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Nicotine and Nicotine Replacement Therapy Use During Myocardial Perfusion Imaging
Chest pain is one of the most common concerns in patients presenting to the emergency department in the United States, accounting for approximately 7.6 million visits annually.1 Given the high mortality rate associated with acute coronary syndromes, prompt evaluation of chest pain is essential.2 Even in mild cases, recognition of newly onset or worsening coronary artery disease (CAD) is crucial to ensure that patients receive optimal medication therapy.
In symptomatic patients with risk factors for CAD, such as advanced age, hypertension, hyperlipidemia, obesity, and diabetes mellitus, myocardial perfusion imaging (MPI) is frequently used as a modality to assess the presence, location, and severity of ischemic or infarcted myocardium.2 MPI requires administration of a radiopharmaceutical before and after the patient undergoes a form of stress.2 This radiopharmaceutical is then detected in the myocardium with a nuclear camera, and images are obtained of the heart to assess myocardial blood flow.2
MPI can be performed using exercise-induced stress via a treadmill, or medication-induced stress (Table 1). In both strategies, healthy coronary arteries dilate to provide the myocardium with more blood flow to meet the increasing myocardial oxygen demand during this period of stress. While healthy vessels are able to dilate appropriately, coronary arteries with flow-limiting stenoses are unable to dilate to the same extent in response to stress.2 Because radioactive isotope uptake by the myocardium is directly related to arterial blood flow, MPI is able to demonstrate a mismatch in coronary blood flow between healthy and diseased coronary arteries indicated by differences in radioisotope uptake.2 The presence of such a mismatch, in conjunction with clinical history, potentially suggests the presence of CAD.
Prior to conducting MPI with a medication, certain substances should be avoided. For instance, methylxanthines, such as caffeine, aminophylline, and theophylline, antagonize adenosine receptors and can have major drug interactions with regadenoson, adenosine, and dipyridamole. Therefore, it is advised that these substances be stopped for at least 12 hours before testing.3 In some cases, other medications that can affect coronary blood flow, such as long-acting nitrates, β-blockers, and calcium channel blockers, are recommended to be avoided for 12 to 48 hours in order to obtain the most accurate depiction of underlying coronary disease.4
Because nicotine and nicotine replacement therapy (NRT) may have substantial effects on coronary circulation, a current area of controversy is whether these should be stopped prior to the use of a stress-inducing medication during MPI. To date, no formal drug interaction studies have been conducted between nicotine and regadenoson.5 Similarly, the ADVANCE MPI 2 Trial, which led to the US Food and Drug Administration approval of regadenoson, did not specify restrictions on the use of nicotine prior to stress testing in the protocol.6 However, as this trial was multicenter, investigators admit that individual study sites could have had their own restrictions on the use of nicotine prior to stress testing with regadenoson, but this information was not collected.6 The current review focuses on how the simultaneous use of nicotine or NRT during MPI with pharmacologic agents, such as regadenoson, may affect the accuracy of imaging results and the clinical impact of this interaction.
Nicotine Coronary Artery Effect
It is well documented that long-term cigarette smoking is a major risk factor for CAD.7 Compared with nonsmokers, cigarette smokers experience 2 times greater risk of morbidity and mortality from ischemic heart disease.7 There are several mechanisms by which nicotine induces damage to the myocardium (Figure). Nicotine has direct effects on both the sympathetic nervous system (SNS) and myocardial endothelium.8 Together, these factors result in reduced coronary blood flow, leading to less oxygen supply to meet an increased oxygen demand, resulting in myocardial ischemia.
Nicotine’s effect on coronary vasomotor tone occurs primarily through noradrenergic stimulation of α and β receptors associated with coronary vasoconstriction or vasodilation, respectively.9,10 These competing influences on coronary blood flow appear to manifest differently based on whether patients are at rest or in a stressed state. A study by Czerin and colleagues demonstrated that in healthy patients with relatively short smoking histories and in a healthy nonsmoker control group, coronary blood flow increased by 25% and 40%, respectively, with nicotine use at rest.9 However, when these patients were stressed with dipyramidole and while smoking during the examination, myocardial blood flow was reduced by 11% in the study group and 14% in the control group.9 This is likely because the patients studied had relatively healthy coronary arteries that were able to maximally dilate when stressed. In this scenario, nicotine’s dilatory effects are offset by nicotine’s α-receptor–mediated vasoconstriction effects.9 Of note, patients in the study group experienced a somewhat diminished increase in coronary blood flow at rest with nicotine use, suggesting that even a short smoking history may damage the myocardial endothelium, rendering it less responsive to nicotine’s vasodilatory effects.9
These principles similarly apply to patients with underlying moderate-to-severe cardiovascular disease (CVD). With nicotine use at rest, patients with significant CAD do not experience as dramatic of an increase in coronary blood flow, which typically decreases or remains the same despite increased myocardial work.10 This may be because patients with moderate-to-severe CAD often have flow-limiting stenoses and damaged endothelium that do not allow vessels to respond as efficiently to increased myocardial demand or to nicotine’s β-receptor–mediated vasodilatory effects.10,11 Moreover, when stressed, diseased coronary arteries are not able to further dilate and nicotine’s α-receptor–mediated vasoconstriction effects dominate.10,11
In a study by Quillen and colleagues of patients with moderate-to-severe CAD, the mean diameter of proximal coronary artery segments decreased by 5%, the distal coronary diameter decreased 8%, and the coronary vascular resistance increased by 21% while smoking at rest.12 The investigators did not analyze how parameters changed when these diseased coronary arteries were stressed using a medication during MPI. However, it can be predicted that coronary arteries would have constricted to a similar or greater degree than observed in Czerin and colleagues’ study, given that the underlying myocardium was diseased and more susceptible to nicotine’s vasoconstriction effects.9 Importantly, these studies have several limitations, most notably that they are older and have small sample sizes. Additionally, while statistically significant differences were found in the degree of changes in coronary circulation with nicotine use at rest and during stress, it is unclear whether this translates to a clinically significant and impactful finding.9-12
Nicotine Replacement Therapy and Stress Testing
Given the association between cigarette smoking and CAD, medical practitioners strongly encourage patients to quit smoking to reduce their risk of adverse cardiovascular outcomes. Various smoking cessation treatments are available for patients. Common, readily accessible forms of therapy include nicotine replacement products (Table 2).
Early studies of NRT in patients with underlying CVD found an increased risk of cardiovascular events, such as myocardial infarction, presumably due to the nicotine content of these products.13,14 However, the concentration of nicotine in NRT is substantially lower than that found in cigarettes and in some formulations, such as transdermal patches, nicotine is delivered over a prolonged period of time.15 For this reason, NRT is thought to be safe in patients with underlying CVD and stable ischemic heart disease. A recent systematic review and meta-analysis found that while NRT may be associated with tachycardia, it did not increase the risk of more serious cardiovascular adverse effects (AEs).16,17
Given the lower nicotine concentration in NRT products, the associated hemodynamic effect of nicotine also is thought to be less pronounced. In a study conducted by Tzivoni and colleagues in patients with CAD using transdermal nicotine patches, no differences in blood pressure, heart rate, ischemia, or arrhythmias were found from baseline to 2 weeks.18 These findings were further confirmed in a small study by Lucini and colleagues, which found that nicotine patches produced slight hemodynamic effects, but to a lesser extent than cigarette smoking.19 For the NRT gum formulation, while a small study found that 4 mg produced coronary vasoconstriction in patients with underlying CAD, a study by Nitenberg and Antony demonstrated that healthy and diseased coronary arteries did not significantly constrict while patients were using nicotine gum both before and after a cold pressor test, suggesting a lesser degree of coronary vasoconstriction than nicotine from cigarette smoking.20,21 Similar findings have been described with the nicotine intranasal spray in a study by Keeley and colleagues, which showed no additional AEs on myocardial demand or vasoconstriction when an intranasal nicotine spray was added to cigarette smoking.22 Importantly, a review of the transdermal and gum formulations found that these less pronounced hemodynamic effects were observed across different doses of NRT; however, further studies are needed to clarify the relationship between NRT dose and cardiovascular effects.23
Overall, NRT does not seem to activate the SNS to the same degree as nicotine obtained via cigarette smoking and likely does not increase the myocardial oxygen demand as much. Additionally, by containing a lower concentration of nicotine, NRT may not impair the myocardium’s ability to supply oxygen to coronary arteries to the same extent as nicotine from cigarette smoking. Therefore, the effects of NRT on MPI using a stress-inducing medication may not be as pronounced. However, due to study limitations, results should be interpreted cautiously.18-23
Conclusions
Because of the close relationship between cigarette smoking and CAD, many patients with underlying CVD are either current smokers or may be using NRT for smoking cessation. Therefore, the question of whether to refrain from nicotine use prior to MPI is clinically relevant. Currently, there is a lack of high-quality studies demonstrating the effects of nicotine and NRT on coronary perfusion. Because of this, the impact of nicotine and NRT use on the accuracy of MPI using stress-inducing medications remains uncertain. Nevertheless, given that nicotine and NRT may largely affect the accuracy of imaging results, several institutions have adopted protocols that prohibit patients from using these drugs on the day of nuclear stress testing.
There are currently no data specifying the number of hours to hold nicotine products prior to cardiac stress testing. It is generally recommended that other medications that affect coronary blood flow be held for 5 half-lives before conducting MPI.4 Following the same guidance for nicotine and NRT may present a reasonable approach to ensure accurate imaging results. Based on the discussed literature, patients should be instructed to refrain from cigarette smoking for at least 5 to 10 hours prior to MPI, given nicotine’s half-life of about 1 to 2 hours.24
The data for NRT are less clear. While use of NRT may not be an absolute contraindication to conducting MPI, it is important to consider that this may affect the accuracy of results. Given this uncertainty, it is likely ideal to hold NRT prior to MPI, based on the specific formulation of NRT and that product's half-life. Further robust studies are needed to analyze the impact of nicotine and NRT on the accuracy of nuclear stress testing using a medication.
1. Rui P, Kang K, Ashman JJ. National Hospital Ambulatory Medical Care Survey: 2016 emergency department summary tables. Published 2016. Accessed March 30, 2020. https://www.cdc.gov/nchs/data/nhamcs/web_tables/2016_ed_web_tables.pdf
2. Lange RA. Cardiovascular testing. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic Approach, 10th ed. McGraw Hill; 2017.
3. Mace S. Observation Medicine: Principles and Protocols. Cambridge University Press; 2017.
4. Currie GM. Pharmacology, part 4: nuclear cardiology. J Nucl Med Technol. 2019;47(2):97-110. doi:10.2967/jnmt.118.219675
5. Regadenoson; Package insert. Astellas Pharma US Inc; 2008.
6. Iskandrian AE, Bateman TM, Belardinelli L, et al. Adenosine versus regadenoson comparative evaluation in myocardial perfusion imaging: results of the ADVANCE phase 3 multicenter international trial. J Nucl Cardiol. 2007;14(5):645-658. doi:10.1016/j.nuclcard.2007.06.114
7. Hajar R. Risk factors for coronary artery disease: historical perspectives. Heart Views. 2017;18(3):109-114. doi:10.4103/HEARTVIEWS.HEARTVIEWS_106_17
8. Benowitz NL, Burbank AD. Cardiovascular toxicity of nicotine: implications for electronic cigarette use. Trends Cardiovasc Med. 2016;26(6):515-523. doi:10.1016/j.tcm.2016.03.001
9. Czernin J, Sun K, Brunken R, Böttcher M, Phelps M, Schelbert H. Effect of acute and long-term smoking on myocardial blood flow and flow reserve. Circulation. 1995;91:2891-2897. doi:10.1161/01.CIR.91.12.2891
10. Winniford MD, Wheelan KR, Kremers MS, et al. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone. Circulation. 1986;73(4):662-667. doi:10.1161/01.cir.73.4.662
11. Klein LW, Ambrose J, Pichard A, Holt J, Gorlin R, Teichholz LE. Acute coronary hemodynamic response to cigarette smoking in patients with coronary artery disease. J Am Coll Cardiol. 1984;3(4):879-886. doi:10.1016/s0735-1097(84)80344-7
12. Quillen JE, Rossen JD, Oskarsson HJ, Minor RL Jr, Lopez AG, Winniford MD. Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels. J Am Coll Cardiol. 1993;22(3):642-647. doi:10.1016/0735-1097(93)90170-6
13. Dacosta A, Guy JM, Tardy B, et al. Myocardial infarction and nicotine patch: a contributing or causative factor?. Eur Heart J. 1993;14(12):1709-1711. doi:10.1093/eurheartj/14.12.1709
14. Ottervanger JP, Festen JM, de Vries AG, Stricker BH. Acute myocardial infarction while using the nicotine patch. Chest. 1995;107(6):1765-1766. doi:10.1378/chest.107.6.1765
15. Dollerup J, Vestbo J, Murray-Thomas T, et al. Cardiovascular risks in smokers treated with nicotine replacement therapy: a historical cohort study. Clin Epidemiol. 2017;9:231-243. Published 2017 Apr 26. doi:10.2147/CLEP.S127775
16. Mills EJ, Wu P, Lockhart I, Wilson K, Ebbert JO. Adverse events associated with nicotine replacement therapy (NRT) for smoking cessation. A systematic review and meta-analysis of one hundred and twenty studies involving 177,390 individuals. Tob Induc Dis. 2010;8(1):8. Published 2010 Jul 13. doi:10.1186/1617-9625-8-8
17. Mills EJ, Thorlund K, Eapen S, Wu P, Prochaska JJ. Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis. Circulation. 2014;129(1):28-41. doi:10.1161/CIRCULATIONAHA.113.003961
18. Tzivoni D, Keren A, Meyler S, Khoury Z, Lerer T, Brunel P. Cardiovascular safety of transdermal nicotine patches in patients with coronary artery disease who try to quit smoking. Cardiovasc Drugs Ther. 1998;12(3):239-244. doi:10.1023/a:1007757530765
19. Lucini D, Bertocchi F, Malliani A, Pagani M. Autonomic effects of nicotine patch administration in habitual cigarette smokers: a double-blind, placebo-controlled study using spectral analysis of RR interval and systolic arterial pressure variabilities. J Cardiovasc Pharmacol. 1998;31(5):714-720. doi:10.1097/00005344-199805000-00010
20. Kaijser L, Berglund B. Effect of nicotine on coronary blood-flow in man. Clin Physiol. 1985;5(6):541-552. doi:10.1111/j.1475-097x.1985.tb00767.x
21. Nitenberg A, Antony I. Effects of nicotine gum on coronary vasomotor responses during sympathetic stimulation in patients with coronary artery stenosis. J Cardiovasc Pharmacol. 1999;34(5):694-699. doi:10.1097/00005344-199911000-00011
22. Keeley EC, Pirwitz MJ, Landau C, et al. Intranasal nicotine spray does not augment the adverse effects of cigarette smoking on myocardial oxygen demand or coronary arterial dimensions. Am J Med. 1996;101(4):357-363. doi:10.1016/s0002-9343(96)00237-9
23. Benowitz NL, Gourlay SG. Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy. J Am Coll Cardiol. 1997;29(7):1422-1431. doi:10.1016/s0735-1097(97)00079-x
24. Flowers L. Nicotine replacement therapy. Amer J Psych. 2017;11(6):4-7.
25. Adenosine; Package insert. Astellas Pharma US Inc; 1989.
26. Dipyridamole; Package insert. Boehringer Ingelheim Pharmaceuticals Inc; 2019.
27. Dobutamine; Package insert. Baxter Healthcare Corporation; 2012.
Chest pain is one of the most common concerns in patients presenting to the emergency department in the United States, accounting for approximately 7.6 million visits annually.1 Given the high mortality rate associated with acute coronary syndromes, prompt evaluation of chest pain is essential.2 Even in mild cases, recognition of newly onset or worsening coronary artery disease (CAD) is crucial to ensure that patients receive optimal medication therapy.
In symptomatic patients with risk factors for CAD, such as advanced age, hypertension, hyperlipidemia, obesity, and diabetes mellitus, myocardial perfusion imaging (MPI) is frequently used as a modality to assess the presence, location, and severity of ischemic or infarcted myocardium.2 MPI requires administration of a radiopharmaceutical before and after the patient undergoes a form of stress.2 This radiopharmaceutical is then detected in the myocardium with a nuclear camera, and images are obtained of the heart to assess myocardial blood flow.2
MPI can be performed using exercise-induced stress via a treadmill, or medication-induced stress (Table 1). In both strategies, healthy coronary arteries dilate to provide the myocardium with more blood flow to meet the increasing myocardial oxygen demand during this period of stress. While healthy vessels are able to dilate appropriately, coronary arteries with flow-limiting stenoses are unable to dilate to the same extent in response to stress.2 Because radioactive isotope uptake by the myocardium is directly related to arterial blood flow, MPI is able to demonstrate a mismatch in coronary blood flow between healthy and diseased coronary arteries indicated by differences in radioisotope uptake.2 The presence of such a mismatch, in conjunction with clinical history, potentially suggests the presence of CAD.
Prior to conducting MPI with a medication, certain substances should be avoided. For instance, methylxanthines, such as caffeine, aminophylline, and theophylline, antagonize adenosine receptors and can have major drug interactions with regadenoson, adenosine, and dipyridamole. Therefore, it is advised that these substances be stopped for at least 12 hours before testing.3 In some cases, other medications that can affect coronary blood flow, such as long-acting nitrates, β-blockers, and calcium channel blockers, are recommended to be avoided for 12 to 48 hours in order to obtain the most accurate depiction of underlying coronary disease.4
Because nicotine and nicotine replacement therapy (NRT) may have substantial effects on coronary circulation, a current area of controversy is whether these should be stopped prior to the use of a stress-inducing medication during MPI. To date, no formal drug interaction studies have been conducted between nicotine and regadenoson.5 Similarly, the ADVANCE MPI 2 Trial, which led to the US Food and Drug Administration approval of regadenoson, did not specify restrictions on the use of nicotine prior to stress testing in the protocol.6 However, as this trial was multicenter, investigators admit that individual study sites could have had their own restrictions on the use of nicotine prior to stress testing with regadenoson, but this information was not collected.6 The current review focuses on how the simultaneous use of nicotine or NRT during MPI with pharmacologic agents, such as regadenoson, may affect the accuracy of imaging results and the clinical impact of this interaction.
Nicotine Coronary Artery Effect
It is well documented that long-term cigarette smoking is a major risk factor for CAD.7 Compared with nonsmokers, cigarette smokers experience 2 times greater risk of morbidity and mortality from ischemic heart disease.7 There are several mechanisms by which nicotine induces damage to the myocardium (Figure). Nicotine has direct effects on both the sympathetic nervous system (SNS) and myocardial endothelium.8 Together, these factors result in reduced coronary blood flow, leading to less oxygen supply to meet an increased oxygen demand, resulting in myocardial ischemia.
Nicotine’s effect on coronary vasomotor tone occurs primarily through noradrenergic stimulation of α and β receptors associated with coronary vasoconstriction or vasodilation, respectively.9,10 These competing influences on coronary blood flow appear to manifest differently based on whether patients are at rest or in a stressed state. A study by Czerin and colleagues demonstrated that in healthy patients with relatively short smoking histories and in a healthy nonsmoker control group, coronary blood flow increased by 25% and 40%, respectively, with nicotine use at rest.9 However, when these patients were stressed with dipyramidole and while smoking during the examination, myocardial blood flow was reduced by 11% in the study group and 14% in the control group.9 This is likely because the patients studied had relatively healthy coronary arteries that were able to maximally dilate when stressed. In this scenario, nicotine’s dilatory effects are offset by nicotine’s α-receptor–mediated vasoconstriction effects.9 Of note, patients in the study group experienced a somewhat diminished increase in coronary blood flow at rest with nicotine use, suggesting that even a short smoking history may damage the myocardial endothelium, rendering it less responsive to nicotine’s vasodilatory effects.9
These principles similarly apply to patients with underlying moderate-to-severe cardiovascular disease (CVD). With nicotine use at rest, patients with significant CAD do not experience as dramatic of an increase in coronary blood flow, which typically decreases or remains the same despite increased myocardial work.10 This may be because patients with moderate-to-severe CAD often have flow-limiting stenoses and damaged endothelium that do not allow vessels to respond as efficiently to increased myocardial demand or to nicotine’s β-receptor–mediated vasodilatory effects.10,11 Moreover, when stressed, diseased coronary arteries are not able to further dilate and nicotine’s α-receptor–mediated vasoconstriction effects dominate.10,11
In a study by Quillen and colleagues of patients with moderate-to-severe CAD, the mean diameter of proximal coronary artery segments decreased by 5%, the distal coronary diameter decreased 8%, and the coronary vascular resistance increased by 21% while smoking at rest.12 The investigators did not analyze how parameters changed when these diseased coronary arteries were stressed using a medication during MPI. However, it can be predicted that coronary arteries would have constricted to a similar or greater degree than observed in Czerin and colleagues’ study, given that the underlying myocardium was diseased and more susceptible to nicotine’s vasoconstriction effects.9 Importantly, these studies have several limitations, most notably that they are older and have small sample sizes. Additionally, while statistically significant differences were found in the degree of changes in coronary circulation with nicotine use at rest and during stress, it is unclear whether this translates to a clinically significant and impactful finding.9-12
Nicotine Replacement Therapy and Stress Testing
Given the association between cigarette smoking and CAD, medical practitioners strongly encourage patients to quit smoking to reduce their risk of adverse cardiovascular outcomes. Various smoking cessation treatments are available for patients. Common, readily accessible forms of therapy include nicotine replacement products (Table 2).
Early studies of NRT in patients with underlying CVD found an increased risk of cardiovascular events, such as myocardial infarction, presumably due to the nicotine content of these products.13,14 However, the concentration of nicotine in NRT is substantially lower than that found in cigarettes and in some formulations, such as transdermal patches, nicotine is delivered over a prolonged period of time.15 For this reason, NRT is thought to be safe in patients with underlying CVD and stable ischemic heart disease. A recent systematic review and meta-analysis found that while NRT may be associated with tachycardia, it did not increase the risk of more serious cardiovascular adverse effects (AEs).16,17
Given the lower nicotine concentration in NRT products, the associated hemodynamic effect of nicotine also is thought to be less pronounced. In a study conducted by Tzivoni and colleagues in patients with CAD using transdermal nicotine patches, no differences in blood pressure, heart rate, ischemia, or arrhythmias were found from baseline to 2 weeks.18 These findings were further confirmed in a small study by Lucini and colleagues, which found that nicotine patches produced slight hemodynamic effects, but to a lesser extent than cigarette smoking.19 For the NRT gum formulation, while a small study found that 4 mg produced coronary vasoconstriction in patients with underlying CAD, a study by Nitenberg and Antony demonstrated that healthy and diseased coronary arteries did not significantly constrict while patients were using nicotine gum both before and after a cold pressor test, suggesting a lesser degree of coronary vasoconstriction than nicotine from cigarette smoking.20,21 Similar findings have been described with the nicotine intranasal spray in a study by Keeley and colleagues, which showed no additional AEs on myocardial demand or vasoconstriction when an intranasal nicotine spray was added to cigarette smoking.22 Importantly, a review of the transdermal and gum formulations found that these less pronounced hemodynamic effects were observed across different doses of NRT; however, further studies are needed to clarify the relationship between NRT dose and cardiovascular effects.23
Overall, NRT does not seem to activate the SNS to the same degree as nicotine obtained via cigarette smoking and likely does not increase the myocardial oxygen demand as much. Additionally, by containing a lower concentration of nicotine, NRT may not impair the myocardium’s ability to supply oxygen to coronary arteries to the same extent as nicotine from cigarette smoking. Therefore, the effects of NRT on MPI using a stress-inducing medication may not be as pronounced. However, due to study limitations, results should be interpreted cautiously.18-23
Conclusions
Because of the close relationship between cigarette smoking and CAD, many patients with underlying CVD are either current smokers or may be using NRT for smoking cessation. Therefore, the question of whether to refrain from nicotine use prior to MPI is clinically relevant. Currently, there is a lack of high-quality studies demonstrating the effects of nicotine and NRT on coronary perfusion. Because of this, the impact of nicotine and NRT use on the accuracy of MPI using stress-inducing medications remains uncertain. Nevertheless, given that nicotine and NRT may largely affect the accuracy of imaging results, several institutions have adopted protocols that prohibit patients from using these drugs on the day of nuclear stress testing.
There are currently no data specifying the number of hours to hold nicotine products prior to cardiac stress testing. It is generally recommended that other medications that affect coronary blood flow be held for 5 half-lives before conducting MPI.4 Following the same guidance for nicotine and NRT may present a reasonable approach to ensure accurate imaging results. Based on the discussed literature, patients should be instructed to refrain from cigarette smoking for at least 5 to 10 hours prior to MPI, given nicotine’s half-life of about 1 to 2 hours.24
The data for NRT are less clear. While use of NRT may not be an absolute contraindication to conducting MPI, it is important to consider that this may affect the accuracy of results. Given this uncertainty, it is likely ideal to hold NRT prior to MPI, based on the specific formulation of NRT and that product's half-life. Further robust studies are needed to analyze the impact of nicotine and NRT on the accuracy of nuclear stress testing using a medication.
Chest pain is one of the most common concerns in patients presenting to the emergency department in the United States, accounting for approximately 7.6 million visits annually.1 Given the high mortality rate associated with acute coronary syndromes, prompt evaluation of chest pain is essential.2 Even in mild cases, recognition of newly onset or worsening coronary artery disease (CAD) is crucial to ensure that patients receive optimal medication therapy.
In symptomatic patients with risk factors for CAD, such as advanced age, hypertension, hyperlipidemia, obesity, and diabetes mellitus, myocardial perfusion imaging (MPI) is frequently used as a modality to assess the presence, location, and severity of ischemic or infarcted myocardium.2 MPI requires administration of a radiopharmaceutical before and after the patient undergoes a form of stress.2 This radiopharmaceutical is then detected in the myocardium with a nuclear camera, and images are obtained of the heart to assess myocardial blood flow.2
MPI can be performed using exercise-induced stress via a treadmill, or medication-induced stress (Table 1). In both strategies, healthy coronary arteries dilate to provide the myocardium with more blood flow to meet the increasing myocardial oxygen demand during this period of stress. While healthy vessels are able to dilate appropriately, coronary arteries with flow-limiting stenoses are unable to dilate to the same extent in response to stress.2 Because radioactive isotope uptake by the myocardium is directly related to arterial blood flow, MPI is able to demonstrate a mismatch in coronary blood flow between healthy and diseased coronary arteries indicated by differences in radioisotope uptake.2 The presence of such a mismatch, in conjunction with clinical history, potentially suggests the presence of CAD.
Prior to conducting MPI with a medication, certain substances should be avoided. For instance, methylxanthines, such as caffeine, aminophylline, and theophylline, antagonize adenosine receptors and can have major drug interactions with regadenoson, adenosine, and dipyridamole. Therefore, it is advised that these substances be stopped for at least 12 hours before testing.3 In some cases, other medications that can affect coronary blood flow, such as long-acting nitrates, β-blockers, and calcium channel blockers, are recommended to be avoided for 12 to 48 hours in order to obtain the most accurate depiction of underlying coronary disease.4
Because nicotine and nicotine replacement therapy (NRT) may have substantial effects on coronary circulation, a current area of controversy is whether these should be stopped prior to the use of a stress-inducing medication during MPI. To date, no formal drug interaction studies have been conducted between nicotine and regadenoson.5 Similarly, the ADVANCE MPI 2 Trial, which led to the US Food and Drug Administration approval of regadenoson, did not specify restrictions on the use of nicotine prior to stress testing in the protocol.6 However, as this trial was multicenter, investigators admit that individual study sites could have had their own restrictions on the use of nicotine prior to stress testing with regadenoson, but this information was not collected.6 The current review focuses on how the simultaneous use of nicotine or NRT during MPI with pharmacologic agents, such as regadenoson, may affect the accuracy of imaging results and the clinical impact of this interaction.
Nicotine Coronary Artery Effect
It is well documented that long-term cigarette smoking is a major risk factor for CAD.7 Compared with nonsmokers, cigarette smokers experience 2 times greater risk of morbidity and mortality from ischemic heart disease.7 There are several mechanisms by which nicotine induces damage to the myocardium (Figure). Nicotine has direct effects on both the sympathetic nervous system (SNS) and myocardial endothelium.8 Together, these factors result in reduced coronary blood flow, leading to less oxygen supply to meet an increased oxygen demand, resulting in myocardial ischemia.
Nicotine’s effect on coronary vasomotor tone occurs primarily through noradrenergic stimulation of α and β receptors associated with coronary vasoconstriction or vasodilation, respectively.9,10 These competing influences on coronary blood flow appear to manifest differently based on whether patients are at rest or in a stressed state. A study by Czerin and colleagues demonstrated that in healthy patients with relatively short smoking histories and in a healthy nonsmoker control group, coronary blood flow increased by 25% and 40%, respectively, with nicotine use at rest.9 However, when these patients were stressed with dipyramidole and while smoking during the examination, myocardial blood flow was reduced by 11% in the study group and 14% in the control group.9 This is likely because the patients studied had relatively healthy coronary arteries that were able to maximally dilate when stressed. In this scenario, nicotine’s dilatory effects are offset by nicotine’s α-receptor–mediated vasoconstriction effects.9 Of note, patients in the study group experienced a somewhat diminished increase in coronary blood flow at rest with nicotine use, suggesting that even a short smoking history may damage the myocardial endothelium, rendering it less responsive to nicotine’s vasodilatory effects.9
These principles similarly apply to patients with underlying moderate-to-severe cardiovascular disease (CVD). With nicotine use at rest, patients with significant CAD do not experience as dramatic of an increase in coronary blood flow, which typically decreases or remains the same despite increased myocardial work.10 This may be because patients with moderate-to-severe CAD often have flow-limiting stenoses and damaged endothelium that do not allow vessels to respond as efficiently to increased myocardial demand or to nicotine’s β-receptor–mediated vasodilatory effects.10,11 Moreover, when stressed, diseased coronary arteries are not able to further dilate and nicotine’s α-receptor–mediated vasoconstriction effects dominate.10,11
In a study by Quillen and colleagues of patients with moderate-to-severe CAD, the mean diameter of proximal coronary artery segments decreased by 5%, the distal coronary diameter decreased 8%, and the coronary vascular resistance increased by 21% while smoking at rest.12 The investigators did not analyze how parameters changed when these diseased coronary arteries were stressed using a medication during MPI. However, it can be predicted that coronary arteries would have constricted to a similar or greater degree than observed in Czerin and colleagues’ study, given that the underlying myocardium was diseased and more susceptible to nicotine’s vasoconstriction effects.9 Importantly, these studies have several limitations, most notably that they are older and have small sample sizes. Additionally, while statistically significant differences were found in the degree of changes in coronary circulation with nicotine use at rest and during stress, it is unclear whether this translates to a clinically significant and impactful finding.9-12
Nicotine Replacement Therapy and Stress Testing
Given the association between cigarette smoking and CAD, medical practitioners strongly encourage patients to quit smoking to reduce their risk of adverse cardiovascular outcomes. Various smoking cessation treatments are available for patients. Common, readily accessible forms of therapy include nicotine replacement products (Table 2).
Early studies of NRT in patients with underlying CVD found an increased risk of cardiovascular events, such as myocardial infarction, presumably due to the nicotine content of these products.13,14 However, the concentration of nicotine in NRT is substantially lower than that found in cigarettes and in some formulations, such as transdermal patches, nicotine is delivered over a prolonged period of time.15 For this reason, NRT is thought to be safe in patients with underlying CVD and stable ischemic heart disease. A recent systematic review and meta-analysis found that while NRT may be associated with tachycardia, it did not increase the risk of more serious cardiovascular adverse effects (AEs).16,17
Given the lower nicotine concentration in NRT products, the associated hemodynamic effect of nicotine also is thought to be less pronounced. In a study conducted by Tzivoni and colleagues in patients with CAD using transdermal nicotine patches, no differences in blood pressure, heart rate, ischemia, or arrhythmias were found from baseline to 2 weeks.18 These findings were further confirmed in a small study by Lucini and colleagues, which found that nicotine patches produced slight hemodynamic effects, but to a lesser extent than cigarette smoking.19 For the NRT gum formulation, while a small study found that 4 mg produced coronary vasoconstriction in patients with underlying CAD, a study by Nitenberg and Antony demonstrated that healthy and diseased coronary arteries did not significantly constrict while patients were using nicotine gum both before and after a cold pressor test, suggesting a lesser degree of coronary vasoconstriction than nicotine from cigarette smoking.20,21 Similar findings have been described with the nicotine intranasal spray in a study by Keeley and colleagues, which showed no additional AEs on myocardial demand or vasoconstriction when an intranasal nicotine spray was added to cigarette smoking.22 Importantly, a review of the transdermal and gum formulations found that these less pronounced hemodynamic effects were observed across different doses of NRT; however, further studies are needed to clarify the relationship between NRT dose and cardiovascular effects.23
Overall, NRT does not seem to activate the SNS to the same degree as nicotine obtained via cigarette smoking and likely does not increase the myocardial oxygen demand as much. Additionally, by containing a lower concentration of nicotine, NRT may not impair the myocardium’s ability to supply oxygen to coronary arteries to the same extent as nicotine from cigarette smoking. Therefore, the effects of NRT on MPI using a stress-inducing medication may not be as pronounced. However, due to study limitations, results should be interpreted cautiously.18-23
Conclusions
Because of the close relationship between cigarette smoking and CAD, many patients with underlying CVD are either current smokers or may be using NRT for smoking cessation. Therefore, the question of whether to refrain from nicotine use prior to MPI is clinically relevant. Currently, there is a lack of high-quality studies demonstrating the effects of nicotine and NRT on coronary perfusion. Because of this, the impact of nicotine and NRT use on the accuracy of MPI using stress-inducing medications remains uncertain. Nevertheless, given that nicotine and NRT may largely affect the accuracy of imaging results, several institutions have adopted protocols that prohibit patients from using these drugs on the day of nuclear stress testing.
There are currently no data specifying the number of hours to hold nicotine products prior to cardiac stress testing. It is generally recommended that other medications that affect coronary blood flow be held for 5 half-lives before conducting MPI.4 Following the same guidance for nicotine and NRT may present a reasonable approach to ensure accurate imaging results. Based on the discussed literature, patients should be instructed to refrain from cigarette smoking for at least 5 to 10 hours prior to MPI, given nicotine’s half-life of about 1 to 2 hours.24
The data for NRT are less clear. While use of NRT may not be an absolute contraindication to conducting MPI, it is important to consider that this may affect the accuracy of results. Given this uncertainty, it is likely ideal to hold NRT prior to MPI, based on the specific formulation of NRT and that product's half-life. Further robust studies are needed to analyze the impact of nicotine and NRT on the accuracy of nuclear stress testing using a medication.
1. Rui P, Kang K, Ashman JJ. National Hospital Ambulatory Medical Care Survey: 2016 emergency department summary tables. Published 2016. Accessed March 30, 2020. https://www.cdc.gov/nchs/data/nhamcs/web_tables/2016_ed_web_tables.pdf
2. Lange RA. Cardiovascular testing. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic Approach, 10th ed. McGraw Hill; 2017.
3. Mace S. Observation Medicine: Principles and Protocols. Cambridge University Press; 2017.
4. Currie GM. Pharmacology, part 4: nuclear cardiology. J Nucl Med Technol. 2019;47(2):97-110. doi:10.2967/jnmt.118.219675
5. Regadenoson; Package insert. Astellas Pharma US Inc; 2008.
6. Iskandrian AE, Bateman TM, Belardinelli L, et al. Adenosine versus regadenoson comparative evaluation in myocardial perfusion imaging: results of the ADVANCE phase 3 multicenter international trial. J Nucl Cardiol. 2007;14(5):645-658. doi:10.1016/j.nuclcard.2007.06.114
7. Hajar R. Risk factors for coronary artery disease: historical perspectives. Heart Views. 2017;18(3):109-114. doi:10.4103/HEARTVIEWS.HEARTVIEWS_106_17
8. Benowitz NL, Burbank AD. Cardiovascular toxicity of nicotine: implications for electronic cigarette use. Trends Cardiovasc Med. 2016;26(6):515-523. doi:10.1016/j.tcm.2016.03.001
9. Czernin J, Sun K, Brunken R, Böttcher M, Phelps M, Schelbert H. Effect of acute and long-term smoking on myocardial blood flow and flow reserve. Circulation. 1995;91:2891-2897. doi:10.1161/01.CIR.91.12.2891
10. Winniford MD, Wheelan KR, Kremers MS, et al. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone. Circulation. 1986;73(4):662-667. doi:10.1161/01.cir.73.4.662
11. Klein LW, Ambrose J, Pichard A, Holt J, Gorlin R, Teichholz LE. Acute coronary hemodynamic response to cigarette smoking in patients with coronary artery disease. J Am Coll Cardiol. 1984;3(4):879-886. doi:10.1016/s0735-1097(84)80344-7
12. Quillen JE, Rossen JD, Oskarsson HJ, Minor RL Jr, Lopez AG, Winniford MD. Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels. J Am Coll Cardiol. 1993;22(3):642-647. doi:10.1016/0735-1097(93)90170-6
13. Dacosta A, Guy JM, Tardy B, et al. Myocardial infarction and nicotine patch: a contributing or causative factor?. Eur Heart J. 1993;14(12):1709-1711. doi:10.1093/eurheartj/14.12.1709
14. Ottervanger JP, Festen JM, de Vries AG, Stricker BH. Acute myocardial infarction while using the nicotine patch. Chest. 1995;107(6):1765-1766. doi:10.1378/chest.107.6.1765
15. Dollerup J, Vestbo J, Murray-Thomas T, et al. Cardiovascular risks in smokers treated with nicotine replacement therapy: a historical cohort study. Clin Epidemiol. 2017;9:231-243. Published 2017 Apr 26. doi:10.2147/CLEP.S127775
16. Mills EJ, Wu P, Lockhart I, Wilson K, Ebbert JO. Adverse events associated with nicotine replacement therapy (NRT) for smoking cessation. A systematic review and meta-analysis of one hundred and twenty studies involving 177,390 individuals. Tob Induc Dis. 2010;8(1):8. Published 2010 Jul 13. doi:10.1186/1617-9625-8-8
17. Mills EJ, Thorlund K, Eapen S, Wu P, Prochaska JJ. Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis. Circulation. 2014;129(1):28-41. doi:10.1161/CIRCULATIONAHA.113.003961
18. Tzivoni D, Keren A, Meyler S, Khoury Z, Lerer T, Brunel P. Cardiovascular safety of transdermal nicotine patches in patients with coronary artery disease who try to quit smoking. Cardiovasc Drugs Ther. 1998;12(3):239-244. doi:10.1023/a:1007757530765
19. Lucini D, Bertocchi F, Malliani A, Pagani M. Autonomic effects of nicotine patch administration in habitual cigarette smokers: a double-blind, placebo-controlled study using spectral analysis of RR interval and systolic arterial pressure variabilities. J Cardiovasc Pharmacol. 1998;31(5):714-720. doi:10.1097/00005344-199805000-00010
20. Kaijser L, Berglund B. Effect of nicotine on coronary blood-flow in man. Clin Physiol. 1985;5(6):541-552. doi:10.1111/j.1475-097x.1985.tb00767.x
21. Nitenberg A, Antony I. Effects of nicotine gum on coronary vasomotor responses during sympathetic stimulation in patients with coronary artery stenosis. J Cardiovasc Pharmacol. 1999;34(5):694-699. doi:10.1097/00005344-199911000-00011
22. Keeley EC, Pirwitz MJ, Landau C, et al. Intranasal nicotine spray does not augment the adverse effects of cigarette smoking on myocardial oxygen demand or coronary arterial dimensions. Am J Med. 1996;101(4):357-363. doi:10.1016/s0002-9343(96)00237-9
23. Benowitz NL, Gourlay SG. Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy. J Am Coll Cardiol. 1997;29(7):1422-1431. doi:10.1016/s0735-1097(97)00079-x
24. Flowers L. Nicotine replacement therapy. Amer J Psych. 2017;11(6):4-7.
25. Adenosine; Package insert. Astellas Pharma US Inc; 1989.
26. Dipyridamole; Package insert. Boehringer Ingelheim Pharmaceuticals Inc; 2019.
27. Dobutamine; Package insert. Baxter Healthcare Corporation; 2012.
1. Rui P, Kang K, Ashman JJ. National Hospital Ambulatory Medical Care Survey: 2016 emergency department summary tables. Published 2016. Accessed March 30, 2020. https://www.cdc.gov/nchs/data/nhamcs/web_tables/2016_ed_web_tables.pdf
2. Lange RA. Cardiovascular testing. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. eds. Pharmacotherapy: A Pathophysiologic Approach, 10th ed. McGraw Hill; 2017.
3. Mace S. Observation Medicine: Principles and Protocols. Cambridge University Press; 2017.
4. Currie GM. Pharmacology, part 4: nuclear cardiology. J Nucl Med Technol. 2019;47(2):97-110. doi:10.2967/jnmt.118.219675
5. Regadenoson; Package insert. Astellas Pharma US Inc; 2008.
6. Iskandrian AE, Bateman TM, Belardinelli L, et al. Adenosine versus regadenoson comparative evaluation in myocardial perfusion imaging: results of the ADVANCE phase 3 multicenter international trial. J Nucl Cardiol. 2007;14(5):645-658. doi:10.1016/j.nuclcard.2007.06.114
7. Hajar R. Risk factors for coronary artery disease: historical perspectives. Heart Views. 2017;18(3):109-114. doi:10.4103/HEARTVIEWS.HEARTVIEWS_106_17
8. Benowitz NL, Burbank AD. Cardiovascular toxicity of nicotine: implications for electronic cigarette use. Trends Cardiovasc Med. 2016;26(6):515-523. doi:10.1016/j.tcm.2016.03.001
9. Czernin J, Sun K, Brunken R, Böttcher M, Phelps M, Schelbert H. Effect of acute and long-term smoking on myocardial blood flow and flow reserve. Circulation. 1995;91:2891-2897. doi:10.1161/01.CIR.91.12.2891
10. Winniford MD, Wheelan KR, Kremers MS, et al. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone. Circulation. 1986;73(4):662-667. doi:10.1161/01.cir.73.4.662
11. Klein LW, Ambrose J, Pichard A, Holt J, Gorlin R, Teichholz LE. Acute coronary hemodynamic response to cigarette smoking in patients with coronary artery disease. J Am Coll Cardiol. 1984;3(4):879-886. doi:10.1016/s0735-1097(84)80344-7
12. Quillen JE, Rossen JD, Oskarsson HJ, Minor RL Jr, Lopez AG, Winniford MD. Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels. J Am Coll Cardiol. 1993;22(3):642-647. doi:10.1016/0735-1097(93)90170-6
13. Dacosta A, Guy JM, Tardy B, et al. Myocardial infarction and nicotine patch: a contributing or causative factor?. Eur Heart J. 1993;14(12):1709-1711. doi:10.1093/eurheartj/14.12.1709
14. Ottervanger JP, Festen JM, de Vries AG, Stricker BH. Acute myocardial infarction while using the nicotine patch. Chest. 1995;107(6):1765-1766. doi:10.1378/chest.107.6.1765
15. Dollerup J, Vestbo J, Murray-Thomas T, et al. Cardiovascular risks in smokers treated with nicotine replacement therapy: a historical cohort study. Clin Epidemiol. 2017;9:231-243. Published 2017 Apr 26. doi:10.2147/CLEP.S127775
16. Mills EJ, Wu P, Lockhart I, Wilson K, Ebbert JO. Adverse events associated with nicotine replacement therapy (NRT) for smoking cessation. A systematic review and meta-analysis of one hundred and twenty studies involving 177,390 individuals. Tob Induc Dis. 2010;8(1):8. Published 2010 Jul 13. doi:10.1186/1617-9625-8-8
17. Mills EJ, Thorlund K, Eapen S, Wu P, Prochaska JJ. Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis. Circulation. 2014;129(1):28-41. doi:10.1161/CIRCULATIONAHA.113.003961
18. Tzivoni D, Keren A, Meyler S, Khoury Z, Lerer T, Brunel P. Cardiovascular safety of transdermal nicotine patches in patients with coronary artery disease who try to quit smoking. Cardiovasc Drugs Ther. 1998;12(3):239-244. doi:10.1023/a:1007757530765
19. Lucini D, Bertocchi F, Malliani A, Pagani M. Autonomic effects of nicotine patch administration in habitual cigarette smokers: a double-blind, placebo-controlled study using spectral analysis of RR interval and systolic arterial pressure variabilities. J Cardiovasc Pharmacol. 1998;31(5):714-720. doi:10.1097/00005344-199805000-00010
20. Kaijser L, Berglund B. Effect of nicotine on coronary blood-flow in man. Clin Physiol. 1985;5(6):541-552. doi:10.1111/j.1475-097x.1985.tb00767.x
21. Nitenberg A, Antony I. Effects of nicotine gum on coronary vasomotor responses during sympathetic stimulation in patients with coronary artery stenosis. J Cardiovasc Pharmacol. 1999;34(5):694-699. doi:10.1097/00005344-199911000-00011
22. Keeley EC, Pirwitz MJ, Landau C, et al. Intranasal nicotine spray does not augment the adverse effects of cigarette smoking on myocardial oxygen demand or coronary arterial dimensions. Am J Med. 1996;101(4):357-363. doi:10.1016/s0002-9343(96)00237-9
23. Benowitz NL, Gourlay SG. Cardiovascular toxicity of nicotine: implications for nicotine replacement therapy. J Am Coll Cardiol. 1997;29(7):1422-1431. doi:10.1016/s0735-1097(97)00079-x
24. Flowers L. Nicotine replacement therapy. Amer J Psych. 2017;11(6):4-7.
25. Adenosine; Package insert. Astellas Pharma US Inc; 1989.
26. Dipyridamole; Package insert. Boehringer Ingelheim Pharmaceuticals Inc; 2019.
27. Dobutamine; Package insert. Baxter Healthcare Corporation; 2012.
Effective alternatives to psychotherapy for borderline personality disorder
Early interventions that focus on clinical case management and psychiatric care, and not necessarily on individual psychotherapy, are effective for young patients with borderline personality disorder (BPD), new research suggests.
Findings from the Monitoring Outcomes of Borderline Personality Disorder in Youth (MOBY) trial also showed improved psychosocial functioning and reduced suicide ideation with these therapies.
The results suggest that, contrary to common belief, psychotherapy is not the only effective approach for early BPD, lead author Andrew M. Chanen, PhD, director of clinical programs and services and head of personality disorder research at Orygen, Melbourne, told this news organization.
“We can say that early diagnosis and early treatment is effective, and the treatment doesn’t need to involve individual psychotherapy but does need to involve clinical case management and psychiatric care,” said Dr. Chanen, a professorial fellow at the Centre for Youth Mental Health, University of Melbourne.
The findings were published online in JAMA Psychiatry.
Extreme sensitivity
Patients with BPD have “extreme sensitivity to interpersonal slights” and often exhibit intense and volatile emotions and impulsive behavior, Dr. Chanen noted. Many will self-harm, abuse drugs, or attempt suicide; the suicide rate among patients with BPD is 8%-10%.
The condition is typically diagnosed in puberty or early adulthood, affecting about 3% of young people and a little more than 1% of adults.
Because of their aggression and interpersonal difficulties, patients with BPD are often discriminated against by health professionals and end up not getting treated, said Dr. Chanen.
Those who are treated often receive individual psychotherapy, such as dialectical behavior therapy (DBT). That type of therapy, which teaches healthy ways to cope with stress and regulate emotions, is very effective, Dr. Chanen said.
The MOBY trial examined three treatment approaches: the Helping Young People Early (HYPE) model, HYPE combined with weekly “befriending,” and a general youth mental health service (YMHS) model combined with befriending.
A key element of HYPE is cognitive analytic therapy, a psychotherapy program focused on understanding problematic self-management and interpersonal relationship patterns. The model includes clinical case management, such as attending to housing, vocational and educational issues, other mental health needs, and physical health needs.
In the second model, the psychotherapy of the HYPE program was replaced with befriending, which involves chatting with a patient about neutral topics such as sports and avoiding emotionally loaded topics such as interpersonal problems.
For YMHS plus befriending, experts trained in treating young people, but not specialized in treating BPD, were involved in managing patients.
‘High satisfaction’
Researchers randomly assigned 139 participants aged 15-25 years (80.6% women; mean age, 19.1 years) with BPD to one of the treatment arms. Of these, 128 (92.1%) were included in the intent-to-treat analysis.
The primary endpoint was psychosocial functioning, as measured by the Inventory of Interpersonal Problems Circumplex Version and the Social Adjustment Scale–Self-Report. Secondary endpoints included suicidal ideation, suicide attempts, nonsuicidal self-injury, depression, substance use, and treatment satisfaction.
The investigators reported group averages, but the study’s noninferiority design did not allow for determining if one treatment had superior efficacy.
All groups improved significantly on the primary endpoint. At 12 months, there was a mean 28.91-point (23.8%) drop in interpersonal problems and a mean 0.55-point (19.3%) drop in social adjustment scores.
For secondary outcomes, mean improvements at 12 months ranged from 40.7% (17.64 points) on the depression scale to 52.7% (6.22 points) for suicide ideation.
“The only area where the treatment didn’t really have an impact was substance use,” said Dr. Chanen. “Satisfaction was high for all three interventions throughout the study, and it’s hard to improve on high satisfaction.”
‘Turns things upside down’
That patients across all groups had marked and sustained improvements “in ways you wouldn’t expect for BPD” supports the conclusion that the interventions had a true effect, Dr. Chanen said.
They also imply there are effective alternatives to psychotherapy, which many individuals in the field insist is the only way to treat BPD. “This study turns things upside down and says actually it’s not. It’s the basics of treatment that are important,” Dr. Chanen said.
When a patient presents at the emergency department following a severe overdose, “it’s a reflex” for clinicians to refer that person to a psychotherapy program. “The problem is, these programs are not plentiful enough to be able to service the needs of this group,” Dr. Chanen noted.
On the other hand, the skills for clinical case management and psychiatric care “are available throughout the mental health systems,” he added.
The researchers are planning another analysis to determine whether age and sex predict better outcomes in these patients with BPD.
Unique contribution
Commenting for this news organization, John M. Oldham, MD, distinguished emeritus professor, Baylor College of Medicine, Houston, said a “unique and important contribution” of the study is the focus on early intervention.
“The general standard approach in psychiatry and the diagnostic world has been to not even consider anything until after somebody is 18 years of age, which is a mistake because these kids can become quite impaired earlier than that,” he said.
Dr. Oldham, who was not involved with the research, chaired the American Psychiatric Association workgroup that developed the 2001 evidence-based practice guideline for treating BPD, which recommended psychotherapy as the primary treatment. The guideline was last updated in 2005 – and another update is currently being developed, he noted.
There is an emerging trend toward “good psychiatric management” that focuses on level of functioning rather than on a specific strategy requiring a certificate of training that “not many people out there have,” said Dr. Oldham.
“You’re not going to make much headway with these kids if you’re going to be searching around for a DBT-certified therapist. What you need is to bring them in, get them to trust you, and in a sense be a kind of overall behavioral medicine navigator for them,” he added.
Dr. Oldham noted that, although the primary study outcome improved between 19% and 24%, “that means three-quarters of the people didn’t improve.”
He also pointed out this was only a 1-year trial. “Sometimes treatment for people with a personality disorder such as borderline takes a lot longer than that,” Dr. Oldham concluded.
The trial was funded by the National Health and Medical Research Council. Dr. Chanen reports receiving grants from the Australian government’s National Health and Medical Research Council during the conduct of the study and other support from the Helping Young People Early (HYPE) translational program outside the submitted work. He and another investigator cofounded and lead the HYPE clinical program, a government-funded program with continuous support, and the HYPE translational program, a not-for-profit training program. Dr. Oldham reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Early interventions that focus on clinical case management and psychiatric care, and not necessarily on individual psychotherapy, are effective for young patients with borderline personality disorder (BPD), new research suggests.
Findings from the Monitoring Outcomes of Borderline Personality Disorder in Youth (MOBY) trial also showed improved psychosocial functioning and reduced suicide ideation with these therapies.
The results suggest that, contrary to common belief, psychotherapy is not the only effective approach for early BPD, lead author Andrew M. Chanen, PhD, director of clinical programs and services and head of personality disorder research at Orygen, Melbourne, told this news organization.
“We can say that early diagnosis and early treatment is effective, and the treatment doesn’t need to involve individual psychotherapy but does need to involve clinical case management and psychiatric care,” said Dr. Chanen, a professorial fellow at the Centre for Youth Mental Health, University of Melbourne.
The findings were published online in JAMA Psychiatry.
Extreme sensitivity
Patients with BPD have “extreme sensitivity to interpersonal slights” and often exhibit intense and volatile emotions and impulsive behavior, Dr. Chanen noted. Many will self-harm, abuse drugs, or attempt suicide; the suicide rate among patients with BPD is 8%-10%.
The condition is typically diagnosed in puberty or early adulthood, affecting about 3% of young people and a little more than 1% of adults.
Because of their aggression and interpersonal difficulties, patients with BPD are often discriminated against by health professionals and end up not getting treated, said Dr. Chanen.
Those who are treated often receive individual psychotherapy, such as dialectical behavior therapy (DBT). That type of therapy, which teaches healthy ways to cope with stress and regulate emotions, is very effective, Dr. Chanen said.
The MOBY trial examined three treatment approaches: the Helping Young People Early (HYPE) model, HYPE combined with weekly “befriending,” and a general youth mental health service (YMHS) model combined with befriending.
A key element of HYPE is cognitive analytic therapy, a psychotherapy program focused on understanding problematic self-management and interpersonal relationship patterns. The model includes clinical case management, such as attending to housing, vocational and educational issues, other mental health needs, and physical health needs.
In the second model, the psychotherapy of the HYPE program was replaced with befriending, which involves chatting with a patient about neutral topics such as sports and avoiding emotionally loaded topics such as interpersonal problems.
For YMHS plus befriending, experts trained in treating young people, but not specialized in treating BPD, were involved in managing patients.
‘High satisfaction’
Researchers randomly assigned 139 participants aged 15-25 years (80.6% women; mean age, 19.1 years) with BPD to one of the treatment arms. Of these, 128 (92.1%) were included in the intent-to-treat analysis.
The primary endpoint was psychosocial functioning, as measured by the Inventory of Interpersonal Problems Circumplex Version and the Social Adjustment Scale–Self-Report. Secondary endpoints included suicidal ideation, suicide attempts, nonsuicidal self-injury, depression, substance use, and treatment satisfaction.
The investigators reported group averages, but the study’s noninferiority design did not allow for determining if one treatment had superior efficacy.
All groups improved significantly on the primary endpoint. At 12 months, there was a mean 28.91-point (23.8%) drop in interpersonal problems and a mean 0.55-point (19.3%) drop in social adjustment scores.
For secondary outcomes, mean improvements at 12 months ranged from 40.7% (17.64 points) on the depression scale to 52.7% (6.22 points) for suicide ideation.
“The only area where the treatment didn’t really have an impact was substance use,” said Dr. Chanen. “Satisfaction was high for all three interventions throughout the study, and it’s hard to improve on high satisfaction.”
‘Turns things upside down’
That patients across all groups had marked and sustained improvements “in ways you wouldn’t expect for BPD” supports the conclusion that the interventions had a true effect, Dr. Chanen said.
They also imply there are effective alternatives to psychotherapy, which many individuals in the field insist is the only way to treat BPD. “This study turns things upside down and says actually it’s not. It’s the basics of treatment that are important,” Dr. Chanen said.
When a patient presents at the emergency department following a severe overdose, “it’s a reflex” for clinicians to refer that person to a psychotherapy program. “The problem is, these programs are not plentiful enough to be able to service the needs of this group,” Dr. Chanen noted.
On the other hand, the skills for clinical case management and psychiatric care “are available throughout the mental health systems,” he added.
The researchers are planning another analysis to determine whether age and sex predict better outcomes in these patients with BPD.
Unique contribution
Commenting for this news organization, John M. Oldham, MD, distinguished emeritus professor, Baylor College of Medicine, Houston, said a “unique and important contribution” of the study is the focus on early intervention.
“The general standard approach in psychiatry and the diagnostic world has been to not even consider anything until after somebody is 18 years of age, which is a mistake because these kids can become quite impaired earlier than that,” he said.
Dr. Oldham, who was not involved with the research, chaired the American Psychiatric Association workgroup that developed the 2001 evidence-based practice guideline for treating BPD, which recommended psychotherapy as the primary treatment. The guideline was last updated in 2005 – and another update is currently being developed, he noted.
There is an emerging trend toward “good psychiatric management” that focuses on level of functioning rather than on a specific strategy requiring a certificate of training that “not many people out there have,” said Dr. Oldham.
“You’re not going to make much headway with these kids if you’re going to be searching around for a DBT-certified therapist. What you need is to bring them in, get them to trust you, and in a sense be a kind of overall behavioral medicine navigator for them,” he added.
Dr. Oldham noted that, although the primary study outcome improved between 19% and 24%, “that means three-quarters of the people didn’t improve.”
He also pointed out this was only a 1-year trial. “Sometimes treatment for people with a personality disorder such as borderline takes a lot longer than that,” Dr. Oldham concluded.
The trial was funded by the National Health and Medical Research Council. Dr. Chanen reports receiving grants from the Australian government’s National Health and Medical Research Council during the conduct of the study and other support from the Helping Young People Early (HYPE) translational program outside the submitted work. He and another investigator cofounded and lead the HYPE clinical program, a government-funded program with continuous support, and the HYPE translational program, a not-for-profit training program. Dr. Oldham reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Early interventions that focus on clinical case management and psychiatric care, and not necessarily on individual psychotherapy, are effective for young patients with borderline personality disorder (BPD), new research suggests.
Findings from the Monitoring Outcomes of Borderline Personality Disorder in Youth (MOBY) trial also showed improved psychosocial functioning and reduced suicide ideation with these therapies.
The results suggest that, contrary to common belief, psychotherapy is not the only effective approach for early BPD, lead author Andrew M. Chanen, PhD, director of clinical programs and services and head of personality disorder research at Orygen, Melbourne, told this news organization.
“We can say that early diagnosis and early treatment is effective, and the treatment doesn’t need to involve individual psychotherapy but does need to involve clinical case management and psychiatric care,” said Dr. Chanen, a professorial fellow at the Centre for Youth Mental Health, University of Melbourne.
The findings were published online in JAMA Psychiatry.
Extreme sensitivity
Patients with BPD have “extreme sensitivity to interpersonal slights” and often exhibit intense and volatile emotions and impulsive behavior, Dr. Chanen noted. Many will self-harm, abuse drugs, or attempt suicide; the suicide rate among patients with BPD is 8%-10%.
The condition is typically diagnosed in puberty or early adulthood, affecting about 3% of young people and a little more than 1% of adults.
Because of their aggression and interpersonal difficulties, patients with BPD are often discriminated against by health professionals and end up not getting treated, said Dr. Chanen.
Those who are treated often receive individual psychotherapy, such as dialectical behavior therapy (DBT). That type of therapy, which teaches healthy ways to cope with stress and regulate emotions, is very effective, Dr. Chanen said.
The MOBY trial examined three treatment approaches: the Helping Young People Early (HYPE) model, HYPE combined with weekly “befriending,” and a general youth mental health service (YMHS) model combined with befriending.
A key element of HYPE is cognitive analytic therapy, a psychotherapy program focused on understanding problematic self-management and interpersonal relationship patterns. The model includes clinical case management, such as attending to housing, vocational and educational issues, other mental health needs, and physical health needs.
In the second model, the psychotherapy of the HYPE program was replaced with befriending, which involves chatting with a patient about neutral topics such as sports and avoiding emotionally loaded topics such as interpersonal problems.
For YMHS plus befriending, experts trained in treating young people, but not specialized in treating BPD, were involved in managing patients.
‘High satisfaction’
Researchers randomly assigned 139 participants aged 15-25 years (80.6% women; mean age, 19.1 years) with BPD to one of the treatment arms. Of these, 128 (92.1%) were included in the intent-to-treat analysis.
The primary endpoint was psychosocial functioning, as measured by the Inventory of Interpersonal Problems Circumplex Version and the Social Adjustment Scale–Self-Report. Secondary endpoints included suicidal ideation, suicide attempts, nonsuicidal self-injury, depression, substance use, and treatment satisfaction.
The investigators reported group averages, but the study’s noninferiority design did not allow for determining if one treatment had superior efficacy.
All groups improved significantly on the primary endpoint. At 12 months, there was a mean 28.91-point (23.8%) drop in interpersonal problems and a mean 0.55-point (19.3%) drop in social adjustment scores.
For secondary outcomes, mean improvements at 12 months ranged from 40.7% (17.64 points) on the depression scale to 52.7% (6.22 points) for suicide ideation.
“The only area where the treatment didn’t really have an impact was substance use,” said Dr. Chanen. “Satisfaction was high for all three interventions throughout the study, and it’s hard to improve on high satisfaction.”
‘Turns things upside down’
That patients across all groups had marked and sustained improvements “in ways you wouldn’t expect for BPD” supports the conclusion that the interventions had a true effect, Dr. Chanen said.
They also imply there are effective alternatives to psychotherapy, which many individuals in the field insist is the only way to treat BPD. “This study turns things upside down and says actually it’s not. It’s the basics of treatment that are important,” Dr. Chanen said.
When a patient presents at the emergency department following a severe overdose, “it’s a reflex” for clinicians to refer that person to a psychotherapy program. “The problem is, these programs are not plentiful enough to be able to service the needs of this group,” Dr. Chanen noted.
On the other hand, the skills for clinical case management and psychiatric care “are available throughout the mental health systems,” he added.
The researchers are planning another analysis to determine whether age and sex predict better outcomes in these patients with BPD.
Unique contribution
Commenting for this news organization, John M. Oldham, MD, distinguished emeritus professor, Baylor College of Medicine, Houston, said a “unique and important contribution” of the study is the focus on early intervention.
“The general standard approach in psychiatry and the diagnostic world has been to not even consider anything until after somebody is 18 years of age, which is a mistake because these kids can become quite impaired earlier than that,” he said.
Dr. Oldham, who was not involved with the research, chaired the American Psychiatric Association workgroup that developed the 2001 evidence-based practice guideline for treating BPD, which recommended psychotherapy as the primary treatment. The guideline was last updated in 2005 – and another update is currently being developed, he noted.
There is an emerging trend toward “good psychiatric management” that focuses on level of functioning rather than on a specific strategy requiring a certificate of training that “not many people out there have,” said Dr. Oldham.
“You’re not going to make much headway with these kids if you’re going to be searching around for a DBT-certified therapist. What you need is to bring them in, get them to trust you, and in a sense be a kind of overall behavioral medicine navigator for them,” he added.
Dr. Oldham noted that, although the primary study outcome improved between 19% and 24%, “that means three-quarters of the people didn’t improve.”
He also pointed out this was only a 1-year trial. “Sometimes treatment for people with a personality disorder such as borderline takes a lot longer than that,” Dr. Oldham concluded.
The trial was funded by the National Health and Medical Research Council. Dr. Chanen reports receiving grants from the Australian government’s National Health and Medical Research Council during the conduct of the study and other support from the Helping Young People Early (HYPE) translational program outside the submitted work. He and another investigator cofounded and lead the HYPE clinical program, a government-funded program with continuous support, and the HYPE translational program, a not-for-profit training program. Dr. Oldham reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Study finds sharp drop in opioid scripts among most specialties
The volume of prescription opioids dispensed at retail pharmacies in the United States dropped by 21% in recent years amid efforts to reduce unnecessary use of the painkillers, but the rate of decline varied greatly among types of patients and by type of clinician, a study found.
In a brief report published by Annals of Internal Medicine, researchers from the nonprofit RAND Corp reported an analysis of opioid prescriptions from two periods, 2008-2009 and 2017-2018.
The researchers sought to assess total opioid use rather than simply track the number of pills dispensed. So they used days’ supply and total daily dose to calculate per capita morphine milligram equivalents (MME) for opioid prescriptions, write Bradley D. Stein, MD, PhD, MPH, the study’s lead author and a senior physician researcher at RAND Corp, and his coauthors in their paper.
For the study, the researchers used data from the consulting firm IQVIA, which they say covers about 90% of U.S. prescriptions. Total opioid volume per capita by prescriptions filled in retail pharmacies decreased from 951.4 MME in 2008-2009 to 749.3 MME in 2017-2018, Dr. Stein’s group found.
(In 2020, IQVIA separately said that prescription opioid use per adult in this country rose from an average of 16 pills, or 134 MMEs, in 1992 to a peak of about 55 pills a person, or 790 MMEs, in 2011. By 2019, opioid use per adult had declined to 29 pills and 366 MMEs per capita.)
The RAND report found substantial variation in opioid volume by type of insurance, including a 41.5% decline (636.5 MME to 372.6 MME) among people covered by commercial health plans. That exceeded the 27.7% drop seen for people enrolled in Medicaid (646.8 MME to 467.7 MME). The decline was smaller (17.5%; 2,780.2 MME to 2,294.2 MME) for those on Medicare, who as a group used the most opioids.
‘Almost functions as a Rorschach test’
The causes of the decline are easy to guess, although definitive conclusions are impossible, Dr. Stein told this news organization.
Significant work has been done in recent years to change attitudes about opioid prescriptions by physicians, researchers, and lawmakers. Aggressive promotion of prescription painkillers, particularly Purdue Pharma’s OxyContin, in the 1990s, is widely cited as the triggering event for the national opioid crisis.
In response, states created databases known as prescription drug monitoring programs. The Centers for Disease Control and Prevention in 2016 issued guidelines intended to curb unnecessary use of opioids. The guidelines noted that other medicines could treat chronic pain without raising the risk of addiction. The Choosing Wisely campaign, run by a foundation of the American Board of Internal Medicine, also offered recommendations about limiting use of opioids. And insurers have restricted access to opioids through the prior authorization process. As a result, researchers will make their own guesses at the causes of the decline in opioid prescriptions, based on their own experiences and research interests, Dr. Stein said.
“It almost functions as a Rorschach test,” he said.
Dr. Stein’s group also looked at trends among medical specialties. They found the largest reduction between 2008-2009 and 2017-2018 among emergency physicians (70.5% drop from 99,254.5 MME to 29,234.3 MME), psychiatrists (67.2% drop from 50,464.3 MME to 16,533.0 MME) and oncologists (59.5% drop from 51,731.2 MME to 20,941.4).
Among surgeons, the RAND researchers found a drop of 49.3% from 220,764.6 to 111,904.4. Among dentists, they found a drop of 41.3% from 22,345.3 to 13,126.1.
Among pain specialists, they found a drop of 15.4% from 1,020,808.4 MME to 863,140.7 MME.
Among adult primary care clinicians, Dr. Stein and his colleagues found a drop of 40% from 651,489.4 MME in 2008-2009 to 390,841.0 MME in 2017-2018.
However, one of the groups tracked in the study increased the volume of opioid prescriptions written: advanced practice providers, among whom scripts for the drugs rose 22.7%, from 112,873.9 MME to 138,459.3 MME.
Dr. Stein said he suspects that this gain reflects a change in the nature of the practice of primary care, with nurse practitioners and physician assistants taking more active roles in treatment of patients. Some of the reduction seen among primary care clinicians who treat adults may reflect a shift in which medical personnel in a practice write the opioid prescriptions.
Still, the trends in general seen by Dr. Stein and coauthors are encouraging, even if further study of these patterns is needed, he said.
“This is one of those papers that I think potentially raises as many questions as it provides answers for,” he said.
What’s missing
Maya Hambright, MD, a family medicine physician in New York’s Hudson Valley, who has been working mainly in addiction in response to the opioid overdose crisis, observed that the drop in total prescribed volume of prescription painkillers does not necessarily translate into a reduction in use of opioids
“No one is taking fewer opioids,” Dr. Hambright told this news organization. “I can say that comfortably. They are just getting them from other sources.”
CDC data support Dr. Hambright’s view.
An estimated 100,306 people in the United States died of a drug overdose in the 12 months that ended in April 2021, an increase of 28.5% from the 78,056 deaths during the same period the year before, according to the CDC.
Dr. Hambright said more physicians need to be involved in prescribing medication-assisted treatment (MAT).
The federal government has in the past year loosened restrictions on a requirement, known as an X waiver. Certain clinicians have been exempted from training requirements, as explained in the frequently asked questions page on the Substance Abuse and Mental Health Services Administration website.
SAMHSA says legislation is required to eliminate the waiver. As of Dec. 30, 2021, more than half of the members of the U.S. House of Representatives were listed as sponsors of the Mainstreaming Addiction Treatment (MAT) Act (HR 1384), which would end the need for X waivers. The bill has the backing of 187 Democrats and 43 Republicans.
At this time, too many physicians shy away from offering MAT, Dr. Hambright said.
“People are still scared of it,” she said. “People don’t want to deal with addicts.”
But Dr. Hambright said it’s well worth the initial time invested in having the needed conversations with patients about MAT.
“Afterwards, it’s so straightforward. People feel better. They’re healthier. It’s amazing,” she said. “You’re changing lives.”
The research was supported by grants from the National Institutes of Health. Dr. Stein and coauthors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The volume of prescription opioids dispensed at retail pharmacies in the United States dropped by 21% in recent years amid efforts to reduce unnecessary use of the painkillers, but the rate of decline varied greatly among types of patients and by type of clinician, a study found.
In a brief report published by Annals of Internal Medicine, researchers from the nonprofit RAND Corp reported an analysis of opioid prescriptions from two periods, 2008-2009 and 2017-2018.
The researchers sought to assess total opioid use rather than simply track the number of pills dispensed. So they used days’ supply and total daily dose to calculate per capita morphine milligram equivalents (MME) for opioid prescriptions, write Bradley D. Stein, MD, PhD, MPH, the study’s lead author and a senior physician researcher at RAND Corp, and his coauthors in their paper.
For the study, the researchers used data from the consulting firm IQVIA, which they say covers about 90% of U.S. prescriptions. Total opioid volume per capita by prescriptions filled in retail pharmacies decreased from 951.4 MME in 2008-2009 to 749.3 MME in 2017-2018, Dr. Stein’s group found.
(In 2020, IQVIA separately said that prescription opioid use per adult in this country rose from an average of 16 pills, or 134 MMEs, in 1992 to a peak of about 55 pills a person, or 790 MMEs, in 2011. By 2019, opioid use per adult had declined to 29 pills and 366 MMEs per capita.)
The RAND report found substantial variation in opioid volume by type of insurance, including a 41.5% decline (636.5 MME to 372.6 MME) among people covered by commercial health plans. That exceeded the 27.7% drop seen for people enrolled in Medicaid (646.8 MME to 467.7 MME). The decline was smaller (17.5%; 2,780.2 MME to 2,294.2 MME) for those on Medicare, who as a group used the most opioids.
‘Almost functions as a Rorschach test’
The causes of the decline are easy to guess, although definitive conclusions are impossible, Dr. Stein told this news organization.
Significant work has been done in recent years to change attitudes about opioid prescriptions by physicians, researchers, and lawmakers. Aggressive promotion of prescription painkillers, particularly Purdue Pharma’s OxyContin, in the 1990s, is widely cited as the triggering event for the national opioid crisis.
In response, states created databases known as prescription drug monitoring programs. The Centers for Disease Control and Prevention in 2016 issued guidelines intended to curb unnecessary use of opioids. The guidelines noted that other medicines could treat chronic pain without raising the risk of addiction. The Choosing Wisely campaign, run by a foundation of the American Board of Internal Medicine, also offered recommendations about limiting use of opioids. And insurers have restricted access to opioids through the prior authorization process. As a result, researchers will make their own guesses at the causes of the decline in opioid prescriptions, based on their own experiences and research interests, Dr. Stein said.
“It almost functions as a Rorschach test,” he said.
Dr. Stein’s group also looked at trends among medical specialties. They found the largest reduction between 2008-2009 and 2017-2018 among emergency physicians (70.5% drop from 99,254.5 MME to 29,234.3 MME), psychiatrists (67.2% drop from 50,464.3 MME to 16,533.0 MME) and oncologists (59.5% drop from 51,731.2 MME to 20,941.4).
Among surgeons, the RAND researchers found a drop of 49.3% from 220,764.6 to 111,904.4. Among dentists, they found a drop of 41.3% from 22,345.3 to 13,126.1.
Among pain specialists, they found a drop of 15.4% from 1,020,808.4 MME to 863,140.7 MME.
Among adult primary care clinicians, Dr. Stein and his colleagues found a drop of 40% from 651,489.4 MME in 2008-2009 to 390,841.0 MME in 2017-2018.
However, one of the groups tracked in the study increased the volume of opioid prescriptions written: advanced practice providers, among whom scripts for the drugs rose 22.7%, from 112,873.9 MME to 138,459.3 MME.
Dr. Stein said he suspects that this gain reflects a change in the nature of the practice of primary care, with nurse practitioners and physician assistants taking more active roles in treatment of patients. Some of the reduction seen among primary care clinicians who treat adults may reflect a shift in which medical personnel in a practice write the opioid prescriptions.
Still, the trends in general seen by Dr. Stein and coauthors are encouraging, even if further study of these patterns is needed, he said.
“This is one of those papers that I think potentially raises as many questions as it provides answers for,” he said.
What’s missing
Maya Hambright, MD, a family medicine physician in New York’s Hudson Valley, who has been working mainly in addiction in response to the opioid overdose crisis, observed that the drop in total prescribed volume of prescription painkillers does not necessarily translate into a reduction in use of opioids
“No one is taking fewer opioids,” Dr. Hambright told this news organization. “I can say that comfortably. They are just getting them from other sources.”
CDC data support Dr. Hambright’s view.
An estimated 100,306 people in the United States died of a drug overdose in the 12 months that ended in April 2021, an increase of 28.5% from the 78,056 deaths during the same period the year before, according to the CDC.
Dr. Hambright said more physicians need to be involved in prescribing medication-assisted treatment (MAT).
The federal government has in the past year loosened restrictions on a requirement, known as an X waiver. Certain clinicians have been exempted from training requirements, as explained in the frequently asked questions page on the Substance Abuse and Mental Health Services Administration website.
SAMHSA says legislation is required to eliminate the waiver. As of Dec. 30, 2021, more than half of the members of the U.S. House of Representatives were listed as sponsors of the Mainstreaming Addiction Treatment (MAT) Act (HR 1384), which would end the need for X waivers. The bill has the backing of 187 Democrats and 43 Republicans.
At this time, too many physicians shy away from offering MAT, Dr. Hambright said.
“People are still scared of it,” she said. “People don’t want to deal with addicts.”
But Dr. Hambright said it’s well worth the initial time invested in having the needed conversations with patients about MAT.
“Afterwards, it’s so straightforward. People feel better. They’re healthier. It’s amazing,” she said. “You’re changing lives.”
The research was supported by grants from the National Institutes of Health. Dr. Stein and coauthors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The volume of prescription opioids dispensed at retail pharmacies in the United States dropped by 21% in recent years amid efforts to reduce unnecessary use of the painkillers, but the rate of decline varied greatly among types of patients and by type of clinician, a study found.
In a brief report published by Annals of Internal Medicine, researchers from the nonprofit RAND Corp reported an analysis of opioid prescriptions from two periods, 2008-2009 and 2017-2018.
The researchers sought to assess total opioid use rather than simply track the number of pills dispensed. So they used days’ supply and total daily dose to calculate per capita morphine milligram equivalents (MME) for opioid prescriptions, write Bradley D. Stein, MD, PhD, MPH, the study’s lead author and a senior physician researcher at RAND Corp, and his coauthors in their paper.
For the study, the researchers used data from the consulting firm IQVIA, which they say covers about 90% of U.S. prescriptions. Total opioid volume per capita by prescriptions filled in retail pharmacies decreased from 951.4 MME in 2008-2009 to 749.3 MME in 2017-2018, Dr. Stein’s group found.
(In 2020, IQVIA separately said that prescription opioid use per adult in this country rose from an average of 16 pills, or 134 MMEs, in 1992 to a peak of about 55 pills a person, or 790 MMEs, in 2011. By 2019, opioid use per adult had declined to 29 pills and 366 MMEs per capita.)
The RAND report found substantial variation in opioid volume by type of insurance, including a 41.5% decline (636.5 MME to 372.6 MME) among people covered by commercial health plans. That exceeded the 27.7% drop seen for people enrolled in Medicaid (646.8 MME to 467.7 MME). The decline was smaller (17.5%; 2,780.2 MME to 2,294.2 MME) for those on Medicare, who as a group used the most opioids.
‘Almost functions as a Rorschach test’
The causes of the decline are easy to guess, although definitive conclusions are impossible, Dr. Stein told this news organization.
Significant work has been done in recent years to change attitudes about opioid prescriptions by physicians, researchers, and lawmakers. Aggressive promotion of prescription painkillers, particularly Purdue Pharma’s OxyContin, in the 1990s, is widely cited as the triggering event for the national opioid crisis.
In response, states created databases known as prescription drug monitoring programs. The Centers for Disease Control and Prevention in 2016 issued guidelines intended to curb unnecessary use of opioids. The guidelines noted that other medicines could treat chronic pain without raising the risk of addiction. The Choosing Wisely campaign, run by a foundation of the American Board of Internal Medicine, also offered recommendations about limiting use of opioids. And insurers have restricted access to opioids through the prior authorization process. As a result, researchers will make their own guesses at the causes of the decline in opioid prescriptions, based on their own experiences and research interests, Dr. Stein said.
“It almost functions as a Rorschach test,” he said.
Dr. Stein’s group also looked at trends among medical specialties. They found the largest reduction between 2008-2009 and 2017-2018 among emergency physicians (70.5% drop from 99,254.5 MME to 29,234.3 MME), psychiatrists (67.2% drop from 50,464.3 MME to 16,533.0 MME) and oncologists (59.5% drop from 51,731.2 MME to 20,941.4).
Among surgeons, the RAND researchers found a drop of 49.3% from 220,764.6 to 111,904.4. Among dentists, they found a drop of 41.3% from 22,345.3 to 13,126.1.
Among pain specialists, they found a drop of 15.4% from 1,020,808.4 MME to 863,140.7 MME.
Among adult primary care clinicians, Dr. Stein and his colleagues found a drop of 40% from 651,489.4 MME in 2008-2009 to 390,841.0 MME in 2017-2018.
However, one of the groups tracked in the study increased the volume of opioid prescriptions written: advanced practice providers, among whom scripts for the drugs rose 22.7%, from 112,873.9 MME to 138,459.3 MME.
Dr. Stein said he suspects that this gain reflects a change in the nature of the practice of primary care, with nurse practitioners and physician assistants taking more active roles in treatment of patients. Some of the reduction seen among primary care clinicians who treat adults may reflect a shift in which medical personnel in a practice write the opioid prescriptions.
Still, the trends in general seen by Dr. Stein and coauthors are encouraging, even if further study of these patterns is needed, he said.
“This is one of those papers that I think potentially raises as many questions as it provides answers for,” he said.
What’s missing
Maya Hambright, MD, a family medicine physician in New York’s Hudson Valley, who has been working mainly in addiction in response to the opioid overdose crisis, observed that the drop in total prescribed volume of prescription painkillers does not necessarily translate into a reduction in use of opioids
“No one is taking fewer opioids,” Dr. Hambright told this news organization. “I can say that comfortably. They are just getting them from other sources.”
CDC data support Dr. Hambright’s view.
An estimated 100,306 people in the United States died of a drug overdose in the 12 months that ended in April 2021, an increase of 28.5% from the 78,056 deaths during the same period the year before, according to the CDC.
Dr. Hambright said more physicians need to be involved in prescribing medication-assisted treatment (MAT).
The federal government has in the past year loosened restrictions on a requirement, known as an X waiver. Certain clinicians have been exempted from training requirements, as explained in the frequently asked questions page on the Substance Abuse and Mental Health Services Administration website.
SAMHSA says legislation is required to eliminate the waiver. As of Dec. 30, 2021, more than half of the members of the U.S. House of Representatives were listed as sponsors of the Mainstreaming Addiction Treatment (MAT) Act (HR 1384), which would end the need for X waivers. The bill has the backing of 187 Democrats and 43 Republicans.
At this time, too many physicians shy away from offering MAT, Dr. Hambright said.
“People are still scared of it,” she said. “People don’t want to deal with addicts.”
But Dr. Hambright said it’s well worth the initial time invested in having the needed conversations with patients about MAT.
“Afterwards, it’s so straightforward. People feel better. They’re healthier. It’s amazing,” she said. “You’re changing lives.”
The research was supported by grants from the National Institutes of Health. Dr. Stein and coauthors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Schizophrenia linked to violent behavior, but experts push back
A new meta-analysis suggests the risk for violence is higher in patients with schizophrenia, but some experts beg to differ, calling out study limitations and urging caution when interpreting the findings.
The study suggests patients with schizophrenia spectrum disorder (SSD) are 4.5 times more likely than individuals in the general population to perpetrate violence against others.
While the results showed comorbid substance misuse was associated with a significantly increased risk for violence in those with SSD, data on medication nonadherence, prior exposure to violence, childhood trauma, or other known risk factors were not included in the study.
“I think one of the main implications of this study is that prevention of violence outcomes really should be a focus for clinical services, because these are important outcomes to prevent and many of the factors that increase risk are modifiable, such as substance misuse and treatment adherence,” study coinvestigator Seena Fazel, MD, professor of forensic psychiatry at the University of Oxford (England), said in an interview.
Still, some experts urge caution when interpreting the findings, which they fear could perpetuate stigma against individuals with serious mental illness if not taken in the context of a study that shows association, not causation.
“While potential for violence is certainly a relevant consideration in assessing persons with schizophrenia spectrum disorder, professor emeritus of psychiatry at the State University of New York, Syracuse, who commented on the findings.
The findings were published online Dec. 22, 2021, in JAMA Psychiatry.
No causal link
The meta-analysis included 24 studies involving 51,309 individuals with SSD from 15 countries over 4 decades.
Risk for violence perpetrated by men with schizophrenia was 4.5 times higher (95% confidence interval, 3.6-5.6) than their counterparts in the general population. Among women, the rate was 10.2 times higher (95% CI, 7.1-14.6) versus those without SSD.
The odds of perpetrating sexual offenses (odds ratio, 5.1; 95% CI, 3.8-6.8) and homicide (OR, 17.7; 95% CI, 13.9-22.6) were also increased.
When restricting analysis to studies that used outcomes only from register-based sources, indicating a criminal arrest or conviction, absolute risks of violence perpetration ranged from 2.3% to 24.7% in men with SSD and from 0% to 5.4% in women up to a 35-year follow-up.
“That means that over a 35-year period most men are not going to be involved in these criminal register-based violent outcomes,” Dr. Fazel said. “And at least 90% of the women are not going to have any register-based violent outcomes.”
When accounting for substance use comorbidity, risk for violence perpetration dropped sharply. Those with no substance misuse were 3.5 times more likely than those in the general population to commit acts of violence versus 9.9 times in those with substance misuse comorbidity.
“In these subgroup studies of people with dual diagnoses of schizophrenia and substance misuse, the risk was increased 10-fold,” Dr. Fazel said. “If you look at people without substance misuse comorbidity, there remains a risk there of between three- to fourfold increase. It doesn’t explain the association completely.”
The investigators were quick to point out that this new study identifies an association between SSD and violence, and not causation.
“One important way to consider the association is to think of clinical services for people presenting with a schizophrenia spectrum disorder: Does the evidence suggest that violence is an important enough potential adverse outcome, for a minority of those individuals, such that support for this clinical need should be improved?” study investigator Daniel Whiting, BM BCh, a doctoral research fellow in psychiatry at the University of Oxford, said in an interview. “We highlight this as an implication of the findings.”
Whether the association would change if researchers controlled for substance misuse in both the study and control groups is unknown. Also unclear from this study is what impact other risk factors may have on increasing violent outcomes in individuals with SSD.
Education, treatment adherence important
Dr. Pies pointed out that, “notably, the risk for violence in the study population declined more than sixfold when comorbid substance abuse was excluded from the analysis.”
That aligns with an earlier study conducted in Sweden by Dr. Fazel, which showed that, after controlling for substance misuse, the rate of violent crime among individuals with schizophrenia was only slightly higher than in the general population.
“The fact is that people with schizophrenia who are compliant with proper medication do not commit violent acts any more than those in the general population,” Lynn DeLisi, MD, professor of psychiatry at Harvard Medical School, Boston, and founding editor of Schizophrenia Research, said in a comment.
Indeed, Dr. Fazel’s own research suggests treatment with antipsychotics cuts in half the risk for violent crime by patients with severe mental illness.
“The goal should be education of school officials, families, and primary care physicians to detect this illness early and treat it. Programs that make sure patients comply with medication once they begin it are equally important,” Dr. DeLisi said.
Treatment adherence is important, but the first step toward violence prevention is high-quality risk assessment, said Dr. Fazel. His research team has developed a web-based, free risk calculator shown to help clinicians evaluate the risk that a patient might become violent.
Dr. Pies agreed with the importance of comprehensive, clinical assessments of modifiable risk factors, including substance use, homelessness, medication adherence, and conflictual relationships.
This kind of assessment, “in my experience, is rarely carried out in most evaluations of persons with psychotic symptoms or SSD,” he said.
Perpetuating stigma?
Another concern raised by Dr. Pies and Dr. DeLisi is how the findings might perpetuate stigma toward individuals with serious mental illness. Results from a recently published study showed that, although attitudes toward those with major depression have improved in the United States over the past few decades, stigma toward those with schizophrenia has actually worsened.
The most effective approach to reducing stigma is to “face up to the evidence, then try and prevent the negative outcomes,” Dr. Fazel said.
“The conclusion of this paper is that it’s all pointing toward a strategy toward prevention by developing high-quality risk assessment and then developing high-quality treatment programs that include not just pharmacological treatments but psychosocial treatments and beyond,” he added. “We know that’s the way it works for other disorders as well.”
Although mental illness stigma is a serious problem, Dr. Pies noted, “the risk is not so much that studies of this sort are carried out and then covered in the media, but that they are decontextualized and reduced to ‘bumper sticker’ headlines.”
“The public needs context and perspective,” he said. “It needs to be informed that violent behavior is relatively rare among persons with psychiatric illness, including persons with schizophrenia and related disorders who do not also have a substance use disorder.”
Indeed, some studies have shown that individuals with mental illness are more often the victims of violence than the perpetrators.
“Frankly, the public is much more at risk from the neighborhood lout who drinks heavily and repeatedly starts bar fights than from the average patient with a schizophrenia spectrum disorder,” Dr. Pies said.
Dr. Fazel reported receiving funding from the Wellcome Trust. Dr. DeLisi and Dr. Pies disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new meta-analysis suggests the risk for violence is higher in patients with schizophrenia, but some experts beg to differ, calling out study limitations and urging caution when interpreting the findings.
The study suggests patients with schizophrenia spectrum disorder (SSD) are 4.5 times more likely than individuals in the general population to perpetrate violence against others.
While the results showed comorbid substance misuse was associated with a significantly increased risk for violence in those with SSD, data on medication nonadherence, prior exposure to violence, childhood trauma, or other known risk factors were not included in the study.
“I think one of the main implications of this study is that prevention of violence outcomes really should be a focus for clinical services, because these are important outcomes to prevent and many of the factors that increase risk are modifiable, such as substance misuse and treatment adherence,” study coinvestigator Seena Fazel, MD, professor of forensic psychiatry at the University of Oxford (England), said in an interview.
Still, some experts urge caution when interpreting the findings, which they fear could perpetuate stigma against individuals with serious mental illness if not taken in the context of a study that shows association, not causation.
“While potential for violence is certainly a relevant consideration in assessing persons with schizophrenia spectrum disorder, professor emeritus of psychiatry at the State University of New York, Syracuse, who commented on the findings.
The findings were published online Dec. 22, 2021, in JAMA Psychiatry.
No causal link
The meta-analysis included 24 studies involving 51,309 individuals with SSD from 15 countries over 4 decades.
Risk for violence perpetrated by men with schizophrenia was 4.5 times higher (95% confidence interval, 3.6-5.6) than their counterparts in the general population. Among women, the rate was 10.2 times higher (95% CI, 7.1-14.6) versus those without SSD.
The odds of perpetrating sexual offenses (odds ratio, 5.1; 95% CI, 3.8-6.8) and homicide (OR, 17.7; 95% CI, 13.9-22.6) were also increased.
When restricting analysis to studies that used outcomes only from register-based sources, indicating a criminal arrest or conviction, absolute risks of violence perpetration ranged from 2.3% to 24.7% in men with SSD and from 0% to 5.4% in women up to a 35-year follow-up.
“That means that over a 35-year period most men are not going to be involved in these criminal register-based violent outcomes,” Dr. Fazel said. “And at least 90% of the women are not going to have any register-based violent outcomes.”
When accounting for substance use comorbidity, risk for violence perpetration dropped sharply. Those with no substance misuse were 3.5 times more likely than those in the general population to commit acts of violence versus 9.9 times in those with substance misuse comorbidity.
“In these subgroup studies of people with dual diagnoses of schizophrenia and substance misuse, the risk was increased 10-fold,” Dr. Fazel said. “If you look at people without substance misuse comorbidity, there remains a risk there of between three- to fourfold increase. It doesn’t explain the association completely.”
The investigators were quick to point out that this new study identifies an association between SSD and violence, and not causation.
“One important way to consider the association is to think of clinical services for people presenting with a schizophrenia spectrum disorder: Does the evidence suggest that violence is an important enough potential adverse outcome, for a minority of those individuals, such that support for this clinical need should be improved?” study investigator Daniel Whiting, BM BCh, a doctoral research fellow in psychiatry at the University of Oxford, said in an interview. “We highlight this as an implication of the findings.”
Whether the association would change if researchers controlled for substance misuse in both the study and control groups is unknown. Also unclear from this study is what impact other risk factors may have on increasing violent outcomes in individuals with SSD.
Education, treatment adherence important
Dr. Pies pointed out that, “notably, the risk for violence in the study population declined more than sixfold when comorbid substance abuse was excluded from the analysis.”
That aligns with an earlier study conducted in Sweden by Dr. Fazel, which showed that, after controlling for substance misuse, the rate of violent crime among individuals with schizophrenia was only slightly higher than in the general population.
“The fact is that people with schizophrenia who are compliant with proper medication do not commit violent acts any more than those in the general population,” Lynn DeLisi, MD, professor of psychiatry at Harvard Medical School, Boston, and founding editor of Schizophrenia Research, said in a comment.
Indeed, Dr. Fazel’s own research suggests treatment with antipsychotics cuts in half the risk for violent crime by patients with severe mental illness.
“The goal should be education of school officials, families, and primary care physicians to detect this illness early and treat it. Programs that make sure patients comply with medication once they begin it are equally important,” Dr. DeLisi said.
Treatment adherence is important, but the first step toward violence prevention is high-quality risk assessment, said Dr. Fazel. His research team has developed a web-based, free risk calculator shown to help clinicians evaluate the risk that a patient might become violent.
Dr. Pies agreed with the importance of comprehensive, clinical assessments of modifiable risk factors, including substance use, homelessness, medication adherence, and conflictual relationships.
This kind of assessment, “in my experience, is rarely carried out in most evaluations of persons with psychotic symptoms or SSD,” he said.
Perpetuating stigma?
Another concern raised by Dr. Pies and Dr. DeLisi is how the findings might perpetuate stigma toward individuals with serious mental illness. Results from a recently published study showed that, although attitudes toward those with major depression have improved in the United States over the past few decades, stigma toward those with schizophrenia has actually worsened.
The most effective approach to reducing stigma is to “face up to the evidence, then try and prevent the negative outcomes,” Dr. Fazel said.
“The conclusion of this paper is that it’s all pointing toward a strategy toward prevention by developing high-quality risk assessment and then developing high-quality treatment programs that include not just pharmacological treatments but psychosocial treatments and beyond,” he added. “We know that’s the way it works for other disorders as well.”
Although mental illness stigma is a serious problem, Dr. Pies noted, “the risk is not so much that studies of this sort are carried out and then covered in the media, but that they are decontextualized and reduced to ‘bumper sticker’ headlines.”
“The public needs context and perspective,” he said. “It needs to be informed that violent behavior is relatively rare among persons with psychiatric illness, including persons with schizophrenia and related disorders who do not also have a substance use disorder.”
Indeed, some studies have shown that individuals with mental illness are more often the victims of violence than the perpetrators.
“Frankly, the public is much more at risk from the neighborhood lout who drinks heavily and repeatedly starts bar fights than from the average patient with a schizophrenia spectrum disorder,” Dr. Pies said.
Dr. Fazel reported receiving funding from the Wellcome Trust. Dr. DeLisi and Dr. Pies disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new meta-analysis suggests the risk for violence is higher in patients with schizophrenia, but some experts beg to differ, calling out study limitations and urging caution when interpreting the findings.
The study suggests patients with schizophrenia spectrum disorder (SSD) are 4.5 times more likely than individuals in the general population to perpetrate violence against others.
While the results showed comorbid substance misuse was associated with a significantly increased risk for violence in those with SSD, data on medication nonadherence, prior exposure to violence, childhood trauma, or other known risk factors were not included in the study.
“I think one of the main implications of this study is that prevention of violence outcomes really should be a focus for clinical services, because these are important outcomes to prevent and many of the factors that increase risk are modifiable, such as substance misuse and treatment adherence,” study coinvestigator Seena Fazel, MD, professor of forensic psychiatry at the University of Oxford (England), said in an interview.
Still, some experts urge caution when interpreting the findings, which they fear could perpetuate stigma against individuals with serious mental illness if not taken in the context of a study that shows association, not causation.
“While potential for violence is certainly a relevant consideration in assessing persons with schizophrenia spectrum disorder, professor emeritus of psychiatry at the State University of New York, Syracuse, who commented on the findings.
The findings were published online Dec. 22, 2021, in JAMA Psychiatry.
No causal link
The meta-analysis included 24 studies involving 51,309 individuals with SSD from 15 countries over 4 decades.
Risk for violence perpetrated by men with schizophrenia was 4.5 times higher (95% confidence interval, 3.6-5.6) than their counterparts in the general population. Among women, the rate was 10.2 times higher (95% CI, 7.1-14.6) versus those without SSD.
The odds of perpetrating sexual offenses (odds ratio, 5.1; 95% CI, 3.8-6.8) and homicide (OR, 17.7; 95% CI, 13.9-22.6) were also increased.
When restricting analysis to studies that used outcomes only from register-based sources, indicating a criminal arrest or conviction, absolute risks of violence perpetration ranged from 2.3% to 24.7% in men with SSD and from 0% to 5.4% in women up to a 35-year follow-up.
“That means that over a 35-year period most men are not going to be involved in these criminal register-based violent outcomes,” Dr. Fazel said. “And at least 90% of the women are not going to have any register-based violent outcomes.”
When accounting for substance use comorbidity, risk for violence perpetration dropped sharply. Those with no substance misuse were 3.5 times more likely than those in the general population to commit acts of violence versus 9.9 times in those with substance misuse comorbidity.
“In these subgroup studies of people with dual diagnoses of schizophrenia and substance misuse, the risk was increased 10-fold,” Dr. Fazel said. “If you look at people without substance misuse comorbidity, there remains a risk there of between three- to fourfold increase. It doesn’t explain the association completely.”
The investigators were quick to point out that this new study identifies an association between SSD and violence, and not causation.
“One important way to consider the association is to think of clinical services for people presenting with a schizophrenia spectrum disorder: Does the evidence suggest that violence is an important enough potential adverse outcome, for a minority of those individuals, such that support for this clinical need should be improved?” study investigator Daniel Whiting, BM BCh, a doctoral research fellow in psychiatry at the University of Oxford, said in an interview. “We highlight this as an implication of the findings.”
Whether the association would change if researchers controlled for substance misuse in both the study and control groups is unknown. Also unclear from this study is what impact other risk factors may have on increasing violent outcomes in individuals with SSD.
Education, treatment adherence important
Dr. Pies pointed out that, “notably, the risk for violence in the study population declined more than sixfold when comorbid substance abuse was excluded from the analysis.”
That aligns with an earlier study conducted in Sweden by Dr. Fazel, which showed that, after controlling for substance misuse, the rate of violent crime among individuals with schizophrenia was only slightly higher than in the general population.
“The fact is that people with schizophrenia who are compliant with proper medication do not commit violent acts any more than those in the general population,” Lynn DeLisi, MD, professor of psychiatry at Harvard Medical School, Boston, and founding editor of Schizophrenia Research, said in a comment.
Indeed, Dr. Fazel’s own research suggests treatment with antipsychotics cuts in half the risk for violent crime by patients with severe mental illness.
“The goal should be education of school officials, families, and primary care physicians to detect this illness early and treat it. Programs that make sure patients comply with medication once they begin it are equally important,” Dr. DeLisi said.
Treatment adherence is important, but the first step toward violence prevention is high-quality risk assessment, said Dr. Fazel. His research team has developed a web-based, free risk calculator shown to help clinicians evaluate the risk that a patient might become violent.
Dr. Pies agreed with the importance of comprehensive, clinical assessments of modifiable risk factors, including substance use, homelessness, medication adherence, and conflictual relationships.
This kind of assessment, “in my experience, is rarely carried out in most evaluations of persons with psychotic symptoms or SSD,” he said.
Perpetuating stigma?
Another concern raised by Dr. Pies and Dr. DeLisi is how the findings might perpetuate stigma toward individuals with serious mental illness. Results from a recently published study showed that, although attitudes toward those with major depression have improved in the United States over the past few decades, stigma toward those with schizophrenia has actually worsened.
The most effective approach to reducing stigma is to “face up to the evidence, then try and prevent the negative outcomes,” Dr. Fazel said.
“The conclusion of this paper is that it’s all pointing toward a strategy toward prevention by developing high-quality risk assessment and then developing high-quality treatment programs that include not just pharmacological treatments but psychosocial treatments and beyond,” he added. “We know that’s the way it works for other disorders as well.”
Although mental illness stigma is a serious problem, Dr. Pies noted, “the risk is not so much that studies of this sort are carried out and then covered in the media, but that they are decontextualized and reduced to ‘bumper sticker’ headlines.”
“The public needs context and perspective,” he said. “It needs to be informed that violent behavior is relatively rare among persons with psychiatric illness, including persons with schizophrenia and related disorders who do not also have a substance use disorder.”
Indeed, some studies have shown that individuals with mental illness are more often the victims of violence than the perpetrators.
“Frankly, the public is much more at risk from the neighborhood lout who drinks heavily and repeatedly starts bar fights than from the average patient with a schizophrenia spectrum disorder,” Dr. Pies said.
Dr. Fazel reported receiving funding from the Wellcome Trust. Dr. DeLisi and Dr. Pies disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Opioid agonist therapy guards against self-harm, suicide
FROM THE LANCET PSYCHIATRY
Cessation of opioid agonist therapy (OAT) significantly increases the risk of self-harm and death by suicide in the first month after stopping the treatment in new findings that highlight the need for “advanced safety planning” during this critical time.
Investigators found that 4 weeks after stopping OAT, the risk of death by suicide was almost five times higher and the risk of hospital admission for self-harm was almost three times higher during this period, compared with the 4 weeks after initiation of OAT to treatment end.
These results highlight the importance of a “transition” period when stopping OAT and highlight the need for better supports for patients coming off this treatment, study investigator Prianka Padmanathan, MD, PhD candidate, Population Health Sciences, University of Bristol (England), told this news organization.
She noted the study supports previous findings that OAT “has an important role” in suicide prevention.
“Suicide and self-harm risk is greatly increased during treatment cessation, and advanced safety planning and additional psychosocial support during this time may be required,” Dr. Padmanathan said.
The findings were published online Dec. 15 in The Lancet Psychiatry.
Suicide, self-harm risk
Previous research shows an increased risk for overdose deaths and death in general during the first few weeks of starting and stopping treatment for opioid dependence.
“We wanted to see if the risk of dying by suicide was also elevated during these times,” said Dr. Padmanathan. As suicides are relatively rare, the researchers also looked at self-harm, “which is an important risk factor for suicide.”
, particularly buprenorphine or methadone.
“We tried to exclude people prescribed these drugs for pain and focused specifically on their prescription for opioid dependence,” Dr. Padmanathan said.
They estimated rates and adjusted risk ratios of hospital admissions for nonfatal self-harm and completed suicide during treatment initiation, maintenance, and cessation.
The study included 8,070 patients (69.3% men; mean baseline age, 33.3 years) who received OAT at least once from January 1998 through November 2018. The median treatment time was 84 days. Most of the participants lived in the most deprived neighborhoods and were White.
There were 807 hospital admissions for self-harm (1.99 per 100 person-years) and 46 suicides (0.11 per 100 person-years).
The investigators examined age, sex, socioeconomic status, number of previous OAT treatment episodes, previous self-harm, previous mental illness, and major chronic illness scores as potential confounders.
Need for psychosocial care
Results showed the risk for self-harm was significantly increased while off OAT (aRR, 1.5; 95% confidence interval, 1.21-1.88).
The overall age- and sex-standardized mortality ratio for suicide was 7.5 times higher (95% CI, 5.5-10) in the study cohort, compared with the general population in England between 1998 and 2017.
There was insufficient evidence to show the risk for suicide was higher off, versus on, treatment, but this may be because suicides are relatively rare, Dr. Padmanathan noted.
“The sample may have been too small to enable a difference to be detected. In contrast, self-harm is more common, so there was power to detect a difference there,” she said.
Risk for self-harm was more than double in the first 4 weeks after stopping OAT versus stable periods on treatment (aRR, 2.60; 95% CI, 1.83-3.7). Risk for suicide more than quadrupled during this period (aRR, 4.68; 95% CI, 1.63-13.42).
These new results suggest additional interventions may be in order, Dr. Padmanathan noted.
“We already knew that extra care – for example, providing naloxone when coming off OAT – was important to prevent overdoses. But this study suggests providing psychosocial care and other extra care may also be important to prevent suicides,” she said.
There was no statistical evidence of difference between buprenorphine and methadone in terms of self-harm and suicide risks. However, this may be because the sample was not large enough to detect a difference, said Dr. Padmanathan.
Although there are currently no guidelines to indicate an ideal OAT period, previous study results have suggested extending treatment to 2 years may be beneficial, perhaps reducing self-harm and, therefore, suicides, she noted.
“We think most of these adverse outcomes likely occur during short treatment episodes with an unplanned ending. Extending OAT sufficiently to enable a planned ending might help to reduce these risks,” she added.
‘A window of vulnerability’
Authors of an accompanying editorial note the study “adds weight” to the evidence that OAT is a “lifesaving” treatment.
“It’s critical to recognize that transitions in and out of care are vulnerable periods” when it comes to suicide, the coauthor of the editorial, Paul S. Nestadt, MD, department of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore, told this news organization.
Official suicide statistics may not reflect the entire story, as many deaths that occur because of overdose after treatment cessation are not counted as suicides, he said. “It can be difficult for medical examiners to determine if an overdose was intentional or not,” Dr. Nestadt added.
After treatment has been established, physicians “would be wise to delay treatment cessation” until the patient is in a stable condition and can be closely followed by mental health professionals, the editorialists note.
“We must consider the month following OAT cessation to be a window of vulnerability, not just for relapse but also for suicide,” they write.
The finding that patients prescribed OAT have such a high rate of suicide, compared with the general population, is “troubling” and “highlights the importance of interventions which address both opioid use and suicide risk,” they add.
The editorialists point out the median treatment period of 84 days is less than what is generally recommended, raising the question of whether longer treatment might lower suicide risk after treatment discontinuation.
They also emphasized the need for further study to test potential suicide prevention interventions in the period after treatment cessation.
Dr. Nestadt added the new findings are “quite generalizable outside of the U.K.” and referred to similar studies carried out in Australia and elsewhere.
The study was funded by the Medical Research Council. Dr. Padmanathan was a coapplicant on an a grant awarded to University of Bristol by Bristol and Weston Hospital Charity focusing on suicide prevention for patients presenting to the emergency department with self-harm and harmful substance use. Dr. Nestadt has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE LANCET PSYCHIATRY
Cessation of opioid agonist therapy (OAT) significantly increases the risk of self-harm and death by suicide in the first month after stopping the treatment in new findings that highlight the need for “advanced safety planning” during this critical time.
Investigators found that 4 weeks after stopping OAT, the risk of death by suicide was almost five times higher and the risk of hospital admission for self-harm was almost three times higher during this period, compared with the 4 weeks after initiation of OAT to treatment end.
These results highlight the importance of a “transition” period when stopping OAT and highlight the need for better supports for patients coming off this treatment, study investigator Prianka Padmanathan, MD, PhD candidate, Population Health Sciences, University of Bristol (England), told this news organization.
She noted the study supports previous findings that OAT “has an important role” in suicide prevention.
“Suicide and self-harm risk is greatly increased during treatment cessation, and advanced safety planning and additional psychosocial support during this time may be required,” Dr. Padmanathan said.
The findings were published online Dec. 15 in The Lancet Psychiatry.
Suicide, self-harm risk
Previous research shows an increased risk for overdose deaths and death in general during the first few weeks of starting and stopping treatment for opioid dependence.
“We wanted to see if the risk of dying by suicide was also elevated during these times,” said Dr. Padmanathan. As suicides are relatively rare, the researchers also looked at self-harm, “which is an important risk factor for suicide.”
, particularly buprenorphine or methadone.
“We tried to exclude people prescribed these drugs for pain and focused specifically on their prescription for opioid dependence,” Dr. Padmanathan said.
They estimated rates and adjusted risk ratios of hospital admissions for nonfatal self-harm and completed suicide during treatment initiation, maintenance, and cessation.
The study included 8,070 patients (69.3% men; mean baseline age, 33.3 years) who received OAT at least once from January 1998 through November 2018. The median treatment time was 84 days. Most of the participants lived in the most deprived neighborhoods and were White.
There were 807 hospital admissions for self-harm (1.99 per 100 person-years) and 46 suicides (0.11 per 100 person-years).
The investigators examined age, sex, socioeconomic status, number of previous OAT treatment episodes, previous self-harm, previous mental illness, and major chronic illness scores as potential confounders.
Need for psychosocial care
Results showed the risk for self-harm was significantly increased while off OAT (aRR, 1.5; 95% confidence interval, 1.21-1.88).
The overall age- and sex-standardized mortality ratio for suicide was 7.5 times higher (95% CI, 5.5-10) in the study cohort, compared with the general population in England between 1998 and 2017.
There was insufficient evidence to show the risk for suicide was higher off, versus on, treatment, but this may be because suicides are relatively rare, Dr. Padmanathan noted.
“The sample may have been too small to enable a difference to be detected. In contrast, self-harm is more common, so there was power to detect a difference there,” she said.
Risk for self-harm was more than double in the first 4 weeks after stopping OAT versus stable periods on treatment (aRR, 2.60; 95% CI, 1.83-3.7). Risk for suicide more than quadrupled during this period (aRR, 4.68; 95% CI, 1.63-13.42).
These new results suggest additional interventions may be in order, Dr. Padmanathan noted.
“We already knew that extra care – for example, providing naloxone when coming off OAT – was important to prevent overdoses. But this study suggests providing psychosocial care and other extra care may also be important to prevent suicides,” she said.
There was no statistical evidence of difference between buprenorphine and methadone in terms of self-harm and suicide risks. However, this may be because the sample was not large enough to detect a difference, said Dr. Padmanathan.
Although there are currently no guidelines to indicate an ideal OAT period, previous study results have suggested extending treatment to 2 years may be beneficial, perhaps reducing self-harm and, therefore, suicides, she noted.
“We think most of these adverse outcomes likely occur during short treatment episodes with an unplanned ending. Extending OAT sufficiently to enable a planned ending might help to reduce these risks,” she added.
‘A window of vulnerability’
Authors of an accompanying editorial note the study “adds weight” to the evidence that OAT is a “lifesaving” treatment.
“It’s critical to recognize that transitions in and out of care are vulnerable periods” when it comes to suicide, the coauthor of the editorial, Paul S. Nestadt, MD, department of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore, told this news organization.
Official suicide statistics may not reflect the entire story, as many deaths that occur because of overdose after treatment cessation are not counted as suicides, he said. “It can be difficult for medical examiners to determine if an overdose was intentional or not,” Dr. Nestadt added.
After treatment has been established, physicians “would be wise to delay treatment cessation” until the patient is in a stable condition and can be closely followed by mental health professionals, the editorialists note.
“We must consider the month following OAT cessation to be a window of vulnerability, not just for relapse but also for suicide,” they write.
The finding that patients prescribed OAT have such a high rate of suicide, compared with the general population, is “troubling” and “highlights the importance of interventions which address both opioid use and suicide risk,” they add.
The editorialists point out the median treatment period of 84 days is less than what is generally recommended, raising the question of whether longer treatment might lower suicide risk after treatment discontinuation.
They also emphasized the need for further study to test potential suicide prevention interventions in the period after treatment cessation.
Dr. Nestadt added the new findings are “quite generalizable outside of the U.K.” and referred to similar studies carried out in Australia and elsewhere.
The study was funded by the Medical Research Council. Dr. Padmanathan was a coapplicant on an a grant awarded to University of Bristol by Bristol and Weston Hospital Charity focusing on suicide prevention for patients presenting to the emergency department with self-harm and harmful substance use. Dr. Nestadt has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE LANCET PSYCHIATRY
Cessation of opioid agonist therapy (OAT) significantly increases the risk of self-harm and death by suicide in the first month after stopping the treatment in new findings that highlight the need for “advanced safety planning” during this critical time.
Investigators found that 4 weeks after stopping OAT, the risk of death by suicide was almost five times higher and the risk of hospital admission for self-harm was almost three times higher during this period, compared with the 4 weeks after initiation of OAT to treatment end.
These results highlight the importance of a “transition” period when stopping OAT and highlight the need for better supports for patients coming off this treatment, study investigator Prianka Padmanathan, MD, PhD candidate, Population Health Sciences, University of Bristol (England), told this news organization.
She noted the study supports previous findings that OAT “has an important role” in suicide prevention.
“Suicide and self-harm risk is greatly increased during treatment cessation, and advanced safety planning and additional psychosocial support during this time may be required,” Dr. Padmanathan said.
The findings were published online Dec. 15 in The Lancet Psychiatry.
Suicide, self-harm risk
Previous research shows an increased risk for overdose deaths and death in general during the first few weeks of starting and stopping treatment for opioid dependence.
“We wanted to see if the risk of dying by suicide was also elevated during these times,” said Dr. Padmanathan. As suicides are relatively rare, the researchers also looked at self-harm, “which is an important risk factor for suicide.”
, particularly buprenorphine or methadone.
“We tried to exclude people prescribed these drugs for pain and focused specifically on their prescription for opioid dependence,” Dr. Padmanathan said.
They estimated rates and adjusted risk ratios of hospital admissions for nonfatal self-harm and completed suicide during treatment initiation, maintenance, and cessation.
The study included 8,070 patients (69.3% men; mean baseline age, 33.3 years) who received OAT at least once from January 1998 through November 2018. The median treatment time was 84 days. Most of the participants lived in the most deprived neighborhoods and were White.
There were 807 hospital admissions for self-harm (1.99 per 100 person-years) and 46 suicides (0.11 per 100 person-years).
The investigators examined age, sex, socioeconomic status, number of previous OAT treatment episodes, previous self-harm, previous mental illness, and major chronic illness scores as potential confounders.
Need for psychosocial care
Results showed the risk for self-harm was significantly increased while off OAT (aRR, 1.5; 95% confidence interval, 1.21-1.88).
The overall age- and sex-standardized mortality ratio for suicide was 7.5 times higher (95% CI, 5.5-10) in the study cohort, compared with the general population in England between 1998 and 2017.
There was insufficient evidence to show the risk for suicide was higher off, versus on, treatment, but this may be because suicides are relatively rare, Dr. Padmanathan noted.
“The sample may have been too small to enable a difference to be detected. In contrast, self-harm is more common, so there was power to detect a difference there,” she said.
Risk for self-harm was more than double in the first 4 weeks after stopping OAT versus stable periods on treatment (aRR, 2.60; 95% CI, 1.83-3.7). Risk for suicide more than quadrupled during this period (aRR, 4.68; 95% CI, 1.63-13.42).
These new results suggest additional interventions may be in order, Dr. Padmanathan noted.
“We already knew that extra care – for example, providing naloxone when coming off OAT – was important to prevent overdoses. But this study suggests providing psychosocial care and other extra care may also be important to prevent suicides,” she said.
There was no statistical evidence of difference between buprenorphine and methadone in terms of self-harm and suicide risks. However, this may be because the sample was not large enough to detect a difference, said Dr. Padmanathan.
Although there are currently no guidelines to indicate an ideal OAT period, previous study results have suggested extending treatment to 2 years may be beneficial, perhaps reducing self-harm and, therefore, suicides, she noted.
“We think most of these adverse outcomes likely occur during short treatment episodes with an unplanned ending. Extending OAT sufficiently to enable a planned ending might help to reduce these risks,” she added.
‘A window of vulnerability’
Authors of an accompanying editorial note the study “adds weight” to the evidence that OAT is a “lifesaving” treatment.
“It’s critical to recognize that transitions in and out of care are vulnerable periods” when it comes to suicide, the coauthor of the editorial, Paul S. Nestadt, MD, department of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore, told this news organization.
Official suicide statistics may not reflect the entire story, as many deaths that occur because of overdose after treatment cessation are not counted as suicides, he said. “It can be difficult for medical examiners to determine if an overdose was intentional or not,” Dr. Nestadt added.
After treatment has been established, physicians “would be wise to delay treatment cessation” until the patient is in a stable condition and can be closely followed by mental health professionals, the editorialists note.
“We must consider the month following OAT cessation to be a window of vulnerability, not just for relapse but also for suicide,” they write.
The finding that patients prescribed OAT have such a high rate of suicide, compared with the general population, is “troubling” and “highlights the importance of interventions which address both opioid use and suicide risk,” they add.
The editorialists point out the median treatment period of 84 days is less than what is generally recommended, raising the question of whether longer treatment might lower suicide risk after treatment discontinuation.
They also emphasized the need for further study to test potential suicide prevention interventions in the period after treatment cessation.
Dr. Nestadt added the new findings are “quite generalizable outside of the U.K.” and referred to similar studies carried out in Australia and elsewhere.
The study was funded by the Medical Research Council. Dr. Padmanathan was a coapplicant on an a grant awarded to University of Bristol by Bristol and Weston Hospital Charity focusing on suicide prevention for patients presenting to the emergency department with self-harm and harmful substance use. Dr. Nestadt has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Pandemic screen time linked to anxiety, depression in older kids
However, the study doesn’t definitively prove that screen time is harmful, and an expert challenged the conclusions.
Still, the findings highlight the potential harms of excessive screen time, especially in the context of pandemic-era virtual learning. Clinicians “really need to advocate for policies that would be protective for children to reduce their screen time and social isolation and increase their involvement with school, sports, and academic activities,” Catherine S. Birken, MD, a pediatrician at the University of Toronto and study coauthor said in an interview.
The study appeared Dec. 28, 2021, in the journal JAMA Network Open (doi: 10.1001/jamanetworkopen.2021.40875).
Dr. Birken and colleagues launched the study to examine whether heightened levels of screen time during the pandemic disrupted mental health in kids. In particular, they wanted to break down different types of screen time, such as virtual learning, watching television, and playing video games.
“The bulk of the literature is supportive of a strong relationship between screen time and mental health symptoms like anxiety,” Dr. Birken said.
For the study, the researchers surveyed parents to track the screen time of 2,026 children between May 2020 and April 2021.
In a cohort of 532 younger children (average age, 5.9 years; 52% male; 58% of European ancestry), the researchers linked each extra daily hour of TV or use of digital media to worse behavior, as measured by the Strengths and Difficulties Questionnaire: 0.22 in an adjusted model for children aged 2-4;(95% confidence interval, 0.10-0.35; P < .001) and 0.07 in an adjusted model in those aged 4 and older (95% CI, 0.02-0.11; P = .007).
However, the researchers observed no statistically significant links to more anxiety/depression or hyperactivity/inattention in this group of children.
Among 1,494 older kids (mean age, 11.3; 57% male; 58% of European ancestry), researchers linked greater daily use of TV or digital media to higher levels of depression symptoms in a dose-dependent relationship, Dr. Birken said (1 hour: beta, 0.21; 95% CI, –1.28 to 0.78; 2-3 hours: beta, 1.81; 95% CI, 0.29-3.33; 4-5 hours: beta, 2.80; 95% CI, 1.15-4.44; 6-8 hours: beta, 5.16; 95% CI, 3.32-7.01; 9 hours: beta, 5.42; 95% CI, 3.30-7.54; overall P < .001).
“Similarly, higher TV or digital media time per day was associated with higher levels of anxiety symptoms,” the researchers reported. “TV or digital media time per day was also significantly associated with differences in symptoms of irritability, inattention, and hyperactivity/inattention.”
More time spent learning virtually was associated with higher levels of depression and anxiety in both groups of children, according to the researchers. Whether this finding reflects an effect of screens themselves or because the children most exposed to virtual learning may also have been the most exposed to the stressful disruptiveness of the pandemic is unclear.
The researchers also found “insufficient evidence” to link more virtual learning to irritability, inattention and hyperactivity, inattention, and hyperactivity/impulsivity in adjusted models.
Video chatting did not appear to have a protective effect, Dr. Birken said. The researchers also specifically analyzed children with autism and found no link between more screen time and various mental health/conduct problems.
Is it possible that kids with more anxiety, depression, and isolation simply turn to screens because they’re anxious, depressed, and isolated? Dr. Birken said the researchers adjusted the findings to account for previous mental health problems. And she noted that the study linked more pandemic-era virtual learning to more depression/anxiety. It’s “hard to imagine” how more mental health problems would cause more virtual learning.
Bad news or bad stats?
Chris Ferguson, PhD, a professor of psychology at Stetson University. DeLand, Fla., who studies screen time, criticized the study in an interview. “The observed effects are so tiny, it’s impossible to know if they are real or a false-positive artifact common to social science research,” he said. “Ultimately, this study is better evidence about how many scholars are bad at statistics than anything having to do with kids and screens.”
Dr. Ferguson said that the results may be confounded because kids turn to screens to reduce their anxiety. “For the most part, screens were a godsend during COVID-19,” he said. “They helped kids stay inside and gave them something to do while social distancing and allowed them to keep in touch with friends and families. Honestly, what else were we expecting kids to do, stare at the wallpaper?”
Children with depression and anxiety often retreat into screens or books to escape the unpleasantries of real life. “That doesn’t mean the screens or books are the culprits,” he said.
Instead of focusing on screen time, Dr. Ferguson suggested parents consider these factors: “Keeping in mind not every kid is a genius, is your kid doing about as well in school as you’d expect, given their natural ability? Are they getting at least some exercise every day? Are they getting adequate sleep? Are they able to socialize with friends in some context, either in real life or online? Are they happy?”
The study was funded by the Canadian Institutes of Health Research, the Center for Brain & Mental Health at The Hospital for Sick Children, the Ontario Ministry of Health, and the Miner’s Lamp Innovation Fund in Prevention and Early Detection of Severe Mental Illness at the University of Toronto. The study authors reported various financial relationships. Dr. Ferguson reported no relevant financial conflicts of interest.
A version of this article first appeared on Medscape.com.
However, the study doesn’t definitively prove that screen time is harmful, and an expert challenged the conclusions.
Still, the findings highlight the potential harms of excessive screen time, especially in the context of pandemic-era virtual learning. Clinicians “really need to advocate for policies that would be protective for children to reduce their screen time and social isolation and increase their involvement with school, sports, and academic activities,” Catherine S. Birken, MD, a pediatrician at the University of Toronto and study coauthor said in an interview.
The study appeared Dec. 28, 2021, in the journal JAMA Network Open (doi: 10.1001/jamanetworkopen.2021.40875).
Dr. Birken and colleagues launched the study to examine whether heightened levels of screen time during the pandemic disrupted mental health in kids. In particular, they wanted to break down different types of screen time, such as virtual learning, watching television, and playing video games.
“The bulk of the literature is supportive of a strong relationship between screen time and mental health symptoms like anxiety,” Dr. Birken said.
For the study, the researchers surveyed parents to track the screen time of 2,026 children between May 2020 and April 2021.
In a cohort of 532 younger children (average age, 5.9 years; 52% male; 58% of European ancestry), the researchers linked each extra daily hour of TV or use of digital media to worse behavior, as measured by the Strengths and Difficulties Questionnaire: 0.22 in an adjusted model for children aged 2-4;(95% confidence interval, 0.10-0.35; P < .001) and 0.07 in an adjusted model in those aged 4 and older (95% CI, 0.02-0.11; P = .007).
However, the researchers observed no statistically significant links to more anxiety/depression or hyperactivity/inattention in this group of children.
Among 1,494 older kids (mean age, 11.3; 57% male; 58% of European ancestry), researchers linked greater daily use of TV or digital media to higher levels of depression symptoms in a dose-dependent relationship, Dr. Birken said (1 hour: beta, 0.21; 95% CI, –1.28 to 0.78; 2-3 hours: beta, 1.81; 95% CI, 0.29-3.33; 4-5 hours: beta, 2.80; 95% CI, 1.15-4.44; 6-8 hours: beta, 5.16; 95% CI, 3.32-7.01; 9 hours: beta, 5.42; 95% CI, 3.30-7.54; overall P < .001).
“Similarly, higher TV or digital media time per day was associated with higher levels of anxiety symptoms,” the researchers reported. “TV or digital media time per day was also significantly associated with differences in symptoms of irritability, inattention, and hyperactivity/inattention.”
More time spent learning virtually was associated with higher levels of depression and anxiety in both groups of children, according to the researchers. Whether this finding reflects an effect of screens themselves or because the children most exposed to virtual learning may also have been the most exposed to the stressful disruptiveness of the pandemic is unclear.
The researchers also found “insufficient evidence” to link more virtual learning to irritability, inattention and hyperactivity, inattention, and hyperactivity/impulsivity in adjusted models.
Video chatting did not appear to have a protective effect, Dr. Birken said. The researchers also specifically analyzed children with autism and found no link between more screen time and various mental health/conduct problems.
Is it possible that kids with more anxiety, depression, and isolation simply turn to screens because they’re anxious, depressed, and isolated? Dr. Birken said the researchers adjusted the findings to account for previous mental health problems. And she noted that the study linked more pandemic-era virtual learning to more depression/anxiety. It’s “hard to imagine” how more mental health problems would cause more virtual learning.
Bad news or bad stats?
Chris Ferguson, PhD, a professor of psychology at Stetson University. DeLand, Fla., who studies screen time, criticized the study in an interview. “The observed effects are so tiny, it’s impossible to know if they are real or a false-positive artifact common to social science research,” he said. “Ultimately, this study is better evidence about how many scholars are bad at statistics than anything having to do with kids and screens.”
Dr. Ferguson said that the results may be confounded because kids turn to screens to reduce their anxiety. “For the most part, screens were a godsend during COVID-19,” he said. “They helped kids stay inside and gave them something to do while social distancing and allowed them to keep in touch with friends and families. Honestly, what else were we expecting kids to do, stare at the wallpaper?”
Children with depression and anxiety often retreat into screens or books to escape the unpleasantries of real life. “That doesn’t mean the screens or books are the culprits,” he said.
Instead of focusing on screen time, Dr. Ferguson suggested parents consider these factors: “Keeping in mind not every kid is a genius, is your kid doing about as well in school as you’d expect, given their natural ability? Are they getting at least some exercise every day? Are they getting adequate sleep? Are they able to socialize with friends in some context, either in real life or online? Are they happy?”
The study was funded by the Canadian Institutes of Health Research, the Center for Brain & Mental Health at The Hospital for Sick Children, the Ontario Ministry of Health, and the Miner’s Lamp Innovation Fund in Prevention and Early Detection of Severe Mental Illness at the University of Toronto. The study authors reported various financial relationships. Dr. Ferguson reported no relevant financial conflicts of interest.
A version of this article first appeared on Medscape.com.
However, the study doesn’t definitively prove that screen time is harmful, and an expert challenged the conclusions.
Still, the findings highlight the potential harms of excessive screen time, especially in the context of pandemic-era virtual learning. Clinicians “really need to advocate for policies that would be protective for children to reduce their screen time and social isolation and increase their involvement with school, sports, and academic activities,” Catherine S. Birken, MD, a pediatrician at the University of Toronto and study coauthor said in an interview.
The study appeared Dec. 28, 2021, in the journal JAMA Network Open (doi: 10.1001/jamanetworkopen.2021.40875).
Dr. Birken and colleagues launched the study to examine whether heightened levels of screen time during the pandemic disrupted mental health in kids. In particular, they wanted to break down different types of screen time, such as virtual learning, watching television, and playing video games.
“The bulk of the literature is supportive of a strong relationship between screen time and mental health symptoms like anxiety,” Dr. Birken said.
For the study, the researchers surveyed parents to track the screen time of 2,026 children between May 2020 and April 2021.
In a cohort of 532 younger children (average age, 5.9 years; 52% male; 58% of European ancestry), the researchers linked each extra daily hour of TV or use of digital media to worse behavior, as measured by the Strengths and Difficulties Questionnaire: 0.22 in an adjusted model for children aged 2-4;(95% confidence interval, 0.10-0.35; P < .001) and 0.07 in an adjusted model in those aged 4 and older (95% CI, 0.02-0.11; P = .007).
However, the researchers observed no statistically significant links to more anxiety/depression or hyperactivity/inattention in this group of children.
Among 1,494 older kids (mean age, 11.3; 57% male; 58% of European ancestry), researchers linked greater daily use of TV or digital media to higher levels of depression symptoms in a dose-dependent relationship, Dr. Birken said (1 hour: beta, 0.21; 95% CI, –1.28 to 0.78; 2-3 hours: beta, 1.81; 95% CI, 0.29-3.33; 4-5 hours: beta, 2.80; 95% CI, 1.15-4.44; 6-8 hours: beta, 5.16; 95% CI, 3.32-7.01; 9 hours: beta, 5.42; 95% CI, 3.30-7.54; overall P < .001).
“Similarly, higher TV or digital media time per day was associated with higher levels of anxiety symptoms,” the researchers reported. “TV or digital media time per day was also significantly associated with differences in symptoms of irritability, inattention, and hyperactivity/inattention.”
More time spent learning virtually was associated with higher levels of depression and anxiety in both groups of children, according to the researchers. Whether this finding reflects an effect of screens themselves or because the children most exposed to virtual learning may also have been the most exposed to the stressful disruptiveness of the pandemic is unclear.
The researchers also found “insufficient evidence” to link more virtual learning to irritability, inattention and hyperactivity, inattention, and hyperactivity/impulsivity in adjusted models.
Video chatting did not appear to have a protective effect, Dr. Birken said. The researchers also specifically analyzed children with autism and found no link between more screen time and various mental health/conduct problems.
Is it possible that kids with more anxiety, depression, and isolation simply turn to screens because they’re anxious, depressed, and isolated? Dr. Birken said the researchers adjusted the findings to account for previous mental health problems. And she noted that the study linked more pandemic-era virtual learning to more depression/anxiety. It’s “hard to imagine” how more mental health problems would cause more virtual learning.
Bad news or bad stats?
Chris Ferguson, PhD, a professor of psychology at Stetson University. DeLand, Fla., who studies screen time, criticized the study in an interview. “The observed effects are so tiny, it’s impossible to know if they are real or a false-positive artifact common to social science research,” he said. “Ultimately, this study is better evidence about how many scholars are bad at statistics than anything having to do with kids and screens.”
Dr. Ferguson said that the results may be confounded because kids turn to screens to reduce their anxiety. “For the most part, screens were a godsend during COVID-19,” he said. “They helped kids stay inside and gave them something to do while social distancing and allowed them to keep in touch with friends and families. Honestly, what else were we expecting kids to do, stare at the wallpaper?”
Children with depression and anxiety often retreat into screens or books to escape the unpleasantries of real life. “That doesn’t mean the screens or books are the culprits,” he said.
Instead of focusing on screen time, Dr. Ferguson suggested parents consider these factors: “Keeping in mind not every kid is a genius, is your kid doing about as well in school as you’d expect, given their natural ability? Are they getting at least some exercise every day? Are they getting adequate sleep? Are they able to socialize with friends in some context, either in real life or online? Are they happy?”
The study was funded by the Canadian Institutes of Health Research, the Center for Brain & Mental Health at The Hospital for Sick Children, the Ontario Ministry of Health, and the Miner’s Lamp Innovation Fund in Prevention and Early Detection of Severe Mental Illness at the University of Toronto. The study authors reported various financial relationships. Dr. Ferguson reported no relevant financial conflicts of interest.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Treating homeless patients: Book offers key insights
As a psychiatrist dedicated to working with people who are experiencing homelessness, I was very impressed with the new book edited by Col. (Ret.) Elspeth Cameron Ritchie, MD, MPH, and Maria D. Llorente, MD, about treating and providing services to this vulnerable population.
The book, “Clinical Management of the Homeless Patient: Social, Psychiatric, and Medical Issues” (Cham, Switzerland: Springer Nature Switzerland, 2021), offers an in-depth review and analysis of the biopsychosocial complexities that affect how medical and behavioral health conditions present in those who are unhoused. Notably, the book recommends with great sensitivity best practices to address these conditions with care, understanding, and love.
This text, invaluable in particular for those of us clinicians who work with people experiencing homelessness (PEH), provides a historical context of homelessness in the United States, an evaluation of the current state, and indispensable guidance for medical and behavioral health practitioners, case managers, housing navigators, and policy makers alike. It also serves as an inspiring source for those who are considering work in the public sector while reminding those of us in the field why we continue to do this challenging and rewarding work.
Tips can provide hope to clinicians
The volume is divided into four clear sections that are easy to navigate depending on your area of expertise and interest. Each chapter consolidates an extensive literature review into an intriguing and thought-provoking analysis. Part I, “The Big Picture – Social and Medical Issues,” focuses on conditions that disproportionately affect those who are unhoused. The authors offer a glimpse into the unique challenges of managing routine health conditions. They also detail the practical knowledge that’s needed to best care for our most vulnerable neighbors; for example, promoting a shared decision-making model; simplifying treatment plans; prescribing, when possible, medications that are dosed daily – instead of multiple times per day; allowing for walk-in appointments; and addressing cultural, linguistic, and educational barriers.
Most chapters highlight informative case examples that bring the text to life. It can be heartbreaking to recognize and witness the inhumane conditions in which PEH live, and these practical tips and suggestions for future policies based on best practices can help prevent burnout and provide hope for those who care for this community.
Part II, “Psychiatric Issues and Treatments,” presents a brief yet comprehensive history on homelessness, beginning with the deep shame that PEH experienced in Colonial times as the result of cultural and religious influences. Sadly, that negative judgment continues to this day.
The authors also explain how deinstitutionalization and transinstitutionalization have shaped the current state of homelessness, including why many PEH receive their care in emergency departments while incarcerated. This section highlights the barriers of care that are created not just by the patient, but also by the clinicians and systems of care – and what’s needed practically to overcome those challenges.
I appreciate the chapter on substance use disorders. It reminds us that the most commonly used substance among PEH is tobacco, which has serious health effects and for which we have treatment; nevertheless, . This section also provides examples of the trauma-informed language to use when addressing difficult and sometimes stigmatizing topics, such as survival sex and trauma history.
The evidence-based discussion continues in Part III with a focus on topics that everyone working with PEH should understand, including food insecurity, the criminal justice system, and sex trafficking. Part IV highlights best practices that should be replicated in every community, including Housing First approaches, medical respite care, and multiple Veterans Administration programs.
Throughout the text, major themes reverberate across the chapters, beginning with empathy. All who work with PEH must understand the conditions and challenges PEH face every day that affect their physical and mental health. The authors offer a stark and pointed reminder that being unhoused amounts to a full-time job just to meet basic needs. In addition, the devastating role of trauma and structural racism in creating and promoting the conditions that lead someone to be unhoused cannot be underestimated.
Fortunately, the primary aim of the book is to highlight solutions, and it’s here that the book shines. While some interventions are well-known, such as the importance of working in multidisciplinary teams, building trust and rapport with our patients, and urging clinicians and institutions to examine their own judgments and biases that might interfere with humane treatment, other suggestions will lead some readers into new territory. The authors, for example, maintain that we need more data and evidence-based research that include PEH. They also make a case for more preventive care and enhanced professional education for all health care workers that centers on trauma-informed care, social determinants of health, and the unique needs of especially vulnerable communities, such as the unhoused LBGTQ+ community and policies that promote best practices, such as Housing First. The book is a stirring read. It offers both inspiration and practical guidance for all who are currently working with or interested in caring for people experiencing homelessness.
Dr. Bird is a psychiatrist with Alameda County Health Care for the Homeless and the TRUST Clinic in Oakland, Calif. She also is a cofounder of StreetHealth, a backpack street medicine team that provides psychiatric and substance use disorder treatment to people experiencing homelessness in downtown Oakland.
Dr. Bird has no disclosures.
As a psychiatrist dedicated to working with people who are experiencing homelessness, I was very impressed with the new book edited by Col. (Ret.) Elspeth Cameron Ritchie, MD, MPH, and Maria D. Llorente, MD, about treating and providing services to this vulnerable population.
The book, “Clinical Management of the Homeless Patient: Social, Psychiatric, and Medical Issues” (Cham, Switzerland: Springer Nature Switzerland, 2021), offers an in-depth review and analysis of the biopsychosocial complexities that affect how medical and behavioral health conditions present in those who are unhoused. Notably, the book recommends with great sensitivity best practices to address these conditions with care, understanding, and love.
This text, invaluable in particular for those of us clinicians who work with people experiencing homelessness (PEH), provides a historical context of homelessness in the United States, an evaluation of the current state, and indispensable guidance for medical and behavioral health practitioners, case managers, housing navigators, and policy makers alike. It also serves as an inspiring source for those who are considering work in the public sector while reminding those of us in the field why we continue to do this challenging and rewarding work.
Tips can provide hope to clinicians
The volume is divided into four clear sections that are easy to navigate depending on your area of expertise and interest. Each chapter consolidates an extensive literature review into an intriguing and thought-provoking analysis. Part I, “The Big Picture – Social and Medical Issues,” focuses on conditions that disproportionately affect those who are unhoused. The authors offer a glimpse into the unique challenges of managing routine health conditions. They also detail the practical knowledge that’s needed to best care for our most vulnerable neighbors; for example, promoting a shared decision-making model; simplifying treatment plans; prescribing, when possible, medications that are dosed daily – instead of multiple times per day; allowing for walk-in appointments; and addressing cultural, linguistic, and educational barriers.
Most chapters highlight informative case examples that bring the text to life. It can be heartbreaking to recognize and witness the inhumane conditions in which PEH live, and these practical tips and suggestions for future policies based on best practices can help prevent burnout and provide hope for those who care for this community.
Part II, “Psychiatric Issues and Treatments,” presents a brief yet comprehensive history on homelessness, beginning with the deep shame that PEH experienced in Colonial times as the result of cultural and religious influences. Sadly, that negative judgment continues to this day.
The authors also explain how deinstitutionalization and transinstitutionalization have shaped the current state of homelessness, including why many PEH receive their care in emergency departments while incarcerated. This section highlights the barriers of care that are created not just by the patient, but also by the clinicians and systems of care – and what’s needed practically to overcome those challenges.
I appreciate the chapter on substance use disorders. It reminds us that the most commonly used substance among PEH is tobacco, which has serious health effects and for which we have treatment; nevertheless, . This section also provides examples of the trauma-informed language to use when addressing difficult and sometimes stigmatizing topics, such as survival sex and trauma history.
The evidence-based discussion continues in Part III with a focus on topics that everyone working with PEH should understand, including food insecurity, the criminal justice system, and sex trafficking. Part IV highlights best practices that should be replicated in every community, including Housing First approaches, medical respite care, and multiple Veterans Administration programs.
Throughout the text, major themes reverberate across the chapters, beginning with empathy. All who work with PEH must understand the conditions and challenges PEH face every day that affect their physical and mental health. The authors offer a stark and pointed reminder that being unhoused amounts to a full-time job just to meet basic needs. In addition, the devastating role of trauma and structural racism in creating and promoting the conditions that lead someone to be unhoused cannot be underestimated.
Fortunately, the primary aim of the book is to highlight solutions, and it’s here that the book shines. While some interventions are well-known, such as the importance of working in multidisciplinary teams, building trust and rapport with our patients, and urging clinicians and institutions to examine their own judgments and biases that might interfere with humane treatment, other suggestions will lead some readers into new territory. The authors, for example, maintain that we need more data and evidence-based research that include PEH. They also make a case for more preventive care and enhanced professional education for all health care workers that centers on trauma-informed care, social determinants of health, and the unique needs of especially vulnerable communities, such as the unhoused LBGTQ+ community and policies that promote best practices, such as Housing First. The book is a stirring read. It offers both inspiration and practical guidance for all who are currently working with or interested in caring for people experiencing homelessness.
Dr. Bird is a psychiatrist with Alameda County Health Care for the Homeless and the TRUST Clinic in Oakland, Calif. She also is a cofounder of StreetHealth, a backpack street medicine team that provides psychiatric and substance use disorder treatment to people experiencing homelessness in downtown Oakland.
Dr. Bird has no disclosures.
As a psychiatrist dedicated to working with people who are experiencing homelessness, I was very impressed with the new book edited by Col. (Ret.) Elspeth Cameron Ritchie, MD, MPH, and Maria D. Llorente, MD, about treating and providing services to this vulnerable population.
The book, “Clinical Management of the Homeless Patient: Social, Psychiatric, and Medical Issues” (Cham, Switzerland: Springer Nature Switzerland, 2021), offers an in-depth review and analysis of the biopsychosocial complexities that affect how medical and behavioral health conditions present in those who are unhoused. Notably, the book recommends with great sensitivity best practices to address these conditions with care, understanding, and love.
This text, invaluable in particular for those of us clinicians who work with people experiencing homelessness (PEH), provides a historical context of homelessness in the United States, an evaluation of the current state, and indispensable guidance for medical and behavioral health practitioners, case managers, housing navigators, and policy makers alike. It also serves as an inspiring source for those who are considering work in the public sector while reminding those of us in the field why we continue to do this challenging and rewarding work.
Tips can provide hope to clinicians
The volume is divided into four clear sections that are easy to navigate depending on your area of expertise and interest. Each chapter consolidates an extensive literature review into an intriguing and thought-provoking analysis. Part I, “The Big Picture – Social and Medical Issues,” focuses on conditions that disproportionately affect those who are unhoused. The authors offer a glimpse into the unique challenges of managing routine health conditions. They also detail the practical knowledge that’s needed to best care for our most vulnerable neighbors; for example, promoting a shared decision-making model; simplifying treatment plans; prescribing, when possible, medications that are dosed daily – instead of multiple times per day; allowing for walk-in appointments; and addressing cultural, linguistic, and educational barriers.
Most chapters highlight informative case examples that bring the text to life. It can be heartbreaking to recognize and witness the inhumane conditions in which PEH live, and these practical tips and suggestions for future policies based on best practices can help prevent burnout and provide hope for those who care for this community.
Part II, “Psychiatric Issues and Treatments,” presents a brief yet comprehensive history on homelessness, beginning with the deep shame that PEH experienced in Colonial times as the result of cultural and religious influences. Sadly, that negative judgment continues to this day.
The authors also explain how deinstitutionalization and transinstitutionalization have shaped the current state of homelessness, including why many PEH receive their care in emergency departments while incarcerated. This section highlights the barriers of care that are created not just by the patient, but also by the clinicians and systems of care – and what’s needed practically to overcome those challenges.
I appreciate the chapter on substance use disorders. It reminds us that the most commonly used substance among PEH is tobacco, which has serious health effects and for which we have treatment; nevertheless, . This section also provides examples of the trauma-informed language to use when addressing difficult and sometimes stigmatizing topics, such as survival sex and trauma history.
The evidence-based discussion continues in Part III with a focus on topics that everyone working with PEH should understand, including food insecurity, the criminal justice system, and sex trafficking. Part IV highlights best practices that should be replicated in every community, including Housing First approaches, medical respite care, and multiple Veterans Administration programs.
Throughout the text, major themes reverberate across the chapters, beginning with empathy. All who work with PEH must understand the conditions and challenges PEH face every day that affect their physical and mental health. The authors offer a stark and pointed reminder that being unhoused amounts to a full-time job just to meet basic needs. In addition, the devastating role of trauma and structural racism in creating and promoting the conditions that lead someone to be unhoused cannot be underestimated.
Fortunately, the primary aim of the book is to highlight solutions, and it’s here that the book shines. While some interventions are well-known, such as the importance of working in multidisciplinary teams, building trust and rapport with our patients, and urging clinicians and institutions to examine their own judgments and biases that might interfere with humane treatment, other suggestions will lead some readers into new territory. The authors, for example, maintain that we need more data and evidence-based research that include PEH. They also make a case for more preventive care and enhanced professional education for all health care workers that centers on trauma-informed care, social determinants of health, and the unique needs of especially vulnerable communities, such as the unhoused LBGTQ+ community and policies that promote best practices, such as Housing First. The book is a stirring read. It offers both inspiration and practical guidance for all who are currently working with or interested in caring for people experiencing homelessness.
Dr. Bird is a psychiatrist with Alameda County Health Care for the Homeless and the TRUST Clinic in Oakland, Calif. She also is a cofounder of StreetHealth, a backpack street medicine team that provides psychiatric and substance use disorder treatment to people experiencing homelessness in downtown Oakland.
Dr. Bird has no disclosures.
Last call? Moderate alcohol’s health benefits look increasingly doubtful
When holiday shoppers recently went to their local liquor stores in search of some liquid spirit, many were instead greeted by the sight of increasingly barren shelves.
Although partly a result of global supply chain issues, this was also yet more evidence of the rising demand for alcohol among adults during these difficult COVID years. It’s a trend that has led to concerns of an echo pandemic of alcohol-related morbidity, which has begun to play out in the form of rising rates of gastrointestinal and liver disease, hospital admissions for alcoholic hepatitis, and alcohol-related incidents of domestic violence.
Those who imbibe alcohol in low to moderate levels may not see themselves reflected in such stories of drinking’s hefty tolls. They’re instead following established health guidance that a little bit of alcohol now and then actually has robust health benefits. Yet the past few of years have seen a notable fraying of this idea, as emerging data calls into question whether alcohol in moderation should really continue to be just what the doctor ordered.
Behind the curve: Alcohol’s diminishing cardioprotective value
Perhaps the most resonant argument for the benefits of light to moderate alcohol consumption – usually defined as between one to two drinks a day – has been its proposed cardioprotective value. In this way, alcohol differs from tobacco, which is unsafe at any level. Alcohol’s proposed cardioprotective effects are often represented as a J-shaped curve, with moderate drinking occupying the sweet spot between teetotaling and heavy/binge drinking when it comes to reduced mortality.
In reality, this association is more likely “a statistical artifact” largely derived from low-quality observational studies, according to Christopher Labos, MD, CM, MSc, an epidemiologist and cardiologist at the Queen Elizabeth Health Complex in Montreal.
“When you look at studies that correct for things like reverse causation, or the fact that some people who drink zero alcohol are former drinkers who used to drink alcohol, then you realize that the protective benefit of alcohol is either minimal or nonexistent and that alcohol does more harm than good to our society,” said Dr. Labos, who detailed the reasons underpinning alcohol’s unearned cardioprotective reputation in a 2020 Medscape commentary.
This statistical limitation was on display in July 2021 when BMC Medicine published results from meta-analyses suggesting that current drinkers need not stop consuming small amounts of alcohol for the secondary prevention of cardiovascular disease (CVD). The study’s own investigators noted that it likely overestimated the reduced risk of CVD by including former heavy drinkers as nondrinkers.
Even if the J-shaped curve exists, its simplicity is deceiving. CVD risk increases alongside alcohol consumption owning to a complicated array of genetic and lifestyle factors. The curve also presents something of a catch-22. If you like alcohol enough to drink it every day, staying at the nadir of the curve where you’d gain the most benefits may prove challenging.
Another factor dimming alcohol’s cardioprotective reputation came via recent data that atrial fibrillation episodes can be triggered by acute alcohol use. A randomized, controlled trial published in the New England Journal of Medicine concluded that abstinence reduced arrhythmia recurrences in regular drinkers with atrial fibrillation.
“If we can replicate that, I think we’ll find that reducing alcohol consumption might be a very effective way to prevent and treat atrial fibrillation,” said Dr. Labos.
However, J-curve proponents will note the publication of study data from the UK Biobank indicating that low levels of alcohol consumption confers the greatest reduction in atrial fibrillation risk.
An overlooked carcinogen no longer
Surveys indicate that less than half of Americans realize alcohol increases cancer risk. That might have changed just a bit this year. In early 2021, an epidemiological analysis estimated that alcohol contributed to 4.8% of cancer cases and 3.2% of cancer deaths in the United States. Then the Lancet Oncology published the results of a high-profile, population-based study on the global burden of cancer as a result of alcoho. Although the main takeaway message was that 4% of new cancer cases worldwide in 2020 were attributable to alcohol, it was also noteworthy that moderate drinking accounted for 103,100 out of 741,300 of these projected annual cases.
“The risk of cancer increases even with low or moderate levels of drinking,” said the study’s lead author Harriet Rumgay, BSc, from the International Agency for Research on Cancer in Lyon, France. “Drinking less means you’ll have a lower risk of cancer than if you drink heavily, but there is no safe limit of alcohol consumption.”
The study linked alcohol consumption with an increased risk of at least seven different cancer types, including cancers of the oral cavity, pharynx, larynx, esophagus, colon, rectum, liver, and breast.
Although in North America men represented about two-thirds of the burden of cancer caused by alcohol, Ms. Rumgay added that “low and moderate levels of drinking [one or two alcoholic drinks per day] contributed relatively more cancer cases among women than among men.”
Yet more negative news for moderate alcohol drinkers arrived in August 2021, when a team of South Korean researchers published data in JAMA Network Open showing that, when it came to the risk of developing gastrointestinal cancers, even binge drinking may be preferable to continuous but moderate consumption.
who in updating its guidelines in 2020 after an 8-year interim offered this succinct piece of advice: “It is best not to drink alcohol.”
Neurotoxic implications
There has similarly been a reconsideration of the effects of moderate alcohol consumption on brain health.
A recent report of multimodal MRI brain and cognitive testing data from over 25,000 participants in the UK Biobank study indicate that alcohol may have no safe dosage . Even moderate consumption reduced gray matter volume and functional connectivity, negative associations that were increased in those with higher blood pressure and body mass index.
Speaking with this news organization in May 2021, an investigator said: “The size of the effect is small, albeit greater than any other modifiable risk factor,” noting that the changes have been linked to decreased memory and dementia.
Louise Mewton, PhD, from the Center for Healthy Brain Aging at the University of New South Wales, Sydney, said that these results provide an interesting comparison with others into the association between alcohol and dementia.
“A recent study of over 1 million dementia cases in France indicated that problematic alcohol use (alcohol use disorders) were one of the strongest risk factors for dementia – even more so than things like high blood pressure and diabetes,” Dr. Mewton said in an interview. In comparison, “the most-recent reviews indicate that 4 drinks/week is associated with the lowest risk for dementia – so we’re talking about very low levels of alcohol use in terms of maintaining brain health.
“Understanding why very small amounts of alcohol appear to be protective in terms of dementia but damaging when we look at brain scans is something that would be really interesting to unpack.”
Dr. Mewton and colleagues recently published data suggesting that there are three periods when the brain might be particularly susceptible to alcohol’s neurotoxic effects: gestation (from conception to birth), later adolescence (15-19 years), and older adulthood (over 65 years). Directing behavioral interventions to patients in these stages may therefore be beneficial.
And there’s no time too soon to promote abstinence among those with alcohol use disorder, as brain damage is shown to still occur even in the immediate period after people cease drinking.
Although in one more argument for the J-shaped curve’s relevance, data from the Massachusetts General Brigham Biobank recently indicated that moderate alcohol use, unlike low and heavy use, lowered both stress-related neurobiological activity and major adverse cardiovascular events.
Getting patients to reconsider alcohol’s ‘benefits’
These new findings mean physicians will find themselves imparting a more nuanced message about the health impacts of moderate alcohol consumption than in prior years. To aid those efforts, Ms. Rumgay advised clinicians to consult a special issue of the journal Nutrients that features review articles of alcohol›s impact on various health outcomes.
Ms. Rumgay also supports broader policy changes.
“There is some evidence that adding cancer warnings to alcohol labels, similar to those used on cigarette packages, might deter people from purchasing alcohol products and increase awareness of the causal link with cancer,” she said. “But the most effective ways of reducing alcohol use in the population are through increasing the price of alcohol through higher taxes, limiting purchasing availability, and reducing marketing of alcohol brands to the public.”
Dr. Mewton recommended various interventions for patients who still find it difficult to curtail their drinking.
“For less severe, problematic use, things like cognitive-behavioral therapy and motivational therapy are very effective in reducing alcohol consumption,” she said in an interview.
For all the discussion about how the COVID-19 pandemic has exacerbated problematic drinking, it has also provided an opportunity for getting patients to reexamine their relationship to alcohol. And as Dr. Labos noted, emerging data on alcohol’s negative effects probably won’t be considered earth-shattering to most patients.
“Deep down, I think most people know that alcohol is not healthy, but it is part of our social culture and so we find ways to justify our own behavior,” he said in an interview.
Dr. Labos suggested that clinicians reframe alcohol in their patients’ minds for what it really is – “an indulgence that we shouldn’t have too much of very often.
“Just like junk food, that doesn’t mean we can’t enjoy small amounts occasionally, but we have to stop presenting that it is good for us, because it isn’t.”
A version of this article first appeared on Medscape.com.
When holiday shoppers recently went to their local liquor stores in search of some liquid spirit, many were instead greeted by the sight of increasingly barren shelves.
Although partly a result of global supply chain issues, this was also yet more evidence of the rising demand for alcohol among adults during these difficult COVID years. It’s a trend that has led to concerns of an echo pandemic of alcohol-related morbidity, which has begun to play out in the form of rising rates of gastrointestinal and liver disease, hospital admissions for alcoholic hepatitis, and alcohol-related incidents of domestic violence.
Those who imbibe alcohol in low to moderate levels may not see themselves reflected in such stories of drinking’s hefty tolls. They’re instead following established health guidance that a little bit of alcohol now and then actually has robust health benefits. Yet the past few of years have seen a notable fraying of this idea, as emerging data calls into question whether alcohol in moderation should really continue to be just what the doctor ordered.
Behind the curve: Alcohol’s diminishing cardioprotective value
Perhaps the most resonant argument for the benefits of light to moderate alcohol consumption – usually defined as between one to two drinks a day – has been its proposed cardioprotective value. In this way, alcohol differs from tobacco, which is unsafe at any level. Alcohol’s proposed cardioprotective effects are often represented as a J-shaped curve, with moderate drinking occupying the sweet spot between teetotaling and heavy/binge drinking when it comes to reduced mortality.
In reality, this association is more likely “a statistical artifact” largely derived from low-quality observational studies, according to Christopher Labos, MD, CM, MSc, an epidemiologist and cardiologist at the Queen Elizabeth Health Complex in Montreal.
“When you look at studies that correct for things like reverse causation, or the fact that some people who drink zero alcohol are former drinkers who used to drink alcohol, then you realize that the protective benefit of alcohol is either minimal or nonexistent and that alcohol does more harm than good to our society,” said Dr. Labos, who detailed the reasons underpinning alcohol’s unearned cardioprotective reputation in a 2020 Medscape commentary.
This statistical limitation was on display in July 2021 when BMC Medicine published results from meta-analyses suggesting that current drinkers need not stop consuming small amounts of alcohol for the secondary prevention of cardiovascular disease (CVD). The study’s own investigators noted that it likely overestimated the reduced risk of CVD by including former heavy drinkers as nondrinkers.
Even if the J-shaped curve exists, its simplicity is deceiving. CVD risk increases alongside alcohol consumption owning to a complicated array of genetic and lifestyle factors. The curve also presents something of a catch-22. If you like alcohol enough to drink it every day, staying at the nadir of the curve where you’d gain the most benefits may prove challenging.
Another factor dimming alcohol’s cardioprotective reputation came via recent data that atrial fibrillation episodes can be triggered by acute alcohol use. A randomized, controlled trial published in the New England Journal of Medicine concluded that abstinence reduced arrhythmia recurrences in regular drinkers with atrial fibrillation.
“If we can replicate that, I think we’ll find that reducing alcohol consumption might be a very effective way to prevent and treat atrial fibrillation,” said Dr. Labos.
However, J-curve proponents will note the publication of study data from the UK Biobank indicating that low levels of alcohol consumption confers the greatest reduction in atrial fibrillation risk.
An overlooked carcinogen no longer
Surveys indicate that less than half of Americans realize alcohol increases cancer risk. That might have changed just a bit this year. In early 2021, an epidemiological analysis estimated that alcohol contributed to 4.8% of cancer cases and 3.2% of cancer deaths in the United States. Then the Lancet Oncology published the results of a high-profile, population-based study on the global burden of cancer as a result of alcoho. Although the main takeaway message was that 4% of new cancer cases worldwide in 2020 were attributable to alcohol, it was also noteworthy that moderate drinking accounted for 103,100 out of 741,300 of these projected annual cases.
“The risk of cancer increases even with low or moderate levels of drinking,” said the study’s lead author Harriet Rumgay, BSc, from the International Agency for Research on Cancer in Lyon, France. “Drinking less means you’ll have a lower risk of cancer than if you drink heavily, but there is no safe limit of alcohol consumption.”
The study linked alcohol consumption with an increased risk of at least seven different cancer types, including cancers of the oral cavity, pharynx, larynx, esophagus, colon, rectum, liver, and breast.
Although in North America men represented about two-thirds of the burden of cancer caused by alcohol, Ms. Rumgay added that “low and moderate levels of drinking [one or two alcoholic drinks per day] contributed relatively more cancer cases among women than among men.”
Yet more negative news for moderate alcohol drinkers arrived in August 2021, when a team of South Korean researchers published data in JAMA Network Open showing that, when it came to the risk of developing gastrointestinal cancers, even binge drinking may be preferable to continuous but moderate consumption.
who in updating its guidelines in 2020 after an 8-year interim offered this succinct piece of advice: “It is best not to drink alcohol.”
Neurotoxic implications
There has similarly been a reconsideration of the effects of moderate alcohol consumption on brain health.
A recent report of multimodal MRI brain and cognitive testing data from over 25,000 participants in the UK Biobank study indicate that alcohol may have no safe dosage . Even moderate consumption reduced gray matter volume and functional connectivity, negative associations that were increased in those with higher blood pressure and body mass index.
Speaking with this news organization in May 2021, an investigator said: “The size of the effect is small, albeit greater than any other modifiable risk factor,” noting that the changes have been linked to decreased memory and dementia.
Louise Mewton, PhD, from the Center for Healthy Brain Aging at the University of New South Wales, Sydney, said that these results provide an interesting comparison with others into the association between alcohol and dementia.
“A recent study of over 1 million dementia cases in France indicated that problematic alcohol use (alcohol use disorders) were one of the strongest risk factors for dementia – even more so than things like high blood pressure and diabetes,” Dr. Mewton said in an interview. In comparison, “the most-recent reviews indicate that 4 drinks/week is associated with the lowest risk for dementia – so we’re talking about very low levels of alcohol use in terms of maintaining brain health.
“Understanding why very small amounts of alcohol appear to be protective in terms of dementia but damaging when we look at brain scans is something that would be really interesting to unpack.”
Dr. Mewton and colleagues recently published data suggesting that there are three periods when the brain might be particularly susceptible to alcohol’s neurotoxic effects: gestation (from conception to birth), later adolescence (15-19 years), and older adulthood (over 65 years). Directing behavioral interventions to patients in these stages may therefore be beneficial.
And there’s no time too soon to promote abstinence among those with alcohol use disorder, as brain damage is shown to still occur even in the immediate period after people cease drinking.
Although in one more argument for the J-shaped curve’s relevance, data from the Massachusetts General Brigham Biobank recently indicated that moderate alcohol use, unlike low and heavy use, lowered both stress-related neurobiological activity and major adverse cardiovascular events.
Getting patients to reconsider alcohol’s ‘benefits’
These new findings mean physicians will find themselves imparting a more nuanced message about the health impacts of moderate alcohol consumption than in prior years. To aid those efforts, Ms. Rumgay advised clinicians to consult a special issue of the journal Nutrients that features review articles of alcohol›s impact on various health outcomes.
Ms. Rumgay also supports broader policy changes.
“There is some evidence that adding cancer warnings to alcohol labels, similar to those used on cigarette packages, might deter people from purchasing alcohol products and increase awareness of the causal link with cancer,” she said. “But the most effective ways of reducing alcohol use in the population are through increasing the price of alcohol through higher taxes, limiting purchasing availability, and reducing marketing of alcohol brands to the public.”
Dr. Mewton recommended various interventions for patients who still find it difficult to curtail their drinking.
“For less severe, problematic use, things like cognitive-behavioral therapy and motivational therapy are very effective in reducing alcohol consumption,” she said in an interview.
For all the discussion about how the COVID-19 pandemic has exacerbated problematic drinking, it has also provided an opportunity for getting patients to reexamine their relationship to alcohol. And as Dr. Labos noted, emerging data on alcohol’s negative effects probably won’t be considered earth-shattering to most patients.
“Deep down, I think most people know that alcohol is not healthy, but it is part of our social culture and so we find ways to justify our own behavior,” he said in an interview.
Dr. Labos suggested that clinicians reframe alcohol in their patients’ minds for what it really is – “an indulgence that we shouldn’t have too much of very often.
“Just like junk food, that doesn’t mean we can’t enjoy small amounts occasionally, but we have to stop presenting that it is good for us, because it isn’t.”
A version of this article first appeared on Medscape.com.
When holiday shoppers recently went to their local liquor stores in search of some liquid spirit, many were instead greeted by the sight of increasingly barren shelves.
Although partly a result of global supply chain issues, this was also yet more evidence of the rising demand for alcohol among adults during these difficult COVID years. It’s a trend that has led to concerns of an echo pandemic of alcohol-related morbidity, which has begun to play out in the form of rising rates of gastrointestinal and liver disease, hospital admissions for alcoholic hepatitis, and alcohol-related incidents of domestic violence.
Those who imbibe alcohol in low to moderate levels may not see themselves reflected in such stories of drinking’s hefty tolls. They’re instead following established health guidance that a little bit of alcohol now and then actually has robust health benefits. Yet the past few of years have seen a notable fraying of this idea, as emerging data calls into question whether alcohol in moderation should really continue to be just what the doctor ordered.
Behind the curve: Alcohol’s diminishing cardioprotective value
Perhaps the most resonant argument for the benefits of light to moderate alcohol consumption – usually defined as between one to two drinks a day – has been its proposed cardioprotective value. In this way, alcohol differs from tobacco, which is unsafe at any level. Alcohol’s proposed cardioprotective effects are often represented as a J-shaped curve, with moderate drinking occupying the sweet spot between teetotaling and heavy/binge drinking when it comes to reduced mortality.
In reality, this association is more likely “a statistical artifact” largely derived from low-quality observational studies, according to Christopher Labos, MD, CM, MSc, an epidemiologist and cardiologist at the Queen Elizabeth Health Complex in Montreal.
“When you look at studies that correct for things like reverse causation, or the fact that some people who drink zero alcohol are former drinkers who used to drink alcohol, then you realize that the protective benefit of alcohol is either minimal or nonexistent and that alcohol does more harm than good to our society,” said Dr. Labos, who detailed the reasons underpinning alcohol’s unearned cardioprotective reputation in a 2020 Medscape commentary.
This statistical limitation was on display in July 2021 when BMC Medicine published results from meta-analyses suggesting that current drinkers need not stop consuming small amounts of alcohol for the secondary prevention of cardiovascular disease (CVD). The study’s own investigators noted that it likely overestimated the reduced risk of CVD by including former heavy drinkers as nondrinkers.
Even if the J-shaped curve exists, its simplicity is deceiving. CVD risk increases alongside alcohol consumption owning to a complicated array of genetic and lifestyle factors. The curve also presents something of a catch-22. If you like alcohol enough to drink it every day, staying at the nadir of the curve where you’d gain the most benefits may prove challenging.
Another factor dimming alcohol’s cardioprotective reputation came via recent data that atrial fibrillation episodes can be triggered by acute alcohol use. A randomized, controlled trial published in the New England Journal of Medicine concluded that abstinence reduced arrhythmia recurrences in regular drinkers with atrial fibrillation.
“If we can replicate that, I think we’ll find that reducing alcohol consumption might be a very effective way to prevent and treat atrial fibrillation,” said Dr. Labos.
However, J-curve proponents will note the publication of study data from the UK Biobank indicating that low levels of alcohol consumption confers the greatest reduction in atrial fibrillation risk.
An overlooked carcinogen no longer
Surveys indicate that less than half of Americans realize alcohol increases cancer risk. That might have changed just a bit this year. In early 2021, an epidemiological analysis estimated that alcohol contributed to 4.8% of cancer cases and 3.2% of cancer deaths in the United States. Then the Lancet Oncology published the results of a high-profile, population-based study on the global burden of cancer as a result of alcoho. Although the main takeaway message was that 4% of new cancer cases worldwide in 2020 were attributable to alcohol, it was also noteworthy that moderate drinking accounted for 103,100 out of 741,300 of these projected annual cases.
“The risk of cancer increases even with low or moderate levels of drinking,” said the study’s lead author Harriet Rumgay, BSc, from the International Agency for Research on Cancer in Lyon, France. “Drinking less means you’ll have a lower risk of cancer than if you drink heavily, but there is no safe limit of alcohol consumption.”
The study linked alcohol consumption with an increased risk of at least seven different cancer types, including cancers of the oral cavity, pharynx, larynx, esophagus, colon, rectum, liver, and breast.
Although in North America men represented about two-thirds of the burden of cancer caused by alcohol, Ms. Rumgay added that “low and moderate levels of drinking [one or two alcoholic drinks per day] contributed relatively more cancer cases among women than among men.”
Yet more negative news for moderate alcohol drinkers arrived in August 2021, when a team of South Korean researchers published data in JAMA Network Open showing that, when it came to the risk of developing gastrointestinal cancers, even binge drinking may be preferable to continuous but moderate consumption.
who in updating its guidelines in 2020 after an 8-year interim offered this succinct piece of advice: “It is best not to drink alcohol.”
Neurotoxic implications
There has similarly been a reconsideration of the effects of moderate alcohol consumption on brain health.
A recent report of multimodal MRI brain and cognitive testing data from over 25,000 participants in the UK Biobank study indicate that alcohol may have no safe dosage . Even moderate consumption reduced gray matter volume and functional connectivity, negative associations that were increased in those with higher blood pressure and body mass index.
Speaking with this news organization in May 2021, an investigator said: “The size of the effect is small, albeit greater than any other modifiable risk factor,” noting that the changes have been linked to decreased memory and dementia.
Louise Mewton, PhD, from the Center for Healthy Brain Aging at the University of New South Wales, Sydney, said that these results provide an interesting comparison with others into the association between alcohol and dementia.
“A recent study of over 1 million dementia cases in France indicated that problematic alcohol use (alcohol use disorders) were one of the strongest risk factors for dementia – even more so than things like high blood pressure and diabetes,” Dr. Mewton said in an interview. In comparison, “the most-recent reviews indicate that 4 drinks/week is associated with the lowest risk for dementia – so we’re talking about very low levels of alcohol use in terms of maintaining brain health.
“Understanding why very small amounts of alcohol appear to be protective in terms of dementia but damaging when we look at brain scans is something that would be really interesting to unpack.”
Dr. Mewton and colleagues recently published data suggesting that there are three periods when the brain might be particularly susceptible to alcohol’s neurotoxic effects: gestation (from conception to birth), later adolescence (15-19 years), and older adulthood (over 65 years). Directing behavioral interventions to patients in these stages may therefore be beneficial.
And there’s no time too soon to promote abstinence among those with alcohol use disorder, as brain damage is shown to still occur even in the immediate period after people cease drinking.
Although in one more argument for the J-shaped curve’s relevance, data from the Massachusetts General Brigham Biobank recently indicated that moderate alcohol use, unlike low and heavy use, lowered both stress-related neurobiological activity and major adverse cardiovascular events.
Getting patients to reconsider alcohol’s ‘benefits’
These new findings mean physicians will find themselves imparting a more nuanced message about the health impacts of moderate alcohol consumption than in prior years. To aid those efforts, Ms. Rumgay advised clinicians to consult a special issue of the journal Nutrients that features review articles of alcohol›s impact on various health outcomes.
Ms. Rumgay also supports broader policy changes.
“There is some evidence that adding cancer warnings to alcohol labels, similar to those used on cigarette packages, might deter people from purchasing alcohol products and increase awareness of the causal link with cancer,” she said. “But the most effective ways of reducing alcohol use in the population are through increasing the price of alcohol through higher taxes, limiting purchasing availability, and reducing marketing of alcohol brands to the public.”
Dr. Mewton recommended various interventions for patients who still find it difficult to curtail their drinking.
“For less severe, problematic use, things like cognitive-behavioral therapy and motivational therapy are very effective in reducing alcohol consumption,” she said in an interview.
For all the discussion about how the COVID-19 pandemic has exacerbated problematic drinking, it has also provided an opportunity for getting patients to reexamine their relationship to alcohol. And as Dr. Labos noted, emerging data on alcohol’s negative effects probably won’t be considered earth-shattering to most patients.
“Deep down, I think most people know that alcohol is not healthy, but it is part of our social culture and so we find ways to justify our own behavior,” he said in an interview.
Dr. Labos suggested that clinicians reframe alcohol in their patients’ minds for what it really is – “an indulgence that we shouldn’t have too much of very often.
“Just like junk food, that doesn’t mean we can’t enjoy small amounts occasionally, but we have to stop presenting that it is good for us, because it isn’t.”
A version of this article first appeared on Medscape.com.
Transcranial magnetic stimulation shows promise for alcohol addiction
Deep, repetitive transcranial magnetic stimulation (TMS) is safe and effective in decreasing symptoms of alcohol addiction and brain reactivity, new research suggests.
In a randomized, double-blind, sham-controlled trial, participants who received TMS targeting the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC) for 3 weeks showed significantly reduced heavy drinking days, compared with a group who received a sham treatment.
and showed less functional connectivity on MRI in areas of the brain that can trigger craving and relapse.
Clinicians should “keep their eyes open” in the wake of this phase 2 trial, cocorresponding author Markus Heilig, MD, PhD, professor of psychiatry and director at the Center for Social and Affective Neuroscience, department of biomedical and clinical sciences, Linköping (Sweden) University, said in an interview.
“If and when this replicates in the equivalent of a phase 3 study, we will actually have a completely novel treatment available for this difficult to treat and very impactful disease,” Dr. Heilig said.
The findings were published online Dec. 5, 2021, in Biological Psychiatry.
Proof of concept
In the proof-of-concept trial, researchers enrolled and randomly assigned 51 treatment-seeking adults with moderate to severe alcohol dependence to receive active or sham treatment. Before treatment, participants completed “craving induction,” which included holding and smelling but not consuming an alcoholic beverage.
Dr. Heilig noted that, before stimulating the brain, “you want to make it as malleable as possible;” and brain networks tend to be more malleable when they are active.
During the 3-week treatment phase, active or sham stimulations were delivered in five 30-minute sessions per week. During the sessions, all participants wore a helmet with a deep TMS coil produced by BrainsWay.
In the active-stimulation group, each session included 100 trains of 30 pulses at 10 Hz (3 seconds) with 15-second intervals, for a total of 3,000 pulses. The sham stimulation produced the same acoustic artifact and generated skin sensations mimicking those of the active stimulation, but it did not involve a magnetic field.
Participants, operators, and raters were blinded to the type of coil used.
Five participants relapsed during the first 3 weeks of treatment and were excluded from the analysis. The mean age of those completing treatment (n = 23 in each group) was 43 years, and two-thirds were men.
The gender makeup of the study reflects “what a real treatment-seeking group looks like,” Dr. Heilig said.
During the 12-week follow-up phase, five additional participants dropped out.
‘Pretty robust’ treatment effect
The primary outcome was reduction in percentage of heavy drinking days (pHDD), defined as consuming at least five drinks of 12 grams of alcohol per day for men and at least four such drinks for women.
Initially, pHDD dropped in both groups, which is something generally seen in alcohol studies, said Dr. Heilig. “The moment people decide to participate in a study, everybody drops their consumption, [which] biases a study like this against picking up an effect.”
However, heavy drinking days increased during follow-up in the sham group but remained low in the active-treatment group. The mean pHDD was significantly lower in the active versus sham groups (2.9% vs. 10.6%, P = .037).
“So despite the bias, a treatment effect does emerge,” and was “pretty robust,” Dr. Heilig said.
This was supported by a significant group difference in weekly alcohol consumption and a trend-level difference in percentage of alcohol-positive urine samples.
A secondary outcome was change in alcohol craving, assessed with the Penn Alcohol Craving Scale; PACS scores decreased in both groups during treatment but was more steeply reduced in the active group. During follow-up, craving levels increased to a lesser extent in the active group.
MRI scans showed reduced connectivity from the mPFC to the subgenual ACC, an area involved in negative emotions that can trigger craving and relapse, said Dr. Heilig. There was also reduced connectivity between the dorsal ACC and caudate, a circuit involved in the reward system.
In treatment trials, researchers look for a biomarker of target engagement. However, “to date, there has been no study using TMS that has actually demonstrated the intervention had a measurable effect on brain activity. So to me, this is a biomarker; it did something to the brain,” Dr. Heilig said.
Delving deeper into the brain
The results underline the importance of stimulating deeper parts of the brain, cocorresponding author Abraham Zangen, PhD, head of the Brain Stimulation and Behavior Lab and chair of the psychobiology brain program, Ben Gurion University, Be’er Sheva, Israel, said in an interview.
Early TMS studies, which involved superficial brain stimulation, reduced cigarette consumption but was not associated with quitting, Dr. Zangen said. “It was only when we targeted deeper parts of the prefrontal cortex that we were able to induce smoking cessation.”
It was this research that led to approval by the Food and Drug Administration of deep TMS for smoking cessation.
This same deep-brain approach was used in the current study. “So the emphasis on the technology that allows penetration into deeper parts of the brain and targeting the relevant pathological circuitry of addiction is a key complement of the success of this study,” Dr. Zangen said.
Results also showed no serious adverse events. Only a few participants reported transient headaches, which all resolved spontaneously; and frequency did not differ between groups.
Dr. Heilig now hopes to carry out a multisite phase 3 study of the intervention and would suggest it involve 4 (instead of 3) weeks of initial treatment and then a weekly booster session. “There are biological reasons to believe that might be more efficient, although we don’t have the data,” he said.
On the other hand, he noted, the longer the trial, the more difficult it might be to recruit patients.
Clinically significant?
Commenting on the study, Derek Blevins, MD, assistant professor of clinical psychiatry at Columbia University and research psychiatrist, division on substance use disorders, New York State Psychiatric Institute, both in New York, called the research “really exciting.”
To date, most TMS studies have been relatively small and looked at a target such as craving. Although these studies did show some effect, the clinical significance of that effect was unclear, said Dr. Blevins, who was not involved with the current research.
“I think this new study actually demonstrated a clinically significant effect of a noninvasive treatment for a disease that’s very difficult to treat,” he said.
A potential limitation of the study, however, was it required abstinence, Dr. Blevins noted. It would be “really helpful” to understand how TMS might aid individuals such as those who relapsed during the study, “because they’re the more treatment-refractory individuals we see in clinical practice.”
If a multicenter trial is launched, Dr. Blevins said he would also like it to include an ethnically and racially diverse population.
The study was supported by grants from the European Union’s Horizon 2020 research and innovation program and the Swedish Research Council. Dr. Heilig reported having received consulting fees, research support, or other compensation from Indivior, Camurus, BrainsWay, Aelis Farma, and Janssen Pharmaceuticals. Dr. Zangen is an inventor of deep TMS coils and has financial interest in BrainsWay, which produces and markets these coils. Dr. Blevins reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Deep, repetitive transcranial magnetic stimulation (TMS) is safe and effective in decreasing symptoms of alcohol addiction and brain reactivity, new research suggests.
In a randomized, double-blind, sham-controlled trial, participants who received TMS targeting the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC) for 3 weeks showed significantly reduced heavy drinking days, compared with a group who received a sham treatment.
and showed less functional connectivity on MRI in areas of the brain that can trigger craving and relapse.
Clinicians should “keep their eyes open” in the wake of this phase 2 trial, cocorresponding author Markus Heilig, MD, PhD, professor of psychiatry and director at the Center for Social and Affective Neuroscience, department of biomedical and clinical sciences, Linköping (Sweden) University, said in an interview.
“If and when this replicates in the equivalent of a phase 3 study, we will actually have a completely novel treatment available for this difficult to treat and very impactful disease,” Dr. Heilig said.
The findings were published online Dec. 5, 2021, in Biological Psychiatry.
Proof of concept
In the proof-of-concept trial, researchers enrolled and randomly assigned 51 treatment-seeking adults with moderate to severe alcohol dependence to receive active or sham treatment. Before treatment, participants completed “craving induction,” which included holding and smelling but not consuming an alcoholic beverage.
Dr. Heilig noted that, before stimulating the brain, “you want to make it as malleable as possible;” and brain networks tend to be more malleable when they are active.
During the 3-week treatment phase, active or sham stimulations were delivered in five 30-minute sessions per week. During the sessions, all participants wore a helmet with a deep TMS coil produced by BrainsWay.
In the active-stimulation group, each session included 100 trains of 30 pulses at 10 Hz (3 seconds) with 15-second intervals, for a total of 3,000 pulses. The sham stimulation produced the same acoustic artifact and generated skin sensations mimicking those of the active stimulation, but it did not involve a magnetic field.
Participants, operators, and raters were blinded to the type of coil used.
Five participants relapsed during the first 3 weeks of treatment and were excluded from the analysis. The mean age of those completing treatment (n = 23 in each group) was 43 years, and two-thirds were men.
The gender makeup of the study reflects “what a real treatment-seeking group looks like,” Dr. Heilig said.
During the 12-week follow-up phase, five additional participants dropped out.
‘Pretty robust’ treatment effect
The primary outcome was reduction in percentage of heavy drinking days (pHDD), defined as consuming at least five drinks of 12 grams of alcohol per day for men and at least four such drinks for women.
Initially, pHDD dropped in both groups, which is something generally seen in alcohol studies, said Dr. Heilig. “The moment people decide to participate in a study, everybody drops their consumption, [which] biases a study like this against picking up an effect.”
However, heavy drinking days increased during follow-up in the sham group but remained low in the active-treatment group. The mean pHDD was significantly lower in the active versus sham groups (2.9% vs. 10.6%, P = .037).
“So despite the bias, a treatment effect does emerge,” and was “pretty robust,” Dr. Heilig said.
This was supported by a significant group difference in weekly alcohol consumption and a trend-level difference in percentage of alcohol-positive urine samples.
A secondary outcome was change in alcohol craving, assessed with the Penn Alcohol Craving Scale; PACS scores decreased in both groups during treatment but was more steeply reduced in the active group. During follow-up, craving levels increased to a lesser extent in the active group.
MRI scans showed reduced connectivity from the mPFC to the subgenual ACC, an area involved in negative emotions that can trigger craving and relapse, said Dr. Heilig. There was also reduced connectivity between the dorsal ACC and caudate, a circuit involved in the reward system.
In treatment trials, researchers look for a biomarker of target engagement. However, “to date, there has been no study using TMS that has actually demonstrated the intervention had a measurable effect on brain activity. So to me, this is a biomarker; it did something to the brain,” Dr. Heilig said.
Delving deeper into the brain
The results underline the importance of stimulating deeper parts of the brain, cocorresponding author Abraham Zangen, PhD, head of the Brain Stimulation and Behavior Lab and chair of the psychobiology brain program, Ben Gurion University, Be’er Sheva, Israel, said in an interview.
Early TMS studies, which involved superficial brain stimulation, reduced cigarette consumption but was not associated with quitting, Dr. Zangen said. “It was only when we targeted deeper parts of the prefrontal cortex that we were able to induce smoking cessation.”
It was this research that led to approval by the Food and Drug Administration of deep TMS for smoking cessation.
This same deep-brain approach was used in the current study. “So the emphasis on the technology that allows penetration into deeper parts of the brain and targeting the relevant pathological circuitry of addiction is a key complement of the success of this study,” Dr. Zangen said.
Results also showed no serious adverse events. Only a few participants reported transient headaches, which all resolved spontaneously; and frequency did not differ between groups.
Dr. Heilig now hopes to carry out a multisite phase 3 study of the intervention and would suggest it involve 4 (instead of 3) weeks of initial treatment and then a weekly booster session. “There are biological reasons to believe that might be more efficient, although we don’t have the data,” he said.
On the other hand, he noted, the longer the trial, the more difficult it might be to recruit patients.
Clinically significant?
Commenting on the study, Derek Blevins, MD, assistant professor of clinical psychiatry at Columbia University and research psychiatrist, division on substance use disorders, New York State Psychiatric Institute, both in New York, called the research “really exciting.”
To date, most TMS studies have been relatively small and looked at a target such as craving. Although these studies did show some effect, the clinical significance of that effect was unclear, said Dr. Blevins, who was not involved with the current research.
“I think this new study actually demonstrated a clinically significant effect of a noninvasive treatment for a disease that’s very difficult to treat,” he said.
A potential limitation of the study, however, was it required abstinence, Dr. Blevins noted. It would be “really helpful” to understand how TMS might aid individuals such as those who relapsed during the study, “because they’re the more treatment-refractory individuals we see in clinical practice.”
If a multicenter trial is launched, Dr. Blevins said he would also like it to include an ethnically and racially diverse population.
The study was supported by grants from the European Union’s Horizon 2020 research and innovation program and the Swedish Research Council. Dr. Heilig reported having received consulting fees, research support, or other compensation from Indivior, Camurus, BrainsWay, Aelis Farma, and Janssen Pharmaceuticals. Dr. Zangen is an inventor of deep TMS coils and has financial interest in BrainsWay, which produces and markets these coils. Dr. Blevins reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Deep, repetitive transcranial magnetic stimulation (TMS) is safe and effective in decreasing symptoms of alcohol addiction and brain reactivity, new research suggests.
In a randomized, double-blind, sham-controlled trial, participants who received TMS targeting the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC) for 3 weeks showed significantly reduced heavy drinking days, compared with a group who received a sham treatment.
and showed less functional connectivity on MRI in areas of the brain that can trigger craving and relapse.
Clinicians should “keep their eyes open” in the wake of this phase 2 trial, cocorresponding author Markus Heilig, MD, PhD, professor of psychiatry and director at the Center for Social and Affective Neuroscience, department of biomedical and clinical sciences, Linköping (Sweden) University, said in an interview.
“If and when this replicates in the equivalent of a phase 3 study, we will actually have a completely novel treatment available for this difficult to treat and very impactful disease,” Dr. Heilig said.
The findings were published online Dec. 5, 2021, in Biological Psychiatry.
Proof of concept
In the proof-of-concept trial, researchers enrolled and randomly assigned 51 treatment-seeking adults with moderate to severe alcohol dependence to receive active or sham treatment. Before treatment, participants completed “craving induction,” which included holding and smelling but not consuming an alcoholic beverage.
Dr. Heilig noted that, before stimulating the brain, “you want to make it as malleable as possible;” and brain networks tend to be more malleable when they are active.
During the 3-week treatment phase, active or sham stimulations were delivered in five 30-minute sessions per week. During the sessions, all participants wore a helmet with a deep TMS coil produced by BrainsWay.
In the active-stimulation group, each session included 100 trains of 30 pulses at 10 Hz (3 seconds) with 15-second intervals, for a total of 3,000 pulses. The sham stimulation produced the same acoustic artifact and generated skin sensations mimicking those of the active stimulation, but it did not involve a magnetic field.
Participants, operators, and raters were blinded to the type of coil used.
Five participants relapsed during the first 3 weeks of treatment and were excluded from the analysis. The mean age of those completing treatment (n = 23 in each group) was 43 years, and two-thirds were men.
The gender makeup of the study reflects “what a real treatment-seeking group looks like,” Dr. Heilig said.
During the 12-week follow-up phase, five additional participants dropped out.
‘Pretty robust’ treatment effect
The primary outcome was reduction in percentage of heavy drinking days (pHDD), defined as consuming at least five drinks of 12 grams of alcohol per day for men and at least four such drinks for women.
Initially, pHDD dropped in both groups, which is something generally seen in alcohol studies, said Dr. Heilig. “The moment people decide to participate in a study, everybody drops their consumption, [which] biases a study like this against picking up an effect.”
However, heavy drinking days increased during follow-up in the sham group but remained low in the active-treatment group. The mean pHDD was significantly lower in the active versus sham groups (2.9% vs. 10.6%, P = .037).
“So despite the bias, a treatment effect does emerge,” and was “pretty robust,” Dr. Heilig said.
This was supported by a significant group difference in weekly alcohol consumption and a trend-level difference in percentage of alcohol-positive urine samples.
A secondary outcome was change in alcohol craving, assessed with the Penn Alcohol Craving Scale; PACS scores decreased in both groups during treatment but was more steeply reduced in the active group. During follow-up, craving levels increased to a lesser extent in the active group.
MRI scans showed reduced connectivity from the mPFC to the subgenual ACC, an area involved in negative emotions that can trigger craving and relapse, said Dr. Heilig. There was also reduced connectivity between the dorsal ACC and caudate, a circuit involved in the reward system.
In treatment trials, researchers look for a biomarker of target engagement. However, “to date, there has been no study using TMS that has actually demonstrated the intervention had a measurable effect on brain activity. So to me, this is a biomarker; it did something to the brain,” Dr. Heilig said.
Delving deeper into the brain
The results underline the importance of stimulating deeper parts of the brain, cocorresponding author Abraham Zangen, PhD, head of the Brain Stimulation and Behavior Lab and chair of the psychobiology brain program, Ben Gurion University, Be’er Sheva, Israel, said in an interview.
Early TMS studies, which involved superficial brain stimulation, reduced cigarette consumption but was not associated with quitting, Dr. Zangen said. “It was only when we targeted deeper parts of the prefrontal cortex that we were able to induce smoking cessation.”
It was this research that led to approval by the Food and Drug Administration of deep TMS for smoking cessation.
This same deep-brain approach was used in the current study. “So the emphasis on the technology that allows penetration into deeper parts of the brain and targeting the relevant pathological circuitry of addiction is a key complement of the success of this study,” Dr. Zangen said.
Results also showed no serious adverse events. Only a few participants reported transient headaches, which all resolved spontaneously; and frequency did not differ between groups.
Dr. Heilig now hopes to carry out a multisite phase 3 study of the intervention and would suggest it involve 4 (instead of 3) weeks of initial treatment and then a weekly booster session. “There are biological reasons to believe that might be more efficient, although we don’t have the data,” he said.
On the other hand, he noted, the longer the trial, the more difficult it might be to recruit patients.
Clinically significant?
Commenting on the study, Derek Blevins, MD, assistant professor of clinical psychiatry at Columbia University and research psychiatrist, division on substance use disorders, New York State Psychiatric Institute, both in New York, called the research “really exciting.”
To date, most TMS studies have been relatively small and looked at a target such as craving. Although these studies did show some effect, the clinical significance of that effect was unclear, said Dr. Blevins, who was not involved with the current research.
“I think this new study actually demonstrated a clinically significant effect of a noninvasive treatment for a disease that’s very difficult to treat,” he said.
A potential limitation of the study, however, was it required abstinence, Dr. Blevins noted. It would be “really helpful” to understand how TMS might aid individuals such as those who relapsed during the study, “because they’re the more treatment-refractory individuals we see in clinical practice.”
If a multicenter trial is launched, Dr. Blevins said he would also like it to include an ethnically and racially diverse population.
The study was supported by grants from the European Union’s Horizon 2020 research and innovation program and the Swedish Research Council. Dr. Heilig reported having received consulting fees, research support, or other compensation from Indivior, Camurus, BrainsWay, Aelis Farma, and Janssen Pharmaceuticals. Dr. Zangen is an inventor of deep TMS coils and has financial interest in BrainsWay, which produces and markets these coils. Dr. Blevins reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM BIOLOGICAL PSYCHIATRY
Many clinicians feel ill-prepared for drug overdose deaths
new research suggests.
However, results from a survey study also showed that colleagues were an important source of support in the wake of this type of event.
“A patient overdose death can change clinical decision-making for providers experiencing high levels of stress related to the overdose death,” noted the investigators, led by Amy Yule, MD, director of adolescent addiction psychiatry, Boston Medical Center, and assistant professor of psychiatry at Boston University Medical Center.
The findings were presented by Dr. Yule at the annual meeting of the American Academy of Addiction Psychiatry.
All-time high
As reported by this news organization, there has recently been a record number of drug overdose deaths. And these deaths affect families, communities, and often providers, Dr. Yule told meeting attendees.
Previous research has looked at the impact of drug overdose deaths and the opioid epidemic on first responders and community health workers in the field of overdose prevention.
“But there’s less in the literature to my knowledge that describes the experience of providers and clinicians who are working in more formalized medical settings,” said Dr. Yule.
In December 2020, researchers sent an email to members of the Providers Clinical Support System (PCSS) inviting them to complete an anonymous survey. The PCSS program was created in response to the opioid overdose epidemic to train primary care clinicians in the prevention and treatment of opioid use disorders.
A total of 12,204 members received the email, 1,064 opened the survey link, and 523 completed the survey.
Participants were mostly White and female, with an average age of 52 years. Respondents had been practicing for an average of about 16 years.
The largest responder group was physicians (47%), followed by counselors (29%), nurse practitioners (17%), and nurses (7%).
Among physician respondents, 41% reported having received additional formal training in addiction.
Only 24% of the respondents indicated they received training in “postvention,” which refers to interventions after a suicide to support the bereaved. Such interventions “could be helpful in potentially preparing them for a drug overdose death in their practice,” said Dr. Yule.
Categories of preparedness
The survey inquired about three categories of preparedness: coping with a drug overdose death, providing support to a colleague, and talking with families who have lost a member to a drug overdose.
Overall, 59% said they felt somewhat or fairly well prepared for the first two categories and 55% for the third category.
“I think it’s notable that there is a higher percentage of people who felt not at all prepared to talk with family members (20.5%), compared to those who felt not at all prepared to cope with a drug overdose death (13.8%) or prepared to support a colleague (12%),” Dr. Yule said.
More than half of respondents (55%) indicated a drug overdose death had occurred in their own practice.
The survey also looked at frequency of consultations with colleagues, critical incident debriefing sessions, and interactions with a patient’s family.
Almost half (48%) of the sample said they consulted with a colleague after most patient overdose deaths. Only 24% said they had a critical incidence debriefing session after most of these events, and 20% said they interacted with the patient’s family.
Asked what resources they found helpful for coping with a recent patient drug overdose death, respondents flagged their colleagues and meetings with families.
The survey also examined provider trauma after a patient drug overdose death, using the Impact of Event Scale–R. “If the score is above a certain cutoff level, there is potential concern” for PTSD, Dr. Yule said.
Among the 141 respondents who had a patient drug overdose death in their practice during the previous year, 121 completed this trauma scale. Of these, 18% had “a very elevated” score, Dr. Yule reported.
Sources of support
Commenting on the survey study, Larissa Mooney, MD, associate professor and director of the addiction psychiatry division in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said it is not surprising that many providers do not feel adequately prepared to cope with an overdose death, or how to support a colleague after such an event.
“This is not routinely covered in training, and patient overdose may occur without warning signs,” said Dr. Mooney, who was not involved with the research.
However, these new findings suggest a range of potential sources of support for providers after a patient overdose death that may be helpful, “including colleagues, friends, therapy, supervision, and meeting with the patient’s family,” she said.
The study received funding from the PCSS. Dr. Yule disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
However, results from a survey study also showed that colleagues were an important source of support in the wake of this type of event.
“A patient overdose death can change clinical decision-making for providers experiencing high levels of stress related to the overdose death,” noted the investigators, led by Amy Yule, MD, director of adolescent addiction psychiatry, Boston Medical Center, and assistant professor of psychiatry at Boston University Medical Center.
The findings were presented by Dr. Yule at the annual meeting of the American Academy of Addiction Psychiatry.
All-time high
As reported by this news organization, there has recently been a record number of drug overdose deaths. And these deaths affect families, communities, and often providers, Dr. Yule told meeting attendees.
Previous research has looked at the impact of drug overdose deaths and the opioid epidemic on first responders and community health workers in the field of overdose prevention.
“But there’s less in the literature to my knowledge that describes the experience of providers and clinicians who are working in more formalized medical settings,” said Dr. Yule.
In December 2020, researchers sent an email to members of the Providers Clinical Support System (PCSS) inviting them to complete an anonymous survey. The PCSS program was created in response to the opioid overdose epidemic to train primary care clinicians in the prevention and treatment of opioid use disorders.
A total of 12,204 members received the email, 1,064 opened the survey link, and 523 completed the survey.
Participants were mostly White and female, with an average age of 52 years. Respondents had been practicing for an average of about 16 years.
The largest responder group was physicians (47%), followed by counselors (29%), nurse practitioners (17%), and nurses (7%).
Among physician respondents, 41% reported having received additional formal training in addiction.
Only 24% of the respondents indicated they received training in “postvention,” which refers to interventions after a suicide to support the bereaved. Such interventions “could be helpful in potentially preparing them for a drug overdose death in their practice,” said Dr. Yule.
Categories of preparedness
The survey inquired about three categories of preparedness: coping with a drug overdose death, providing support to a colleague, and talking with families who have lost a member to a drug overdose.
Overall, 59% said they felt somewhat or fairly well prepared for the first two categories and 55% for the third category.
“I think it’s notable that there is a higher percentage of people who felt not at all prepared to talk with family members (20.5%), compared to those who felt not at all prepared to cope with a drug overdose death (13.8%) or prepared to support a colleague (12%),” Dr. Yule said.
More than half of respondents (55%) indicated a drug overdose death had occurred in their own practice.
The survey also looked at frequency of consultations with colleagues, critical incident debriefing sessions, and interactions with a patient’s family.
Almost half (48%) of the sample said they consulted with a colleague after most patient overdose deaths. Only 24% said they had a critical incidence debriefing session after most of these events, and 20% said they interacted with the patient’s family.
Asked what resources they found helpful for coping with a recent patient drug overdose death, respondents flagged their colleagues and meetings with families.
The survey also examined provider trauma after a patient drug overdose death, using the Impact of Event Scale–R. “If the score is above a certain cutoff level, there is potential concern” for PTSD, Dr. Yule said.
Among the 141 respondents who had a patient drug overdose death in their practice during the previous year, 121 completed this trauma scale. Of these, 18% had “a very elevated” score, Dr. Yule reported.
Sources of support
Commenting on the survey study, Larissa Mooney, MD, associate professor and director of the addiction psychiatry division in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said it is not surprising that many providers do not feel adequately prepared to cope with an overdose death, or how to support a colleague after such an event.
“This is not routinely covered in training, and patient overdose may occur without warning signs,” said Dr. Mooney, who was not involved with the research.
However, these new findings suggest a range of potential sources of support for providers after a patient overdose death that may be helpful, “including colleagues, friends, therapy, supervision, and meeting with the patient’s family,” she said.
The study received funding from the PCSS. Dr. Yule disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
However, results from a survey study also showed that colleagues were an important source of support in the wake of this type of event.
“A patient overdose death can change clinical decision-making for providers experiencing high levels of stress related to the overdose death,” noted the investigators, led by Amy Yule, MD, director of adolescent addiction psychiatry, Boston Medical Center, and assistant professor of psychiatry at Boston University Medical Center.
The findings were presented by Dr. Yule at the annual meeting of the American Academy of Addiction Psychiatry.
All-time high
As reported by this news organization, there has recently been a record number of drug overdose deaths. And these deaths affect families, communities, and often providers, Dr. Yule told meeting attendees.
Previous research has looked at the impact of drug overdose deaths and the opioid epidemic on first responders and community health workers in the field of overdose prevention.
“But there’s less in the literature to my knowledge that describes the experience of providers and clinicians who are working in more formalized medical settings,” said Dr. Yule.
In December 2020, researchers sent an email to members of the Providers Clinical Support System (PCSS) inviting them to complete an anonymous survey. The PCSS program was created in response to the opioid overdose epidemic to train primary care clinicians in the prevention and treatment of opioid use disorders.
A total of 12,204 members received the email, 1,064 opened the survey link, and 523 completed the survey.
Participants were mostly White and female, with an average age of 52 years. Respondents had been practicing for an average of about 16 years.
The largest responder group was physicians (47%), followed by counselors (29%), nurse practitioners (17%), and nurses (7%).
Among physician respondents, 41% reported having received additional formal training in addiction.
Only 24% of the respondents indicated they received training in “postvention,” which refers to interventions after a suicide to support the bereaved. Such interventions “could be helpful in potentially preparing them for a drug overdose death in their practice,” said Dr. Yule.
Categories of preparedness
The survey inquired about three categories of preparedness: coping with a drug overdose death, providing support to a colleague, and talking with families who have lost a member to a drug overdose.
Overall, 59% said they felt somewhat or fairly well prepared for the first two categories and 55% for the third category.
“I think it’s notable that there is a higher percentage of people who felt not at all prepared to talk with family members (20.5%), compared to those who felt not at all prepared to cope with a drug overdose death (13.8%) or prepared to support a colleague (12%),” Dr. Yule said.
More than half of respondents (55%) indicated a drug overdose death had occurred in their own practice.
The survey also looked at frequency of consultations with colleagues, critical incident debriefing sessions, and interactions with a patient’s family.
Almost half (48%) of the sample said they consulted with a colleague after most patient overdose deaths. Only 24% said they had a critical incidence debriefing session after most of these events, and 20% said they interacted with the patient’s family.
Asked what resources they found helpful for coping with a recent patient drug overdose death, respondents flagged their colleagues and meetings with families.
The survey also examined provider trauma after a patient drug overdose death, using the Impact of Event Scale–R. “If the score is above a certain cutoff level, there is potential concern” for PTSD, Dr. Yule said.
Among the 141 respondents who had a patient drug overdose death in their practice during the previous year, 121 completed this trauma scale. Of these, 18% had “a very elevated” score, Dr. Yule reported.
Sources of support
Commenting on the survey study, Larissa Mooney, MD, associate professor and director of the addiction psychiatry division in the department of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said it is not surprising that many providers do not feel adequately prepared to cope with an overdose death, or how to support a colleague after such an event.
“This is not routinely covered in training, and patient overdose may occur without warning signs,” said Dr. Mooney, who was not involved with the research.
However, these new findings suggest a range of potential sources of support for providers after a patient overdose death that may be helpful, “including colleagues, friends, therapy, supervision, and meeting with the patient’s family,” she said.
The study received funding from the PCSS. Dr. Yule disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM AAAP 2021