Old, Frail Patients: Study More, Intervene Less?

Article Type
Changed

Lessons From SENIOR-RITA

 

The ability to save cardiac muscle during an acute coronary syndrome with percutaneous coronary intervention (PCI) made cardiology one of the most popular fields in medicine.

But acute coronary syndromes come in different categories. While rapid PCI clearly benefits patients with ST-segment elevation myocardial infarction (STEMI), the best use of angiography and PCI for patients with non–ST-segment elevation myocardial infarction (NSTEMI) is more complex.

The evidence for early invasive vs conservative strategies in patients with NSTEMI is mixed. There have been many trials and meta-analyses, and generally, outcomes are similar with either approach. Perhaps if one looks with enough optimism, there is a benefit for the more aggressive approach in higher-risk patients.

Despite the similar outcomes with the two strategies, most patients are treated with the early invasive approach. Early and invasive fit the spirit of modern cardiology.

Yet, older patients with acute coronary syndromes present a different challenge. NSTEMI trials, like most trials, enrolled mostly younger adults. 

Whether evidence obtained in young people applies to older patients is one of the most common and important questions in all of medical practice. Older patients may be at higher risk for a primary outcome, but they also have greater risks for harm from therapy as well as more competing causes of morbidity and mortality. 

Only a handful of smaller trials have enrolled older patients with NSTEMI. These trials have produced little evidence that an early invasive approach should be preferred.
 

The SENIOR-RITA Trial

At ESC, Vijay Kunadian, MD, from Newcastle, England, presented results of SENIOR-RITA, a large trial comparing an invasive vs conservative strategy in NSTEMI patients 75 years of age or older. 

In the conservative arm, coronary angiography was allowed if the patient deteriorated and the procedure was clinically indicated in the judgment of the treating physicians.

Slightly more than 1500 patients with NSTEMI were randomly assigned to either strategy in 48 centers in the United Kingdom. Their mean age was 82 years, nearly half were women, and about a third were frail. 

Over 4 years of follow-up, the primary outcome of cardiovascular (CV) death or MI occurred at a similar rate in both arms: 25.6% vs 26.3% for invasive vs conservative, respectively (HR, 0.94; 95% CI, 0.77-1.14; P =.53). 

Rates of CV death were also not significantly different (15.8% vs 14.2%; HR, 1.11; 95% CI, 0.86-1.44). 

The rate of nonfatal MI was slightly lower in the invasive arm (11.7% vs 15.0%; HR, 0.75; 95% CI, 0.57-0.99).

Some other notable findings: Fewer than half of patients in the invasive arm underwent revascularization. Coronary angiography was done in about a quarter of patients in the conservative arm, and revascularization in only 14%. 

 

Comments

Because medicine has improved and patients live longer, cardiologists increasingly see older adults with frailty. It’s important to study these patients. 

The authors tell us that 1 in 5 patients screened were enrolled, and those not enrolled were similar in age and were treated nearly equally with either strategy. Not all trials offer this information; it’s important because knowing that patients in a trial are representative helps us translate evidence to our actual patients. 

Another positive was the investigators’ smart choice of cardiovascular death and MI as their primary outcome. Strategy trials are usually open label. If they had included an outcome that requires a decision from a clinician, such as unplanned revascularization, then bias becomes a possibility when patients and clinicians are aware of the treatment assignment. (I wrote about poor endpoint choice in the ABYSS trial.) 

The most notable finding in SENIOR-RITA was that approximately 76% of patients in the conservative arm did not have a coronary angiogram and 86% were not revascularized. 

Yet, the rate of CV death and MI were similar during 4 years of follow-up. This observation is nearly identical to the findings in chronic stable disease, seen in the ISCHEMIA trial. (See Figure 6a in the paper’s supplement.) 

I take two messages from this consistent observation: One is that medical therapy is quite good at treating coronary artery disease not associated with acute vessel closure in STEMI. 

The other is that using coronary angiography and revascularization as a bailout, in only a fraction of cases, achieves the same result, so the conservative strategy should be preferred.

I am not sure that the SENIOR-RITA researchers see it this way. They write in their discussion that “clinicians are often reluctant to offer an invasive strategy to frail older adults.” They then remind readers that modern PCI techniques (radial approach) have low rates of adverse events. 

Perhaps I misread their message, but that paragraph seemed like it was reinforcing our tendency to offer invasive approaches to patients with NSTEMI. 

I feel differently. When a trial reports similar outcomes with two strategies, I think we should favor the one with less intervention. I feel even more strongly about this philosophy in older patients with frailty.

Are we not in the business of helping people with the least amount of intervention?

The greatest challenge for the cardiologist of today is not a lack of treatment options, but whether we should use all options in older, frailer adults. 

Good on the SENIOR-RITA investigators, for they have shown that we can avoid intervention in the vast majority of older adults presenting with NSTEMI. 

Dr. Mandrola practices cardiac electrophysiology in Louisville, Kentucky, and is a writer and podcaster for Medscape. He espouses a conservative approach to medical practice. He participates in clinical research and writes often about the state of medical evidence. He has disclosed no relevant financial relationships.

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

Publications
Topics
Sections

Lessons From SENIOR-RITA

Lessons From SENIOR-RITA

 

The ability to save cardiac muscle during an acute coronary syndrome with percutaneous coronary intervention (PCI) made cardiology one of the most popular fields in medicine.

But acute coronary syndromes come in different categories. While rapid PCI clearly benefits patients with ST-segment elevation myocardial infarction (STEMI), the best use of angiography and PCI for patients with non–ST-segment elevation myocardial infarction (NSTEMI) is more complex.

The evidence for early invasive vs conservative strategies in patients with NSTEMI is mixed. There have been many trials and meta-analyses, and generally, outcomes are similar with either approach. Perhaps if one looks with enough optimism, there is a benefit for the more aggressive approach in higher-risk patients.

Despite the similar outcomes with the two strategies, most patients are treated with the early invasive approach. Early and invasive fit the spirit of modern cardiology.

Yet, older patients with acute coronary syndromes present a different challenge. NSTEMI trials, like most trials, enrolled mostly younger adults. 

Whether evidence obtained in young people applies to older patients is one of the most common and important questions in all of medical practice. Older patients may be at higher risk for a primary outcome, but they also have greater risks for harm from therapy as well as more competing causes of morbidity and mortality. 

Only a handful of smaller trials have enrolled older patients with NSTEMI. These trials have produced little evidence that an early invasive approach should be preferred.
 

The SENIOR-RITA Trial

At ESC, Vijay Kunadian, MD, from Newcastle, England, presented results of SENIOR-RITA, a large trial comparing an invasive vs conservative strategy in NSTEMI patients 75 years of age or older. 

In the conservative arm, coronary angiography was allowed if the patient deteriorated and the procedure was clinically indicated in the judgment of the treating physicians.

Slightly more than 1500 patients with NSTEMI were randomly assigned to either strategy in 48 centers in the United Kingdom. Their mean age was 82 years, nearly half were women, and about a third were frail. 

Over 4 years of follow-up, the primary outcome of cardiovascular (CV) death or MI occurred at a similar rate in both arms: 25.6% vs 26.3% for invasive vs conservative, respectively (HR, 0.94; 95% CI, 0.77-1.14; P =.53). 

Rates of CV death were also not significantly different (15.8% vs 14.2%; HR, 1.11; 95% CI, 0.86-1.44). 

The rate of nonfatal MI was slightly lower in the invasive arm (11.7% vs 15.0%; HR, 0.75; 95% CI, 0.57-0.99).

Some other notable findings: Fewer than half of patients in the invasive arm underwent revascularization. Coronary angiography was done in about a quarter of patients in the conservative arm, and revascularization in only 14%. 

 

Comments

Because medicine has improved and patients live longer, cardiologists increasingly see older adults with frailty. It’s important to study these patients. 

The authors tell us that 1 in 5 patients screened were enrolled, and those not enrolled were similar in age and were treated nearly equally with either strategy. Not all trials offer this information; it’s important because knowing that patients in a trial are representative helps us translate evidence to our actual patients. 

Another positive was the investigators’ smart choice of cardiovascular death and MI as their primary outcome. Strategy trials are usually open label. If they had included an outcome that requires a decision from a clinician, such as unplanned revascularization, then bias becomes a possibility when patients and clinicians are aware of the treatment assignment. (I wrote about poor endpoint choice in the ABYSS trial.) 

The most notable finding in SENIOR-RITA was that approximately 76% of patients in the conservative arm did not have a coronary angiogram and 86% were not revascularized. 

Yet, the rate of CV death and MI were similar during 4 years of follow-up. This observation is nearly identical to the findings in chronic stable disease, seen in the ISCHEMIA trial. (See Figure 6a in the paper’s supplement.) 

I take two messages from this consistent observation: One is that medical therapy is quite good at treating coronary artery disease not associated with acute vessel closure in STEMI. 

The other is that using coronary angiography and revascularization as a bailout, in only a fraction of cases, achieves the same result, so the conservative strategy should be preferred.

I am not sure that the SENIOR-RITA researchers see it this way. They write in their discussion that “clinicians are often reluctant to offer an invasive strategy to frail older adults.” They then remind readers that modern PCI techniques (radial approach) have low rates of adverse events. 

Perhaps I misread their message, but that paragraph seemed like it was reinforcing our tendency to offer invasive approaches to patients with NSTEMI. 

I feel differently. When a trial reports similar outcomes with two strategies, I think we should favor the one with less intervention. I feel even more strongly about this philosophy in older patients with frailty.

Are we not in the business of helping people with the least amount of intervention?

The greatest challenge for the cardiologist of today is not a lack of treatment options, but whether we should use all options in older, frailer adults. 

Good on the SENIOR-RITA investigators, for they have shown that we can avoid intervention in the vast majority of older adults presenting with NSTEMI. 

Dr. Mandrola practices cardiac electrophysiology in Louisville, Kentucky, and is a writer and podcaster for Medscape. He espouses a conservative approach to medical practice. He participates in clinical research and writes often about the state of medical evidence. He has disclosed no relevant financial relationships.

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

 

The ability to save cardiac muscle during an acute coronary syndrome with percutaneous coronary intervention (PCI) made cardiology one of the most popular fields in medicine.

But acute coronary syndromes come in different categories. While rapid PCI clearly benefits patients with ST-segment elevation myocardial infarction (STEMI), the best use of angiography and PCI for patients with non–ST-segment elevation myocardial infarction (NSTEMI) is more complex.

The evidence for early invasive vs conservative strategies in patients with NSTEMI is mixed. There have been many trials and meta-analyses, and generally, outcomes are similar with either approach. Perhaps if one looks with enough optimism, there is a benefit for the more aggressive approach in higher-risk patients.

Despite the similar outcomes with the two strategies, most patients are treated with the early invasive approach. Early and invasive fit the spirit of modern cardiology.

Yet, older patients with acute coronary syndromes present a different challenge. NSTEMI trials, like most trials, enrolled mostly younger adults. 

Whether evidence obtained in young people applies to older patients is one of the most common and important questions in all of medical practice. Older patients may be at higher risk for a primary outcome, but they also have greater risks for harm from therapy as well as more competing causes of morbidity and mortality. 

Only a handful of smaller trials have enrolled older patients with NSTEMI. These trials have produced little evidence that an early invasive approach should be preferred.
 

The SENIOR-RITA Trial

At ESC, Vijay Kunadian, MD, from Newcastle, England, presented results of SENIOR-RITA, a large trial comparing an invasive vs conservative strategy in NSTEMI patients 75 years of age or older. 

In the conservative arm, coronary angiography was allowed if the patient deteriorated and the procedure was clinically indicated in the judgment of the treating physicians.

Slightly more than 1500 patients with NSTEMI were randomly assigned to either strategy in 48 centers in the United Kingdom. Their mean age was 82 years, nearly half were women, and about a third were frail. 

Over 4 years of follow-up, the primary outcome of cardiovascular (CV) death or MI occurred at a similar rate in both arms: 25.6% vs 26.3% for invasive vs conservative, respectively (HR, 0.94; 95% CI, 0.77-1.14; P =.53). 

Rates of CV death were also not significantly different (15.8% vs 14.2%; HR, 1.11; 95% CI, 0.86-1.44). 

The rate of nonfatal MI was slightly lower in the invasive arm (11.7% vs 15.0%; HR, 0.75; 95% CI, 0.57-0.99).

Some other notable findings: Fewer than half of patients in the invasive arm underwent revascularization. Coronary angiography was done in about a quarter of patients in the conservative arm, and revascularization in only 14%. 

 

Comments

Because medicine has improved and patients live longer, cardiologists increasingly see older adults with frailty. It’s important to study these patients. 

The authors tell us that 1 in 5 patients screened were enrolled, and those not enrolled were similar in age and were treated nearly equally with either strategy. Not all trials offer this information; it’s important because knowing that patients in a trial are representative helps us translate evidence to our actual patients. 

Another positive was the investigators’ smart choice of cardiovascular death and MI as their primary outcome. Strategy trials are usually open label. If they had included an outcome that requires a decision from a clinician, such as unplanned revascularization, then bias becomes a possibility when patients and clinicians are aware of the treatment assignment. (I wrote about poor endpoint choice in the ABYSS trial.) 

The most notable finding in SENIOR-RITA was that approximately 76% of patients in the conservative arm did not have a coronary angiogram and 86% were not revascularized. 

Yet, the rate of CV death and MI were similar during 4 years of follow-up. This observation is nearly identical to the findings in chronic stable disease, seen in the ISCHEMIA trial. (See Figure 6a in the paper’s supplement.) 

I take two messages from this consistent observation: One is that medical therapy is quite good at treating coronary artery disease not associated with acute vessel closure in STEMI. 

The other is that using coronary angiography and revascularization as a bailout, in only a fraction of cases, achieves the same result, so the conservative strategy should be preferred.

I am not sure that the SENIOR-RITA researchers see it this way. They write in their discussion that “clinicians are often reluctant to offer an invasive strategy to frail older adults.” They then remind readers that modern PCI techniques (radial approach) have low rates of adverse events. 

Perhaps I misread their message, but that paragraph seemed like it was reinforcing our tendency to offer invasive approaches to patients with NSTEMI. 

I feel differently. When a trial reports similar outcomes with two strategies, I think we should favor the one with less intervention. I feel even more strongly about this philosophy in older patients with frailty.

Are we not in the business of helping people with the least amount of intervention?

The greatest challenge for the cardiologist of today is not a lack of treatment options, but whether we should use all options in older, frailer adults. 

Good on the SENIOR-RITA investigators, for they have shown that we can avoid intervention in the vast majority of older adults presenting with NSTEMI. 

Dr. Mandrola practices cardiac electrophysiology in Louisville, Kentucky, and is a writer and podcaster for Medscape. He espouses a conservative approach to medical practice. He participates in clinical research and writes often about the state of medical evidence. He has disclosed no relevant financial relationships.

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

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

Navigating Ethical and Clinical Considerations Relating to Percutaneous Gastrostomy (PEG) Tubes

Article Type
Changed

 

Cases

Consults for percutaneous gastrostomy (PEG) tube placement for a patient ...

  • With dysphagia after stroke: A 70-year-old female with a history of hypertension presented to the hospital with altered mental status and left-sided weakness. She was previously active and independently living. MRI of the brain revealed a right basal ganglia infarct. As a result, she developed dysphagia. She was evaluated by speech and language pathology and underwent a modified barium swallow. Given concerns for aspiration, the recommendation was made for gastroenterology (GI) consultation to place PEG tube for nutrition and medication administration.
  • With advanced dementia: An 85-year-old male with an extensive medical history including advanced dementia was admitted from his nursing home for decreased oral intake. His baseline mental status is awake and alert, but he is nonverbal and does not follow commands. Upon 72-hour calorie count, the nutrition consultants determined that he cannot independently meet his nutrition goals. His family wants “everything done” and are asking about a “feeding tube.” The primary team has now consulted GI for PEG tube placement.
  • Who is being discharged to a long-term care facility: A 45-year-old male was admitted to the ICU after a heroin overdose. CPR was initiated in the field and return of spontaneous circulation was obtained after 25 minutes. The patient has minimal brainstem reflexes. He is ventilator dependent. He has no family, and now is status-post tracheostomy placement by two-physician consent. The patient is ready for discharge to a long-term care facility that will not accept patients with nasogastric tubes. GI is consulted for PEG tube placement.

Discussion

Gastroenterologists are often consulted for PEG tube placement. However, the circumstances surrounding and the implications of PEG tube placement are often complicated for reasons beyond nutritional or technical considerations. This is rooted in the fact that, as one expert wrote, “feeding, unlike any other medical treatment, has a moral and emotional significance derived from culture.”1 Understanding the evidence, ethical considerations, and team dynamic behind PEG tube placement is critical for every gastroenterologist. Herein we review these topics and offer guidelines for having patient-centered conversations involving these fundamental concepts.

courtesy Paul Nguyen
Dr. Emily Seltzer

First, the gastroenterologist should understand the evidence to debunk myths and clarify truths surrounding PEG tube placement. While PEG tubes may help patients with amyotrophic lateral sclerosis stabilize their weight and can even be prophylactically placed in select patients with head and neck cancer,2,3 they are not always appropriate in patients in early recovery from stroke and have not been shown to improve outcomes in patients with advanced dementia. At least 50% of stroke-related dysphagia resolves within 1-2 weeks, and so the American Heart Association Stroke Council recommends continuing nasogastric tube feeding for 2-3 weeks in patients such as the one presented in case 1 before considering PEG tube placement.4

In situations of advanced dementia such as in case,2 several studies demonstrate that PEG tubes do not reduce or prevent aspiration pneumonia, prevent consequences of malnutrition, prolong life, reduce pressure ulcers, reduce urinary of gastrointestinal tract infections, lead to functional improvement, mitigate decline, or even improve comfort or quality of life for patients or their caregivers.5-7 Despite this evidence, as demonstrated in case,3 it is true that many American skilled nursing facilities will not accept a patient without a PEG if enteral feeding is needed. This restriction may vary by state: One study found that skilled nursing facilities in New York City are much less likely to accept patients with nasogastric feeding tubes than randomly selected skilled nursing facilities throughout the country.6 Nonetheless, gastroenterologists should look to the literature to understand the outcomes of populations of patients after PEG tube placement and use that data to guide decision-making.

courtesy Ohio State University Wexner Medical Center
Dr. Antoinette Pusateri

Secondly, the five ethical principles that inform all medical decision making – autonomy, beneficence, nonmaleficence, justice, and futility – should also inform the gastroenterologist’s rationale in offering PEG placement.8

Autonomy implies that the medical team has determined who is able to make the decision regarding PEG tube placement for the patient. Beneficence connects the patient’s medical diagnosis and technical parameters of PEG tube placement with his or her goals of care. Nonmaleficence ensures the decision-making party understands the benefits and risks of the procedure, including anticipatory guidance on possible PEG tube management, complications, risks, and need for replacement. Justice incorporates the context of the patient’s life, including family dynamics, religious, cultural, and financial factors. Futility connects the patient’s prognosis with practical aspects of having a PEG tube.

The complexity of PEG placement lies in the fact that these ethical principles are often at odds with each other. For example, case 2 highlights the conflicting principles of autonomy and futility for elderly dementia patients: While PEG tube placements do not improve comfort or quality of life in advanced dementia (futility), the family representing the patient has stated they want everything done for his care, including PEG tube placement (autonomy). Navigating these ethical principles can be difficult, but having a framework to organize the different factors offers sound guidance for the gastroenterologist.

courtesy Rusty Schramm
Dr. Anh Nguyen

Finally, the gastroenterologist should recognize the roles of the multidisciplinary team members, including the patient and their representatives, regarding PEG tube placement consults. While gastroenterologists can be viewed as the technicians consulted to simply “place the tube,” they must seek to understand the members of the team representing the patient to be stewards of their skill set. Consulting team physicians carry great responsibility in organizing the medical and psychosocial aspects of each patient’s care, and their proper goals to relieve suffering and prevent death may color their judgment regarding who they believe is a candidate for a PEG tube. Nutritionists, speech therapists, and case managers can help provide objective data on the practicality and feasibility of a PEG tube in their patients. The healthcare system may influence the decision to consult heavily, as seen in the rules of the long-term care facility in case.3 While it is the job of the multidisciplinary medical team to explain the evidence and ethical considerations of PEG tube placement in a patient-centered manner, ultimately the decision belongs to the patient and their family or representatives.

The moral burden of not pursuing PEG placement may supersede the medical advice in many situations. There is an emotionally taxing perception that withholding nutrition via PEG is “starving the patient,” despite literature showing many terminally ill patients do not experience thirst or hunger, and those who do have alleviation of these symptoms with small amounts of food or liquid, not with PEG placement.5 As every patient is unique, PEG tube consultation guidelines created with input from all stakeholders have been utilized to ensure that patients are medically optimized for PEG tube placement and that evidence and ethics-based considerations are evaluated by the multidisciplinary team. An example of such a guideline is shown in Figure 1.

courtesy Dr. Emily Seltzer
Figure 1. Navigating Percutaneous Gastrostomy Tube Placements: A Reference Guide for Gastroenterologists

If the gastroenterologist encounters more contentious consultations, there are ways to build consensus to both alleviate patient and family suffering as well as elevate the discussions between teams.

First, identify the type of consult that is repeatedly bringing differing viewpoints and differing ethical principles into play. Second, get representatives from teams together in a neutral environment to understand stakeholders needs. New data suggest, in stroke cases like case 1, there may be dramatic benefit in long-term ability to recover if patients can get early intensive rehabilitation.9 This intense daily rehabilitation is not available within the hospital setting at many locations, and facilitation of discharge may be requested earlier than usually advised tube placement. Third, build a common language for requests and responses between teams. For instance, neurologists can identify and document which patients have less likelihood of early spontaneous recovery, and this can allow gastroenterologists to understand that those patients with little potential for early swallowing recovery can safely be targeted for PEG earlier during the hospital course. Other patients described as having a potential for spontaneous improvement should be given time to recover before an intervention is considered.10 Having a common understanding of goals and a better-informed decision pathway helps each team member feel fulfilled and rewarded, which will ultimately help reduce compassion fatigue and moral burden on providers.

courtesy Robert Wood Johnson University Hospital
Dr. Ellen Stein

In conclusion, PEG tube placement can be a challenging consultation for gastroenterologists because of the clinical, social, and ethical ramifications at stake for the patient. Even when PEG tube placement is technically feasible, the gastroenterologist should feel empowered to address the evidence-based outcomes of PEG tube placement, discuss the ethical principles of the decision-making process, and communicate with a multidisciplinary team using guidelines as set forth by this paper to best serve the patient.

Dr. Seltzer is based in the Department of Internal Medicine, Mount Sinai Morningside-West, New York City. Dr. Pusateri is based in the Division of Gastroenterology, Hepatology and Nutrition, Ohio State University Wexner Medical Center, Columbus. Dr. Nguyen is based in the Division of Gastroenterology and Center for Esophageal Diseases, Baylor Scott & White Health, Dallas, Texas. Dr. Stein is based in the Division of Gastroenterology, Robert Wood Johnson University Hospital, Rutgers University, New Brunswick, New Jersey. All authors contributed equally to this manuscript, and have no disclosures related to this article.

References

1. Mackie S. Gastroenterol Nurs. 2001 May-Jun;24(3):138-42.

2. Miller RG et al. Neurology. 2009 Oct. doi: 10.1212/WNL.0b013e3181bc0141.

3. Colevas AD et al. J Natl Compr Canc Netw. 2018 May. doi: 10.6004/jnccn.2018.0026.

4. Holloway RG et al. Stroke. 2014 Jun. doi: 10.1161/STR.0000000000000015.

5. Finucane TE et al. JAMA. 1999 Oct. doi: 10.1001/jama.282.14.1365.

6. Burgermaster M et al. Nutr Clin Pract. 2016 Jun. doi: 10.1177/0884533616629636.

7. American Geriatrics Society Ethics C, Clinical P, Models of Care C. J Am Geriatr Soc. 2014 Aug. doi: 10.1111/jgs.12924.

8. Beauchamp TL. Principlism in Bioethics. In: Serna P, eds. Bioethical Decision Making and Argumentation. International Library of Ethics, Law, and the New Medicine, vol 70. Springer; Cham. 2016 Sept:1-16. doi: 10.1007/978-3-319-43419-3_1.

9. Powers WJ et al. Stroke. 2019 Oct. doi: 10.1161/STR.0000000000000211.

10. Galovic M et al. JAMA Neurol. 2019 May. doi: 10.1001/jamaneurol.2018.4858.

Publications
Topics
Sections

 

Cases

Consults for percutaneous gastrostomy (PEG) tube placement for a patient ...

  • With dysphagia after stroke: A 70-year-old female with a history of hypertension presented to the hospital with altered mental status and left-sided weakness. She was previously active and independently living. MRI of the brain revealed a right basal ganglia infarct. As a result, she developed dysphagia. She was evaluated by speech and language pathology and underwent a modified barium swallow. Given concerns for aspiration, the recommendation was made for gastroenterology (GI) consultation to place PEG tube for nutrition and medication administration.
  • With advanced dementia: An 85-year-old male with an extensive medical history including advanced dementia was admitted from his nursing home for decreased oral intake. His baseline mental status is awake and alert, but he is nonverbal and does not follow commands. Upon 72-hour calorie count, the nutrition consultants determined that he cannot independently meet his nutrition goals. His family wants “everything done” and are asking about a “feeding tube.” The primary team has now consulted GI for PEG tube placement.
  • Who is being discharged to a long-term care facility: A 45-year-old male was admitted to the ICU after a heroin overdose. CPR was initiated in the field and return of spontaneous circulation was obtained after 25 minutes. The patient has minimal brainstem reflexes. He is ventilator dependent. He has no family, and now is status-post tracheostomy placement by two-physician consent. The patient is ready for discharge to a long-term care facility that will not accept patients with nasogastric tubes. GI is consulted for PEG tube placement.

Discussion

Gastroenterologists are often consulted for PEG tube placement. However, the circumstances surrounding and the implications of PEG tube placement are often complicated for reasons beyond nutritional or technical considerations. This is rooted in the fact that, as one expert wrote, “feeding, unlike any other medical treatment, has a moral and emotional significance derived from culture.”1 Understanding the evidence, ethical considerations, and team dynamic behind PEG tube placement is critical for every gastroenterologist. Herein we review these topics and offer guidelines for having patient-centered conversations involving these fundamental concepts.

courtesy Paul Nguyen
Dr. Emily Seltzer

First, the gastroenterologist should understand the evidence to debunk myths and clarify truths surrounding PEG tube placement. While PEG tubes may help patients with amyotrophic lateral sclerosis stabilize their weight and can even be prophylactically placed in select patients with head and neck cancer,2,3 they are not always appropriate in patients in early recovery from stroke and have not been shown to improve outcomes in patients with advanced dementia. At least 50% of stroke-related dysphagia resolves within 1-2 weeks, and so the American Heart Association Stroke Council recommends continuing nasogastric tube feeding for 2-3 weeks in patients such as the one presented in case 1 before considering PEG tube placement.4

In situations of advanced dementia such as in case,2 several studies demonstrate that PEG tubes do not reduce or prevent aspiration pneumonia, prevent consequences of malnutrition, prolong life, reduce pressure ulcers, reduce urinary of gastrointestinal tract infections, lead to functional improvement, mitigate decline, or even improve comfort or quality of life for patients or their caregivers.5-7 Despite this evidence, as demonstrated in case,3 it is true that many American skilled nursing facilities will not accept a patient without a PEG if enteral feeding is needed. This restriction may vary by state: One study found that skilled nursing facilities in New York City are much less likely to accept patients with nasogastric feeding tubes than randomly selected skilled nursing facilities throughout the country.6 Nonetheless, gastroenterologists should look to the literature to understand the outcomes of populations of patients after PEG tube placement and use that data to guide decision-making.

courtesy Ohio State University Wexner Medical Center
Dr. Antoinette Pusateri

Secondly, the five ethical principles that inform all medical decision making – autonomy, beneficence, nonmaleficence, justice, and futility – should also inform the gastroenterologist’s rationale in offering PEG placement.8

Autonomy implies that the medical team has determined who is able to make the decision regarding PEG tube placement for the patient. Beneficence connects the patient’s medical diagnosis and technical parameters of PEG tube placement with his or her goals of care. Nonmaleficence ensures the decision-making party understands the benefits and risks of the procedure, including anticipatory guidance on possible PEG tube management, complications, risks, and need for replacement. Justice incorporates the context of the patient’s life, including family dynamics, religious, cultural, and financial factors. Futility connects the patient’s prognosis with practical aspects of having a PEG tube.

The complexity of PEG placement lies in the fact that these ethical principles are often at odds with each other. For example, case 2 highlights the conflicting principles of autonomy and futility for elderly dementia patients: While PEG tube placements do not improve comfort or quality of life in advanced dementia (futility), the family representing the patient has stated they want everything done for his care, including PEG tube placement (autonomy). Navigating these ethical principles can be difficult, but having a framework to organize the different factors offers sound guidance for the gastroenterologist.

courtesy Rusty Schramm
Dr. Anh Nguyen

Finally, the gastroenterologist should recognize the roles of the multidisciplinary team members, including the patient and their representatives, regarding PEG tube placement consults. While gastroenterologists can be viewed as the technicians consulted to simply “place the tube,” they must seek to understand the members of the team representing the patient to be stewards of their skill set. Consulting team physicians carry great responsibility in organizing the medical and psychosocial aspects of each patient’s care, and their proper goals to relieve suffering and prevent death may color their judgment regarding who they believe is a candidate for a PEG tube. Nutritionists, speech therapists, and case managers can help provide objective data on the practicality and feasibility of a PEG tube in their patients. The healthcare system may influence the decision to consult heavily, as seen in the rules of the long-term care facility in case.3 While it is the job of the multidisciplinary medical team to explain the evidence and ethical considerations of PEG tube placement in a patient-centered manner, ultimately the decision belongs to the patient and their family or representatives.

The moral burden of not pursuing PEG placement may supersede the medical advice in many situations. There is an emotionally taxing perception that withholding nutrition via PEG is “starving the patient,” despite literature showing many terminally ill patients do not experience thirst or hunger, and those who do have alleviation of these symptoms with small amounts of food or liquid, not with PEG placement.5 As every patient is unique, PEG tube consultation guidelines created with input from all stakeholders have been utilized to ensure that patients are medically optimized for PEG tube placement and that evidence and ethics-based considerations are evaluated by the multidisciplinary team. An example of such a guideline is shown in Figure 1.

courtesy Dr. Emily Seltzer
Figure 1. Navigating Percutaneous Gastrostomy Tube Placements: A Reference Guide for Gastroenterologists

If the gastroenterologist encounters more contentious consultations, there are ways to build consensus to both alleviate patient and family suffering as well as elevate the discussions between teams.

First, identify the type of consult that is repeatedly bringing differing viewpoints and differing ethical principles into play. Second, get representatives from teams together in a neutral environment to understand stakeholders needs. New data suggest, in stroke cases like case 1, there may be dramatic benefit in long-term ability to recover if patients can get early intensive rehabilitation.9 This intense daily rehabilitation is not available within the hospital setting at many locations, and facilitation of discharge may be requested earlier than usually advised tube placement. Third, build a common language for requests and responses between teams. For instance, neurologists can identify and document which patients have less likelihood of early spontaneous recovery, and this can allow gastroenterologists to understand that those patients with little potential for early swallowing recovery can safely be targeted for PEG earlier during the hospital course. Other patients described as having a potential for spontaneous improvement should be given time to recover before an intervention is considered.10 Having a common understanding of goals and a better-informed decision pathway helps each team member feel fulfilled and rewarded, which will ultimately help reduce compassion fatigue and moral burden on providers.

courtesy Robert Wood Johnson University Hospital
Dr. Ellen Stein

In conclusion, PEG tube placement can be a challenging consultation for gastroenterologists because of the clinical, social, and ethical ramifications at stake for the patient. Even when PEG tube placement is technically feasible, the gastroenterologist should feel empowered to address the evidence-based outcomes of PEG tube placement, discuss the ethical principles of the decision-making process, and communicate with a multidisciplinary team using guidelines as set forth by this paper to best serve the patient.

Dr. Seltzer is based in the Department of Internal Medicine, Mount Sinai Morningside-West, New York City. Dr. Pusateri is based in the Division of Gastroenterology, Hepatology and Nutrition, Ohio State University Wexner Medical Center, Columbus. Dr. Nguyen is based in the Division of Gastroenterology and Center for Esophageal Diseases, Baylor Scott & White Health, Dallas, Texas. Dr. Stein is based in the Division of Gastroenterology, Robert Wood Johnson University Hospital, Rutgers University, New Brunswick, New Jersey. All authors contributed equally to this manuscript, and have no disclosures related to this article.

References

1. Mackie S. Gastroenterol Nurs. 2001 May-Jun;24(3):138-42.

2. Miller RG et al. Neurology. 2009 Oct. doi: 10.1212/WNL.0b013e3181bc0141.

3. Colevas AD et al. J Natl Compr Canc Netw. 2018 May. doi: 10.6004/jnccn.2018.0026.

4. Holloway RG et al. Stroke. 2014 Jun. doi: 10.1161/STR.0000000000000015.

5. Finucane TE et al. JAMA. 1999 Oct. doi: 10.1001/jama.282.14.1365.

6. Burgermaster M et al. Nutr Clin Pract. 2016 Jun. doi: 10.1177/0884533616629636.

7. American Geriatrics Society Ethics C, Clinical P, Models of Care C. J Am Geriatr Soc. 2014 Aug. doi: 10.1111/jgs.12924.

8. Beauchamp TL. Principlism in Bioethics. In: Serna P, eds. Bioethical Decision Making and Argumentation. International Library of Ethics, Law, and the New Medicine, vol 70. Springer; Cham. 2016 Sept:1-16. doi: 10.1007/978-3-319-43419-3_1.

9. Powers WJ et al. Stroke. 2019 Oct. doi: 10.1161/STR.0000000000000211.

10. Galovic M et al. JAMA Neurol. 2019 May. doi: 10.1001/jamaneurol.2018.4858.

 

Cases

Consults for percutaneous gastrostomy (PEG) tube placement for a patient ...

  • With dysphagia after stroke: A 70-year-old female with a history of hypertension presented to the hospital with altered mental status and left-sided weakness. She was previously active and independently living. MRI of the brain revealed a right basal ganglia infarct. As a result, she developed dysphagia. She was evaluated by speech and language pathology and underwent a modified barium swallow. Given concerns for aspiration, the recommendation was made for gastroenterology (GI) consultation to place PEG tube for nutrition and medication administration.
  • With advanced dementia: An 85-year-old male with an extensive medical history including advanced dementia was admitted from his nursing home for decreased oral intake. His baseline mental status is awake and alert, but he is nonverbal and does not follow commands. Upon 72-hour calorie count, the nutrition consultants determined that he cannot independently meet his nutrition goals. His family wants “everything done” and are asking about a “feeding tube.” The primary team has now consulted GI for PEG tube placement.
  • Who is being discharged to a long-term care facility: A 45-year-old male was admitted to the ICU after a heroin overdose. CPR was initiated in the field and return of spontaneous circulation was obtained after 25 minutes. The patient has minimal brainstem reflexes. He is ventilator dependent. He has no family, and now is status-post tracheostomy placement by two-physician consent. The patient is ready for discharge to a long-term care facility that will not accept patients with nasogastric tubes. GI is consulted for PEG tube placement.

Discussion

Gastroenterologists are often consulted for PEG tube placement. However, the circumstances surrounding and the implications of PEG tube placement are often complicated for reasons beyond nutritional or technical considerations. This is rooted in the fact that, as one expert wrote, “feeding, unlike any other medical treatment, has a moral and emotional significance derived from culture.”1 Understanding the evidence, ethical considerations, and team dynamic behind PEG tube placement is critical for every gastroenterologist. Herein we review these topics and offer guidelines for having patient-centered conversations involving these fundamental concepts.

courtesy Paul Nguyen
Dr. Emily Seltzer

First, the gastroenterologist should understand the evidence to debunk myths and clarify truths surrounding PEG tube placement. While PEG tubes may help patients with amyotrophic lateral sclerosis stabilize their weight and can even be prophylactically placed in select patients with head and neck cancer,2,3 they are not always appropriate in patients in early recovery from stroke and have not been shown to improve outcomes in patients with advanced dementia. At least 50% of stroke-related dysphagia resolves within 1-2 weeks, and so the American Heart Association Stroke Council recommends continuing nasogastric tube feeding for 2-3 weeks in patients such as the one presented in case 1 before considering PEG tube placement.4

In situations of advanced dementia such as in case,2 several studies demonstrate that PEG tubes do not reduce or prevent aspiration pneumonia, prevent consequences of malnutrition, prolong life, reduce pressure ulcers, reduce urinary of gastrointestinal tract infections, lead to functional improvement, mitigate decline, or even improve comfort or quality of life for patients or their caregivers.5-7 Despite this evidence, as demonstrated in case,3 it is true that many American skilled nursing facilities will not accept a patient without a PEG if enteral feeding is needed. This restriction may vary by state: One study found that skilled nursing facilities in New York City are much less likely to accept patients with nasogastric feeding tubes than randomly selected skilled nursing facilities throughout the country.6 Nonetheless, gastroenterologists should look to the literature to understand the outcomes of populations of patients after PEG tube placement and use that data to guide decision-making.

courtesy Ohio State University Wexner Medical Center
Dr. Antoinette Pusateri

Secondly, the five ethical principles that inform all medical decision making – autonomy, beneficence, nonmaleficence, justice, and futility – should also inform the gastroenterologist’s rationale in offering PEG placement.8

Autonomy implies that the medical team has determined who is able to make the decision regarding PEG tube placement for the patient. Beneficence connects the patient’s medical diagnosis and technical parameters of PEG tube placement with his or her goals of care. Nonmaleficence ensures the decision-making party understands the benefits and risks of the procedure, including anticipatory guidance on possible PEG tube management, complications, risks, and need for replacement. Justice incorporates the context of the patient’s life, including family dynamics, religious, cultural, and financial factors. Futility connects the patient’s prognosis with practical aspects of having a PEG tube.

The complexity of PEG placement lies in the fact that these ethical principles are often at odds with each other. For example, case 2 highlights the conflicting principles of autonomy and futility for elderly dementia patients: While PEG tube placements do not improve comfort or quality of life in advanced dementia (futility), the family representing the patient has stated they want everything done for his care, including PEG tube placement (autonomy). Navigating these ethical principles can be difficult, but having a framework to organize the different factors offers sound guidance for the gastroenterologist.

courtesy Rusty Schramm
Dr. Anh Nguyen

Finally, the gastroenterologist should recognize the roles of the multidisciplinary team members, including the patient and their representatives, regarding PEG tube placement consults. While gastroenterologists can be viewed as the technicians consulted to simply “place the tube,” they must seek to understand the members of the team representing the patient to be stewards of their skill set. Consulting team physicians carry great responsibility in organizing the medical and psychosocial aspects of each patient’s care, and their proper goals to relieve suffering and prevent death may color their judgment regarding who they believe is a candidate for a PEG tube. Nutritionists, speech therapists, and case managers can help provide objective data on the practicality and feasibility of a PEG tube in their patients. The healthcare system may influence the decision to consult heavily, as seen in the rules of the long-term care facility in case.3 While it is the job of the multidisciplinary medical team to explain the evidence and ethical considerations of PEG tube placement in a patient-centered manner, ultimately the decision belongs to the patient and their family or representatives.

The moral burden of not pursuing PEG placement may supersede the medical advice in many situations. There is an emotionally taxing perception that withholding nutrition via PEG is “starving the patient,” despite literature showing many terminally ill patients do not experience thirst or hunger, and those who do have alleviation of these symptoms with small amounts of food or liquid, not with PEG placement.5 As every patient is unique, PEG tube consultation guidelines created with input from all stakeholders have been utilized to ensure that patients are medically optimized for PEG tube placement and that evidence and ethics-based considerations are evaluated by the multidisciplinary team. An example of such a guideline is shown in Figure 1.

courtesy Dr. Emily Seltzer
Figure 1. Navigating Percutaneous Gastrostomy Tube Placements: A Reference Guide for Gastroenterologists

If the gastroenterologist encounters more contentious consultations, there are ways to build consensus to both alleviate patient and family suffering as well as elevate the discussions between teams.

First, identify the type of consult that is repeatedly bringing differing viewpoints and differing ethical principles into play. Second, get representatives from teams together in a neutral environment to understand stakeholders needs. New data suggest, in stroke cases like case 1, there may be dramatic benefit in long-term ability to recover if patients can get early intensive rehabilitation.9 This intense daily rehabilitation is not available within the hospital setting at many locations, and facilitation of discharge may be requested earlier than usually advised tube placement. Third, build a common language for requests and responses between teams. For instance, neurologists can identify and document which patients have less likelihood of early spontaneous recovery, and this can allow gastroenterologists to understand that those patients with little potential for early swallowing recovery can safely be targeted for PEG earlier during the hospital course. Other patients described as having a potential for spontaneous improvement should be given time to recover before an intervention is considered.10 Having a common understanding of goals and a better-informed decision pathway helps each team member feel fulfilled and rewarded, which will ultimately help reduce compassion fatigue and moral burden on providers.

courtesy Robert Wood Johnson University Hospital
Dr. Ellen Stein

In conclusion, PEG tube placement can be a challenging consultation for gastroenterologists because of the clinical, social, and ethical ramifications at stake for the patient. Even when PEG tube placement is technically feasible, the gastroenterologist should feel empowered to address the evidence-based outcomes of PEG tube placement, discuss the ethical principles of the decision-making process, and communicate with a multidisciplinary team using guidelines as set forth by this paper to best serve the patient.

Dr. Seltzer is based in the Department of Internal Medicine, Mount Sinai Morningside-West, New York City. Dr. Pusateri is based in the Division of Gastroenterology, Hepatology and Nutrition, Ohio State University Wexner Medical Center, Columbus. Dr. Nguyen is based in the Division of Gastroenterology and Center for Esophageal Diseases, Baylor Scott & White Health, Dallas, Texas. Dr. Stein is based in the Division of Gastroenterology, Robert Wood Johnson University Hospital, Rutgers University, New Brunswick, New Jersey. All authors contributed equally to this manuscript, and have no disclosures related to this article.

References

1. Mackie S. Gastroenterol Nurs. 2001 May-Jun;24(3):138-42.

2. Miller RG et al. Neurology. 2009 Oct. doi: 10.1212/WNL.0b013e3181bc0141.

3. Colevas AD et al. J Natl Compr Canc Netw. 2018 May. doi: 10.6004/jnccn.2018.0026.

4. Holloway RG et al. Stroke. 2014 Jun. doi: 10.1161/STR.0000000000000015.

5. Finucane TE et al. JAMA. 1999 Oct. doi: 10.1001/jama.282.14.1365.

6. Burgermaster M et al. Nutr Clin Pract. 2016 Jun. doi: 10.1177/0884533616629636.

7. American Geriatrics Society Ethics C, Clinical P, Models of Care C. J Am Geriatr Soc. 2014 Aug. doi: 10.1111/jgs.12924.

8. Beauchamp TL. Principlism in Bioethics. In: Serna P, eds. Bioethical Decision Making and Argumentation. International Library of Ethics, Law, and the New Medicine, vol 70. Springer; Cham. 2016 Sept:1-16. doi: 10.1007/978-3-319-43419-3_1.

9. Powers WJ et al. Stroke. 2019 Oct. doi: 10.1161/STR.0000000000000211.

10. Galovic M et al. JAMA Neurol. 2019 May. doi: 10.1001/jamaneurol.2018.4858.

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

ANA Testing: When to Tap the Brakes

Article Type
Changed

 

This transcript has been edited for clarity

There are five reasons you do not want to order that notorious antinuclear antibody (ANA) test — when a patient comes into your office and you say, “Let’s just run a wellness check” and you order the ANA test, or the patient comes in and says, “Hey doc, order everything, okay?” — without really thinking these things through.

1. I’m sure you know that the ANA test, if positive, does not exclude other conditions. For instance, older women could have a positive ANA test; it’s very common in this group. 

2. There’s a high false-positive rate for an ANA test. For instance, cancers and viral infections can cause an ANA test to be positive, and certain medications can cause a false-positive ANA test. 

3. Context matters. If you have a patient that has particular symptoms, joint swelling, a strong family history of autoimmune disease, a luminal rash that you can’t understand, hair loss, those kind of things, then yes, when you order that ANA test, it’s going to be valuable. If the patient does not have those symptoms, you are just running down this rabbit hole that causes worry for you and your patient. 

4. The ANA test on its own is not helpful until you order the subtypes. Double-stranded DNA and anti-SSA or anti-SSB antibodies are just a few examples of the subtypes of the ANA test that really help you understand what you ordered. 

5. The elephant in the room: What is the pretest probability of your diagnostic test — all the symptoms, the hair loss, the malar rash, the sores in the mouth, the joint swelling, the blood in the urine? Fluid around the heart, pericarditis, pleurisy, those kinds of symptoms, right? When you have those symptoms and you order an ANA test, then you have basically put directions into your GPS. So now you know that if the test is positive, these are the things you’re going to do with the test going forward.

I hope that these five things have told you: Hey, before you order that ANA test, let’s make sure that we’re not causing unnecessary stress for our patients and also minimizing unnecessary testing.

Dr. Dada, CEO, Overlake Arthritis and Osteoporosis Center, Bellevue, Washington, disclosed ties with Horizon Pharmaceuticals.

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

Publications
Topics
Sections

 

This transcript has been edited for clarity

There are five reasons you do not want to order that notorious antinuclear antibody (ANA) test — when a patient comes into your office and you say, “Let’s just run a wellness check” and you order the ANA test, or the patient comes in and says, “Hey doc, order everything, okay?” — without really thinking these things through.

1. I’m sure you know that the ANA test, if positive, does not exclude other conditions. For instance, older women could have a positive ANA test; it’s very common in this group. 

2. There’s a high false-positive rate for an ANA test. For instance, cancers and viral infections can cause an ANA test to be positive, and certain medications can cause a false-positive ANA test. 

3. Context matters. If you have a patient that has particular symptoms, joint swelling, a strong family history of autoimmune disease, a luminal rash that you can’t understand, hair loss, those kind of things, then yes, when you order that ANA test, it’s going to be valuable. If the patient does not have those symptoms, you are just running down this rabbit hole that causes worry for you and your patient. 

4. The ANA test on its own is not helpful until you order the subtypes. Double-stranded DNA and anti-SSA or anti-SSB antibodies are just a few examples of the subtypes of the ANA test that really help you understand what you ordered. 

5. The elephant in the room: What is the pretest probability of your diagnostic test — all the symptoms, the hair loss, the malar rash, the sores in the mouth, the joint swelling, the blood in the urine? Fluid around the heart, pericarditis, pleurisy, those kinds of symptoms, right? When you have those symptoms and you order an ANA test, then you have basically put directions into your GPS. So now you know that if the test is positive, these are the things you’re going to do with the test going forward.

I hope that these five things have told you: Hey, before you order that ANA test, let’s make sure that we’re not causing unnecessary stress for our patients and also minimizing unnecessary testing.

Dr. Dada, CEO, Overlake Arthritis and Osteoporosis Center, Bellevue, Washington, disclosed ties with Horizon Pharmaceuticals.

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

 

This transcript has been edited for clarity

There are five reasons you do not want to order that notorious antinuclear antibody (ANA) test — when a patient comes into your office and you say, “Let’s just run a wellness check” and you order the ANA test, or the patient comes in and says, “Hey doc, order everything, okay?” — without really thinking these things through.

1. I’m sure you know that the ANA test, if positive, does not exclude other conditions. For instance, older women could have a positive ANA test; it’s very common in this group. 

2. There’s a high false-positive rate for an ANA test. For instance, cancers and viral infections can cause an ANA test to be positive, and certain medications can cause a false-positive ANA test. 

3. Context matters. If you have a patient that has particular symptoms, joint swelling, a strong family history of autoimmune disease, a luminal rash that you can’t understand, hair loss, those kind of things, then yes, when you order that ANA test, it’s going to be valuable. If the patient does not have those symptoms, you are just running down this rabbit hole that causes worry for you and your patient. 

4. The ANA test on its own is not helpful until you order the subtypes. Double-stranded DNA and anti-SSA or anti-SSB antibodies are just a few examples of the subtypes of the ANA test that really help you understand what you ordered. 

5. The elephant in the room: What is the pretest probability of your diagnostic test — all the symptoms, the hair loss, the malar rash, the sores in the mouth, the joint swelling, the blood in the urine? Fluid around the heart, pericarditis, pleurisy, those kinds of symptoms, right? When you have those symptoms and you order an ANA test, then you have basically put directions into your GPS. So now you know that if the test is positive, these are the things you’re going to do with the test going forward.

I hope that these five things have told you: Hey, before you order that ANA test, let’s make sure that we’re not causing unnecessary stress for our patients and also minimizing unnecessary testing.

Dr. Dada, CEO, Overlake Arthritis and Osteoporosis Center, Bellevue, Washington, disclosed ties with Horizon Pharmaceuticals.

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

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

Diabetes Increases Injury Risk: A Troubling Trend

Article Type
Changed

 

In 2024, a record number of people are celebrating their 65th birthdays. Increasing age is associated with a higher risk for falls, fractures, and other injuries that may require hospitalization. 

In older adults with type 1 and type 2 diabetes, the risk for falls is double that seen in older people without these conditions. Increased clinician awareness of the many factors that result in this higher risk in people with diabetes, and timely implementation of strategies to prevent falls, are essential.

The annual incidence of falls in people with diabetes older than 65 years is about 39%, compared with 19% among those without diabetes. People with diabetes on insulin face an even greater increased risk for falls compared with those who are not using insulin (94% vs 27% increased risk).

Many well-known aspects of diabetes contribute to this greater risk. These include decreased sensorimotor function, musculoskeletal and neuromuscular deficits, foot and body pain, poor vision, hypoglycemic episodes, pharmacologic complications, and problems with hearing and balance. 

Optimal management of diabetes and its complications is essential, and the American Diabetes Association has developed clear guidelines for clinicians to follow to reduce the risk for diabetes related complications and manage these conditions.

The prevalence of diabetic peripheral neuropathy increases with age and duration of diabetes. People with diabetic peripheral neuropathy and diminished sensation on their feet are at increased risk for loss of postural control. Loss of proprioceptive feedback (the ability to sense movement, action and location) during standing and walking leads increases the risk for falls.

In addition, less physical activity, impaired muscle strength, and suboptimal postural control all influence gait patterns and increase the risk for falling. Adults with diabetes have a two to three times higher risk for sarcopenia (decreased muscle strength and muscle mass). They also have low plantar flexion strength, causing increased displacement of their center of gravity, which in turn reduces their maximum forward stride and may result in falls and injury.

Many people with diabetes experience neuropathic foot and body pain, requiring psychotropic and other medications that may exacerbate the risk, such as amitriptyline and duloxetine. Furthermore, older adults with diabetes are more likely to take more prescription medications and may be more sensitive to effects of multiple medications than are individuals without diabetes.

A hazard of managing diabetes, particularly with insulin, is the increased risk for unexpected low blood glucose levels. These episodes can also occur in patients taking certain kinds of oral diabetes medications, but they are more common in those on insulin. Low blood glucose can cause dizziness, confusion, and postural instability, increasing the risk for falling.

Diabetic eye complications include retinopathy, macular edema, cataracts, and glaucoma. In a study of close to 10,000 middle-aged and older adults with diabetes, those with moderate eye complications had almost double the risk of falls as those without eye complications.

Another concern with diabetes is its effect on nerves and blood vessels in the inner ear, leading to a negative effect on balance and hearing loss, both of which are also associated with a higher risk for falling and injury.

Clinicians can reduce the risk for falls in patients by taking measures to improve diabetes control and reduce the risk for microvascular disease affecting the nerves, eyes, and ears. 

In addition, exercises that optimize muscle mass, bone strength, gait, and balance, and use of specialized footwear in people with neuropathy, may reduce fall risk. Chair yoga and tai chi have also been shown to be helpful. Clinicians can also advise patients on commonsense strategies to implement in their homes, such as ensuring proper lighting, reducing, clutter and minimizing the use of floor rugs.

The risk for falls and the associated risk for fracture and possible hospitalization are of significant concern in older adults — particularly those with diabetes, and even more so in those with diabetes who are on insulin. It is our responsibility as clinicians to implement strategies to optimize diabetes control in our patients and monitor them for microvascular and other complications that may increase this risk, and manage them appropriately if and when these complications occur.

Madhusmita Misra, Professor, Chair, Physician-in-Chief, Department of Pediatrics, University of Virginia and UVA Health Children’s, Charlottesville, has disclosed being a key opinion leader for Lumos Pharma. Sidhartha Pani, Assistant Professor, Department of Internal Medicine, UVA School of Medicine; Medical Director, Department of General Medicine, Same Day Care Clinic, Charlottesville, disclosed no relevant financial relationships.

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

Publications
Topics
Sections

 

In 2024, a record number of people are celebrating their 65th birthdays. Increasing age is associated with a higher risk for falls, fractures, and other injuries that may require hospitalization. 

In older adults with type 1 and type 2 diabetes, the risk for falls is double that seen in older people without these conditions. Increased clinician awareness of the many factors that result in this higher risk in people with diabetes, and timely implementation of strategies to prevent falls, are essential.

The annual incidence of falls in people with diabetes older than 65 years is about 39%, compared with 19% among those without diabetes. People with diabetes on insulin face an even greater increased risk for falls compared with those who are not using insulin (94% vs 27% increased risk).

Many well-known aspects of diabetes contribute to this greater risk. These include decreased sensorimotor function, musculoskeletal and neuromuscular deficits, foot and body pain, poor vision, hypoglycemic episodes, pharmacologic complications, and problems with hearing and balance. 

Optimal management of diabetes and its complications is essential, and the American Diabetes Association has developed clear guidelines for clinicians to follow to reduce the risk for diabetes related complications and manage these conditions.

The prevalence of diabetic peripheral neuropathy increases with age and duration of diabetes. People with diabetic peripheral neuropathy and diminished sensation on their feet are at increased risk for loss of postural control. Loss of proprioceptive feedback (the ability to sense movement, action and location) during standing and walking leads increases the risk for falls.

In addition, less physical activity, impaired muscle strength, and suboptimal postural control all influence gait patterns and increase the risk for falling. Adults with diabetes have a two to three times higher risk for sarcopenia (decreased muscle strength and muscle mass). They also have low plantar flexion strength, causing increased displacement of their center of gravity, which in turn reduces their maximum forward stride and may result in falls and injury.

Many people with diabetes experience neuropathic foot and body pain, requiring psychotropic and other medications that may exacerbate the risk, such as amitriptyline and duloxetine. Furthermore, older adults with diabetes are more likely to take more prescription medications and may be more sensitive to effects of multiple medications than are individuals without diabetes.

A hazard of managing diabetes, particularly with insulin, is the increased risk for unexpected low blood glucose levels. These episodes can also occur in patients taking certain kinds of oral diabetes medications, but they are more common in those on insulin. Low blood glucose can cause dizziness, confusion, and postural instability, increasing the risk for falling.

Diabetic eye complications include retinopathy, macular edema, cataracts, and glaucoma. In a study of close to 10,000 middle-aged and older adults with diabetes, those with moderate eye complications had almost double the risk of falls as those without eye complications.

Another concern with diabetes is its effect on nerves and blood vessels in the inner ear, leading to a negative effect on balance and hearing loss, both of which are also associated with a higher risk for falling and injury.

Clinicians can reduce the risk for falls in patients by taking measures to improve diabetes control and reduce the risk for microvascular disease affecting the nerves, eyes, and ears. 

In addition, exercises that optimize muscle mass, bone strength, gait, and balance, and use of specialized footwear in people with neuropathy, may reduce fall risk. Chair yoga and tai chi have also been shown to be helpful. Clinicians can also advise patients on commonsense strategies to implement in their homes, such as ensuring proper lighting, reducing, clutter and minimizing the use of floor rugs.

The risk for falls and the associated risk for fracture and possible hospitalization are of significant concern in older adults — particularly those with diabetes, and even more so in those with diabetes who are on insulin. It is our responsibility as clinicians to implement strategies to optimize diabetes control in our patients and monitor them for microvascular and other complications that may increase this risk, and manage them appropriately if and when these complications occur.

Madhusmita Misra, Professor, Chair, Physician-in-Chief, Department of Pediatrics, University of Virginia and UVA Health Children’s, Charlottesville, has disclosed being a key opinion leader for Lumos Pharma. Sidhartha Pani, Assistant Professor, Department of Internal Medicine, UVA School of Medicine; Medical Director, Department of General Medicine, Same Day Care Clinic, Charlottesville, disclosed no relevant financial relationships.

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

 

In 2024, a record number of people are celebrating their 65th birthdays. Increasing age is associated with a higher risk for falls, fractures, and other injuries that may require hospitalization. 

In older adults with type 1 and type 2 diabetes, the risk for falls is double that seen in older people without these conditions. Increased clinician awareness of the many factors that result in this higher risk in people with diabetes, and timely implementation of strategies to prevent falls, are essential.

The annual incidence of falls in people with diabetes older than 65 years is about 39%, compared with 19% among those without diabetes. People with diabetes on insulin face an even greater increased risk for falls compared with those who are not using insulin (94% vs 27% increased risk).

Many well-known aspects of diabetes contribute to this greater risk. These include decreased sensorimotor function, musculoskeletal and neuromuscular deficits, foot and body pain, poor vision, hypoglycemic episodes, pharmacologic complications, and problems with hearing and balance. 

Optimal management of diabetes and its complications is essential, and the American Diabetes Association has developed clear guidelines for clinicians to follow to reduce the risk for diabetes related complications and manage these conditions.

The prevalence of diabetic peripheral neuropathy increases with age and duration of diabetes. People with diabetic peripheral neuropathy and diminished sensation on their feet are at increased risk for loss of postural control. Loss of proprioceptive feedback (the ability to sense movement, action and location) during standing and walking leads increases the risk for falls.

In addition, less physical activity, impaired muscle strength, and suboptimal postural control all influence gait patterns and increase the risk for falling. Adults with diabetes have a two to three times higher risk for sarcopenia (decreased muscle strength and muscle mass). They also have low plantar flexion strength, causing increased displacement of their center of gravity, which in turn reduces their maximum forward stride and may result in falls and injury.

Many people with diabetes experience neuropathic foot and body pain, requiring psychotropic and other medications that may exacerbate the risk, such as amitriptyline and duloxetine. Furthermore, older adults with diabetes are more likely to take more prescription medications and may be more sensitive to effects of multiple medications than are individuals without diabetes.

A hazard of managing diabetes, particularly with insulin, is the increased risk for unexpected low blood glucose levels. These episodes can also occur in patients taking certain kinds of oral diabetes medications, but they are more common in those on insulin. Low blood glucose can cause dizziness, confusion, and postural instability, increasing the risk for falling.

Diabetic eye complications include retinopathy, macular edema, cataracts, and glaucoma. In a study of close to 10,000 middle-aged and older adults with diabetes, those with moderate eye complications had almost double the risk of falls as those without eye complications.

Another concern with diabetes is its effect on nerves and blood vessels in the inner ear, leading to a negative effect on balance and hearing loss, both of which are also associated with a higher risk for falling and injury.

Clinicians can reduce the risk for falls in patients by taking measures to improve diabetes control and reduce the risk for microvascular disease affecting the nerves, eyes, and ears. 

In addition, exercises that optimize muscle mass, bone strength, gait, and balance, and use of specialized footwear in people with neuropathy, may reduce fall risk. Chair yoga and tai chi have also been shown to be helpful. Clinicians can also advise patients on commonsense strategies to implement in their homes, such as ensuring proper lighting, reducing, clutter and minimizing the use of floor rugs.

The risk for falls and the associated risk for fracture and possible hospitalization are of significant concern in older adults — particularly those with diabetes, and even more so in those with diabetes who are on insulin. It is our responsibility as clinicians to implement strategies to optimize diabetes control in our patients and monitor them for microvascular and other complications that may increase this risk, and manage them appropriately if and when these complications occur.

Madhusmita Misra, Professor, Chair, Physician-in-Chief, Department of Pediatrics, University of Virginia and UVA Health Children’s, Charlottesville, has disclosed being a key opinion leader for Lumos Pharma. Sidhartha Pani, Assistant Professor, Department of Internal Medicine, UVA School of Medicine; Medical Director, Department of General Medicine, Same Day Care Clinic, Charlottesville, disclosed no relevant financial relationships.

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

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

GLP-1 RA Therapy for Alcohol Use Disorder?

Article Type
Changed

 

This transcript has been edited for clarity. 

Akshay B. Jain, MD: Today we are very excited to have Dr. Leggio join us all the way from the National Institutes of Health (NIH). He is an addiction physician scientist in the intramural research program at NIH. Welcome, Dr. Leggio. Thanks for joining us. 

Lorenzo Leggio, MD, PhD: Thank you so much. 

Dr. Jain: We’ll get right into this. Your session was, in my mind, extremely informative. The session looked at glucagon-like peptide 1 receptor agonist (GLP-1 RA) therapy and its potential effects on mitigating alcohol misuse syndrome, so, reduction of alcohol addiction potentially. 

We’ve seen in some previous clinical trials, including many from your group, that alcohol use is known to be reduced — the overall risk of incidence, as well as recurrence of alcohol use — in individuals who are on GLP-1 RA therapy.

Can you share more insights about the data already out there? 

Dr. Leggio: At the preclinical level, we have a very robust line of studies, experiments, and publications looking at the effect of GLP-1 RAs, starting from exenatide up to, more recently, semaglutide. They show that these GLP-1 RAs do reduce alcohol drinking. They used different animal models of excessive alcohol drinking, using different species — for example, mice, rats, nonhuman primates — models that reflect the excessive alcohol drinking behavior that we see in patients, like physical alcohol dependence or binge-like alcohol drinking, and other behaviors in animal models that reflect the human condition.

In addition to that, we recently have seen an increase in human evidence that GLP-1 RAs may reduce alcohol drinking. For example, there is some anecdotal evidence and some analyses using social media showing that people on GLP-1 RAs report drinking less alcohol. 

There are also some pharmacoepidemiology studies which are very intriguing and quite promising. In this case, people have been looking at electronic medical records; they have used the pharmacoepidemiology approaches to match patients on GLP-1 RAs because of diabetes or obesity, and have compared and matched to patients on different drugs as the controls.

A study was recently published Nature Communications by a group in Cleveland in collaboration with Dr. Nora Volkow from the National Institute on Drug Abuse. This study shows the association between being on a GLP-1 RA and the lower incidence of alcohol use disorder and lower drinking.

There is also some promise from prospective randomized clinical trials. In particular, there was one clinical trial from Denmark, a well-known and -conducted clinical trial where they looked at exenatide, and they didn’t see an effect of exenatide compared with placebo in the main analysis. But in a subanalysis, they did see that exenatide reduced alcohol drinking, but only in patients with alcohol use disorder and obesity.

This suggests that these medications may work for some patients and not for other patients. That’s fine, because just like in any other field in medicine, including diabetes, obesity, hypertension, Parkinson’s, and depression, not all medications work for everybody. If these medications will work for alcohol addiction, we do not expect that they will work for everybody.

One ongoing question in the field is to try to identify the phenotypes or the subgroup of people who may be more responsive to these medications. 

Dr. Jain: This is such a fascinating field, and all these studies are coming out. In your review of all the literature so far, do you think this is dose dependent? Also, we see that, for instance, with certain individuals, when they take GLP-1 RA therapy, they might have a lot of gastrointestinal (GI) side effects. Recent studies have shown that the rate of these GI side effects does not necessarily correlate with the amount of weight loss. In the alcohol addiction field, do you think that the GI side effects, things like nausea, could also have a potential role in mitigating the alcohol addiction?

Dr. Leggio: This is a great question. They may play a role; they may contribute, too, but we don’t think that they are the driving mechanism of why people drink less, for at least a couple of reasons. 

One is that, similar to the obesity field, the data we have so far don’t necessarily show a relationship between the GI side effects and the reduction in drinking. Plus, the reduction in drinking is likely to happen later when many GI side effects are gone or attenuated. 

The second reason is from the neuroscience field. We are starting to better understand the mechanism at the brain level as to how these medications work. We don’t see that the nausea or, more generally, not feeling well — malaise, etc. — are driving mechanisms for how these medications work.

Again, it’s not to discount completely that the GI side effects may play a role, but I would say that, if anything, they may be more contributing to. And if they do, that will not be unique to this class of medication. For example, we have three medications approved by the US Food and Drug Administration (FDA) for alcohol use disorder.

One challenge we have in the addiction field is that many people don’t know that these medications exist — many primary care providers don’t know — and they are completely underutilized. Everybody here who is listening to us knows that roughly 85% of people with diabetes receive a medication for diabetes. For alcohol use disorder, the number is 2%. These are medications approved by the FDA. 

One of them is naltrexone, which does give GI symptoms — in particular, nausea and vomiting. The other medication is acamprosate, which does give diarrhea.

You have medications approved for alcohol disorder where you do have some GI symptoms, but they are not the mechanism either for how these medications help people to curb craving and reduce alcohol drinking.

Dr. Jain: What about the dose-dependent action? Do you think that GLP-1 RAs, at a lower dose, may not have an effect on alcohol use disorder vs at a higher dose, or is everyone a little different? 

Dr. Leggio: That’s a wonderful question. The short answer is, we don’t know, to be honest. Now, in some of the animal studies — my team has been in collaboration with other scientists in the NIH intramural research program, and also with scientists in academia, for example, at Scripps, UCLA — we see a dose response where the higher the dose, the higher the effect of the drug. In this case, semaglutide reduced binge drinking in a rat model of a physical alcohol dependence.

That said, I would be very cautious about claiming, based on the rodent data, that humans will have a dose response. It’s an open question. We really don’t know. Some of the pharmacoepidemiology data suggested that even lower doses — for example, using semaglutide for diabetes without going up to the obesity dose — may be just as effective as a higher dose in reducing the incidence of alcohol use disorder. 

It’s important also to keep in mind that the pharmacoepidemiology data are always an association. Reduction in alcohol disorder is associated with the prescription GLP-1 RA, but they don’t really replace the more gold-standard, double-blind, placebo-controlled randomized clinical trial. Nonetheless, with the pharmacoepidemiology data, I think there is an argument to at least hypothesize that people may respond well, even to lower doses. 

This also may be important from a safety standpoint. 

Basically, we need to wait for results in the next years to come from randomized clinical trials to better unfold the question about doses. For example, just anecdotally, I will tell you that in the clinical trial we are conducting right now at the NIH Intramural Research Program, for which I’m the principal investigator (PI), we are going up to 2.4 mg — the highest dose of semaglutide.

We are collaborating with Kyle Simmons, PhD, from Oklahoma State University. Our two studies are not like a two-site clinical trial, but they are harmonized. In Dr. Simmons’ clinical trial, they’re going up to 1.0 mg. We are excited about this team approach because the trials are slightly different, but they’re harmonized to the point that, once the studies are done, we’ll be able to combine and compare data to better answer the question about dosing, and many other questions.

Dr. Jain: From a clinical perspective, we see that many people who are battling alcohol use disorder may not have obesity. They might actually be on the leaner side, and hence, we may not want to use a high dose of GLP-1 RA therapy. It’ll be very exciting to see when these results come out.

This brings me to the next question. I think everyone would love to know why this happens. Why is GLP-1 RA having this effect on alcohol use disorder? I know that your group has done many animal studies, as you pointed out, and one of the postulated theories was the effect on the GABA neurotransmission pathway.

Can you tell us more about what you feel is the underlying mechanism of action here?

Dr. Leggio: I will start by saying that we don’t fully know. There are many open questions. If I can sidetrack for one second: We come up with the idea that, first of all, alcohol use disorder and substance use disorder are addictive behaviors, addictive disorders. We define addiction as a brain disease. 

Granted that addiction is a brain disease, it doesn’t mean that addiction works just in the brain in isolation. As we all know, the brain works in concert with the rest of the body. One specific approach my team has been taking is working on the analogy and the similarities between obesity and addiction to try to understand how the body-brain connection, such as the gut-brain-neuroendocrine pathway, may play a role in patients with addiction.

 

 

With that in mind, a large amount of work in my lab in the past 20 years — since I’ve been a PI — has been focused on studying this neuroendocrine pathways related to the gut-brain axis. For example, we have done work on insulin and leptin, primarily; we had done work on ghrelin, and since 2015 on the GLP-1 RAs.

With that in mind, the framework we are working on, which is also substantiated by many studies done by our team and other teams in the neuroscience field, kind of supports the idea that, similar to what we see in obesity, these medications may work by affecting what we call reward processing, or the seeking for addictive drugs, such as alcohol, and also the drugs such as the stimulants, opioids, nicotine, and so on.

The idea is that the mechanism is driven by the ability of the medication — semaglutide and all the GLP-1 RAs — to reduce the rewarding properties of alcohol and drugs. To maybe make the example more pragmatic, what does that mean? It means, for example, that a patient who typically has 10 drinks per day in the afternoon and night, while they are on the medication they may feel the lack of need to drink up to 10 to feel the same reward. 

They may be able to stop after two or three drinks, which means a significant harm reduction and a beneficial outcome. This also brings us to another mechanism, which may be related to society. We don’t fully understand how much the society mechanism, including society mechanism related to GI motility, may also play a role.

With that said, we don’t think that the effect of the GLP-1 RAs is merely due to alcohol being a calorie-based nutrient because, in fact, we see alcohol as an addictive drug, not as a nutrient. Also, the GLP-1 RAs, at least in animal models, seem to work on other addictive drugs that don’t have calories, such as nicotine, and possibly with cannabis, opioids, and stimulants.

Then on the molecular level, our team recently showed, in collaboration with Dr. Marisa Roberto from Scripps in La Jolla, California, that semaglutide may in fact change the GABA transmission at the level of some brain regions, such as the amygdala and the prefrontal cortex. These are brain regions that are well-established hubs that play a role in the mechanism underlying addiction. 

There are also some very exciting recent data showing how these medications may work not just on GABA or just on dopamine, which is the canonical way we conceive of reward processing, but by working on both by modulating GABA transmission — for example, at the ventral tegmental area and dopamine transmission at the nucleus accumbens.

Bottom line, if I summarize all of this, is that the mechanism is not fully understood, but there is definitely a contribution of this medication to effect and reward processing, possibly by altering the balance between GABA and dopamine. There are still some unknown questions, such as, are these mechanisms all brain driven or are they signaling from the periphery to the brain, or maybe both?

Also, as we all know, there are many differences across all these GLP-1 analogs in brain penetrance. Whether the drug needs to go to the brain to have an effect on alcohol drinking, cocaine seeking, or smoking is really an open question.

Dr. Jain: This is so thought-provoking. I guess the more we uncover, the more mesmerized we get with all the potential crosstalk. There is a large amount of overlap in the brain with each of these different things and how it all interplays with each other. 

Speaking of interplay, I’m thinking about how many people prone to having alcohol use disorder can potentially develop complications, one of these being chronic pancreatitis. This is a well-known complication that can occur in people having alcohol addiction. Along that same line, we know that previous history of pancreatitis is considered a use-with-caution, or we don’t want to use GLP-1 RA therapy in people who have had pancreatitis. 

Now it becomes this quagmire where people may have chronic pancreatitis, but we may want to consider GLP-1 RA therapy for management of alcohol use disorder. What are your thoughts about this, and the safety, potentially, in using it in these patients? 

Dr. Leggio: This is another wonderful question. That’s definitely a top priority in our mind, to address these kinds of questions. For example, our RCT does have, as core primary outcomes, not only the efficacy defined as a reduction in alcohol drinking, but also safety.

The reason is exactly what you just explained. There are many unanswered questions, including whether giving a GLP-1 RA and alcohol together may have synergistic effects and increase the likelihood of having pancreatitis. 

The good news is that, so far, based on the published literature, including the RCT done with exenatide in Denmark and published in 2022 and also the ongoing clinical trials — including my own clinical trial, but of course we are blind — pancreatitis has not been coming out as an adverse event.

However, it’s also true that it often happens in clinical medication development. Of course, we screen and select our population well. For example, we do exclude people who have a history of pancreatitis. We exclude people with high lipase or with any of the clinical symptomatology that makes us concerned about these people having pancreatitis. 

As often happens when you move a medication from clinical trials to clinical practice, we still need to understand whether this medication works in patients. I’m just speculating, but even if the clinical trials do not raise red flags in terms of increased risk for some side effects such as pancreatitis, I think it will be very important for practitioners to keep a close eye on the death risk regardless. 

It’s very interesting that it’s similar to alcohol liver disease. With pancreatitis, not every single patient with alcohol addiction has pancreatitis. We don’t really fully understand why some people develop pancreatitis and some people do not. The point being that there are many patients with alcohol addiction who don’t have pancreatitis and may benefit from these medications if they work. Again, we have to prove that in patients.

On the other side, as we all know, pancreatitis is a potentially life-threatening condition for those people who either have it or are at risk for it. I think we have to be very careful before we consider giving them a GLP-1 RA.

One could argue that alcohol is the leading cause of mortality and morbidity in the world. For example, right now, alcohol is the leading cause of liver disease. It’s the main reason for liver transplantation in our country. Alcohol is affecting thousands of people in terms of death and emergency room visits.

You could argue that the downside is not treating these people and they die because of alcohol addiction. A GLP-1 RA is not going to be for everybody. I will remind everybody that (1) we do have FDA-approved medications for alcohol addiction; and (2) there are also other medications not approved by the FDA, but with a proven efficacy in some clinical trials — for example, topiramate and gabapentin — and they’ve been endorsed by the American Psychiatric Association. 

There is also some evidence for another medication, baclofen, which has been endorsed by the American College of Gastroenterology for patients with alcohol addiction and liver disease.

The point I’m making is that it’s not that either we use the GLP-1 RAs or we have no other tools. We have other tools. I think we have to personalize the treatment based on the patient’s profile from a safety standpoint and from a phenotypic standpoint. 

Dr. Jain: I love that thought. I think individualization is the key here.

We know that people with diabetes have a higher risk for pancreatitis by virtue of having diabetes. People with obesity also have a higher risk for pancreatitis by virtue of having obesity. These are the two conditions where we are using a large amount of GLP-1 RA therapy. Again, the idea is looking at the person in front of us and then deciding, based on their past medical history and their current risk, whether or not a medication is a right fit for them.

I think more individualization here will come as we start using these medications that might be having potential effects on different organ systems. You mentioned a little bit about the liver, so a thought came in my mind. We know that people with diabetes who have alcohol use disorder are at a higher risk for potential hypoglycemia. If they have events when they have increased consumption of alcohol, there can be more hypoglycemia.

We now could potentially be using semaglutide or other GLP-1 RA therapy for management of alcohol use disorder. In your own experience in the studies that you’ve done or the literature that’s out there, has that been associated with an even higher risk for hypoglycemia? 

Dr. Leggio: It’s a wonderful question. I’m not aware of any formal and published report of that association. That said, your thinking from a physiopathologist standpoint makes total sense. I could not agree more. The fact that nothing has been published, at least to my knowledge, doesn’t mean that the death risk doesn’t exist. In fact, I agree with you that it does exist. 

Alcohol use disorder is interesting and tricky clinically because chronically, alcohol addiction or alcohol use disorder is associated with an increased risk for diabetes. Acutely, as you point out; and this could be with or without alcohol use disorder. An episode of a high volume of binge drinking may lead to hypoglycemia.

This is one of the reasons why people may show up to the emergency room with intoxication, and one of the symptoms detected at the emergency room is that they also have hypoglycemia in addition to vomiting, nausea, and everything else that we see in patients with acute intoxication.

Similar to the discussion about pancreatitis, as we work on understanding the possible role of GLP-1 RA in patients with alcohol use disorder, we do have to keep a close eye on the risk for hypoglycemia. The short answer is that this is not well established, but based on the simple concept of “first, do no harm,” I think we need to track that very carefully. 

In the ongoing clinical trial we’re doing in Maryland in my program at the NIH, we do just that. We are tracking glucose levels. Of course, patients come to clinic weekly, so unless they have symptoms, typically we don’t see anything at the time.

 

 

More important, we educate our patients when they go through the consent process. We tell them that this medication per se does not give hypoglycemia. In fact, we’re including people with diabetes, so for people on other medications like metformin, we explain to them that technically such a risk should not exist, but because you’re drinking alcohol in excessive amounts, you do have a potential higher risk. We just don’t know how significant that risk could be. 

We do a large amount of education at baseline when they enroll in our study. We also educate our patients on how to recognize early on the potential risk for hypoglycemia, exactly for the reasons you said. We explain to them the unknown potential that the GLP-1 RAs and alcohol together may synergize and give hypoglycemia.

Dr. Jain: I don’t know if you got this feeling at the ADA conference, but I felt, when attending all these sessions, that it seems like GLP-1 RA is the gift that keeps giving. We see the effect on diabetes, obesity, metabolic-associated steatotic liver disease, possibly with Alzheimer’s, chronic obstructive pulmonary disease, and so many things.

Now, of course, there’s potential use in alcohol use disorder. Do you think that using GLP-1 RA therapy is ready for prime time? Do you think we are now ready to prescribe this in people with alcohol use disorder?

Dr. Leggio: I would say we’re not there yet. As I mentioned at the beginning, the evidence keeps on growing. It’s getting stronger and stronger because the positive data keep on coming up. We have data from animal models, including the different species, ranging from rodents to nonhuman primates. We have anecdotal evidence and machine-learning approaches using, for example, big data and social media data. Now we have pharmacoepidemiology data and some small, initial, but still good randomized clinical trials.

What we are missing is the final step of having a substantial number of prospective, double-blind, placebo-controlled clinical trials to really prove or disprove whether these medications work, and to also better understand which patients may respond to these medications.

The good news is that there are many ongoing clinical trials. We are conducting a clinical trial in Maryland at the NIH. Dr. Simmons is doing a clinical trial at Oklahoma State University. Dr. Christian Hendershot at UNC is conducting a study at Chapel Hill. Dr. Josh Gowin is doing a study in Colorado. Dr. Anders Fink-Jensen is doing a study in Denmark. The momentum is very high. 

I’m only mentioning those people who are doing alcohol-semaglutide clinical trials. There are also people doing clinical trials on smoking, stimulants, and opioids. There are actually some very fresh, still unpublished data from Penn State that were presented publicly at conferences, showing how these drugs may reduce opioid craving, which is, of course, critically important, given that we’re in the middle of a fentanyl pandemic that is killing one person every 7 minutes, for example, in Baltimore. It’s very alarming and we need more treatments.

The bottom line is that it’s very promising, but we need to wait for these clinical trials to have a definitive answer. I would say that if you have a patient with diabetes, obesity, and also alcohol addiction, and they are on semaglutide or any other GLP-1 RA, and in addition to using the medication for diabetes and obesity, they also have a beneficial effect on their alcohol drinking, then that’s fantastic. At the end of the day, that’s the mission we all share: helping people. 

If it’s someone without obesity and diabetes, personally, at this stage, I will go with other medications that either have FDA approval or at least very solid evidence of efficacy from RCTs rather than going with the GLP-1 RA, at least until I see more definitive data from randomized clinical trials. 

There is a large amount of hope. We are hoping that these clinical trials will be positive. We are very enthusiastic and we’re also very thrilled to see that Novo Nordisk recently launched a gigantic multisite clinical trial with — I forgot how many sites, but it’s very large across Europe, America, and maybe other continents as well.

Their primary outcome is improvement in alcohol-related liver disease, but they’re also looking at alcohol drinking as a secondary outcome. That’s very important because, unlike in the diabetes field, in the addiction field, we do struggle to build partnership with the private sector because sometimes the addiction field is not seen as an appetitive field from pharma. 

We all know that the best success in any medication development story is when you put academia, the government, and pharma together. Think about the COVID-19 vaccine development. That’s unfortunately the exception rather than rule in the addiction field. 

With the company doing a large clinical trial in the alcohol field, although they focus more on the liver but they also looked at drinking, I really hope we’ll see more and more companies in the private sector take more and more interest in addiction. Also, I hope to see more and more partnership between the private sector, the government, and academia. 

Dr. Jain: Such exciting times, indeed. We can’t wait enough for the results of these and many other trials to come out. Dr. Leggio, it was an absolute delight chatting with you today. Thank you so much for joining us from ADA 2024.

Akshay B. Jain, MD, Clinical Instructor, Department of Endocrinology, University of British Columbia; Endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Care to Know; CCRN; Connected in Motion; CPD Network; Dexcom; Diabetes Canada; Eli Lilly; GSK; HLS Therapeutics; Janssen; Master Clinician Alliance; MDBriefcase; Merck; Medtronic; Moderna; Novartis; Novo Nordisk; Partners in Progressive Medical Education; Pfizer; Sanofi Aventis; Timed Right; WebMD. Received research grants/research support from: Abbott; Amgen; Novo Nordisk. Received consulting fees from: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Dexcom; Eli Lilly; Gilead Sciences; GSK; HLS Therapeutics; Insulet; Janssen; Medtronic; Novo Nordisk; Partners in Progressive Medical Education; PocketPills; Roche; Sanofi Aventis; Takeda. Lorenzo Leggio, MD, PhD, Clinical Director, Deputy Scientific Director, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland, has disclosed the following relevant financial relationships: Serve(d) as a US federal employee for: National Institutes of Health. He had received income in an amount equal to or greater than $250 from: UK Medical Council on Alcohol for his service as editor-in-chief for Alcohol and Alcoholism and received royalties from Rutledge as an editor for a textbook.

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

Publications
Topics
Sections

 

This transcript has been edited for clarity. 

Akshay B. Jain, MD: Today we are very excited to have Dr. Leggio join us all the way from the National Institutes of Health (NIH). He is an addiction physician scientist in the intramural research program at NIH. Welcome, Dr. Leggio. Thanks for joining us. 

Lorenzo Leggio, MD, PhD: Thank you so much. 

Dr. Jain: We’ll get right into this. Your session was, in my mind, extremely informative. The session looked at glucagon-like peptide 1 receptor agonist (GLP-1 RA) therapy and its potential effects on mitigating alcohol misuse syndrome, so, reduction of alcohol addiction potentially. 

We’ve seen in some previous clinical trials, including many from your group, that alcohol use is known to be reduced — the overall risk of incidence, as well as recurrence of alcohol use — in individuals who are on GLP-1 RA therapy.

Can you share more insights about the data already out there? 

Dr. Leggio: At the preclinical level, we have a very robust line of studies, experiments, and publications looking at the effect of GLP-1 RAs, starting from exenatide up to, more recently, semaglutide. They show that these GLP-1 RAs do reduce alcohol drinking. They used different animal models of excessive alcohol drinking, using different species — for example, mice, rats, nonhuman primates — models that reflect the excessive alcohol drinking behavior that we see in patients, like physical alcohol dependence or binge-like alcohol drinking, and other behaviors in animal models that reflect the human condition.

In addition to that, we recently have seen an increase in human evidence that GLP-1 RAs may reduce alcohol drinking. For example, there is some anecdotal evidence and some analyses using social media showing that people on GLP-1 RAs report drinking less alcohol. 

There are also some pharmacoepidemiology studies which are very intriguing and quite promising. In this case, people have been looking at electronic medical records; they have used the pharmacoepidemiology approaches to match patients on GLP-1 RAs because of diabetes or obesity, and have compared and matched to patients on different drugs as the controls.

A study was recently published Nature Communications by a group in Cleveland in collaboration with Dr. Nora Volkow from the National Institute on Drug Abuse. This study shows the association between being on a GLP-1 RA and the lower incidence of alcohol use disorder and lower drinking.

There is also some promise from prospective randomized clinical trials. In particular, there was one clinical trial from Denmark, a well-known and -conducted clinical trial where they looked at exenatide, and they didn’t see an effect of exenatide compared with placebo in the main analysis. But in a subanalysis, they did see that exenatide reduced alcohol drinking, but only in patients with alcohol use disorder and obesity.

This suggests that these medications may work for some patients and not for other patients. That’s fine, because just like in any other field in medicine, including diabetes, obesity, hypertension, Parkinson’s, and depression, not all medications work for everybody. If these medications will work for alcohol addiction, we do not expect that they will work for everybody.

One ongoing question in the field is to try to identify the phenotypes or the subgroup of people who may be more responsive to these medications. 

Dr. Jain: This is such a fascinating field, and all these studies are coming out. In your review of all the literature so far, do you think this is dose dependent? Also, we see that, for instance, with certain individuals, when they take GLP-1 RA therapy, they might have a lot of gastrointestinal (GI) side effects. Recent studies have shown that the rate of these GI side effects does not necessarily correlate with the amount of weight loss. In the alcohol addiction field, do you think that the GI side effects, things like nausea, could also have a potential role in mitigating the alcohol addiction?

Dr. Leggio: This is a great question. They may play a role; they may contribute, too, but we don’t think that they are the driving mechanism of why people drink less, for at least a couple of reasons. 

One is that, similar to the obesity field, the data we have so far don’t necessarily show a relationship between the GI side effects and the reduction in drinking. Plus, the reduction in drinking is likely to happen later when many GI side effects are gone or attenuated. 

The second reason is from the neuroscience field. We are starting to better understand the mechanism at the brain level as to how these medications work. We don’t see that the nausea or, more generally, not feeling well — malaise, etc. — are driving mechanisms for how these medications work.

Again, it’s not to discount completely that the GI side effects may play a role, but I would say that, if anything, they may be more contributing to. And if they do, that will not be unique to this class of medication. For example, we have three medications approved by the US Food and Drug Administration (FDA) for alcohol use disorder.

One challenge we have in the addiction field is that many people don’t know that these medications exist — many primary care providers don’t know — and they are completely underutilized. Everybody here who is listening to us knows that roughly 85% of people with diabetes receive a medication for diabetes. For alcohol use disorder, the number is 2%. These are medications approved by the FDA. 

One of them is naltrexone, which does give GI symptoms — in particular, nausea and vomiting. The other medication is acamprosate, which does give diarrhea.

You have medications approved for alcohol disorder where you do have some GI symptoms, but they are not the mechanism either for how these medications help people to curb craving and reduce alcohol drinking.

Dr. Jain: What about the dose-dependent action? Do you think that GLP-1 RAs, at a lower dose, may not have an effect on alcohol use disorder vs at a higher dose, or is everyone a little different? 

Dr. Leggio: That’s a wonderful question. The short answer is, we don’t know, to be honest. Now, in some of the animal studies — my team has been in collaboration with other scientists in the NIH intramural research program, and also with scientists in academia, for example, at Scripps, UCLA — we see a dose response where the higher the dose, the higher the effect of the drug. In this case, semaglutide reduced binge drinking in a rat model of a physical alcohol dependence.

That said, I would be very cautious about claiming, based on the rodent data, that humans will have a dose response. It’s an open question. We really don’t know. Some of the pharmacoepidemiology data suggested that even lower doses — for example, using semaglutide for diabetes without going up to the obesity dose — may be just as effective as a higher dose in reducing the incidence of alcohol use disorder. 

It’s important also to keep in mind that the pharmacoepidemiology data are always an association. Reduction in alcohol disorder is associated with the prescription GLP-1 RA, but they don’t really replace the more gold-standard, double-blind, placebo-controlled randomized clinical trial. Nonetheless, with the pharmacoepidemiology data, I think there is an argument to at least hypothesize that people may respond well, even to lower doses. 

This also may be important from a safety standpoint. 

Basically, we need to wait for results in the next years to come from randomized clinical trials to better unfold the question about doses. For example, just anecdotally, I will tell you that in the clinical trial we are conducting right now at the NIH Intramural Research Program, for which I’m the principal investigator (PI), we are going up to 2.4 mg — the highest dose of semaglutide.

We are collaborating with Kyle Simmons, PhD, from Oklahoma State University. Our two studies are not like a two-site clinical trial, but they are harmonized. In Dr. Simmons’ clinical trial, they’re going up to 1.0 mg. We are excited about this team approach because the trials are slightly different, but they’re harmonized to the point that, once the studies are done, we’ll be able to combine and compare data to better answer the question about dosing, and many other questions.

Dr. Jain: From a clinical perspective, we see that many people who are battling alcohol use disorder may not have obesity. They might actually be on the leaner side, and hence, we may not want to use a high dose of GLP-1 RA therapy. It’ll be very exciting to see when these results come out.

This brings me to the next question. I think everyone would love to know why this happens. Why is GLP-1 RA having this effect on alcohol use disorder? I know that your group has done many animal studies, as you pointed out, and one of the postulated theories was the effect on the GABA neurotransmission pathway.

Can you tell us more about what you feel is the underlying mechanism of action here?

Dr. Leggio: I will start by saying that we don’t fully know. There are many open questions. If I can sidetrack for one second: We come up with the idea that, first of all, alcohol use disorder and substance use disorder are addictive behaviors, addictive disorders. We define addiction as a brain disease. 

Granted that addiction is a brain disease, it doesn’t mean that addiction works just in the brain in isolation. As we all know, the brain works in concert with the rest of the body. One specific approach my team has been taking is working on the analogy and the similarities between obesity and addiction to try to understand how the body-brain connection, such as the gut-brain-neuroendocrine pathway, may play a role in patients with addiction.

 

 

With that in mind, a large amount of work in my lab in the past 20 years — since I’ve been a PI — has been focused on studying this neuroendocrine pathways related to the gut-brain axis. For example, we have done work on insulin and leptin, primarily; we had done work on ghrelin, and since 2015 on the GLP-1 RAs.

With that in mind, the framework we are working on, which is also substantiated by many studies done by our team and other teams in the neuroscience field, kind of supports the idea that, similar to what we see in obesity, these medications may work by affecting what we call reward processing, or the seeking for addictive drugs, such as alcohol, and also the drugs such as the stimulants, opioids, nicotine, and so on.

The idea is that the mechanism is driven by the ability of the medication — semaglutide and all the GLP-1 RAs — to reduce the rewarding properties of alcohol and drugs. To maybe make the example more pragmatic, what does that mean? It means, for example, that a patient who typically has 10 drinks per day in the afternoon and night, while they are on the medication they may feel the lack of need to drink up to 10 to feel the same reward. 

They may be able to stop after two or three drinks, which means a significant harm reduction and a beneficial outcome. This also brings us to another mechanism, which may be related to society. We don’t fully understand how much the society mechanism, including society mechanism related to GI motility, may also play a role.

With that said, we don’t think that the effect of the GLP-1 RAs is merely due to alcohol being a calorie-based nutrient because, in fact, we see alcohol as an addictive drug, not as a nutrient. Also, the GLP-1 RAs, at least in animal models, seem to work on other addictive drugs that don’t have calories, such as nicotine, and possibly with cannabis, opioids, and stimulants.

Then on the molecular level, our team recently showed, in collaboration with Dr. Marisa Roberto from Scripps in La Jolla, California, that semaglutide may in fact change the GABA transmission at the level of some brain regions, such as the amygdala and the prefrontal cortex. These are brain regions that are well-established hubs that play a role in the mechanism underlying addiction. 

There are also some very exciting recent data showing how these medications may work not just on GABA or just on dopamine, which is the canonical way we conceive of reward processing, but by working on both by modulating GABA transmission — for example, at the ventral tegmental area and dopamine transmission at the nucleus accumbens.

Bottom line, if I summarize all of this, is that the mechanism is not fully understood, but there is definitely a contribution of this medication to effect and reward processing, possibly by altering the balance between GABA and dopamine. There are still some unknown questions, such as, are these mechanisms all brain driven or are they signaling from the periphery to the brain, or maybe both?

Also, as we all know, there are many differences across all these GLP-1 analogs in brain penetrance. Whether the drug needs to go to the brain to have an effect on alcohol drinking, cocaine seeking, or smoking is really an open question.

Dr. Jain: This is so thought-provoking. I guess the more we uncover, the more mesmerized we get with all the potential crosstalk. There is a large amount of overlap in the brain with each of these different things and how it all interplays with each other. 

Speaking of interplay, I’m thinking about how many people prone to having alcohol use disorder can potentially develop complications, one of these being chronic pancreatitis. This is a well-known complication that can occur in people having alcohol addiction. Along that same line, we know that previous history of pancreatitis is considered a use-with-caution, or we don’t want to use GLP-1 RA therapy in people who have had pancreatitis. 

Now it becomes this quagmire where people may have chronic pancreatitis, but we may want to consider GLP-1 RA therapy for management of alcohol use disorder. What are your thoughts about this, and the safety, potentially, in using it in these patients? 

Dr. Leggio: This is another wonderful question. That’s definitely a top priority in our mind, to address these kinds of questions. For example, our RCT does have, as core primary outcomes, not only the efficacy defined as a reduction in alcohol drinking, but also safety.

The reason is exactly what you just explained. There are many unanswered questions, including whether giving a GLP-1 RA and alcohol together may have synergistic effects and increase the likelihood of having pancreatitis. 

The good news is that, so far, based on the published literature, including the RCT done with exenatide in Denmark and published in 2022 and also the ongoing clinical trials — including my own clinical trial, but of course we are blind — pancreatitis has not been coming out as an adverse event.

However, it’s also true that it often happens in clinical medication development. Of course, we screen and select our population well. For example, we do exclude people who have a history of pancreatitis. We exclude people with high lipase or with any of the clinical symptomatology that makes us concerned about these people having pancreatitis. 

As often happens when you move a medication from clinical trials to clinical practice, we still need to understand whether this medication works in patients. I’m just speculating, but even if the clinical trials do not raise red flags in terms of increased risk for some side effects such as pancreatitis, I think it will be very important for practitioners to keep a close eye on the death risk regardless. 

It’s very interesting that it’s similar to alcohol liver disease. With pancreatitis, not every single patient with alcohol addiction has pancreatitis. We don’t really fully understand why some people develop pancreatitis and some people do not. The point being that there are many patients with alcohol addiction who don’t have pancreatitis and may benefit from these medications if they work. Again, we have to prove that in patients.

On the other side, as we all know, pancreatitis is a potentially life-threatening condition for those people who either have it or are at risk for it. I think we have to be very careful before we consider giving them a GLP-1 RA.

One could argue that alcohol is the leading cause of mortality and morbidity in the world. For example, right now, alcohol is the leading cause of liver disease. It’s the main reason for liver transplantation in our country. Alcohol is affecting thousands of people in terms of death and emergency room visits.

You could argue that the downside is not treating these people and they die because of alcohol addiction. A GLP-1 RA is not going to be for everybody. I will remind everybody that (1) we do have FDA-approved medications for alcohol addiction; and (2) there are also other medications not approved by the FDA, but with a proven efficacy in some clinical trials — for example, topiramate and gabapentin — and they’ve been endorsed by the American Psychiatric Association. 

There is also some evidence for another medication, baclofen, which has been endorsed by the American College of Gastroenterology for patients with alcohol addiction and liver disease.

The point I’m making is that it’s not that either we use the GLP-1 RAs or we have no other tools. We have other tools. I think we have to personalize the treatment based on the patient’s profile from a safety standpoint and from a phenotypic standpoint. 

Dr. Jain: I love that thought. I think individualization is the key here.

We know that people with diabetes have a higher risk for pancreatitis by virtue of having diabetes. People with obesity also have a higher risk for pancreatitis by virtue of having obesity. These are the two conditions where we are using a large amount of GLP-1 RA therapy. Again, the idea is looking at the person in front of us and then deciding, based on their past medical history and their current risk, whether or not a medication is a right fit for them.

I think more individualization here will come as we start using these medications that might be having potential effects on different organ systems. You mentioned a little bit about the liver, so a thought came in my mind. We know that people with diabetes who have alcohol use disorder are at a higher risk for potential hypoglycemia. If they have events when they have increased consumption of alcohol, there can be more hypoglycemia.

We now could potentially be using semaglutide or other GLP-1 RA therapy for management of alcohol use disorder. In your own experience in the studies that you’ve done or the literature that’s out there, has that been associated with an even higher risk for hypoglycemia? 

Dr. Leggio: It’s a wonderful question. I’m not aware of any formal and published report of that association. That said, your thinking from a physiopathologist standpoint makes total sense. I could not agree more. The fact that nothing has been published, at least to my knowledge, doesn’t mean that the death risk doesn’t exist. In fact, I agree with you that it does exist. 

Alcohol use disorder is interesting and tricky clinically because chronically, alcohol addiction or alcohol use disorder is associated with an increased risk for diabetes. Acutely, as you point out; and this could be with or without alcohol use disorder. An episode of a high volume of binge drinking may lead to hypoglycemia.

This is one of the reasons why people may show up to the emergency room with intoxication, and one of the symptoms detected at the emergency room is that they also have hypoglycemia in addition to vomiting, nausea, and everything else that we see in patients with acute intoxication.

Similar to the discussion about pancreatitis, as we work on understanding the possible role of GLP-1 RA in patients with alcohol use disorder, we do have to keep a close eye on the risk for hypoglycemia. The short answer is that this is not well established, but based on the simple concept of “first, do no harm,” I think we need to track that very carefully. 

In the ongoing clinical trial we’re doing in Maryland in my program at the NIH, we do just that. We are tracking glucose levels. Of course, patients come to clinic weekly, so unless they have symptoms, typically we don’t see anything at the time.

 

 

More important, we educate our patients when they go through the consent process. We tell them that this medication per se does not give hypoglycemia. In fact, we’re including people with diabetes, so for people on other medications like metformin, we explain to them that technically such a risk should not exist, but because you’re drinking alcohol in excessive amounts, you do have a potential higher risk. We just don’t know how significant that risk could be. 

We do a large amount of education at baseline when they enroll in our study. We also educate our patients on how to recognize early on the potential risk for hypoglycemia, exactly for the reasons you said. We explain to them the unknown potential that the GLP-1 RAs and alcohol together may synergize and give hypoglycemia.

Dr. Jain: I don’t know if you got this feeling at the ADA conference, but I felt, when attending all these sessions, that it seems like GLP-1 RA is the gift that keeps giving. We see the effect on diabetes, obesity, metabolic-associated steatotic liver disease, possibly with Alzheimer’s, chronic obstructive pulmonary disease, and so many things.

Now, of course, there’s potential use in alcohol use disorder. Do you think that using GLP-1 RA therapy is ready for prime time? Do you think we are now ready to prescribe this in people with alcohol use disorder?

Dr. Leggio: I would say we’re not there yet. As I mentioned at the beginning, the evidence keeps on growing. It’s getting stronger and stronger because the positive data keep on coming up. We have data from animal models, including the different species, ranging from rodents to nonhuman primates. We have anecdotal evidence and machine-learning approaches using, for example, big data and social media data. Now we have pharmacoepidemiology data and some small, initial, but still good randomized clinical trials.

What we are missing is the final step of having a substantial number of prospective, double-blind, placebo-controlled clinical trials to really prove or disprove whether these medications work, and to also better understand which patients may respond to these medications.

The good news is that there are many ongoing clinical trials. We are conducting a clinical trial in Maryland at the NIH. Dr. Simmons is doing a clinical trial at Oklahoma State University. Dr. Christian Hendershot at UNC is conducting a study at Chapel Hill. Dr. Josh Gowin is doing a study in Colorado. Dr. Anders Fink-Jensen is doing a study in Denmark. The momentum is very high. 

I’m only mentioning those people who are doing alcohol-semaglutide clinical trials. There are also people doing clinical trials on smoking, stimulants, and opioids. There are actually some very fresh, still unpublished data from Penn State that were presented publicly at conferences, showing how these drugs may reduce opioid craving, which is, of course, critically important, given that we’re in the middle of a fentanyl pandemic that is killing one person every 7 minutes, for example, in Baltimore. It’s very alarming and we need more treatments.

The bottom line is that it’s very promising, but we need to wait for these clinical trials to have a definitive answer. I would say that if you have a patient with diabetes, obesity, and also alcohol addiction, and they are on semaglutide or any other GLP-1 RA, and in addition to using the medication for diabetes and obesity, they also have a beneficial effect on their alcohol drinking, then that’s fantastic. At the end of the day, that’s the mission we all share: helping people. 

If it’s someone without obesity and diabetes, personally, at this stage, I will go with other medications that either have FDA approval or at least very solid evidence of efficacy from RCTs rather than going with the GLP-1 RA, at least until I see more definitive data from randomized clinical trials. 

There is a large amount of hope. We are hoping that these clinical trials will be positive. We are very enthusiastic and we’re also very thrilled to see that Novo Nordisk recently launched a gigantic multisite clinical trial with — I forgot how many sites, but it’s very large across Europe, America, and maybe other continents as well.

Their primary outcome is improvement in alcohol-related liver disease, but they’re also looking at alcohol drinking as a secondary outcome. That’s very important because, unlike in the diabetes field, in the addiction field, we do struggle to build partnership with the private sector because sometimes the addiction field is not seen as an appetitive field from pharma. 

We all know that the best success in any medication development story is when you put academia, the government, and pharma together. Think about the COVID-19 vaccine development. That’s unfortunately the exception rather than rule in the addiction field. 

With the company doing a large clinical trial in the alcohol field, although they focus more on the liver but they also looked at drinking, I really hope we’ll see more and more companies in the private sector take more and more interest in addiction. Also, I hope to see more and more partnership between the private sector, the government, and academia. 

Dr. Jain: Such exciting times, indeed. We can’t wait enough for the results of these and many other trials to come out. Dr. Leggio, it was an absolute delight chatting with you today. Thank you so much for joining us from ADA 2024.

Akshay B. Jain, MD, Clinical Instructor, Department of Endocrinology, University of British Columbia; Endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Care to Know; CCRN; Connected in Motion; CPD Network; Dexcom; Diabetes Canada; Eli Lilly; GSK; HLS Therapeutics; Janssen; Master Clinician Alliance; MDBriefcase; Merck; Medtronic; Moderna; Novartis; Novo Nordisk; Partners in Progressive Medical Education; Pfizer; Sanofi Aventis; Timed Right; WebMD. Received research grants/research support from: Abbott; Amgen; Novo Nordisk. Received consulting fees from: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Dexcom; Eli Lilly; Gilead Sciences; GSK; HLS Therapeutics; Insulet; Janssen; Medtronic; Novo Nordisk; Partners in Progressive Medical Education; PocketPills; Roche; Sanofi Aventis; Takeda. Lorenzo Leggio, MD, PhD, Clinical Director, Deputy Scientific Director, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland, has disclosed the following relevant financial relationships: Serve(d) as a US federal employee for: National Institutes of Health. He had received income in an amount equal to or greater than $250 from: UK Medical Council on Alcohol for his service as editor-in-chief for Alcohol and Alcoholism and received royalties from Rutledge as an editor for a textbook.

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

 

This transcript has been edited for clarity. 

Akshay B. Jain, MD: Today we are very excited to have Dr. Leggio join us all the way from the National Institutes of Health (NIH). He is an addiction physician scientist in the intramural research program at NIH. Welcome, Dr. Leggio. Thanks for joining us. 

Lorenzo Leggio, MD, PhD: Thank you so much. 

Dr. Jain: We’ll get right into this. Your session was, in my mind, extremely informative. The session looked at glucagon-like peptide 1 receptor agonist (GLP-1 RA) therapy and its potential effects on mitigating alcohol misuse syndrome, so, reduction of alcohol addiction potentially. 

We’ve seen in some previous clinical trials, including many from your group, that alcohol use is known to be reduced — the overall risk of incidence, as well as recurrence of alcohol use — in individuals who are on GLP-1 RA therapy.

Can you share more insights about the data already out there? 

Dr. Leggio: At the preclinical level, we have a very robust line of studies, experiments, and publications looking at the effect of GLP-1 RAs, starting from exenatide up to, more recently, semaglutide. They show that these GLP-1 RAs do reduce alcohol drinking. They used different animal models of excessive alcohol drinking, using different species — for example, mice, rats, nonhuman primates — models that reflect the excessive alcohol drinking behavior that we see in patients, like physical alcohol dependence or binge-like alcohol drinking, and other behaviors in animal models that reflect the human condition.

In addition to that, we recently have seen an increase in human evidence that GLP-1 RAs may reduce alcohol drinking. For example, there is some anecdotal evidence and some analyses using social media showing that people on GLP-1 RAs report drinking less alcohol. 

There are also some pharmacoepidemiology studies which are very intriguing and quite promising. In this case, people have been looking at electronic medical records; they have used the pharmacoepidemiology approaches to match patients on GLP-1 RAs because of diabetes or obesity, and have compared and matched to patients on different drugs as the controls.

A study was recently published Nature Communications by a group in Cleveland in collaboration with Dr. Nora Volkow from the National Institute on Drug Abuse. This study shows the association between being on a GLP-1 RA and the lower incidence of alcohol use disorder and lower drinking.

There is also some promise from prospective randomized clinical trials. In particular, there was one clinical trial from Denmark, a well-known and -conducted clinical trial where they looked at exenatide, and they didn’t see an effect of exenatide compared with placebo in the main analysis. But in a subanalysis, they did see that exenatide reduced alcohol drinking, but only in patients with alcohol use disorder and obesity.

This suggests that these medications may work for some patients and not for other patients. That’s fine, because just like in any other field in medicine, including diabetes, obesity, hypertension, Parkinson’s, and depression, not all medications work for everybody. If these medications will work for alcohol addiction, we do not expect that they will work for everybody.

One ongoing question in the field is to try to identify the phenotypes or the subgroup of people who may be more responsive to these medications. 

Dr. Jain: This is such a fascinating field, and all these studies are coming out. In your review of all the literature so far, do you think this is dose dependent? Also, we see that, for instance, with certain individuals, when they take GLP-1 RA therapy, they might have a lot of gastrointestinal (GI) side effects. Recent studies have shown that the rate of these GI side effects does not necessarily correlate with the amount of weight loss. In the alcohol addiction field, do you think that the GI side effects, things like nausea, could also have a potential role in mitigating the alcohol addiction?

Dr. Leggio: This is a great question. They may play a role; they may contribute, too, but we don’t think that they are the driving mechanism of why people drink less, for at least a couple of reasons. 

One is that, similar to the obesity field, the data we have so far don’t necessarily show a relationship between the GI side effects and the reduction in drinking. Plus, the reduction in drinking is likely to happen later when many GI side effects are gone or attenuated. 

The second reason is from the neuroscience field. We are starting to better understand the mechanism at the brain level as to how these medications work. We don’t see that the nausea or, more generally, not feeling well — malaise, etc. — are driving mechanisms for how these medications work.

Again, it’s not to discount completely that the GI side effects may play a role, but I would say that, if anything, they may be more contributing to. And if they do, that will not be unique to this class of medication. For example, we have three medications approved by the US Food and Drug Administration (FDA) for alcohol use disorder.

One challenge we have in the addiction field is that many people don’t know that these medications exist — many primary care providers don’t know — and they are completely underutilized. Everybody here who is listening to us knows that roughly 85% of people with diabetes receive a medication for diabetes. For alcohol use disorder, the number is 2%. These are medications approved by the FDA. 

One of them is naltrexone, which does give GI symptoms — in particular, nausea and vomiting. The other medication is acamprosate, which does give diarrhea.

You have medications approved for alcohol disorder where you do have some GI symptoms, but they are not the mechanism either for how these medications help people to curb craving and reduce alcohol drinking.

Dr. Jain: What about the dose-dependent action? Do you think that GLP-1 RAs, at a lower dose, may not have an effect on alcohol use disorder vs at a higher dose, or is everyone a little different? 

Dr. Leggio: That’s a wonderful question. The short answer is, we don’t know, to be honest. Now, in some of the animal studies — my team has been in collaboration with other scientists in the NIH intramural research program, and also with scientists in academia, for example, at Scripps, UCLA — we see a dose response where the higher the dose, the higher the effect of the drug. In this case, semaglutide reduced binge drinking in a rat model of a physical alcohol dependence.

That said, I would be very cautious about claiming, based on the rodent data, that humans will have a dose response. It’s an open question. We really don’t know. Some of the pharmacoepidemiology data suggested that even lower doses — for example, using semaglutide for diabetes without going up to the obesity dose — may be just as effective as a higher dose in reducing the incidence of alcohol use disorder. 

It’s important also to keep in mind that the pharmacoepidemiology data are always an association. Reduction in alcohol disorder is associated with the prescription GLP-1 RA, but they don’t really replace the more gold-standard, double-blind, placebo-controlled randomized clinical trial. Nonetheless, with the pharmacoepidemiology data, I think there is an argument to at least hypothesize that people may respond well, even to lower doses. 

This also may be important from a safety standpoint. 

Basically, we need to wait for results in the next years to come from randomized clinical trials to better unfold the question about doses. For example, just anecdotally, I will tell you that in the clinical trial we are conducting right now at the NIH Intramural Research Program, for which I’m the principal investigator (PI), we are going up to 2.4 mg — the highest dose of semaglutide.

We are collaborating with Kyle Simmons, PhD, from Oklahoma State University. Our two studies are not like a two-site clinical trial, but they are harmonized. In Dr. Simmons’ clinical trial, they’re going up to 1.0 mg. We are excited about this team approach because the trials are slightly different, but they’re harmonized to the point that, once the studies are done, we’ll be able to combine and compare data to better answer the question about dosing, and many other questions.

Dr. Jain: From a clinical perspective, we see that many people who are battling alcohol use disorder may not have obesity. They might actually be on the leaner side, and hence, we may not want to use a high dose of GLP-1 RA therapy. It’ll be very exciting to see when these results come out.

This brings me to the next question. I think everyone would love to know why this happens. Why is GLP-1 RA having this effect on alcohol use disorder? I know that your group has done many animal studies, as you pointed out, and one of the postulated theories was the effect on the GABA neurotransmission pathway.

Can you tell us more about what you feel is the underlying mechanism of action here?

Dr. Leggio: I will start by saying that we don’t fully know. There are many open questions. If I can sidetrack for one second: We come up with the idea that, first of all, alcohol use disorder and substance use disorder are addictive behaviors, addictive disorders. We define addiction as a brain disease. 

Granted that addiction is a brain disease, it doesn’t mean that addiction works just in the brain in isolation. As we all know, the brain works in concert with the rest of the body. One specific approach my team has been taking is working on the analogy and the similarities between obesity and addiction to try to understand how the body-brain connection, such as the gut-brain-neuroendocrine pathway, may play a role in patients with addiction.

 

 

With that in mind, a large amount of work in my lab in the past 20 years — since I’ve been a PI — has been focused on studying this neuroendocrine pathways related to the gut-brain axis. For example, we have done work on insulin and leptin, primarily; we had done work on ghrelin, and since 2015 on the GLP-1 RAs.

With that in mind, the framework we are working on, which is also substantiated by many studies done by our team and other teams in the neuroscience field, kind of supports the idea that, similar to what we see in obesity, these medications may work by affecting what we call reward processing, or the seeking for addictive drugs, such as alcohol, and also the drugs such as the stimulants, opioids, nicotine, and so on.

The idea is that the mechanism is driven by the ability of the medication — semaglutide and all the GLP-1 RAs — to reduce the rewarding properties of alcohol and drugs. To maybe make the example more pragmatic, what does that mean? It means, for example, that a patient who typically has 10 drinks per day in the afternoon and night, while they are on the medication they may feel the lack of need to drink up to 10 to feel the same reward. 

They may be able to stop after two or three drinks, which means a significant harm reduction and a beneficial outcome. This also brings us to another mechanism, which may be related to society. We don’t fully understand how much the society mechanism, including society mechanism related to GI motility, may also play a role.

With that said, we don’t think that the effect of the GLP-1 RAs is merely due to alcohol being a calorie-based nutrient because, in fact, we see alcohol as an addictive drug, not as a nutrient. Also, the GLP-1 RAs, at least in animal models, seem to work on other addictive drugs that don’t have calories, such as nicotine, and possibly with cannabis, opioids, and stimulants.

Then on the molecular level, our team recently showed, in collaboration with Dr. Marisa Roberto from Scripps in La Jolla, California, that semaglutide may in fact change the GABA transmission at the level of some brain regions, such as the amygdala and the prefrontal cortex. These are brain regions that are well-established hubs that play a role in the mechanism underlying addiction. 

There are also some very exciting recent data showing how these medications may work not just on GABA or just on dopamine, which is the canonical way we conceive of reward processing, but by working on both by modulating GABA transmission — for example, at the ventral tegmental area and dopamine transmission at the nucleus accumbens.

Bottom line, if I summarize all of this, is that the mechanism is not fully understood, but there is definitely a contribution of this medication to effect and reward processing, possibly by altering the balance between GABA and dopamine. There are still some unknown questions, such as, are these mechanisms all brain driven or are they signaling from the periphery to the brain, or maybe both?

Also, as we all know, there are many differences across all these GLP-1 analogs in brain penetrance. Whether the drug needs to go to the brain to have an effect on alcohol drinking, cocaine seeking, or smoking is really an open question.

Dr. Jain: This is so thought-provoking. I guess the more we uncover, the more mesmerized we get with all the potential crosstalk. There is a large amount of overlap in the brain with each of these different things and how it all interplays with each other. 

Speaking of interplay, I’m thinking about how many people prone to having alcohol use disorder can potentially develop complications, one of these being chronic pancreatitis. This is a well-known complication that can occur in people having alcohol addiction. Along that same line, we know that previous history of pancreatitis is considered a use-with-caution, or we don’t want to use GLP-1 RA therapy in people who have had pancreatitis. 

Now it becomes this quagmire where people may have chronic pancreatitis, but we may want to consider GLP-1 RA therapy for management of alcohol use disorder. What are your thoughts about this, and the safety, potentially, in using it in these patients? 

Dr. Leggio: This is another wonderful question. That’s definitely a top priority in our mind, to address these kinds of questions. For example, our RCT does have, as core primary outcomes, not only the efficacy defined as a reduction in alcohol drinking, but also safety.

The reason is exactly what you just explained. There are many unanswered questions, including whether giving a GLP-1 RA and alcohol together may have synergistic effects and increase the likelihood of having pancreatitis. 

The good news is that, so far, based on the published literature, including the RCT done with exenatide in Denmark and published in 2022 and also the ongoing clinical trials — including my own clinical trial, but of course we are blind — pancreatitis has not been coming out as an adverse event.

However, it’s also true that it often happens in clinical medication development. Of course, we screen and select our population well. For example, we do exclude people who have a history of pancreatitis. We exclude people with high lipase or with any of the clinical symptomatology that makes us concerned about these people having pancreatitis. 

As often happens when you move a medication from clinical trials to clinical practice, we still need to understand whether this medication works in patients. I’m just speculating, but even if the clinical trials do not raise red flags in terms of increased risk for some side effects such as pancreatitis, I think it will be very important for practitioners to keep a close eye on the death risk regardless. 

It’s very interesting that it’s similar to alcohol liver disease. With pancreatitis, not every single patient with alcohol addiction has pancreatitis. We don’t really fully understand why some people develop pancreatitis and some people do not. The point being that there are many patients with alcohol addiction who don’t have pancreatitis and may benefit from these medications if they work. Again, we have to prove that in patients.

On the other side, as we all know, pancreatitis is a potentially life-threatening condition for those people who either have it or are at risk for it. I think we have to be very careful before we consider giving them a GLP-1 RA.

One could argue that alcohol is the leading cause of mortality and morbidity in the world. For example, right now, alcohol is the leading cause of liver disease. It’s the main reason for liver transplantation in our country. Alcohol is affecting thousands of people in terms of death and emergency room visits.

You could argue that the downside is not treating these people and they die because of alcohol addiction. A GLP-1 RA is not going to be for everybody. I will remind everybody that (1) we do have FDA-approved medications for alcohol addiction; and (2) there are also other medications not approved by the FDA, but with a proven efficacy in some clinical trials — for example, topiramate and gabapentin — and they’ve been endorsed by the American Psychiatric Association. 

There is also some evidence for another medication, baclofen, which has been endorsed by the American College of Gastroenterology for patients with alcohol addiction and liver disease.

The point I’m making is that it’s not that either we use the GLP-1 RAs or we have no other tools. We have other tools. I think we have to personalize the treatment based on the patient’s profile from a safety standpoint and from a phenotypic standpoint. 

Dr. Jain: I love that thought. I think individualization is the key here.

We know that people with diabetes have a higher risk for pancreatitis by virtue of having diabetes. People with obesity also have a higher risk for pancreatitis by virtue of having obesity. These are the two conditions where we are using a large amount of GLP-1 RA therapy. Again, the idea is looking at the person in front of us and then deciding, based on their past medical history and their current risk, whether or not a medication is a right fit for them.

I think more individualization here will come as we start using these medications that might be having potential effects on different organ systems. You mentioned a little bit about the liver, so a thought came in my mind. We know that people with diabetes who have alcohol use disorder are at a higher risk for potential hypoglycemia. If they have events when they have increased consumption of alcohol, there can be more hypoglycemia.

We now could potentially be using semaglutide or other GLP-1 RA therapy for management of alcohol use disorder. In your own experience in the studies that you’ve done or the literature that’s out there, has that been associated with an even higher risk for hypoglycemia? 

Dr. Leggio: It’s a wonderful question. I’m not aware of any formal and published report of that association. That said, your thinking from a physiopathologist standpoint makes total sense. I could not agree more. The fact that nothing has been published, at least to my knowledge, doesn’t mean that the death risk doesn’t exist. In fact, I agree with you that it does exist. 

Alcohol use disorder is interesting and tricky clinically because chronically, alcohol addiction or alcohol use disorder is associated with an increased risk for diabetes. Acutely, as you point out; and this could be with or without alcohol use disorder. An episode of a high volume of binge drinking may lead to hypoglycemia.

This is one of the reasons why people may show up to the emergency room with intoxication, and one of the symptoms detected at the emergency room is that they also have hypoglycemia in addition to vomiting, nausea, and everything else that we see in patients with acute intoxication.

Similar to the discussion about pancreatitis, as we work on understanding the possible role of GLP-1 RA in patients with alcohol use disorder, we do have to keep a close eye on the risk for hypoglycemia. The short answer is that this is not well established, but based on the simple concept of “first, do no harm,” I think we need to track that very carefully. 

In the ongoing clinical trial we’re doing in Maryland in my program at the NIH, we do just that. We are tracking glucose levels. Of course, patients come to clinic weekly, so unless they have symptoms, typically we don’t see anything at the time.

 

 

More important, we educate our patients when they go through the consent process. We tell them that this medication per se does not give hypoglycemia. In fact, we’re including people with diabetes, so for people on other medications like metformin, we explain to them that technically such a risk should not exist, but because you’re drinking alcohol in excessive amounts, you do have a potential higher risk. We just don’t know how significant that risk could be. 

We do a large amount of education at baseline when they enroll in our study. We also educate our patients on how to recognize early on the potential risk for hypoglycemia, exactly for the reasons you said. We explain to them the unknown potential that the GLP-1 RAs and alcohol together may synergize and give hypoglycemia.

Dr. Jain: I don’t know if you got this feeling at the ADA conference, but I felt, when attending all these sessions, that it seems like GLP-1 RA is the gift that keeps giving. We see the effect on diabetes, obesity, metabolic-associated steatotic liver disease, possibly with Alzheimer’s, chronic obstructive pulmonary disease, and so many things.

Now, of course, there’s potential use in alcohol use disorder. Do you think that using GLP-1 RA therapy is ready for prime time? Do you think we are now ready to prescribe this in people with alcohol use disorder?

Dr. Leggio: I would say we’re not there yet. As I mentioned at the beginning, the evidence keeps on growing. It’s getting stronger and stronger because the positive data keep on coming up. We have data from animal models, including the different species, ranging from rodents to nonhuman primates. We have anecdotal evidence and machine-learning approaches using, for example, big data and social media data. Now we have pharmacoepidemiology data and some small, initial, but still good randomized clinical trials.

What we are missing is the final step of having a substantial number of prospective, double-blind, placebo-controlled clinical trials to really prove or disprove whether these medications work, and to also better understand which patients may respond to these medications.

The good news is that there are many ongoing clinical trials. We are conducting a clinical trial in Maryland at the NIH. Dr. Simmons is doing a clinical trial at Oklahoma State University. Dr. Christian Hendershot at UNC is conducting a study at Chapel Hill. Dr. Josh Gowin is doing a study in Colorado. Dr. Anders Fink-Jensen is doing a study in Denmark. The momentum is very high. 

I’m only mentioning those people who are doing alcohol-semaglutide clinical trials. There are also people doing clinical trials on smoking, stimulants, and opioids. There are actually some very fresh, still unpublished data from Penn State that were presented publicly at conferences, showing how these drugs may reduce opioid craving, which is, of course, critically important, given that we’re in the middle of a fentanyl pandemic that is killing one person every 7 minutes, for example, in Baltimore. It’s very alarming and we need more treatments.

The bottom line is that it’s very promising, but we need to wait for these clinical trials to have a definitive answer. I would say that if you have a patient with diabetes, obesity, and also alcohol addiction, and they are on semaglutide or any other GLP-1 RA, and in addition to using the medication for diabetes and obesity, they also have a beneficial effect on their alcohol drinking, then that’s fantastic. At the end of the day, that’s the mission we all share: helping people. 

If it’s someone without obesity and diabetes, personally, at this stage, I will go with other medications that either have FDA approval or at least very solid evidence of efficacy from RCTs rather than going with the GLP-1 RA, at least until I see more definitive data from randomized clinical trials. 

There is a large amount of hope. We are hoping that these clinical trials will be positive. We are very enthusiastic and we’re also very thrilled to see that Novo Nordisk recently launched a gigantic multisite clinical trial with — I forgot how many sites, but it’s very large across Europe, America, and maybe other continents as well.

Their primary outcome is improvement in alcohol-related liver disease, but they’re also looking at alcohol drinking as a secondary outcome. That’s very important because, unlike in the diabetes field, in the addiction field, we do struggle to build partnership with the private sector because sometimes the addiction field is not seen as an appetitive field from pharma. 

We all know that the best success in any medication development story is when you put academia, the government, and pharma together. Think about the COVID-19 vaccine development. That’s unfortunately the exception rather than rule in the addiction field. 

With the company doing a large clinical trial in the alcohol field, although they focus more on the liver but they also looked at drinking, I really hope we’ll see more and more companies in the private sector take more and more interest in addiction. Also, I hope to see more and more partnership between the private sector, the government, and academia. 

Dr. Jain: Such exciting times, indeed. We can’t wait enough for the results of these and many other trials to come out. Dr. Leggio, it was an absolute delight chatting with you today. Thank you so much for joining us from ADA 2024.

Akshay B. Jain, MD, Clinical Instructor, Department of Endocrinology, University of British Columbia; Endocrinologist, TLC Diabetes and Endocrinology, Vancouver, British Columbia, Canada, has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Care to Know; CCRN; Connected in Motion; CPD Network; Dexcom; Diabetes Canada; Eli Lilly; GSK; HLS Therapeutics; Janssen; Master Clinician Alliance; MDBriefcase; Merck; Medtronic; Moderna; Novartis; Novo Nordisk; Partners in Progressive Medical Education; Pfizer; Sanofi Aventis; Timed Right; WebMD. Received research grants/research support from: Abbott; Amgen; Novo Nordisk. Received consulting fees from: Abbott; Acerus; AstraZeneca; Amgen; Bausch Healthcare; Bayer; Boehringer Ingelheim; Dexcom; Eli Lilly; Gilead Sciences; GSK; HLS Therapeutics; Insulet; Janssen; Medtronic; Novo Nordisk; Partners in Progressive Medical Education; PocketPills; Roche; Sanofi Aventis; Takeda. Lorenzo Leggio, MD, PhD, Clinical Director, Deputy Scientific Director, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, Maryland, has disclosed the following relevant financial relationships: Serve(d) as a US federal employee for: National Institutes of Health. He had received income in an amount equal to or greater than $250 from: UK Medical Council on Alcohol for his service as editor-in-chief for Alcohol and Alcoholism and received royalties from Rutledge as an editor for a textbook.

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

Publications
Publications
Topics
Article Type
Sections
Article Source

FROM ADA 2024

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Gate On Date
Un-Gate On Date
Use ProPublica
CFC Schedule Remove Status
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article
survey writer start date

Baby-Led Weaning

Article Type
Changed

 

I first heard the term “baby-led weaning” about 20 years ago, which turns out was just a few years after the concept was introduced to the public by a public health/midwife in Britain. Starting infants on solid foods when they could feed themselves didn’t sound as off-the-wall to me as it did to most other folks, but I chose not to include it in my list of standard recommendations at the 4- and 6-month well child visits. If any parent had asked me my opinion I would have told them to give it a try with a few specific cautions about what and how. But, I don’t recall any parents asking me. The ones who knew me well or had read, or at least heard about, my book on picky eating must have already figured out what my answer would be. The parents who didn’t know me may have been afraid I would tell them it was a crazy idea.

Twelve years ago I retired from office practice and hadn’t heard a peep about baby-led weaning until last week when I encountered a story in The New York Times. It appears that while I have been reveling in my post-practice existence, baby-led weaning has become a “thing.” As the author of the article observed: “The concept seems to appeal to millennials who favor parenting philosophies that prioritize child autonomy.”

Dr. William G. Wilkoff

Baby-led weaning’s traction has been so robust that the largest manufacturer of baby food in this country has been labeling some of its products “baby-led friendly since 2021.” There are several online businesses that have tapped into the growing market. One offers a very detailed free directory that lists almost any edible you can imagine with recommendations of when and how they can be presented in a safe and appealing matter to little hand feeders. Of course the company has also figured out a way to monetize the product.

Not surprisingly the American Academy of Pediatrics (AAP) has remained silent on baby-led weaning. However, in The New York Times article, Dr. Mark R. Corkins, chair of the AAP nutrition committee, is quoted as describing baby-led weaning is “a social media–driven invention.”

While I was interested to learn about the concept’s growth and commercialization, I was troubled to find that like co-sleeping, sleep training, and exclusive breastfeeding, baby-led weaning has become one of those angst-producing topics that is torturing new parents who live every day in fear that they “aren’t doing it right.” We pediatricians might deserve a small dose of blame for not vigorously emphasizing that there are numerous ways to skin that cat known as parenting. However, social media websites and Mom chat rooms are probably more responsible for creating an atmosphere in which parents are afraid of being ostracized for the decisions they have made in good faith whether it is about weaning or when to start toilet training.

In isolated cultures, weaning a baby to solids was probably never a topic for discussion or debate. New parents did what their parents did, or more likely a child’s grandmother advised or took over the process herself. The child was fed what the rest of the family ate. If it was something the infant could handle himself you gave it to him. If not you mashed it up or maybe you chewed it for him into a consistency he could manage.

However, most new parents have become so distanced from their own parents’ childrearing practices geographically, temporally, and philosophically, that they must rely on folks like us and others whom they believe are, or at least claim to be, experts. Young adults are no longer hesitant to cross ethnic thresholds when they decide to be co-parents, meaning that any remnant of family tradition is either diluted or lost outright. In the void created by this abandonment of tradition, corporations were happy to step in with easy-to-prepare baby food that lacks in nutritional and dietary variety. Baby-led weaning is just one more logical step in the metamorphosis of our society’s infant feeding patterns.

I still have no problem with baby-led weaning as an option for parents, particularly if with just a click of a mouse they can access safe and healthy advice to make up for generations of grandmotherly experience acquired over hundreds of years. However, I am deeply concerned when baby-led weaning is confused with the all-too-common disaster of child-led family meals.

It is one thing when parents hoping to encourage the process of self-feeding offer their infants an edible that may not be in the family’s usual diet. However, it is a totally different matter when a family allows itself to become dietary contortionists to a accommodate a 4-year-old whose diet consists of a monotonous rotation of three pasta shapes topped with grated Parmesan cheese, and on a good day a raw carrot slice or two. Parents living in this nutritional wasteland may have given up on managing their children’s pickiness, and may find it is less stressful to join the child and eat a few forkfuls of pasta to preserve some semblance of a family dinner. Then after the child has been put to bed they have their own balanced meal.

Almost by definition family meals are a compromise. Even adults without children negotiate often unspoken menu patterns with their partners. “This evening we’ll have your favorite, I may have my favorite next week.”

Most parents of young children understand that their diet may be a bit heavier on pasta than they might prefer and a little less varied when it comes to vegetables. It is just part of the deal. However, when mealtimes become totally dictated by the pickiness of a child there is a problem. While a poorly structured child-led family diet may be nutritionally deficient, the bigger problem is that it is expensive in time and labor, two resources usually in short supply in young families.

Theoretically, infants who have led their own weaning are more likely to have been introduced to a broad variety of flavors and textures and this may carry them into childhood as more adventuresome eaters. Picky eating can be managed successfully and result in a family that can enjoy the psychological and emotional benefits of nutritionally balanced family meals, but it requires a combination of parental courage and patience.

It is unclear exactly how we got into a situation in which a generation of parents makes things more difficult for themselves by favoring practices that overemphasize child autonomy. It may be that the parents had suffered under autocratic parents themselves, or more likely they have read too many novels or watched too many movies and TV shows in which the parents were portrayed as overbearing or controlling. Or, it may simply be that they haven’t had enough exposure to young children to realize that they all benefit from clear limits to a varying degree.

In the process of watching tens of thousands of parents, it has become clear to me that those who are the most successful are leaders and that they lead primarily by example. They have learned to be masters in the art of deception by creating a safe environment with sensible limits while at the same time fostering an atmosphere in which the child sees himself as participating in the process.

The biblical prophet Isaiah (11:6-9) in his description of how things will be different after the Lord acts to help his people predicts: “and a little child shall lead them.” This prediction fits nicely as the last in a string of crazy situations that includes a wolf living with a lamb and a leopard lying down with a calf.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Publications
Topics
Sections

 

I first heard the term “baby-led weaning” about 20 years ago, which turns out was just a few years after the concept was introduced to the public by a public health/midwife in Britain. Starting infants on solid foods when they could feed themselves didn’t sound as off-the-wall to me as it did to most other folks, but I chose not to include it in my list of standard recommendations at the 4- and 6-month well child visits. If any parent had asked me my opinion I would have told them to give it a try with a few specific cautions about what and how. But, I don’t recall any parents asking me. The ones who knew me well or had read, or at least heard about, my book on picky eating must have already figured out what my answer would be. The parents who didn’t know me may have been afraid I would tell them it was a crazy idea.

Twelve years ago I retired from office practice and hadn’t heard a peep about baby-led weaning until last week when I encountered a story in The New York Times. It appears that while I have been reveling in my post-practice existence, baby-led weaning has become a “thing.” As the author of the article observed: “The concept seems to appeal to millennials who favor parenting philosophies that prioritize child autonomy.”

Dr. William G. Wilkoff

Baby-led weaning’s traction has been so robust that the largest manufacturer of baby food in this country has been labeling some of its products “baby-led friendly since 2021.” There are several online businesses that have tapped into the growing market. One offers a very detailed free directory that lists almost any edible you can imagine with recommendations of when and how they can be presented in a safe and appealing matter to little hand feeders. Of course the company has also figured out a way to monetize the product.

Not surprisingly the American Academy of Pediatrics (AAP) has remained silent on baby-led weaning. However, in The New York Times article, Dr. Mark R. Corkins, chair of the AAP nutrition committee, is quoted as describing baby-led weaning is “a social media–driven invention.”

While I was interested to learn about the concept’s growth and commercialization, I was troubled to find that like co-sleeping, sleep training, and exclusive breastfeeding, baby-led weaning has become one of those angst-producing topics that is torturing new parents who live every day in fear that they “aren’t doing it right.” We pediatricians might deserve a small dose of blame for not vigorously emphasizing that there are numerous ways to skin that cat known as parenting. However, social media websites and Mom chat rooms are probably more responsible for creating an atmosphere in which parents are afraid of being ostracized for the decisions they have made in good faith whether it is about weaning or when to start toilet training.

In isolated cultures, weaning a baby to solids was probably never a topic for discussion or debate. New parents did what their parents did, or more likely a child’s grandmother advised or took over the process herself. The child was fed what the rest of the family ate. If it was something the infant could handle himself you gave it to him. If not you mashed it up or maybe you chewed it for him into a consistency he could manage.

However, most new parents have become so distanced from their own parents’ childrearing practices geographically, temporally, and philosophically, that they must rely on folks like us and others whom they believe are, or at least claim to be, experts. Young adults are no longer hesitant to cross ethnic thresholds when they decide to be co-parents, meaning that any remnant of family tradition is either diluted or lost outright. In the void created by this abandonment of tradition, corporations were happy to step in with easy-to-prepare baby food that lacks in nutritional and dietary variety. Baby-led weaning is just one more logical step in the metamorphosis of our society’s infant feeding patterns.

I still have no problem with baby-led weaning as an option for parents, particularly if with just a click of a mouse they can access safe and healthy advice to make up for generations of grandmotherly experience acquired over hundreds of years. However, I am deeply concerned when baby-led weaning is confused with the all-too-common disaster of child-led family meals.

It is one thing when parents hoping to encourage the process of self-feeding offer their infants an edible that may not be in the family’s usual diet. However, it is a totally different matter when a family allows itself to become dietary contortionists to a accommodate a 4-year-old whose diet consists of a monotonous rotation of three pasta shapes topped with grated Parmesan cheese, and on a good day a raw carrot slice or two. Parents living in this nutritional wasteland may have given up on managing their children’s pickiness, and may find it is less stressful to join the child and eat a few forkfuls of pasta to preserve some semblance of a family dinner. Then after the child has been put to bed they have their own balanced meal.

Almost by definition family meals are a compromise. Even adults without children negotiate often unspoken menu patterns with their partners. “This evening we’ll have your favorite, I may have my favorite next week.”

Most parents of young children understand that their diet may be a bit heavier on pasta than they might prefer and a little less varied when it comes to vegetables. It is just part of the deal. However, when mealtimes become totally dictated by the pickiness of a child there is a problem. While a poorly structured child-led family diet may be nutritionally deficient, the bigger problem is that it is expensive in time and labor, two resources usually in short supply in young families.

Theoretically, infants who have led their own weaning are more likely to have been introduced to a broad variety of flavors and textures and this may carry them into childhood as more adventuresome eaters. Picky eating can be managed successfully and result in a family that can enjoy the psychological and emotional benefits of nutritionally balanced family meals, but it requires a combination of parental courage and patience.

It is unclear exactly how we got into a situation in which a generation of parents makes things more difficult for themselves by favoring practices that overemphasize child autonomy. It may be that the parents had suffered under autocratic parents themselves, or more likely they have read too many novels or watched too many movies and TV shows in which the parents were portrayed as overbearing or controlling. Or, it may simply be that they haven’t had enough exposure to young children to realize that they all benefit from clear limits to a varying degree.

In the process of watching tens of thousands of parents, it has become clear to me that those who are the most successful are leaders and that they lead primarily by example. They have learned to be masters in the art of deception by creating a safe environment with sensible limits while at the same time fostering an atmosphere in which the child sees himself as participating in the process.

The biblical prophet Isaiah (11:6-9) in his description of how things will be different after the Lord acts to help his people predicts: “and a little child shall lead them.” This prediction fits nicely as the last in a string of crazy situations that includes a wolf living with a lamb and a leopard lying down with a calf.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

 

I first heard the term “baby-led weaning” about 20 years ago, which turns out was just a few years after the concept was introduced to the public by a public health/midwife in Britain. Starting infants on solid foods when they could feed themselves didn’t sound as off-the-wall to me as it did to most other folks, but I chose not to include it in my list of standard recommendations at the 4- and 6-month well child visits. If any parent had asked me my opinion I would have told them to give it a try with a few specific cautions about what and how. But, I don’t recall any parents asking me. The ones who knew me well or had read, or at least heard about, my book on picky eating must have already figured out what my answer would be. The parents who didn’t know me may have been afraid I would tell them it was a crazy idea.

Twelve years ago I retired from office practice and hadn’t heard a peep about baby-led weaning until last week when I encountered a story in The New York Times. It appears that while I have been reveling in my post-practice existence, baby-led weaning has become a “thing.” As the author of the article observed: “The concept seems to appeal to millennials who favor parenting philosophies that prioritize child autonomy.”

Dr. William G. Wilkoff

Baby-led weaning’s traction has been so robust that the largest manufacturer of baby food in this country has been labeling some of its products “baby-led friendly since 2021.” There are several online businesses that have tapped into the growing market. One offers a very detailed free directory that lists almost any edible you can imagine with recommendations of when and how they can be presented in a safe and appealing matter to little hand feeders. Of course the company has also figured out a way to monetize the product.

Not surprisingly the American Academy of Pediatrics (AAP) has remained silent on baby-led weaning. However, in The New York Times article, Dr. Mark R. Corkins, chair of the AAP nutrition committee, is quoted as describing baby-led weaning is “a social media–driven invention.”

While I was interested to learn about the concept’s growth and commercialization, I was troubled to find that like co-sleeping, sleep training, and exclusive breastfeeding, baby-led weaning has become one of those angst-producing topics that is torturing new parents who live every day in fear that they “aren’t doing it right.” We pediatricians might deserve a small dose of blame for not vigorously emphasizing that there are numerous ways to skin that cat known as parenting. However, social media websites and Mom chat rooms are probably more responsible for creating an atmosphere in which parents are afraid of being ostracized for the decisions they have made in good faith whether it is about weaning or when to start toilet training.

In isolated cultures, weaning a baby to solids was probably never a topic for discussion or debate. New parents did what their parents did, or more likely a child’s grandmother advised or took over the process herself. The child was fed what the rest of the family ate. If it was something the infant could handle himself you gave it to him. If not you mashed it up or maybe you chewed it for him into a consistency he could manage.

However, most new parents have become so distanced from their own parents’ childrearing practices geographically, temporally, and philosophically, that they must rely on folks like us and others whom they believe are, or at least claim to be, experts. Young adults are no longer hesitant to cross ethnic thresholds when they decide to be co-parents, meaning that any remnant of family tradition is either diluted or lost outright. In the void created by this abandonment of tradition, corporations were happy to step in with easy-to-prepare baby food that lacks in nutritional and dietary variety. Baby-led weaning is just one more logical step in the metamorphosis of our society’s infant feeding patterns.

I still have no problem with baby-led weaning as an option for parents, particularly if with just a click of a mouse they can access safe and healthy advice to make up for generations of grandmotherly experience acquired over hundreds of years. However, I am deeply concerned when baby-led weaning is confused with the all-too-common disaster of child-led family meals.

It is one thing when parents hoping to encourage the process of self-feeding offer their infants an edible that may not be in the family’s usual diet. However, it is a totally different matter when a family allows itself to become dietary contortionists to a accommodate a 4-year-old whose diet consists of a monotonous rotation of three pasta shapes topped with grated Parmesan cheese, and on a good day a raw carrot slice or two. Parents living in this nutritional wasteland may have given up on managing their children’s pickiness, and may find it is less stressful to join the child and eat a few forkfuls of pasta to preserve some semblance of a family dinner. Then after the child has been put to bed they have their own balanced meal.

Almost by definition family meals are a compromise. Even adults without children negotiate often unspoken menu patterns with their partners. “This evening we’ll have your favorite, I may have my favorite next week.”

Most parents of young children understand that their diet may be a bit heavier on pasta than they might prefer and a little less varied when it comes to vegetables. It is just part of the deal. However, when mealtimes become totally dictated by the pickiness of a child there is a problem. While a poorly structured child-led family diet may be nutritionally deficient, the bigger problem is that it is expensive in time and labor, two resources usually in short supply in young families.

Theoretically, infants who have led their own weaning are more likely to have been introduced to a broad variety of flavors and textures and this may carry them into childhood as more adventuresome eaters. Picky eating can be managed successfully and result in a family that can enjoy the psychological and emotional benefits of nutritionally balanced family meals, but it requires a combination of parental courage and patience.

It is unclear exactly how we got into a situation in which a generation of parents makes things more difficult for themselves by favoring practices that overemphasize child autonomy. It may be that the parents had suffered under autocratic parents themselves, or more likely they have read too many novels or watched too many movies and TV shows in which the parents were portrayed as overbearing or controlling. Or, it may simply be that they haven’t had enough exposure to young children to realize that they all benefit from clear limits to a varying degree.

In the process of watching tens of thousands of parents, it has become clear to me that those who are the most successful are leaders and that they lead primarily by example. They have learned to be masters in the art of deception by creating a safe environment with sensible limits while at the same time fostering an atmosphere in which the child sees himself as participating in the process.

The biblical prophet Isaiah (11:6-9) in his description of how things will be different after the Lord acts to help his people predicts: “and a little child shall lead them.” This prediction fits nicely as the last in a string of crazy situations that includes a wolf living with a lamb and a leopard lying down with a calf.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

The Small Business of Medicine

Article Type
Changed

 

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Dr. Allan M. Block

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Publications
Topics
Sections

 

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Dr. Allan M. Block

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

 

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Dr. Allan M. Block

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

Long COVID and Blame Hunting

Article Type
Changed

 

I suspect that many of you have seen or read about a recent study regarding the “long COVID” enigma. The investigators surveyed the records of more than 4000 pediatric patients who had been infected and nearly 1400 who had not. The researchers then developed models in which 14 symptoms were more common in previous SARS-CoV2–infected individuals in all age groups, compared with the uninfected. There were four additional symptoms in children only and three additional symptoms in the adolescents.

Using these data, the investigators created research indices that “correlated with poor overall health and quality of life” and emphasized “neurocognitive, pain, and gastrointestinal symptoms in school-age children” and a “change or loss in smell or taste, pain, and fatigue/malaise-related symptoms in adolescents.”

Dr. William G. Wilkoff

So now thanks to these investigators we have research indices for characterizing PASC (post-acute sequelae of SARS-CoV-2, aka. long COVID). What should we to do with them? I’m not sure these results move us any further if our goal is finding something to help patients who believe, or have been told, that they have long COVID.

Even to a non-statistician like myself there appear to be some problems with this study. In an editorial accompanying this study, Suchitra Rao, MBBS, MSCS in the Department of Pediatrics, University of Colorado School of Medicine, Aurora, noted the study has the potential for ascertainment bias. For example, the researchers’ subject recruitment procedure resulted in a higher “proportion of neurocognitive/behavioral manifestations” may have skewed the results.

Also, some of the patient evaluations were not done at a consistent interval after the initial infection, which could result in recall bias. And, more importantly, because there were no baseline measurements to determine preinfection status, the investigators had no way of determining to what degree the patients’ underlying conditions may have reflected the quality of life scores.

Although I wouldn’t consider it a bias, I wonder if the investigators have a preconceived vision of what long COVID is going to look like once it is better understood. The fact that they undertook this project suggests that they believe the truth about the phenomenon will be discoverable using data based on collections of vague symptoms.

Or, do the researchers share my vision of long COVID that if it exists it will be something akin to the burst of Parkinson’s disease seen decades later in survivors of the 1918-1920 flu pandemic. Or, maybe it is something like post-polio syndrome, in which survivors in childhood develop atrophy and muscle weakness as they age. Do the researchers believe that COVID survivors are harboring some remnant of SARS-CoV-2 or its genome inside their bodies ticking like a time bomb ready to surface in the future? Think shingles.

I suspect that there are some folks who may or not share my ticking time bomb vision, but who, like me, wonder if there is really such a thing as long COVID – at least one in the form characterized by the work of these investigators. Unfortunately, the $1 billion the National Institutes of Health has invested in the Researching COVID to Enhance Recovery (RECOVER) initiative is not going to discover delayed sequelae until time is ready to tell us. What researchers are looking at now is a collection of patients, some who were not well to begin with but now describe a collection of vague symptoms, some of which are unique to COVID, but most are not. The loss of taste and smell being the one notable and important exception.

It is easy to understand why patients and their physicians would like to have a diagnosis like “long COVID” to at least validate their symptoms that up until now have eluded explanation or remedy. Not surprisingly, they may feel that, if researchers can’t find a cure, let’s at least have something we can lay the blame on.

A major flaw in this current attempt to characterize long COVID is the lack of a true control group. Yes, the subjects the researchers labeled as “uninfected” lived contemporaneously with the patients unfortunate enough to have acquired the virus. However, this illness was mysterious from its first appearance, continued to be more frightening as we struggled to learn more about it, and was clumsily managed in a way that turned our way of life upside down. This was particularly true for school-age children. It unmasked previously unsuspected underlying conditions and quickly acquired a poorly documented reputation for having a “long” variety.

Of course the “uninfected” also lived through these same tumultuous times. But knowing that you harbored, and may still harbor, this mysterious invader moves the infected and their families into a whole new level of concern and anxiety the rest of us who were more fortunate don’t share.

We must not ignore the fact that patients and their caregivers may receive some comfort when they have something to blame for their symptoms. However, we must shift our focus away from blame hunting, which up to this point has been fruitless. Instead, we must invest our energies into helping those struggling with long COVID find a manageable pathway toward improvement. Each patient should be treated as an individual and not part of a group with similar symptoms cobbled together with data acquired under a cloud of bias.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Publications
Topics
Sections

 

I suspect that many of you have seen or read about a recent study regarding the “long COVID” enigma. The investigators surveyed the records of more than 4000 pediatric patients who had been infected and nearly 1400 who had not. The researchers then developed models in which 14 symptoms were more common in previous SARS-CoV2–infected individuals in all age groups, compared with the uninfected. There were four additional symptoms in children only and three additional symptoms in the adolescents.

Using these data, the investigators created research indices that “correlated with poor overall health and quality of life” and emphasized “neurocognitive, pain, and gastrointestinal symptoms in school-age children” and a “change or loss in smell or taste, pain, and fatigue/malaise-related symptoms in adolescents.”

Dr. William G. Wilkoff

So now thanks to these investigators we have research indices for characterizing PASC (post-acute sequelae of SARS-CoV-2, aka. long COVID). What should we to do with them? I’m not sure these results move us any further if our goal is finding something to help patients who believe, or have been told, that they have long COVID.

Even to a non-statistician like myself there appear to be some problems with this study. In an editorial accompanying this study, Suchitra Rao, MBBS, MSCS in the Department of Pediatrics, University of Colorado School of Medicine, Aurora, noted the study has the potential for ascertainment bias. For example, the researchers’ subject recruitment procedure resulted in a higher “proportion of neurocognitive/behavioral manifestations” may have skewed the results.

Also, some of the patient evaluations were not done at a consistent interval after the initial infection, which could result in recall bias. And, more importantly, because there were no baseline measurements to determine preinfection status, the investigators had no way of determining to what degree the patients’ underlying conditions may have reflected the quality of life scores.

Although I wouldn’t consider it a bias, I wonder if the investigators have a preconceived vision of what long COVID is going to look like once it is better understood. The fact that they undertook this project suggests that they believe the truth about the phenomenon will be discoverable using data based on collections of vague symptoms.

Or, do the researchers share my vision of long COVID that if it exists it will be something akin to the burst of Parkinson’s disease seen decades later in survivors of the 1918-1920 flu pandemic. Or, maybe it is something like post-polio syndrome, in which survivors in childhood develop atrophy and muscle weakness as they age. Do the researchers believe that COVID survivors are harboring some remnant of SARS-CoV-2 or its genome inside their bodies ticking like a time bomb ready to surface in the future? Think shingles.

I suspect that there are some folks who may or not share my ticking time bomb vision, but who, like me, wonder if there is really such a thing as long COVID – at least one in the form characterized by the work of these investigators. Unfortunately, the $1 billion the National Institutes of Health has invested in the Researching COVID to Enhance Recovery (RECOVER) initiative is not going to discover delayed sequelae until time is ready to tell us. What researchers are looking at now is a collection of patients, some who were not well to begin with but now describe a collection of vague symptoms, some of which are unique to COVID, but most are not. The loss of taste and smell being the one notable and important exception.

It is easy to understand why patients and their physicians would like to have a diagnosis like “long COVID” to at least validate their symptoms that up until now have eluded explanation or remedy. Not surprisingly, they may feel that, if researchers can’t find a cure, let’s at least have something we can lay the blame on.

A major flaw in this current attempt to characterize long COVID is the lack of a true control group. Yes, the subjects the researchers labeled as “uninfected” lived contemporaneously with the patients unfortunate enough to have acquired the virus. However, this illness was mysterious from its first appearance, continued to be more frightening as we struggled to learn more about it, and was clumsily managed in a way that turned our way of life upside down. This was particularly true for school-age children. It unmasked previously unsuspected underlying conditions and quickly acquired a poorly documented reputation for having a “long” variety.

Of course the “uninfected” also lived through these same tumultuous times. But knowing that you harbored, and may still harbor, this mysterious invader moves the infected and their families into a whole new level of concern and anxiety the rest of us who were more fortunate don’t share.

We must not ignore the fact that patients and their caregivers may receive some comfort when they have something to blame for their symptoms. However, we must shift our focus away from blame hunting, which up to this point has been fruitless. Instead, we must invest our energies into helping those struggling with long COVID find a manageable pathway toward improvement. Each patient should be treated as an individual and not part of a group with similar symptoms cobbled together with data acquired under a cloud of bias.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

 

I suspect that many of you have seen or read about a recent study regarding the “long COVID” enigma. The investigators surveyed the records of more than 4000 pediatric patients who had been infected and nearly 1400 who had not. The researchers then developed models in which 14 symptoms were more common in previous SARS-CoV2–infected individuals in all age groups, compared with the uninfected. There were four additional symptoms in children only and three additional symptoms in the adolescents.

Using these data, the investigators created research indices that “correlated with poor overall health and quality of life” and emphasized “neurocognitive, pain, and gastrointestinal symptoms in school-age children” and a “change or loss in smell or taste, pain, and fatigue/malaise-related symptoms in adolescents.”

Dr. William G. Wilkoff

So now thanks to these investigators we have research indices for characterizing PASC (post-acute sequelae of SARS-CoV-2, aka. long COVID). What should we to do with them? I’m not sure these results move us any further if our goal is finding something to help patients who believe, or have been told, that they have long COVID.

Even to a non-statistician like myself there appear to be some problems with this study. In an editorial accompanying this study, Suchitra Rao, MBBS, MSCS in the Department of Pediatrics, University of Colorado School of Medicine, Aurora, noted the study has the potential for ascertainment bias. For example, the researchers’ subject recruitment procedure resulted in a higher “proportion of neurocognitive/behavioral manifestations” may have skewed the results.

Also, some of the patient evaluations were not done at a consistent interval after the initial infection, which could result in recall bias. And, more importantly, because there were no baseline measurements to determine preinfection status, the investigators had no way of determining to what degree the patients’ underlying conditions may have reflected the quality of life scores.

Although I wouldn’t consider it a bias, I wonder if the investigators have a preconceived vision of what long COVID is going to look like once it is better understood. The fact that they undertook this project suggests that they believe the truth about the phenomenon will be discoverable using data based on collections of vague symptoms.

Or, do the researchers share my vision of long COVID that if it exists it will be something akin to the burst of Parkinson’s disease seen decades later in survivors of the 1918-1920 flu pandemic. Or, maybe it is something like post-polio syndrome, in which survivors in childhood develop atrophy and muscle weakness as they age. Do the researchers believe that COVID survivors are harboring some remnant of SARS-CoV-2 or its genome inside their bodies ticking like a time bomb ready to surface in the future? Think shingles.

I suspect that there are some folks who may or not share my ticking time bomb vision, but who, like me, wonder if there is really such a thing as long COVID – at least one in the form characterized by the work of these investigators. Unfortunately, the $1 billion the National Institutes of Health has invested in the Researching COVID to Enhance Recovery (RECOVER) initiative is not going to discover delayed sequelae until time is ready to tell us. What researchers are looking at now is a collection of patients, some who were not well to begin with but now describe a collection of vague symptoms, some of which are unique to COVID, but most are not. The loss of taste and smell being the one notable and important exception.

It is easy to understand why patients and their physicians would like to have a diagnosis like “long COVID” to at least validate their symptoms that up until now have eluded explanation or remedy. Not surprisingly, they may feel that, if researchers can’t find a cure, let’s at least have something we can lay the blame on.

A major flaw in this current attempt to characterize long COVID is the lack of a true control group. Yes, the subjects the researchers labeled as “uninfected” lived contemporaneously with the patients unfortunate enough to have acquired the virus. However, this illness was mysterious from its first appearance, continued to be more frightening as we struggled to learn more about it, and was clumsily managed in a way that turned our way of life upside down. This was particularly true for school-age children. It unmasked previously unsuspected underlying conditions and quickly acquired a poorly documented reputation for having a “long” variety.

Of course the “uninfected” also lived through these same tumultuous times. But knowing that you harbored, and may still harbor, this mysterious invader moves the infected and their families into a whole new level of concern and anxiety the rest of us who were more fortunate don’t share.

We must not ignore the fact that patients and their caregivers may receive some comfort when they have something to blame for their symptoms. However, we must shift our focus away from blame hunting, which up to this point has been fruitless. Instead, we must invest our energies into helping those struggling with long COVID find a manageable pathway toward improvement. Each patient should be treated as an individual and not part of a group with similar symptoms cobbled together with data acquired under a cloud of bias.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

Being An Outsider

Article Type
Changed

Our son works for a Maine-based company that produces and sells clothing and outdoor recreation equipment. One of its tag lines is “Be an Outsider.” In his role as chief marketing officer, he was recently given an app for his phone that can calculate how many minutes he spends outside each day. He assured me: “Dad, you don’t need one of these on your phone. Your weather-beaten skin says you are already logging in way more than enough minutes outdoors.”

But, it got me thinking about several avenues of research where an app like that would be useful. As luck would have it, the following week I stumbled across a paper describing just such a study.

Dr. William G. Wilkoff

Researchers in Shanghai, China, placed smartwatches with technology similar to my son’s phone on nearly 3000 children and found “that outdoor exposure patterns characterized by a continuous period of at least 15 minutes, accompanied by a sunlight intensity of more than 2000 lux, were associated with less myopic shift.” In other words, children getting more time outside were less likely to become nearsighted.” Whether this was an effect of being outside instead of staring at a screen indoors is an interesting question.

I have alway suspected that being outdoors was important for wellness and this paper meshed nicely with an article I had recently read in The Washington Post titled, “How time in nature builds happier, healthier and more social children” (Jamie Friedlander Serrano, 2024 Aug 4). The reporter quotes numerous experts in child health and includes links to several articles that tout the benefits of outdoor experiences, particularly ones in a natural environment. There are the vitamin D effects on growth and bone health. There are studies suggesting that being out in nature can reduce stress, anxiety, and aggression, and improve working memory and attention.

In this country there is a small but growing group of schools modeling themselves after the “Forest kindergartens” that have become popular in Europe in which a large portion of the students’ days are spent outside surrounded by nature. It will be interesting to see how robustly this trend grows here in the United States. However, in a nation like ours in which the Environmental Protection Agency estimates that the average American spends 90% of his day indoors, it’s going to require a seismic shift in our societal norms.

I think my mother always knew that being outdoors was healthy for children. I also suspect that she and most my friends’ mothers were primarily motivated by a desire to have the house to themselves. This was primarily to allow them to get the housework done unimpeded by pestering children. But, there may have been times when a busy housewife simply needed to sit down with a book in the peace and quiet of a childless environment. We kids were told to get out of the house and return for lunch and dinner, hopefully not in the tow of a police officer. There were few rules and for the most part we were left to invent our own amusement.

Yes, you’ve heard this old-fogey legend before. But it was true. Those were the halcyon days of the 1950s in a small suburban town of 5000 of a little more than 1 square mile with its own swimming pool. My particular idyll was aptly named Pleasantville but I know we were not alone as the only community where children were allowed – or let’s say “encouraged” – to be outdoors if they weren’t in school. It was a different time.

I am not so naive to believe that we will ever return to those good old days when children roamed free, but it is worth considering what has changed to drive children inside and away from all the health benefits of being outdoors. Is there anything we can do to reverse this unfortunate trend?

First, we must first face up to the reality that our society has become so focused on the potential downsides of everything that we seem to be driven primarily by risk avoidance. We hear how things can go terribly wrong in the world outside, a world we can’t control. Although the data from the pandemic don’t support it, more of us believe children are safer indoors. Parents in particular seem to worry more now than they did 75 years ago. I don’t think we can point to a single event such as the tragedies of September 11 to explain the shift.

While bad news has always traveled fast, today (with communication being almost instantaneous) a story about a child abduction at 6 in the morning in Nevada can be on my local TV channel by lunchtime here in Maine. Parents worry that if bad stuff can happen to a child in Mount Elsewhere, it could happen to my child playing in the backyard across the street.

I think we pediatricians should consider how large a role we may be playing in driving parental anxiety with our frequent warnings about the dangers a child can encounter outdoors whether they come in the form of accidents or exposure to the elements.

While parents have grown more hesitant to send their children outside to play, as a society we have failed to adequately acknowledge and respond to the role that unhealthy attraction of indoor alternatives to outdoor play may be contributing to indoorism. Here we’re talking about television, smartphones, and the internet.

So, what can we do as pediatricians to get our patients outside? First, we can set an example and cover our office walls with pictures of ourselves and our families enjoying the outdoors. We can be vocal advocates for creating and maintaining accessible outdoor spaces in our community. We can advocate for more outside time during recess in school and encourage the school officials to consider having more courses taught outside.

We can be more diligent in asking families about their screen use and not be afraid to express our concern when we hear how little outdoor time their child is getting. Finally, we can strive for more balance in our messaging. For example for every warning we give about playing outside on poor air quality days there should be a reminder of the health benefits of being outdoors on the other days. Every message about the importance of sunscreen should be preceded by a few sentences promoting outdoor activities in wooded environments where sun exposure is less of a concern.

We should all be looking for ways in which our communities can remove the barriers that prevent our patients for reaping the health benefits of being outdoors. Being an outsider is just as important as getting enough sleep, eating the right food and staying physically active.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Publications
Topics
Sections

Our son works for a Maine-based company that produces and sells clothing and outdoor recreation equipment. One of its tag lines is “Be an Outsider.” In his role as chief marketing officer, he was recently given an app for his phone that can calculate how many minutes he spends outside each day. He assured me: “Dad, you don’t need one of these on your phone. Your weather-beaten skin says you are already logging in way more than enough minutes outdoors.”

But, it got me thinking about several avenues of research where an app like that would be useful. As luck would have it, the following week I stumbled across a paper describing just such a study.

Dr. William G. Wilkoff

Researchers in Shanghai, China, placed smartwatches with technology similar to my son’s phone on nearly 3000 children and found “that outdoor exposure patterns characterized by a continuous period of at least 15 minutes, accompanied by a sunlight intensity of more than 2000 lux, were associated with less myopic shift.” In other words, children getting more time outside were less likely to become nearsighted.” Whether this was an effect of being outside instead of staring at a screen indoors is an interesting question.

I have alway suspected that being outdoors was important for wellness and this paper meshed nicely with an article I had recently read in The Washington Post titled, “How time in nature builds happier, healthier and more social children” (Jamie Friedlander Serrano, 2024 Aug 4). The reporter quotes numerous experts in child health and includes links to several articles that tout the benefits of outdoor experiences, particularly ones in a natural environment. There are the vitamin D effects on growth and bone health. There are studies suggesting that being out in nature can reduce stress, anxiety, and aggression, and improve working memory and attention.

In this country there is a small but growing group of schools modeling themselves after the “Forest kindergartens” that have become popular in Europe in which a large portion of the students’ days are spent outside surrounded by nature. It will be interesting to see how robustly this trend grows here in the United States. However, in a nation like ours in which the Environmental Protection Agency estimates that the average American spends 90% of his day indoors, it’s going to require a seismic shift in our societal norms.

I think my mother always knew that being outdoors was healthy for children. I also suspect that she and most my friends’ mothers were primarily motivated by a desire to have the house to themselves. This was primarily to allow them to get the housework done unimpeded by pestering children. But, there may have been times when a busy housewife simply needed to sit down with a book in the peace and quiet of a childless environment. We kids were told to get out of the house and return for lunch and dinner, hopefully not in the tow of a police officer. There were few rules and for the most part we were left to invent our own amusement.

Yes, you’ve heard this old-fogey legend before. But it was true. Those were the halcyon days of the 1950s in a small suburban town of 5000 of a little more than 1 square mile with its own swimming pool. My particular idyll was aptly named Pleasantville but I know we were not alone as the only community where children were allowed – or let’s say “encouraged” – to be outdoors if they weren’t in school. It was a different time.

I am not so naive to believe that we will ever return to those good old days when children roamed free, but it is worth considering what has changed to drive children inside and away from all the health benefits of being outdoors. Is there anything we can do to reverse this unfortunate trend?

First, we must first face up to the reality that our society has become so focused on the potential downsides of everything that we seem to be driven primarily by risk avoidance. We hear how things can go terribly wrong in the world outside, a world we can’t control. Although the data from the pandemic don’t support it, more of us believe children are safer indoors. Parents in particular seem to worry more now than they did 75 years ago. I don’t think we can point to a single event such as the tragedies of September 11 to explain the shift.

While bad news has always traveled fast, today (with communication being almost instantaneous) a story about a child abduction at 6 in the morning in Nevada can be on my local TV channel by lunchtime here in Maine. Parents worry that if bad stuff can happen to a child in Mount Elsewhere, it could happen to my child playing in the backyard across the street.

I think we pediatricians should consider how large a role we may be playing in driving parental anxiety with our frequent warnings about the dangers a child can encounter outdoors whether they come in the form of accidents or exposure to the elements.

While parents have grown more hesitant to send their children outside to play, as a society we have failed to adequately acknowledge and respond to the role that unhealthy attraction of indoor alternatives to outdoor play may be contributing to indoorism. Here we’re talking about television, smartphones, and the internet.

So, what can we do as pediatricians to get our patients outside? First, we can set an example and cover our office walls with pictures of ourselves and our families enjoying the outdoors. We can be vocal advocates for creating and maintaining accessible outdoor spaces in our community. We can advocate for more outside time during recess in school and encourage the school officials to consider having more courses taught outside.

We can be more diligent in asking families about their screen use and not be afraid to express our concern when we hear how little outdoor time their child is getting. Finally, we can strive for more balance in our messaging. For example for every warning we give about playing outside on poor air quality days there should be a reminder of the health benefits of being outdoors on the other days. Every message about the importance of sunscreen should be preceded by a few sentences promoting outdoor activities in wooded environments where sun exposure is less of a concern.

We should all be looking for ways in which our communities can remove the barriers that prevent our patients for reaping the health benefits of being outdoors. Being an outsider is just as important as getting enough sleep, eating the right food and staying physically active.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Our son works for a Maine-based company that produces and sells clothing and outdoor recreation equipment. One of its tag lines is “Be an Outsider.” In his role as chief marketing officer, he was recently given an app for his phone that can calculate how many minutes he spends outside each day. He assured me: “Dad, you don’t need one of these on your phone. Your weather-beaten skin says you are already logging in way more than enough minutes outdoors.”

But, it got me thinking about several avenues of research where an app like that would be useful. As luck would have it, the following week I stumbled across a paper describing just such a study.

Dr. William G. Wilkoff

Researchers in Shanghai, China, placed smartwatches with technology similar to my son’s phone on nearly 3000 children and found “that outdoor exposure patterns characterized by a continuous period of at least 15 minutes, accompanied by a sunlight intensity of more than 2000 lux, were associated with less myopic shift.” In other words, children getting more time outside were less likely to become nearsighted.” Whether this was an effect of being outside instead of staring at a screen indoors is an interesting question.

I have alway suspected that being outdoors was important for wellness and this paper meshed nicely with an article I had recently read in The Washington Post titled, “How time in nature builds happier, healthier and more social children” (Jamie Friedlander Serrano, 2024 Aug 4). The reporter quotes numerous experts in child health and includes links to several articles that tout the benefits of outdoor experiences, particularly ones in a natural environment. There are the vitamin D effects on growth and bone health. There are studies suggesting that being out in nature can reduce stress, anxiety, and aggression, and improve working memory and attention.

In this country there is a small but growing group of schools modeling themselves after the “Forest kindergartens” that have become popular in Europe in which a large portion of the students’ days are spent outside surrounded by nature. It will be interesting to see how robustly this trend grows here in the United States. However, in a nation like ours in which the Environmental Protection Agency estimates that the average American spends 90% of his day indoors, it’s going to require a seismic shift in our societal norms.

I think my mother always knew that being outdoors was healthy for children. I also suspect that she and most my friends’ mothers were primarily motivated by a desire to have the house to themselves. This was primarily to allow them to get the housework done unimpeded by pestering children. But, there may have been times when a busy housewife simply needed to sit down with a book in the peace and quiet of a childless environment. We kids were told to get out of the house and return for lunch and dinner, hopefully not in the tow of a police officer. There were few rules and for the most part we were left to invent our own amusement.

Yes, you’ve heard this old-fogey legend before. But it was true. Those were the halcyon days of the 1950s in a small suburban town of 5000 of a little more than 1 square mile with its own swimming pool. My particular idyll was aptly named Pleasantville but I know we were not alone as the only community where children were allowed – or let’s say “encouraged” – to be outdoors if they weren’t in school. It was a different time.

I am not so naive to believe that we will ever return to those good old days when children roamed free, but it is worth considering what has changed to drive children inside and away from all the health benefits of being outdoors. Is there anything we can do to reverse this unfortunate trend?

First, we must first face up to the reality that our society has become so focused on the potential downsides of everything that we seem to be driven primarily by risk avoidance. We hear how things can go terribly wrong in the world outside, a world we can’t control. Although the data from the pandemic don’t support it, more of us believe children are safer indoors. Parents in particular seem to worry more now than they did 75 years ago. I don’t think we can point to a single event such as the tragedies of September 11 to explain the shift.

While bad news has always traveled fast, today (with communication being almost instantaneous) a story about a child abduction at 6 in the morning in Nevada can be on my local TV channel by lunchtime here in Maine. Parents worry that if bad stuff can happen to a child in Mount Elsewhere, it could happen to my child playing in the backyard across the street.

I think we pediatricians should consider how large a role we may be playing in driving parental anxiety with our frequent warnings about the dangers a child can encounter outdoors whether they come in the form of accidents or exposure to the elements.

While parents have grown more hesitant to send their children outside to play, as a society we have failed to adequately acknowledge and respond to the role that unhealthy attraction of indoor alternatives to outdoor play may be contributing to indoorism. Here we’re talking about television, smartphones, and the internet.

So, what can we do as pediatricians to get our patients outside? First, we can set an example and cover our office walls with pictures of ourselves and our families enjoying the outdoors. We can be vocal advocates for creating and maintaining accessible outdoor spaces in our community. We can advocate for more outside time during recess in school and encourage the school officials to consider having more courses taught outside.

We can be more diligent in asking families about their screen use and not be afraid to express our concern when we hear how little outdoor time their child is getting. Finally, we can strive for more balance in our messaging. For example for every warning we give about playing outside on poor air quality days there should be a reminder of the health benefits of being outdoors on the other days. Every message about the importance of sunscreen should be preceded by a few sentences promoting outdoor activities in wooded environments where sun exposure is less of a concern.

We should all be looking for ways in which our communities can remove the barriers that prevent our patients for reaping the health benefits of being outdoors. Being an outsider is just as important as getting enough sleep, eating the right food and staying physically active.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article

Depiction of Cancer in Movies: Not an Accurate Portrayal

Article Type
Changed

 

This transcript has been edited for clarity. 

I’d like to talk about a very different topic from what I normally discuss, which is probably relatively rarely addressed in clinical conversations among clinicians. There was a very provocative commentary that appeared in JCO Oncology Practice, titled “Hollywood’s Take on Oncology: Portrayal of Cancer in Movies, 2010-2020.”

All of us, as we grow up — as kids, adolescents, young adults, adults, and older individuals — watch television and movies. The older of us know that the doctor in everybody’s home that we all wanted was Marcus Welby. Of course, there was Dr. Kildare, ER, Grey’s Anatomy, and St. Elsewhere. There was Love Story and Brian’s Song. We all know about these. 

This particular review was fascinating. The authors looked at 100 English-language movies that had cancer included in the storyline over the past decade. They asked some relatively simple questions: How did they discuss it? What were the tumor types they discussed? What were the outcomes? 

The question is, what is the public seeing? If you watch these movies and you don’t have family experience or personal experience with cancer, what do you think about cancer? Maybe this is what you know about it. Despite what the National Cancer Institute or the American Society of Clinical Oncology tells you, this may be what you know.

What they showed was really quite interesting. Only one third of the movies even said the cancer type, so in two thirds, you just knew they had “cancer.”

There is another very interesting phenomenon. What do you think was the most common cancer type when they did define the cancer? It was brain tumors, even though we know that brain tumors are certainly not even within the top 10. They’re obviously very serious cancers, but if you’re talking about common cancers, brain cancer doesn’t rank in the top 10, and it was the most common cancer on these shows.

The authors of this paper made the point of whether this would be an opportunity for filmmakers. Again, with the storyline, they’re trying to sell a product here, but wouldn’t this be the opportunity to provide some information about the reality of cancer? They could emphasize the fact that smokers get lung cancer. In my opinion, they could discuss cervical cancer and comment that if HPV vaccination had been done, maybe this would not have happened.

They noted that the majority of cancers in these movies were incurable, and they commented that that’s not the reality today. Today, obviously, many of our cancers that weren’t curable have become quite curable for a percentage of patients, in addition to which, obviously, with early detection, we have a very high cure rate. How about trying to get that message out, too, that we’ve actually had increasing success?

They commented that there was very rarely, if ever, a conversation about multidisciplinary care, that somehow there are multiple doctors with multiple specialties involved. They noted that this is potentially a very important message to give out. They commented that in 12 of these movies, the patient refused cancer care. Again, that happens, but it’s clearly a rare event today. Maybe this is not really a very accurate depiction of what’s going on.

They commented on the fact that, obviously, we’re going back through the past 10 years, so there were no patients who received immunotherapy or targeted therapy. Again, the goal here is not to sell oncology care but to be accurate, or more accurate, about the state of treatment to the extent you can.

They noted that, in fact, there was essentially very little, if any, comment on palliative care or hospice care. The final point they made is that there was very little conversation in these movies about what we now recognize as financial distress in many of our patients. That’s an unfortunate reality and perhaps that might come in the future.

Again, the point of this was not to tell Hollywood how to make their movies but to have the oncology community recognize that if their patients or the families of their patients are seeing these movies, they are not getting a very accurate picture of what is happening in the oncology world today and that some education may very well be required.

Maurie Markman is Professor, Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, California, and President of Medicine & Science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed the following relevant financial relationships: income in an amount equal to or greater than $250 from: GlaxoSmithKline; AstraZeneca.

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

Publications
Topics
Sections

 

This transcript has been edited for clarity. 

I’d like to talk about a very different topic from what I normally discuss, which is probably relatively rarely addressed in clinical conversations among clinicians. There was a very provocative commentary that appeared in JCO Oncology Practice, titled “Hollywood’s Take on Oncology: Portrayal of Cancer in Movies, 2010-2020.”

All of us, as we grow up — as kids, adolescents, young adults, adults, and older individuals — watch television and movies. The older of us know that the doctor in everybody’s home that we all wanted was Marcus Welby. Of course, there was Dr. Kildare, ER, Grey’s Anatomy, and St. Elsewhere. There was Love Story and Brian’s Song. We all know about these. 

This particular review was fascinating. The authors looked at 100 English-language movies that had cancer included in the storyline over the past decade. They asked some relatively simple questions: How did they discuss it? What were the tumor types they discussed? What were the outcomes? 

The question is, what is the public seeing? If you watch these movies and you don’t have family experience or personal experience with cancer, what do you think about cancer? Maybe this is what you know about it. Despite what the National Cancer Institute or the American Society of Clinical Oncology tells you, this may be what you know.

What they showed was really quite interesting. Only one third of the movies even said the cancer type, so in two thirds, you just knew they had “cancer.”

There is another very interesting phenomenon. What do you think was the most common cancer type when they did define the cancer? It was brain tumors, even though we know that brain tumors are certainly not even within the top 10. They’re obviously very serious cancers, but if you’re talking about common cancers, brain cancer doesn’t rank in the top 10, and it was the most common cancer on these shows.

The authors of this paper made the point of whether this would be an opportunity for filmmakers. Again, with the storyline, they’re trying to sell a product here, but wouldn’t this be the opportunity to provide some information about the reality of cancer? They could emphasize the fact that smokers get lung cancer. In my opinion, they could discuss cervical cancer and comment that if HPV vaccination had been done, maybe this would not have happened.

They noted that the majority of cancers in these movies were incurable, and they commented that that’s not the reality today. Today, obviously, many of our cancers that weren’t curable have become quite curable for a percentage of patients, in addition to which, obviously, with early detection, we have a very high cure rate. How about trying to get that message out, too, that we’ve actually had increasing success?

They commented that there was very rarely, if ever, a conversation about multidisciplinary care, that somehow there are multiple doctors with multiple specialties involved. They noted that this is potentially a very important message to give out. They commented that in 12 of these movies, the patient refused cancer care. Again, that happens, but it’s clearly a rare event today. Maybe this is not really a very accurate depiction of what’s going on.

They commented on the fact that, obviously, we’re going back through the past 10 years, so there were no patients who received immunotherapy or targeted therapy. Again, the goal here is not to sell oncology care but to be accurate, or more accurate, about the state of treatment to the extent you can.

They noted that, in fact, there was essentially very little, if any, comment on palliative care or hospice care. The final point they made is that there was very little conversation in these movies about what we now recognize as financial distress in many of our patients. That’s an unfortunate reality and perhaps that might come in the future.

Again, the point of this was not to tell Hollywood how to make their movies but to have the oncology community recognize that if their patients or the families of their patients are seeing these movies, they are not getting a very accurate picture of what is happening in the oncology world today and that some education may very well be required.

Maurie Markman is Professor, Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, California, and President of Medicine & Science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed the following relevant financial relationships: income in an amount equal to or greater than $250 from: GlaxoSmithKline; AstraZeneca.

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

 

This transcript has been edited for clarity. 

I’d like to talk about a very different topic from what I normally discuss, which is probably relatively rarely addressed in clinical conversations among clinicians. There was a very provocative commentary that appeared in JCO Oncology Practice, titled “Hollywood’s Take on Oncology: Portrayal of Cancer in Movies, 2010-2020.”

All of us, as we grow up — as kids, adolescents, young adults, adults, and older individuals — watch television and movies. The older of us know that the doctor in everybody’s home that we all wanted was Marcus Welby. Of course, there was Dr. Kildare, ER, Grey’s Anatomy, and St. Elsewhere. There was Love Story and Brian’s Song. We all know about these. 

This particular review was fascinating. The authors looked at 100 English-language movies that had cancer included in the storyline over the past decade. They asked some relatively simple questions: How did they discuss it? What were the tumor types they discussed? What were the outcomes? 

The question is, what is the public seeing? If you watch these movies and you don’t have family experience or personal experience with cancer, what do you think about cancer? Maybe this is what you know about it. Despite what the National Cancer Institute or the American Society of Clinical Oncology tells you, this may be what you know.

What they showed was really quite interesting. Only one third of the movies even said the cancer type, so in two thirds, you just knew they had “cancer.”

There is another very interesting phenomenon. What do you think was the most common cancer type when they did define the cancer? It was brain tumors, even though we know that brain tumors are certainly not even within the top 10. They’re obviously very serious cancers, but if you’re talking about common cancers, brain cancer doesn’t rank in the top 10, and it was the most common cancer on these shows.

The authors of this paper made the point of whether this would be an opportunity for filmmakers. Again, with the storyline, they’re trying to sell a product here, but wouldn’t this be the opportunity to provide some information about the reality of cancer? They could emphasize the fact that smokers get lung cancer. In my opinion, they could discuss cervical cancer and comment that if HPV vaccination had been done, maybe this would not have happened.

They noted that the majority of cancers in these movies were incurable, and they commented that that’s not the reality today. Today, obviously, many of our cancers that weren’t curable have become quite curable for a percentage of patients, in addition to which, obviously, with early detection, we have a very high cure rate. How about trying to get that message out, too, that we’ve actually had increasing success?

They commented that there was very rarely, if ever, a conversation about multidisciplinary care, that somehow there are multiple doctors with multiple specialties involved. They noted that this is potentially a very important message to give out. They commented that in 12 of these movies, the patient refused cancer care. Again, that happens, but it’s clearly a rare event today. Maybe this is not really a very accurate depiction of what’s going on.

They commented on the fact that, obviously, we’re going back through the past 10 years, so there were no patients who received immunotherapy or targeted therapy. Again, the goal here is not to sell oncology care but to be accurate, or more accurate, about the state of treatment to the extent you can.

They noted that, in fact, there was essentially very little, if any, comment on palliative care or hospice care. The final point they made is that there was very little conversation in these movies about what we now recognize as financial distress in many of our patients. That’s an unfortunate reality and perhaps that might come in the future.

Again, the point of this was not to tell Hollywood how to make their movies but to have the oncology community recognize that if their patients or the families of their patients are seeing these movies, they are not getting a very accurate picture of what is happening in the oncology world today and that some education may very well be required.

Maurie Markman is Professor, Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, California, and President of Medicine & Science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed the following relevant financial relationships: income in an amount equal to or greater than $250 from: GlaxoSmithKline; AstraZeneca.

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

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Disqus Comments
Default
Use ProPublica
Hide sidebar & use full width
render the right sidebar.
Conference Recap Checkbox
Not Conference Recap
Clinical Edge
Display the Slideshow in this Article
Medscape Article
Display survey writer
Reuters content
Disable Inline Native ads
WebMD Article