.

This issue includes our annual supplement, “Gastroenterology Data Trends.” It features a collection of contributions on GI and climate change, long COVID and the GI tract, and the evolution of targeted therapies for C. difficile, among others.

We hope you enjoy this, and all the exciting content included in our October issue.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

AGA has long been a powerful voice in advocating locally and nationally for issues of critical importance to our profession and patients.

While AGA’s advocacy efforts related to access to colorectal cancer screening are frequently highlighted, this is one aspect of a larger advocacy agenda.

This month, I wish to highlight AGA’s extensive advocacy efforts focused on expanding access to obesity treatment. More than 2 in 5 adults in the U.S. have obesity, and weight management has been shown to be beneficial in patients with comorbid gastrointestinal diseases, such as metabolic dysfunction–associated steatotic liver disease, gastroesophageal reflux disease, gallbladder disease, pancreatitis, and GI malignancy.

In 2022, Inside Scope, a podcast by AGA, featured a 6-part seriescalled “Obesity in GI.” In July, Drs. Octavia Pickett-Blakely and Naresh Gunaratnam moderated a Gastro Bites lunch-and-learn session on “Obesity in GI Care – Embracing and Putting It into Practice” in which they discussed models of care delivery supporting obesity management in GI practice.

In November 2022, AGA released “AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity,” (https://shorturl.at/bDNOV) to aid clinicians in appropriately prescribing obesity pharmacotherapy on the front lines of care.

On the policy front, in June, AGA held a Capitol Hill briefing in support of H.R.1577 - Treat and Reduce Obesity Act of 2021 (TROA), a bipartisan bill that would improve access to obesity treatment and care by expanding coverage under Medicare Part D for FDA-approved obesity pharmacotherapy, as well as related services such as behavioral, nutrition, and other counseling. Please check out our new obesity advocacy toolkit for more information.

This month we update you on important multi-society guidance regarding peri-endoscopic management of GLP-1 receptor agonists. We highlight new AGA Clinical Practice Updates on ostomy management and use of gastric POEM for treatment of gastroparesis, as well as a randomized controlled trial from Gastroenterology showing the effectiveness of hemostatic powder in the management of malignant GI bleeding as compared with standard care.

In our Member Spotlight, we feature gastroenterologist Sameer Berry, MD, MBA, who discusses his role as a physician-entrepreneur seeking to transform GI care delivery through his AGA GI Opportunity Fund–supported company, Oshi Health.

This issue includes our annual supplement, “Gastroenterology Data Trends.” It features a collection of contributions on GI and climate change, long COVID and the GI tract, and the evolution of targeted therapies for C. difficile, among others.

We hope you enjoy this, and all the exciting content included in our October issue.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

AGA has long been a powerful voice in advocating locally and nationally for issues of critical importance to our profession and patients.

While AGA’s advocacy efforts related to access to colorectal cancer screening are frequently highlighted, this is one aspect of a larger advocacy agenda.

This month, I wish to highlight AGA’s extensive advocacy efforts focused on expanding access to obesity treatment. More than 2 in 5 adults in the U.S. have obesity, and weight management has been shown to be beneficial in patients with comorbid gastrointestinal diseases, such as metabolic dysfunction–associated steatotic liver disease, gastroesophageal reflux disease, gallbladder disease, pancreatitis, and GI malignancy.

In 2022, Inside Scope, a podcast by AGA, featured a 6-part seriescalled “Obesity in GI.” In July, Drs. Octavia Pickett-Blakely and Naresh Gunaratnam moderated a Gastro Bites lunch-and-learn session on “Obesity in GI Care – Embracing and Putting It into Practice” in which they discussed models of care delivery supporting obesity management in GI practice.

In November 2022, AGA released “AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity,” (https://shorturl.at/bDNOV) to aid clinicians in appropriately prescribing obesity pharmacotherapy on the front lines of care.

On the policy front, in June, AGA held a Capitol Hill briefing in support of H.R.1577 - Treat and Reduce Obesity Act of 2021 (TROA), a bipartisan bill that would improve access to obesity treatment and care by expanding coverage under Medicare Part D for FDA-approved obesity pharmacotherapy, as well as related services such as behavioral, nutrition, and other counseling. Please check out our new obesity advocacy toolkit for more information.

This month we update you on important multi-society guidance regarding peri-endoscopic management of GLP-1 receptor agonists. We highlight new AGA Clinical Practice Updates on ostomy management and use of gastric POEM for treatment of gastroparesis, as well as a randomized controlled trial from Gastroenterology showing the effectiveness of hemostatic powder in the management of malignant GI bleeding as compared with standard care.

In our Member Spotlight, we feature gastroenterologist Sameer Berry, MD, MBA, who discusses his role as a physician-entrepreneur seeking to transform GI care delivery through his AGA GI Opportunity Fund–supported company, Oshi Health.

This issue includes our annual supplement, “Gastroenterology Data Trends.” It features a collection of contributions on GI and climate change, long COVID and the GI tract, and the evolution of targeted therapies for C. difficile, among others.

We hope you enjoy this, and all the exciting content included in our October issue.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Massachusetts General Hospital

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

A version of this article first appeared on Medscape.com.

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Massachusetts General Hospital

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

A version of this article first appeared on Medscape.com.

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Massachusetts General Hospital

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The complex pathophysiology of obesity requires a multidisciplinary approach that includes lifestyle and medical interventions for successful management. Antiobesity medications (AOMs) have emerged as a powerful and life-changing tool for many individuals with obesity who are unable to sustain long-term weight loss through lifestyle changes alone. As with other chronic diseases such as hypertension and hyperlipidemia, the goal of decades of research has been to develop antiobesity medications with long-term efficacy and safety. Recent groundbreaking findings from a phase 2 trial show immense potential for a new AOM.

Here are five things to know about the role of agonists in the management of obesity.

1. Gut hormone physiology informs the development of AOMs.

The three hormones associated with obesity or diabetes are glucagonlike peptide 1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), and glucagon. GLP-1, a peptide released from the intestines in response to food ingestion, increases insulin production, reduces gut motility, and suppresses appetite. GIP is also an intestinal hormone that increases meal-stimulated insulin production and additionally facilitates lipolysis. Glucagon is known to increase hepatic glucose output but will also increase insulin secretion in the setting of hyperglycemia. Glucagon also promotes lipolysis.

Though these hormones are more commonly thought of as incretins, gut hormones that stimulate postprandial insulin secretion, their role in energy physiology is more diverse. Because of multiple mechanisms of action, incretins are increasingly referred to as nutrient-stimulated hormones (NuSH), a term which encompasses other peptides with therapeutic potential (e.g., amylin, oxyntomodulin, peptide tyrosine–tyrosine).

2. Studies have shown that NuSH therapies are highly effective AOMs.

In 2021 the Food and Drug Administration approved subcutaneous semaglutide 2.4 mg, a GLP-1 receptor agonist, for the treatment of obesity. Clinical trials demonstrating an average weight loss of 15% in patients taking semaglutide ushered in a new era of AOMs associated with significant weight loss that not only improve disease activity but also have the potential to achieve diabetes remission. Recent findings from the OASIS I trial demonstrated an average weight loss of 15.1% from baseline in patients treated with oral semaglutide for 68 weeks. Medical societies, including the American Diabetes Association and the American Association for the Study of Liver Diseases, recommend 10%-15% weight loss to fully treat weight-related comorbidities like type 2 diabetes and nonalcoholic fatty liver disease. In 2022, tirzepatide, a dual GLP-1 and GIP receptor agonist, demonstrated an average weight loss of 22.5% in phase 3 of the SURMOUNT-1 trial for obesity – a weight loss approaching that of some bariatric surgeries.

3. Clinical trial data show that the novel triple agonist retatrutide induces significant weight loss.

Preclinical studies on the newest NuSH therapy, triple GLP-1–GIP–glucagon receptor agonist retatrutide, showed predominant activity at the GIP receptor, with less GLP-1– and glucagon-receptor agonism than that of endogenous GLP-1 and GIP. Results from a phase 2 trial published in June 2023 showed a weight loss of 24% at 48 weeks in adults with obesity treated with retatrutide, which is the greatest weight loss reported in an obesity trial so far. Moreover, for the first time in obesity pharmacotherapy research, 100% of participants achieved clinically significant weight loss (defined as ≥ 5% of baseline weight).

4. Retatrutide may improve lipid metabolism.

In the phase 2 trial, retatrutide reduced low-density lipoprotein cholesterol levels by approximately 20%. This degree of reduced plasma LDL-C is dramatic in weight loss studies. Typically, weight loss significantly reduces triglyceride levels, increases high-density lipoprotein cholesterol levels, and has a modest effect on LDL-C reduction of about 5%.

A 20% reduction in LDL-C with retatrutide is hypothesis generating. Preclinical studies have shown glucagon to be an important regulator of proprotein convertase subtilisin/kexin type 9 degradation, with the lack of glucagon resulting in increased PCSK9 levels, decreased LDL receptors, and increased plasma LDL; conversely, treatment with glucagon decreased plasma LDL.

5. The long-term safety of retatrutide still needs to be determined.

In the 48-week phase 2 trial, retatrutide was observed to have a side-effect profile largely similar to other NuSH therapies (e.g., semaglutide 2.4 mg, tirzepatide), with a predominance of gastrointestinal symptoms including nausea, diarrhea, vomiting, and constipation. However, side effects potentially unique to retatrutide also emerged. Cutaneous hyperesthesia and skin sensitivity were reported in 7% of participants in the retatrutide group vs. 1% in the placebo group; none of these effects were associated with physical skin findings. Of note, 17 out of 198 (9%) participants in the retatrutide group developed cardiac arrhythmia vs. two out of 70 (3%) in the placebo group. There was no consistent pattern of arrhythmia type (e.g., supraventricular, ventricular) observed, and some of these events were reported as “palpitations” or “increased heart rate” without further detail. Phase 3 clinical trial data will provide further insight into the long-term safety of retatrutide.

Dr. Tchang is assistant professor of clinical medicine, division of endocrinology, Weill Cornell Medicine and physician, department of medicine, New York-Presbyterian/Weill Cornell Medical Center, both in New York. She has disclosed ties with Gelesis and Novo Nordisk.

A version of this article appeared on Medscape.com.

The complex pathophysiology of obesity requires a multidisciplinary approach that includes lifestyle and medical interventions for successful management. Antiobesity medications (AOMs) have emerged as a powerful and life-changing tool for many individuals with obesity who are unable to sustain long-term weight loss through lifestyle changes alone. As with other chronic diseases such as hypertension and hyperlipidemia, the goal of decades of research has been to develop antiobesity medications with long-term efficacy and safety. Recent groundbreaking findings from a phase 2 trial show immense potential for a new AOM.

Here are five things to know about the role of agonists in the management of obesity.

1. Gut hormone physiology informs the development of AOMs.

The three hormones associated with obesity or diabetes are glucagonlike peptide 1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), and glucagon. GLP-1, a peptide released from the intestines in response to food ingestion, increases insulin production, reduces gut motility, and suppresses appetite. GIP is also an intestinal hormone that increases meal-stimulated insulin production and additionally facilitates lipolysis. Glucagon is known to increase hepatic glucose output but will also increase insulin secretion in the setting of hyperglycemia. Glucagon also promotes lipolysis.

Though these hormones are more commonly thought of as incretins, gut hormones that stimulate postprandial insulin secretion, their role in energy physiology is more diverse. Because of multiple mechanisms of action, incretins are increasingly referred to as nutrient-stimulated hormones (NuSH), a term which encompasses other peptides with therapeutic potential (e.g., amylin, oxyntomodulin, peptide tyrosine–tyrosine).

2. Studies have shown that NuSH therapies are highly effective AOMs.

In 2021 the Food and Drug Administration approved subcutaneous semaglutide 2.4 mg, a GLP-1 receptor agonist, for the treatment of obesity. Clinical trials demonstrating an average weight loss of 15% in patients taking semaglutide ushered in a new era of AOMs associated with significant weight loss that not only improve disease activity but also have the potential to achieve diabetes remission. Recent findings from the OASIS I trial demonstrated an average weight loss of 15.1% from baseline in patients treated with oral semaglutide for 68 weeks. Medical societies, including the American Diabetes Association and the American Association for the Study of Liver Diseases, recommend 10%-15% weight loss to fully treat weight-related comorbidities like type 2 diabetes and nonalcoholic fatty liver disease. In 2022, tirzepatide, a dual GLP-1 and GIP receptor agonist, demonstrated an average weight loss of 22.5% in phase 3 of the SURMOUNT-1 trial for obesity – a weight loss approaching that of some bariatric surgeries.

3. Clinical trial data show that the novel triple agonist retatrutide induces significant weight loss.

Preclinical studies on the newest NuSH therapy, triple GLP-1–GIP–glucagon receptor agonist retatrutide, showed predominant activity at the GIP receptor, with less GLP-1– and glucagon-receptor agonism than that of endogenous GLP-1 and GIP. Results from a phase 2 trial published in June 2023 showed a weight loss of 24% at 48 weeks in adults with obesity treated with retatrutide, which is the greatest weight loss reported in an obesity trial so far. Moreover, for the first time in obesity pharmacotherapy research, 100% of participants achieved clinically significant weight loss (defined as ≥ 5% of baseline weight).

4. Retatrutide may improve lipid metabolism.

In the phase 2 trial, retatrutide reduced low-density lipoprotein cholesterol levels by approximately 20%. This degree of reduced plasma LDL-C is dramatic in weight loss studies. Typically, weight loss significantly reduces triglyceride levels, increases high-density lipoprotein cholesterol levels, and has a modest effect on LDL-C reduction of about 5%.

A 20% reduction in LDL-C with retatrutide is hypothesis generating. Preclinical studies have shown glucagon to be an important regulator of proprotein convertase subtilisin/kexin type 9 degradation, with the lack of glucagon resulting in increased PCSK9 levels, decreased LDL receptors, and increased plasma LDL; conversely, treatment with glucagon decreased plasma LDL.

5. The long-term safety of retatrutide still needs to be determined.

In the 48-week phase 2 trial, retatrutide was observed to have a side-effect profile largely similar to other NuSH therapies (e.g., semaglutide 2.4 mg, tirzepatide), with a predominance of gastrointestinal symptoms including nausea, diarrhea, vomiting, and constipation. However, side effects potentially unique to retatrutide also emerged. Cutaneous hyperesthesia and skin sensitivity were reported in 7% of participants in the retatrutide group vs. 1% in the placebo group; none of these effects were associated with physical skin findings. Of note, 17 out of 198 (9%) participants in the retatrutide group developed cardiac arrhythmia vs. two out of 70 (3%) in the placebo group. There was no consistent pattern of arrhythmia type (e.g., supraventricular, ventricular) observed, and some of these events were reported as “palpitations” or “increased heart rate” without further detail. Phase 3 clinical trial data will provide further insight into the long-term safety of retatrutide.

Dr. Tchang is assistant professor of clinical medicine, division of endocrinology, Weill Cornell Medicine and physician, department of medicine, New York-Presbyterian/Weill Cornell Medical Center, both in New York. She has disclosed ties with Gelesis and Novo Nordisk.

A version of this article appeared on Medscape.com.

The complex pathophysiology of obesity requires a multidisciplinary approach that includes lifestyle and medical interventions for successful management. Antiobesity medications (AOMs) have emerged as a powerful and life-changing tool for many individuals with obesity who are unable to sustain long-term weight loss through lifestyle changes alone. As with other chronic diseases such as hypertension and hyperlipidemia, the goal of decades of research has been to develop antiobesity medications with long-term efficacy and safety. Recent groundbreaking findings from a phase 2 trial show immense potential for a new AOM.

Here are five things to know about the role of agonists in the management of obesity.

1. Gut hormone physiology informs the development of AOMs.

The three hormones associated with obesity or diabetes are glucagonlike peptide 1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), and glucagon. GLP-1, a peptide released from the intestines in response to food ingestion, increases insulin production, reduces gut motility, and suppresses appetite. GIP is also an intestinal hormone that increases meal-stimulated insulin production and additionally facilitates lipolysis. Glucagon is known to increase hepatic glucose output but will also increase insulin secretion in the setting of hyperglycemia. Glucagon also promotes lipolysis.

Though these hormones are more commonly thought of as incretins, gut hormones that stimulate postprandial insulin secretion, their role in energy physiology is more diverse. Because of multiple mechanisms of action, incretins are increasingly referred to as nutrient-stimulated hormones (NuSH), a term which encompasses other peptides with therapeutic potential (e.g., amylin, oxyntomodulin, peptide tyrosine–tyrosine).

2. Studies have shown that NuSH therapies are highly effective AOMs.

In 2021 the Food and Drug Administration approved subcutaneous semaglutide 2.4 mg, a GLP-1 receptor agonist, for the treatment of obesity. Clinical trials demonstrating an average weight loss of 15% in patients taking semaglutide ushered in a new era of AOMs associated with significant weight loss that not only improve disease activity but also have the potential to achieve diabetes remission. Recent findings from the OASIS I trial demonstrated an average weight loss of 15.1% from baseline in patients treated with oral semaglutide for 68 weeks. Medical societies, including the American Diabetes Association and the American Association for the Study of Liver Diseases, recommend 10%-15% weight loss to fully treat weight-related comorbidities like type 2 diabetes and nonalcoholic fatty liver disease. In 2022, tirzepatide, a dual GLP-1 and GIP receptor agonist, demonstrated an average weight loss of 22.5% in phase 3 of the SURMOUNT-1 trial for obesity – a weight loss approaching that of some bariatric surgeries.

3. Clinical trial data show that the novel triple agonist retatrutide induces significant weight loss.

Preclinical studies on the newest NuSH therapy, triple GLP-1–GIP–glucagon receptor agonist retatrutide, showed predominant activity at the GIP receptor, with less GLP-1– and glucagon-receptor agonism than that of endogenous GLP-1 and GIP. Results from a phase 2 trial published in June 2023 showed a weight loss of 24% at 48 weeks in adults with obesity treated with retatrutide, which is the greatest weight loss reported in an obesity trial so far. Moreover, for the first time in obesity pharmacotherapy research, 100% of participants achieved clinically significant weight loss (defined as ≥ 5% of baseline weight).

4. Retatrutide may improve lipid metabolism.

In the phase 2 trial, retatrutide reduced low-density lipoprotein cholesterol levels by approximately 20%. This degree of reduced plasma LDL-C is dramatic in weight loss studies. Typically, weight loss significantly reduces triglyceride levels, increases high-density lipoprotein cholesterol levels, and has a modest effect on LDL-C reduction of about 5%.

A 20% reduction in LDL-C with retatrutide is hypothesis generating. Preclinical studies have shown glucagon to be an important regulator of proprotein convertase subtilisin/kexin type 9 degradation, with the lack of glucagon resulting in increased PCSK9 levels, decreased LDL receptors, and increased plasma LDL; conversely, treatment with glucagon decreased plasma LDL.

5. The long-term safety of retatrutide still needs to be determined.

In the 48-week phase 2 trial, retatrutide was observed to have a side-effect profile largely similar to other NuSH therapies (e.g., semaglutide 2.4 mg, tirzepatide), with a predominance of gastrointestinal symptoms including nausea, diarrhea, vomiting, and constipation. However, side effects potentially unique to retatrutide also emerged. Cutaneous hyperesthesia and skin sensitivity were reported in 7% of participants in the retatrutide group vs. 1% in the placebo group; none of these effects were associated with physical skin findings. Of note, 17 out of 198 (9%) participants in the retatrutide group developed cardiac arrhythmia vs. two out of 70 (3%) in the placebo group. There was no consistent pattern of arrhythmia type (e.g., supraventricular, ventricular) observed, and some of these events were reported as “palpitations” or “increased heart rate” without further detail. Phase 3 clinical trial data will provide further insight into the long-term safety of retatrutide.

Dr. Tchang is assistant professor of clinical medicine, division of endocrinology, Weill Cornell Medicine and physician, department of medicine, New York-Presbyterian/Weill Cornell Medical Center, both in New York. She has disclosed ties with Gelesis and Novo Nordisk.

A version of this article appeared on Medscape.com.

A significant mortality gap persists between patients with type 2 diabetes and cardiovascular disease and similarly aged patients with neither condition. Data from the Emerging Risk Factors Collaboration showed that on average, a 60-year-old female patient with type 2 diabetes and a history of myocardial infarction dies around 14 years earlier than a similarly aged patient with neither of these conditions.

Therefore, I was keen to hear the key new recommendations from the 2023 European Society of Cardiology (ESC) guidelines for the management of cardiovascular disease in patients with diabetes. These recommendations were presented at the recent ESC 2023 congress in Amsterdam, which I was fortunate enough to attend.

The comprehensive guideline cemented the fact that our primary goal in type 2 diabetes management is a reduction in cardiovascular events and mortality, rather than the glucocentric goals that have been followed previously. Of course, good glycemic control remains important to protect against the microvascular complications of diabetes, but glycemic control has only a modest impact on macrovascular complications such as cardiovascular disease.

The updated guideline recommends that all patients with type 2 diabetes without symptomatic atherosclerotic cardiovascular disease or severe target-organ damage be screened for the risk for cardiovascular disease using a new 10-year cardiovascular risk calculator called SCORE2-Diabetes. This calculator extends the well-established SCORE2 cardiovascular risk-prediction tool with added predictors specifically related to type 2 diabetes. It also accounts for variation in risk across Europe.

Using SCORE2 Diabetes will be a change in practice for me, as I have been using QRISK3, which is a United Kingdom–based cardiovascular risk tool that has been less extensively validated in patients with type 2 diabetes. Helpfully, an ESC CVD Risk Calculation app is available and can be tailored to your geographical region to calculate a SCORE2-Diabetes risk score easily. For example, Eastern Europe has a higher cardiovascular risk profile than Western Europe.

Cardiovascular risk categories are now defined on the basis of the presence of atherosclerotic cardiovascular disease, severe target-organ damage, or the 10-year cardiovascular risk using SCORE2-Diabetes.

For patients at very high cardiovascular risk (for example, those with type 2 diabetes and established atherosclerotic cardiovascular disease), the ESC guidance recommends dual therapy with a GLP-1 receptor agonist and an SGLT2 inhibitor to reduce cardiovascular risk independent of glucose control (that is, A1c). This dual therapy is recommended in addition to standard-of-care antiplatelet, antihypertensive, and lipid-lowering therapies.

There is no doubt that the evidence for GLP-1 receptor agonist use and reduction in atherosclerotic cardiovascular disease in type 2 diabetes is compelling, perhaps more so than the evidence for SGLT2 inhibitor use. However, this recommendation will be challenging to implement, given the current global supply issues with GLP-1 receptor agonists, which are driven by the off-label use of these medications for the management of obesity. GLP-1 receptor agonist supplies are not expected to stabilize until mid-2024.

Controversially, the updated ESC guidance suggests the use of metformin only in patients with type 2 diabetes and atherosclerotic cardiovascular disease if additional glucose control is required. This is a misstep, in my opinion, as insulin resistance is one of the key pathophysiologic abnormalities in patients with type 2 diabetes. One of the key advantages of metformin is an improvement in insulin sensitivity. This recommendation will not change my practice, and I will continue to prescribe metformin alongside GLP-1 receptor agonists or SGLT2 inhibitors for my patients at highest cardiovascular risk.

The updated ESC guidance also explicitly reminds healthcare professionals to look for significant comorbidities, such as heart failure of all subtypes and chronic kidney disease.

The ESC guidance recommends a systematic survey for heart failure symptoms and signs at each clinical encounter in all patients with type 2 diabetes. Although I agree that heart failure is underdiagnosed in this population, the recommendation will be challenging to implement and has significant workload implications, as heart failure often presents in insidious, nonspecific ways in primary care.

For patients with type 2 diabetes and heart failure with reduced ejection fraction, SGLT2 inhibitors are recommended to reduce the risk for heart failure hospitalization and cardiovascular death. Again, this recommendation is independent of glycemic control. In addition, for patients with type 2 diabetes and heart failure with mid-range ejection fraction or heart failure with preserved ejection fraction (that is, left ventricular ejection fraction > 40%), SGLT2 inhibitors are also recommended to reduce the risk for heart failure hospitalization or cardiovascular death independent of glycemic control. This recommendation is consistent with other updated global heart failure guidance. Increasingly, the pillars of heart failure therapy are being challenged with the early initiation of SGLT2 inhibitors, given their compelling evidence base, early symptomatic benefit, and ease of use, with less requirement of routine blood monitoring.

Finally, for patients with type 2 diabetes and chronic kidney disease, SGLT2 inhibitors and finerenone are now recommended to reduce the risk for kidney failure and cardiovascular disease, independent of glycemic control and in addition to standard of care.

Finerenone is a nonsteroidal selective mineralocorticoid receptor antagonist with quite different pharmacokinetics and clinical effects, compared with those of spironolactone and eplerenone, which are steroidal MRAs. Specifically, finerenone does not significantly lower blood pressure and has fewer steroid-induced adverse effects such as gynecomastia, impotence, and low libido. However, like steroidal MRAs, finerenone can result in hyperkalemia.

Finerenone has demonstrated significant kidney and cardiovascular benefits across the spectrum of chronic kidney disease in patients with type 2 diabetes. It entails no significant imbalance in adverse events, hence this recommendation. This observation reinforces the importance of measuring urinary albumin–creatinine ratio in patients with type 2 diabetes and preserved kidney function.

In conclusion, the 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes are forward-thinking recommendations. They look beyond glycemia and reflect the current evidence for newer glucose-lowering therapies with proven cardiorenal benefits. Nevertheless, the implementation of these guidelines will be challenging, given their workload implications, the unstable supply of GLP-1 receptor agonists, and a persisting glucocentric approach to type 2 diabetes care in some areas. Implementation will require ongoing education for health care professionals about the risk-benefit ratios of SGLT2 inhibitors and GLP-1 receptor agonists. It also will require a re-evaluation of workforce strategy to support the development of a skilled and sustainable workforce.

Dr. Fernando is a general practitioner partner with North Berwick (Scotland) Health Centre, with a specialist interest in diabetes; cardiovascular, renal, and metabolic diseases; and medical education. He disclosed receiving speakers’ fees from Eli Lilly and Novo Nordisk.

A version of this article appeared on Medscape.com.

A significant mortality gap persists between patients with type 2 diabetes and cardiovascular disease and similarly aged patients with neither condition. Data from the Emerging Risk Factors Collaboration showed that on average, a 60-year-old female patient with type 2 diabetes and a history of myocardial infarction dies around 14 years earlier than a similarly aged patient with neither of these conditions.

Therefore, I was keen to hear the key new recommendations from the 2023 European Society of Cardiology (ESC) guidelines for the management of cardiovascular disease in patients with diabetes. These recommendations were presented at the recent ESC 2023 congress in Amsterdam, which I was fortunate enough to attend.

The comprehensive guideline cemented the fact that our primary goal in type 2 diabetes management is a reduction in cardiovascular events and mortality, rather than the glucocentric goals that have been followed previously. Of course, good glycemic control remains important to protect against the microvascular complications of diabetes, but glycemic control has only a modest impact on macrovascular complications such as cardiovascular disease.

The updated guideline recommends that all patients with type 2 diabetes without symptomatic atherosclerotic cardiovascular disease or severe target-organ damage be screened for the risk for cardiovascular disease using a new 10-year cardiovascular risk calculator called SCORE2-Diabetes. This calculator extends the well-established SCORE2 cardiovascular risk-prediction tool with added predictors specifically related to type 2 diabetes. It also accounts for variation in risk across Europe.

Using SCORE2 Diabetes will be a change in practice for me, as I have been using QRISK3, which is a United Kingdom–based cardiovascular risk tool that has been less extensively validated in patients with type 2 diabetes. Helpfully, an ESC CVD Risk Calculation app is available and can be tailored to your geographical region to calculate a SCORE2-Diabetes risk score easily. For example, Eastern Europe has a higher cardiovascular risk profile than Western Europe.

Cardiovascular risk categories are now defined on the basis of the presence of atherosclerotic cardiovascular disease, severe target-organ damage, or the 10-year cardiovascular risk using SCORE2-Diabetes.

For patients at very high cardiovascular risk (for example, those with type 2 diabetes and established atherosclerotic cardiovascular disease), the ESC guidance recommends dual therapy with a GLP-1 receptor agonist and an SGLT2 inhibitor to reduce cardiovascular risk independent of glucose control (that is, A1c). This dual therapy is recommended in addition to standard-of-care antiplatelet, antihypertensive, and lipid-lowering therapies.

There is no doubt that the evidence for GLP-1 receptor agonist use and reduction in atherosclerotic cardiovascular disease in type 2 diabetes is compelling, perhaps more so than the evidence for SGLT2 inhibitor use. However, this recommendation will be challenging to implement, given the current global supply issues with GLP-1 receptor agonists, which are driven by the off-label use of these medications for the management of obesity. GLP-1 receptor agonist supplies are not expected to stabilize until mid-2024.

Controversially, the updated ESC guidance suggests the use of metformin only in patients with type 2 diabetes and atherosclerotic cardiovascular disease if additional glucose control is required. This is a misstep, in my opinion, as insulin resistance is one of the key pathophysiologic abnormalities in patients with type 2 diabetes. One of the key advantages of metformin is an improvement in insulin sensitivity. This recommendation will not change my practice, and I will continue to prescribe metformin alongside GLP-1 receptor agonists or SGLT2 inhibitors for my patients at highest cardiovascular risk.

The updated ESC guidance also explicitly reminds healthcare professionals to look for significant comorbidities, such as heart failure of all subtypes and chronic kidney disease.

The ESC guidance recommends a systematic survey for heart failure symptoms and signs at each clinical encounter in all patients with type 2 diabetes. Although I agree that heart failure is underdiagnosed in this population, the recommendation will be challenging to implement and has significant workload implications, as heart failure often presents in insidious, nonspecific ways in primary care.

For patients with type 2 diabetes and heart failure with reduced ejection fraction, SGLT2 inhibitors are recommended to reduce the risk for heart failure hospitalization and cardiovascular death. Again, this recommendation is independent of glycemic control. In addition, for patients with type 2 diabetes and heart failure with mid-range ejection fraction or heart failure with preserved ejection fraction (that is, left ventricular ejection fraction > 40%), SGLT2 inhibitors are also recommended to reduce the risk for heart failure hospitalization or cardiovascular death independent of glycemic control. This recommendation is consistent with other updated global heart failure guidance. Increasingly, the pillars of heart failure therapy are being challenged with the early initiation of SGLT2 inhibitors, given their compelling evidence base, early symptomatic benefit, and ease of use, with less requirement of routine blood monitoring.

Finally, for patients with type 2 diabetes and chronic kidney disease, SGLT2 inhibitors and finerenone are now recommended to reduce the risk for kidney failure and cardiovascular disease, independent of glycemic control and in addition to standard of care.

Finerenone is a nonsteroidal selective mineralocorticoid receptor antagonist with quite different pharmacokinetics and clinical effects, compared with those of spironolactone and eplerenone, which are steroidal MRAs. Specifically, finerenone does not significantly lower blood pressure and has fewer steroid-induced adverse effects such as gynecomastia, impotence, and low libido. However, like steroidal MRAs, finerenone can result in hyperkalemia.

Finerenone has demonstrated significant kidney and cardiovascular benefits across the spectrum of chronic kidney disease in patients with type 2 diabetes. It entails no significant imbalance in adverse events, hence this recommendation. This observation reinforces the importance of measuring urinary albumin–creatinine ratio in patients with type 2 diabetes and preserved kidney function.

In conclusion, the 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes are forward-thinking recommendations. They look beyond glycemia and reflect the current evidence for newer glucose-lowering therapies with proven cardiorenal benefits. Nevertheless, the implementation of these guidelines will be challenging, given their workload implications, the unstable supply of GLP-1 receptor agonists, and a persisting glucocentric approach to type 2 diabetes care in some areas. Implementation will require ongoing education for health care professionals about the risk-benefit ratios of SGLT2 inhibitors and GLP-1 receptor agonists. It also will require a re-evaluation of workforce strategy to support the development of a skilled and sustainable workforce.

Dr. Fernando is a general practitioner partner with North Berwick (Scotland) Health Centre, with a specialist interest in diabetes; cardiovascular, renal, and metabolic diseases; and medical education. He disclosed receiving speakers’ fees from Eli Lilly and Novo Nordisk.

A version of this article appeared on Medscape.com.

A significant mortality gap persists between patients with type 2 diabetes and cardiovascular disease and similarly aged patients with neither condition. Data from the Emerging Risk Factors Collaboration showed that on average, a 60-year-old female patient with type 2 diabetes and a history of myocardial infarction dies around 14 years earlier than a similarly aged patient with neither of these conditions.

Therefore, I was keen to hear the key new recommendations from the 2023 European Society of Cardiology (ESC) guidelines for the management of cardiovascular disease in patients with diabetes. These recommendations were presented at the recent ESC 2023 congress in Amsterdam, which I was fortunate enough to attend.

The comprehensive guideline cemented the fact that our primary goal in type 2 diabetes management is a reduction in cardiovascular events and mortality, rather than the glucocentric goals that have been followed previously. Of course, good glycemic control remains important to protect against the microvascular complications of diabetes, but glycemic control has only a modest impact on macrovascular complications such as cardiovascular disease.

The updated guideline recommends that all patients with type 2 diabetes without symptomatic atherosclerotic cardiovascular disease or severe target-organ damage be screened for the risk for cardiovascular disease using a new 10-year cardiovascular risk calculator called SCORE2-Diabetes. This calculator extends the well-established SCORE2 cardiovascular risk-prediction tool with added predictors specifically related to type 2 diabetes. It also accounts for variation in risk across Europe.

Using SCORE2 Diabetes will be a change in practice for me, as I have been using QRISK3, which is a United Kingdom–based cardiovascular risk tool that has been less extensively validated in patients with type 2 diabetes. Helpfully, an ESC CVD Risk Calculation app is available and can be tailored to your geographical region to calculate a SCORE2-Diabetes risk score easily. For example, Eastern Europe has a higher cardiovascular risk profile than Western Europe.

Cardiovascular risk categories are now defined on the basis of the presence of atherosclerotic cardiovascular disease, severe target-organ damage, or the 10-year cardiovascular risk using SCORE2-Diabetes.

For patients at very high cardiovascular risk (for example, those with type 2 diabetes and established atherosclerotic cardiovascular disease), the ESC guidance recommends dual therapy with a GLP-1 receptor agonist and an SGLT2 inhibitor to reduce cardiovascular risk independent of glucose control (that is, A1c). This dual therapy is recommended in addition to standard-of-care antiplatelet, antihypertensive, and lipid-lowering therapies.

There is no doubt that the evidence for GLP-1 receptor agonist use and reduction in atherosclerotic cardiovascular disease in type 2 diabetes is compelling, perhaps more so than the evidence for SGLT2 inhibitor use. However, this recommendation will be challenging to implement, given the current global supply issues with GLP-1 receptor agonists, which are driven by the off-label use of these medications for the management of obesity. GLP-1 receptor agonist supplies are not expected to stabilize until mid-2024.

Controversially, the updated ESC guidance suggests the use of metformin only in patients with type 2 diabetes and atherosclerotic cardiovascular disease if additional glucose control is required. This is a misstep, in my opinion, as insulin resistance is one of the key pathophysiologic abnormalities in patients with type 2 diabetes. One of the key advantages of metformin is an improvement in insulin sensitivity. This recommendation will not change my practice, and I will continue to prescribe metformin alongside GLP-1 receptor agonists or SGLT2 inhibitors for my patients at highest cardiovascular risk.

The updated ESC guidance also explicitly reminds healthcare professionals to look for significant comorbidities, such as heart failure of all subtypes and chronic kidney disease.

The ESC guidance recommends a systematic survey for heart failure symptoms and signs at each clinical encounter in all patients with type 2 diabetes. Although I agree that heart failure is underdiagnosed in this population, the recommendation will be challenging to implement and has significant workload implications, as heart failure often presents in insidious, nonspecific ways in primary care.

For patients with type 2 diabetes and heart failure with reduced ejection fraction, SGLT2 inhibitors are recommended to reduce the risk for heart failure hospitalization and cardiovascular death. Again, this recommendation is independent of glycemic control. In addition, for patients with type 2 diabetes and heart failure with mid-range ejection fraction or heart failure with preserved ejection fraction (that is, left ventricular ejection fraction > 40%), SGLT2 inhibitors are also recommended to reduce the risk for heart failure hospitalization or cardiovascular death independent of glycemic control. This recommendation is consistent with other updated global heart failure guidance. Increasingly, the pillars of heart failure therapy are being challenged with the early initiation of SGLT2 inhibitors, given their compelling evidence base, early symptomatic benefit, and ease of use, with less requirement of routine blood monitoring.

Finally, for patients with type 2 diabetes and chronic kidney disease, SGLT2 inhibitors and finerenone are now recommended to reduce the risk for kidney failure and cardiovascular disease, independent of glycemic control and in addition to standard of care.

Finerenone is a nonsteroidal selective mineralocorticoid receptor antagonist with quite different pharmacokinetics and clinical effects, compared with those of spironolactone and eplerenone, which are steroidal MRAs. Specifically, finerenone does not significantly lower blood pressure and has fewer steroid-induced adverse effects such as gynecomastia, impotence, and low libido. However, like steroidal MRAs, finerenone can result in hyperkalemia.

Finerenone has demonstrated significant kidney and cardiovascular benefits across the spectrum of chronic kidney disease in patients with type 2 diabetes. It entails no significant imbalance in adverse events, hence this recommendation. This observation reinforces the importance of measuring urinary albumin–creatinine ratio in patients with type 2 diabetes and preserved kidney function.

In conclusion, the 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes are forward-thinking recommendations. They look beyond glycemia and reflect the current evidence for newer glucose-lowering therapies with proven cardiorenal benefits. Nevertheless, the implementation of these guidelines will be challenging, given their workload implications, the unstable supply of GLP-1 receptor agonists, and a persisting glucocentric approach to type 2 diabetes care in some areas. Implementation will require ongoing education for health care professionals about the risk-benefit ratios of SGLT2 inhibitors and GLP-1 receptor agonists. It also will require a re-evaluation of workforce strategy to support the development of a skilled and sustainable workforce.

Dr. Fernando is a general practitioner partner with North Berwick (Scotland) Health Centre, with a specialist interest in diabetes; cardiovascular, renal, and metabolic diseases; and medical education. He disclosed receiving speakers’ fees from Eli Lilly and Novo Nordisk.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hello. It’s Mark Kris from Memorial Sloan-Kettering, still musing on things I learned at ASCO 2023.

I learned that there is a new C word.

People used to be afraid to use the word “cancer,” so they would call it the C word. Hopefully we’ve gotten over that stigma, that cancer is an illness that can be fought like any other illness.

There’s a new C word now that people seem, again, afraid to use, and that word is “cure.” It’s almost a true rarity that – again, I’m talking about the lung cancer world in particular – folks use the word “cure.” I didn’t hear it at ASCO, but the truth of the matter is that’s a word we should be using and be using more.

What do our patients want? I think if you truly ask a patient what their goal of care should be, it would be to cure the illness. What I mean by “cure” is to eradicate the cancer that is in their body, keep the cancer and its effects from interfering with their ability to continue their lives, and to do it for the length of their natural life. That’s what our patients want. Yes, overall survival is important, but not as much as a life free of cancer and the burden that it puts on people having cancer in the body.

When you start thinking about cure and how to make it a goal of care, a number of issues immediately crop up. The first one is defining what is meant by “cure.” We don’t have a strict definition of cure. Again, I would probably go to the patients and ask them what they mean by it. There may be some landmark part of the definition that needs to be discussed and addressed, but again, to me it’s having your life not disturbed by cancer, and that generally comes by eradicating cancer. Living with cancer is harder than the living after cancer has been cured. But we don’t have a good definition.

We also don’t have a good way of designing clinical trials to assess whether the regimen is curative. I don’t think I’ve ever seen a trial in lung cancer that looked at the ability of any given treatment to cure patients. We need to come up with ways to design trials to do that. Now, in addition to clinical trials, we don’t have a good body of evidence to design our preclinical experiments to look for those treatments that can lead to cures, or total eradication of cancer in whatever model system might be used. If we make cure the goal, then we need to find ways preclinically to identify those strategies that could lead to that.

Also in the realm of clinical trials, we need a very clear statistical underpinning to show that one or another treatment has a better chance of cure and to show with scientific rigor that one treatment is better than the other when it comes to cure. I think there needs to be more attention to this, and as we think about revamping the clinical trial process, we need to focus more on cure.

I’m saving the most important step for last. None of this can happen unless we try to make it happen and we say cure is possible. My mentor, George Boswell, always taught us that we would, in every single patient with cancer, try to develop a curative strategy. Is there a curative strategy for this patient? If so, pursue it with all the tools and vigor that we have. We really need to think that way.

Obviously, not every patient with cancer can be cured with our current armamentarium of anticancer treatments, but we need to make sure we put it on the table. We need to [confirm] that a strategy does not currently exist that could lead to cure. And of course, if we do find that strategy, we need to pursue it with all the energy and resources that we have.

Please don’t be afraid to use the word “cure.” Our patients want that. They deserve it. We should work hard to try to provide it and work toward developing strategies that we can propose and cure more patients.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York. His research interests include targeted therapies for lung cancer, multimodality therapy, the development of new anticancer drugs, and symptom management with a focus on preventing emesis.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello. It’s Mark Kris from Memorial Sloan-Kettering, still musing on things I learned at ASCO 2023.

I learned that there is a new C word.

People used to be afraid to use the word “cancer,” so they would call it the C word. Hopefully we’ve gotten over that stigma, that cancer is an illness that can be fought like any other illness.

There’s a new C word now that people seem, again, afraid to use, and that word is “cure.” It’s almost a true rarity that – again, I’m talking about the lung cancer world in particular – folks use the word “cure.” I didn’t hear it at ASCO, but the truth of the matter is that’s a word we should be using and be using more.

What do our patients want? I think if you truly ask a patient what their goal of care should be, it would be to cure the illness. What I mean by “cure” is to eradicate the cancer that is in their body, keep the cancer and its effects from interfering with their ability to continue their lives, and to do it for the length of their natural life. That’s what our patients want. Yes, overall survival is important, but not as much as a life free of cancer and the burden that it puts on people having cancer in the body.

When you start thinking about cure and how to make it a goal of care, a number of issues immediately crop up. The first one is defining what is meant by “cure.” We don’t have a strict definition of cure. Again, I would probably go to the patients and ask them what they mean by it. There may be some landmark part of the definition that needs to be discussed and addressed, but again, to me it’s having your life not disturbed by cancer, and that generally comes by eradicating cancer. Living with cancer is harder than the living after cancer has been cured. But we don’t have a good definition.

We also don’t have a good way of designing clinical trials to assess whether the regimen is curative. I don’t think I’ve ever seen a trial in lung cancer that looked at the ability of any given treatment to cure patients. We need to come up with ways to design trials to do that. Now, in addition to clinical trials, we don’t have a good body of evidence to design our preclinical experiments to look for those treatments that can lead to cures, or total eradication of cancer in whatever model system might be used. If we make cure the goal, then we need to find ways preclinically to identify those strategies that could lead to that.

Also in the realm of clinical trials, we need a very clear statistical underpinning to show that one or another treatment has a better chance of cure and to show with scientific rigor that one treatment is better than the other when it comes to cure. I think there needs to be more attention to this, and as we think about revamping the clinical trial process, we need to focus more on cure.

I’m saving the most important step for last. None of this can happen unless we try to make it happen and we say cure is possible. My mentor, George Boswell, always taught us that we would, in every single patient with cancer, try to develop a curative strategy. Is there a curative strategy for this patient? If so, pursue it with all the tools and vigor that we have. We really need to think that way.

Obviously, not every patient with cancer can be cured with our current armamentarium of anticancer treatments, but we need to make sure we put it on the table. We need to [confirm] that a strategy does not currently exist that could lead to cure. And of course, if we do find that strategy, we need to pursue it with all the energy and resources that we have.

Please don’t be afraid to use the word “cure.” Our patients want that. They deserve it. We should work hard to try to provide it and work toward developing strategies that we can propose and cure more patients.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York. His research interests include targeted therapies for lung cancer, multimodality therapy, the development of new anticancer drugs, and symptom management with a focus on preventing emesis.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello. It’s Mark Kris from Memorial Sloan-Kettering, still musing on things I learned at ASCO 2023.

I learned that there is a new C word.

People used to be afraid to use the word “cancer,” so they would call it the C word. Hopefully we’ve gotten over that stigma, that cancer is an illness that can be fought like any other illness.

There’s a new C word now that people seem, again, afraid to use, and that word is “cure.” It’s almost a true rarity that – again, I’m talking about the lung cancer world in particular – folks use the word “cure.” I didn’t hear it at ASCO, but the truth of the matter is that’s a word we should be using and be using more.

What do our patients want? I think if you truly ask a patient what their goal of care should be, it would be to cure the illness. What I mean by “cure” is to eradicate the cancer that is in their body, keep the cancer and its effects from interfering with their ability to continue their lives, and to do it for the length of their natural life. That’s what our patients want. Yes, overall survival is important, but not as much as a life free of cancer and the burden that it puts on people having cancer in the body.

When you start thinking about cure and how to make it a goal of care, a number of issues immediately crop up. The first one is defining what is meant by “cure.” We don’t have a strict definition of cure. Again, I would probably go to the patients and ask them what they mean by it. There may be some landmark part of the definition that needs to be discussed and addressed, but again, to me it’s having your life not disturbed by cancer, and that generally comes by eradicating cancer. Living with cancer is harder than the living after cancer has been cured. But we don’t have a good definition.

We also don’t have a good way of designing clinical trials to assess whether the regimen is curative. I don’t think I’ve ever seen a trial in lung cancer that looked at the ability of any given treatment to cure patients. We need to come up with ways to design trials to do that. Now, in addition to clinical trials, we don’t have a good body of evidence to design our preclinical experiments to look for those treatments that can lead to cures, or total eradication of cancer in whatever model system might be used. If we make cure the goal, then we need to find ways preclinically to identify those strategies that could lead to that.

Also in the realm of clinical trials, we need a very clear statistical underpinning to show that one or another treatment has a better chance of cure and to show with scientific rigor that one treatment is better than the other when it comes to cure. I think there needs to be more attention to this, and as we think about revamping the clinical trial process, we need to focus more on cure.

I’m saving the most important step for last. None of this can happen unless we try to make it happen and we say cure is possible. My mentor, George Boswell, always taught us that we would, in every single patient with cancer, try to develop a curative strategy. Is there a curative strategy for this patient? If so, pursue it with all the tools and vigor that we have. We really need to think that way.

Obviously, not every patient with cancer can be cured with our current armamentarium of anticancer treatments, but we need to make sure we put it on the table. We need to [confirm] that a strategy does not currently exist that could lead to cure. And of course, if we do find that strategy, we need to pursue it with all the energy and resources that we have.

Please don’t be afraid to use the word “cure.” Our patients want that. They deserve it. We should work hard to try to provide it and work toward developing strategies that we can propose and cure more patients.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York. His research interests include targeted therapies for lung cancer, multimodality therapy, the development of new anticancer drugs, and symptom management with a focus on preventing emesis.

A version of this article first appeared on Medscape.com.

Editor’s note: As of this writing, the following proposed health insurance policy from Blue Cross and Blue Shield of North Carolina is still active. The Coalition of State Rheumatology Organizations and other rheumatology advocacy groups are in ongoing discussions with the health insurer and hope to have major changes to this policy implemented.

While AI has been in our world for years, it is expanding by the minute, perhaps by the nanosecond, within the health care sector. The $6.7 billion dollar health care AI market in 2020 is expected to climb to more than $120 billion by 2028. There are many questions regarding the application of AI in our world. Is it a mere instructional algorithm that computes things in a much faster way, or does it create a new story based on the information it has access to? Does it engender excitement or fear ... or both? Remember HAL? As we have seen throughout history with new inventions and technologies, there are risks and rewards. Even the best can have harmful unintended consequences. AI is no different, particularly when it comes to health care. In this case, AI can get a bad name if it is utilized along with biased data input and bad policy.

Shared savings

Here is where “shared savings” comes into play. A shared savings program starts with a baseline cost analysis of a particular care plan and then tracks costs (performance) going forward after certain changes to the original care plan are instituted. If savings are accrued when compared with baseline spending, those savings are shared with the providers of the care. Depending on how the shared savings program is implemented, the optics can be very bad if it appears as though physicians are being paid to reduce care.

‘The volunteer opportunity’

Recently, Blue Cross and Blue Shield of North Carolina, in partnership with Outcomes Matter Innovations, a data analysis company that uses AI/machine-learning technology, offered rheumatologists a new voluntary shared savings, value-based care (VBC) “opportunity.” Rheumatologists would be able to “utilize a web-based machine-learning technology platform that suggests evidence-based care pathways” in the treatment of rheumatoid arthritis and psoriatic arthritis (PsA). The VBC/shared savings model uses the AI platform to propose two different pathways. One model would delay the start of biologics or Janus kinase inhibitors (JAKi), and the second model would taper and/or stop biologics or JAKi altogether.

Delaying the start of biologics/JAKi would be achieved through “methotrexate optimization” and/or the use of triple therapy with methotrexate, sulfasalazine, and hydroxychloroquine. The other model would recommend tapering biologic/JAKi dosing in patients in remission or low disease activity and might even suggest a “medication holiday.”

The intention of this 3-year VBC/shared savings program is to reduce costs and create savings by reducing the use of biologics or JAKi. A tangential question might be, “Reduce costs and create savings for whom?” Apparently, the patients will not reap any of the cost savings, as this is proposed to be a shared savings program with the savings going to the physicians and the insurance company. Perhaps the idea is that patients will benefit by reducing unneeded expensive medications.
 

How will it work?

A cost baseline will be established on biologic and JAKi use prior to the start of the program. Once started, there will be a calculation of savings based on biologic/JAKi use going forward. It was stated that physicians would receive 22% of the total costs saved. In one flyer, it was estimated that, with methotrexate optimization, rheumatologists could be paid an average of $1,527 a month per patient per month of delay before starting a biologic or JAKi.

The American College of Rheumatology has guidelines for the treatment of RA and PsA, and while optimizing methotrexate and triple therapy is mentioned, tapering or stopping treatment with biologics or JAKi is not. Additionally, after lack of response at 3 months, the standard of care is to change to a more effective treatment, which for most patients is a biologic disease-modifying antirheumatic drug (DMARD). It could be construed that rheumatologists are being monetarily incentivized to reduce the use of expensive medications through ways that are not included in ACR guidelines and are not standard of care.

What if after the medication holiday the patient cannot recapture control of their disease? Is there a liability concern? Remember, there is no institutional review board or informed patient consent for this VBC data gathering model.

How will a patient feel knowing that their physician was paid to withhold care, or even worse, if a patient is not told of this and then finds out later? Not only are the optics for this suboptimal (at best), where does the liability fall if the patient does not do well and it comes out that their rheumatologist was paid to reduce the care, particularly in a way that is not supported in the guideline. Clearly, this appears to be a clinical study without an institutional review board and without patient consent.

There are also the data that are collected from this voluntary “opportunity.” A valid question would be, “What kind of data will this produce if rheumatologists are paid to delay, reduce, or stop the use of biologics/JAKi?” Is it possible that physicians may subconsciously delay putting patients on a biologic and taper more rapidly because of the reimbursement? This could lead to faulty, biased, AI-generated data that erroneously show this type of care is working. It would not be unheard of to wonder whether this once-voluntary opportunity might evolve into mandatory policy because now, they have “data to prove it.” … only this time there is no shared savings.
 

Low disease activity results in long-term savings

This is not meant to be an indictment of AI in health care, value-based care, or shared savings programs. In reality, AI had very little to do with how poorly this program was presented. Hopefully, it will bring about further discussions on how to achieve savings without sacrificing care. In fact, optimal care in RA and PsA is probably one of the best ways to save money in the long run. Nowhere in this program is there any mention of the high cost associated with uncontrolled disease activity in patients with RA or PsA. The downstream costs can be enormous when long- and short-term sequelae are taken into consideration: joint replacements, cardiovascular disease, certain kinds of malignancies, and all the side effects of increased steroid usage are just a few of the consequences we see with uncontrolled disease activity. It is only recently that we have been able to achieve low disease activity and remission in our patients. The rush to get patients off these medications is not the answer to achieving long-term savings. In addition to the very bad optics of paying rheumatologists to delay, taper, or stop using expensive mediations in their patients, the ultimate data achieved will be biased, and the only real winner will be the health insurance company.

Again, AI machine-learning and shared saving programs are not the guilty parties here. In fact, AI may be helpful in coming up with solutions to long-term health care costs, whether in the realm of economics or scientific research. CSRO and our state member organizations continue to educate the health insurance company on the significant drawbacks to this “volunteer opportunity.” Let’s hope a more reasonable program is put forward with AI-generated data that can be trusted. Hopefully not with a platform named “HAL,” for those of you old enough to remember “2001: A Space Odyssey.”

Dr. Feldman is a rheumatologist in private practice with The Rheumatology Group in New Orleans. She is the CSRO’s vice president of advocacy and government affairs and its immediate past president, as well as past chair of the Alliance for Safe Biologic Medicines and a past member of the American College of Rheumatology insurance subcommittee. You can reach her at [email protected].

Editor’s note: As of this writing, the following proposed health insurance policy from Blue Cross and Blue Shield of North Carolina is still active. The Coalition of State Rheumatology Organizations and other rheumatology advocacy groups are in ongoing discussions with the health insurer and hope to have major changes to this policy implemented.

While AI has been in our world for years, it is expanding by the minute, perhaps by the nanosecond, within the health care sector. The $6.7 billion dollar health care AI market in 2020 is expected to climb to more than $120 billion by 2028. There are many questions regarding the application of AI in our world. Is it a mere instructional algorithm that computes things in a much faster way, or does it create a new story based on the information it has access to? Does it engender excitement or fear ... or both? Remember HAL? As we have seen throughout history with new inventions and technologies, there are risks and rewards. Even the best can have harmful unintended consequences. AI is no different, particularly when it comes to health care. In this case, AI can get a bad name if it is utilized along with biased data input and bad policy.

Shared savings

Here is where “shared savings” comes into play. A shared savings program starts with a baseline cost analysis of a particular care plan and then tracks costs (performance) going forward after certain changes to the original care plan are instituted. If savings are accrued when compared with baseline spending, those savings are shared with the providers of the care. Depending on how the shared savings program is implemented, the optics can be very bad if it appears as though physicians are being paid to reduce care.

‘The volunteer opportunity’

Recently, Blue Cross and Blue Shield of North Carolina, in partnership with Outcomes Matter Innovations, a data analysis company that uses AI/machine-learning technology, offered rheumatologists a new voluntary shared savings, value-based care (VBC) “opportunity.” Rheumatologists would be able to “utilize a web-based machine-learning technology platform that suggests evidence-based care pathways” in the treatment of rheumatoid arthritis and psoriatic arthritis (PsA). The VBC/shared savings model uses the AI platform to propose two different pathways. One model would delay the start of biologics or Janus kinase inhibitors (JAKi), and the second model would taper and/or stop biologics or JAKi altogether.

Delaying the start of biologics/JAKi would be achieved through “methotrexate optimization” and/or the use of triple therapy with methotrexate, sulfasalazine, and hydroxychloroquine. The other model would recommend tapering biologic/JAKi dosing in patients in remission or low disease activity and might even suggest a “medication holiday.”

The intention of this 3-year VBC/shared savings program is to reduce costs and create savings by reducing the use of biologics or JAKi. A tangential question might be, “Reduce costs and create savings for whom?” Apparently, the patients will not reap any of the cost savings, as this is proposed to be a shared savings program with the savings going to the physicians and the insurance company. Perhaps the idea is that patients will benefit by reducing unneeded expensive medications.
 

How will it work?

A cost baseline will be established on biologic and JAKi use prior to the start of the program. Once started, there will be a calculation of savings based on biologic/JAKi use going forward. It was stated that physicians would receive 22% of the total costs saved. In one flyer, it was estimated that, with methotrexate optimization, rheumatologists could be paid an average of $1,527 a month per patient per month of delay before starting a biologic or JAKi.

The American College of Rheumatology has guidelines for the treatment of RA and PsA, and while optimizing methotrexate and triple therapy is mentioned, tapering or stopping treatment with biologics or JAKi is not. Additionally, after lack of response at 3 months, the standard of care is to change to a more effective treatment, which for most patients is a biologic disease-modifying antirheumatic drug (DMARD). It could be construed that rheumatologists are being monetarily incentivized to reduce the use of expensive medications through ways that are not included in ACR guidelines and are not standard of care.

What if after the medication holiday the patient cannot recapture control of their disease? Is there a liability concern? Remember, there is no institutional review board or informed patient consent for this VBC data gathering model.

How will a patient feel knowing that their physician was paid to withhold care, or even worse, if a patient is not told of this and then finds out later? Not only are the optics for this suboptimal (at best), where does the liability fall if the patient does not do well and it comes out that their rheumatologist was paid to reduce the care, particularly in a way that is not supported in the guideline. Clearly, this appears to be a clinical study without an institutional review board and without patient consent.

There are also the data that are collected from this voluntary “opportunity.” A valid question would be, “What kind of data will this produce if rheumatologists are paid to delay, reduce, or stop the use of biologics/JAKi?” Is it possible that physicians may subconsciously delay putting patients on a biologic and taper more rapidly because of the reimbursement? This could lead to faulty, biased, AI-generated data that erroneously show this type of care is working. It would not be unheard of to wonder whether this once-voluntary opportunity might evolve into mandatory policy because now, they have “data to prove it.” … only this time there is no shared savings.
 

Low disease activity results in long-term savings

This is not meant to be an indictment of AI in health care, value-based care, or shared savings programs. In reality, AI had very little to do with how poorly this program was presented. Hopefully, it will bring about further discussions on how to achieve savings without sacrificing care. In fact, optimal care in RA and PsA is probably one of the best ways to save money in the long run. Nowhere in this program is there any mention of the high cost associated with uncontrolled disease activity in patients with RA or PsA. The downstream costs can be enormous when long- and short-term sequelae are taken into consideration: joint replacements, cardiovascular disease, certain kinds of malignancies, and all the side effects of increased steroid usage are just a few of the consequences we see with uncontrolled disease activity. It is only recently that we have been able to achieve low disease activity and remission in our patients. The rush to get patients off these medications is not the answer to achieving long-term savings. In addition to the very bad optics of paying rheumatologists to delay, taper, or stop using expensive mediations in their patients, the ultimate data achieved will be biased, and the only real winner will be the health insurance company.

Again, AI machine-learning and shared saving programs are not the guilty parties here. In fact, AI may be helpful in coming up with solutions to long-term health care costs, whether in the realm of economics or scientific research. CSRO and our state member organizations continue to educate the health insurance company on the significant drawbacks to this “volunteer opportunity.” Let’s hope a more reasonable program is put forward with AI-generated data that can be trusted. Hopefully not with a platform named “HAL,” for those of you old enough to remember “2001: A Space Odyssey.”

Dr. Feldman is a rheumatologist in private practice with The Rheumatology Group in New Orleans. She is the CSRO’s vice president of advocacy and government affairs and its immediate past president, as well as past chair of the Alliance for Safe Biologic Medicines and a past member of the American College of Rheumatology insurance subcommittee. You can reach her at [email protected].

Editor’s note: As of this writing, the following proposed health insurance policy from Blue Cross and Blue Shield of North Carolina is still active. The Coalition of State Rheumatology Organizations and other rheumatology advocacy groups are in ongoing discussions with the health insurer and hope to have major changes to this policy implemented.

While AI has been in our world for years, it is expanding by the minute, perhaps by the nanosecond, within the health care sector. The $6.7 billion dollar health care AI market in 2020 is expected to climb to more than $120 billion by 2028. There are many questions regarding the application of AI in our world. Is it a mere instructional algorithm that computes things in a much faster way, or does it create a new story based on the information it has access to? Does it engender excitement or fear ... or both? Remember HAL? As we have seen throughout history with new inventions and technologies, there are risks and rewards. Even the best can have harmful unintended consequences. AI is no different, particularly when it comes to health care. In this case, AI can get a bad name if it is utilized along with biased data input and bad policy.

Shared savings

Here is where “shared savings” comes into play. A shared savings program starts with a baseline cost analysis of a particular care plan and then tracks costs (performance) going forward after certain changes to the original care plan are instituted. If savings are accrued when compared with baseline spending, those savings are shared with the providers of the care. Depending on how the shared savings program is implemented, the optics can be very bad if it appears as though physicians are being paid to reduce care.

‘The volunteer opportunity’

Recently, Blue Cross and Blue Shield of North Carolina, in partnership with Outcomes Matter Innovations, a data analysis company that uses AI/machine-learning technology, offered rheumatologists a new voluntary shared savings, value-based care (VBC) “opportunity.” Rheumatologists would be able to “utilize a web-based machine-learning technology platform that suggests evidence-based care pathways” in the treatment of rheumatoid arthritis and psoriatic arthritis (PsA). The VBC/shared savings model uses the AI platform to propose two different pathways. One model would delay the start of biologics or Janus kinase inhibitors (JAKi), and the second model would taper and/or stop biologics or JAKi altogether.

Delaying the start of biologics/JAKi would be achieved through “methotrexate optimization” and/or the use of triple therapy with methotrexate, sulfasalazine, and hydroxychloroquine. The other model would recommend tapering biologic/JAKi dosing in patients in remission or low disease activity and might even suggest a “medication holiday.”

The intention of this 3-year VBC/shared savings program is to reduce costs and create savings by reducing the use of biologics or JAKi. A tangential question might be, “Reduce costs and create savings for whom?” Apparently, the patients will not reap any of the cost savings, as this is proposed to be a shared savings program with the savings going to the physicians and the insurance company. Perhaps the idea is that patients will benefit by reducing unneeded expensive medications.
 

How will it work?

A cost baseline will be established on biologic and JAKi use prior to the start of the program. Once started, there will be a calculation of savings based on biologic/JAKi use going forward. It was stated that physicians would receive 22% of the total costs saved. In one flyer, it was estimated that, with methotrexate optimization, rheumatologists could be paid an average of $1,527 a month per patient per month of delay before starting a biologic or JAKi.

The American College of Rheumatology has guidelines for the treatment of RA and PsA, and while optimizing methotrexate and triple therapy is mentioned, tapering or stopping treatment with biologics or JAKi is not. Additionally, after lack of response at 3 months, the standard of care is to change to a more effective treatment, which for most patients is a biologic disease-modifying antirheumatic drug (DMARD). It could be construed that rheumatologists are being monetarily incentivized to reduce the use of expensive medications through ways that are not included in ACR guidelines and are not standard of care.

What if after the medication holiday the patient cannot recapture control of their disease? Is there a liability concern? Remember, there is no institutional review board or informed patient consent for this VBC data gathering model.

How will a patient feel knowing that their physician was paid to withhold care, or even worse, if a patient is not told of this and then finds out later? Not only are the optics for this suboptimal (at best), where does the liability fall if the patient does not do well and it comes out that their rheumatologist was paid to reduce the care, particularly in a way that is not supported in the guideline. Clearly, this appears to be a clinical study without an institutional review board and without patient consent.

There are also the data that are collected from this voluntary “opportunity.” A valid question would be, “What kind of data will this produce if rheumatologists are paid to delay, reduce, or stop the use of biologics/JAKi?” Is it possible that physicians may subconsciously delay putting patients on a biologic and taper more rapidly because of the reimbursement? This could lead to faulty, biased, AI-generated data that erroneously show this type of care is working. It would not be unheard of to wonder whether this once-voluntary opportunity might evolve into mandatory policy because now, they have “data to prove it.” … only this time there is no shared savings.
 

Low disease activity results in long-term savings

This is not meant to be an indictment of AI in health care, value-based care, or shared savings programs. In reality, AI had very little to do with how poorly this program was presented. Hopefully, it will bring about further discussions on how to achieve savings without sacrificing care. In fact, optimal care in RA and PsA is probably one of the best ways to save money in the long run. Nowhere in this program is there any mention of the high cost associated with uncontrolled disease activity in patients with RA or PsA. The downstream costs can be enormous when long- and short-term sequelae are taken into consideration: joint replacements, cardiovascular disease, certain kinds of malignancies, and all the side effects of increased steroid usage are just a few of the consequences we see with uncontrolled disease activity. It is only recently that we have been able to achieve low disease activity and remission in our patients. The rush to get patients off these medications is not the answer to achieving long-term savings. In addition to the very bad optics of paying rheumatologists to delay, taper, or stop using expensive mediations in their patients, the ultimate data achieved will be biased, and the only real winner will be the health insurance company.

Again, AI machine-learning and shared saving programs are not the guilty parties here. In fact, AI may be helpful in coming up with solutions to long-term health care costs, whether in the realm of economics or scientific research. CSRO and our state member organizations continue to educate the health insurance company on the significant drawbacks to this “volunteer opportunity.” Let’s hope a more reasonable program is put forward with AI-generated data that can be trusted. Hopefully not with a platform named “HAL,” for those of you old enough to remember “2001: A Space Odyssey.”

Dr. Feldman is a rheumatologist in private practice with The Rheumatology Group in New Orleans. She is the CSRO’s vice president of advocacy and government affairs and its immediate past president, as well as past chair of the Alliance for Safe Biologic Medicines and a past member of the American College of Rheumatology insurance subcommittee. You can reach her at [email protected].