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Alternative antirejection regimen is efficacious in pediatric heart transplant
Study challenges everolimus boxed warning
according to the first phase 3 trial to compare antirejection strategies in the pediatric setting.
Even though MMF and tacrolimus have never been evaluated for pediatric cardiac transplant in a controlled trial, this combination is widely considered a standard based on adult data, said Christopher Almond, MD, a professor of pediatric cardiology at Stanford (Calif.) Medicine.
Everolimus has not been widely used in an antirejection regimen in children following heart transplant in part because of a boxed warning. The warning was added to labeling when this agent was associated with increased infection and increased mortality in adults if given within 3 months of transplant.
In this non-inferiority trial, called TEAMMATE, patients were randomized to the MMF-based or everolimus-based regimen 6 months after transplant.
Everolimus- vs. MMF-based antirejection
The study enrolled 210 children and adolescents 21 years of age or younger. The control arm treatment consisted of MMF (660 mg/m2 every 12 hours) plus standard dose of tacrolimus (initially 7-10 ng/mL followed at 6 months by 5-8 ng/mL).
In the experimental arm, patients received everolimus (3-8 ng/mL) plus a low dose of tacrolimus (initially 3-5 ng/mL followed at 6 months by 2.5-4.5 ng/mL).
The primary endpoint was score on the major adverse transplant event (MATE-6) tool. Based on gradations of severity, this assigns values for cardiac allograft vasculopathy (CAV), chronic kidney disease (CKD), acute cellular rejection (ACR), antibody-mediated rejection, infection, and posttransplant lymphoproliferative disorder (PTLD).
Thirty months after randomization, the MATE-6 scores were 1.96 in the everolimus group and 2.18 in the MMF group, which conferred the everolimus-based regimen with a numerical but not a significant advantage over the MMF-based regimen. For the goal of noninferiority, the everolimus regimen “met the prespecified safety criterion for success,” Dr. Almond said.
Numerical advantage for everolimus on efficacy
The primary efficacy endpoint was the MATE-3 score, which is limited to CAV, CKD, and ACR. Again, the mean score on this metric (0.93 vs. 1.25) was lower on the everolimus-based regimen but not significantly different.
Looking at specific events in the MATE-6 score, the everolimus-based regimen was associated with lower numerical rates of CAV and CKD, but a higher rate of PTLD, Dr. Almond reported.
On the MATE-3 efficacy analysis, the everolimus-based regimen was again associated with lower numerical rates of CAV and CKD but higher rates of ACR.
In terms of adverse events, including those involving the gastrointestinal tract, blood cells, proteinuria, and interstitial lung disease, most did not differ markedly even if many were numerically more common in the MMF-based arm. The exception was aphthous stomatitis, which was more common on everolimus (32% vs. 7%; P < .001). There were more discontinuations for an adverse event in the MMF arm (21% vs. 12%; P < .001).
Other differences included a lower proportion of patients in the everolimus arm with anti-HLA antibodies (17% vs. 30%; P < .05). Total cholesterol levels at the end of the study were lower but not significantly different in the MMF group, while the higher median glomerular filtration rate was higher on everolimus, and this did reach statistical significance (P < .05).
Infection rates overall were similar, but cytomegalovirus (CMV) infection was more common on the MMF-based regimen. The 30% lower rate of CMV infection in the everolimus proved to be potentially clinically meaningful when it was considered in the context of MATE-3. When these two endpoints were combined (MATE-3 and CMV infection as a prespecified secondary endpoint, the difference was statistically significant (P = .03) in favor of the everolimus-based regimen,
Study supports safety of everolimus regimen
The take-home message is that the everolimus-based regimen, which “is safe in children and young adults when initiated at 6 months after transplant,” can be considered as an alternative to MFF, Dr. Almond concluded.
However, one of the coauthors of the study, Joseph Rossano, MD, chief of the division of cardiology, Children’s Hospital of Philadelphia, suggested a stronger message.
“These data provide compelling reasons to consider initiation of the combination of everolimus and tacrolimus at 6 months post transplant in pediatric heart transplant recipients,” Dr. Rossano said.
Even though the everolimus-based regimen met the terms of noninferiority overall, patients who received this combination rather than the MMF-based regimen “were less likely to have the combined endpoints of vasculopathy, CKD, rejection and CMV infection. Additionally, they were less likely to make donor specific antibodies,” he said.
He also said that this study challenges the current boxed warning for everolimus. He pointed out that the warning, based on early use of everolimus in adults, does not appear to be an issue for children treated at 6 months.
Early mortality based on infection “was not observed in our study,” he said.
The AHA-invited discussant, Antonio G. Cabrera, MD, division chief of pediatric cardiology, University of Utah, Salt Lake City, drew the same conclusions. Based on the study, the everolimus-based regimen can only be described as noninferior to the MMF-based regimen, but Dr. Cabrera listed the same relative advantages as Dr. Rossano, including better kidney function.
Overall, either regimen might be more appealing based on several variables, but Dr. Cabrera said these data suggest everolimus-based treatment “should be considered” as one of two evidence-based options,
Dr. Almond reported no potential financial conflicts of interest. Dr. Rossano reports financial relationships with Abiomed, Bayer, Cytokinetics, Merck, and Myokardia. Dr. Cabrera reported no potential financial conflicts of interest.
Study challenges everolimus boxed warning
Study challenges everolimus boxed warning
according to the first phase 3 trial to compare antirejection strategies in the pediatric setting.
Even though MMF and tacrolimus have never been evaluated for pediatric cardiac transplant in a controlled trial, this combination is widely considered a standard based on adult data, said Christopher Almond, MD, a professor of pediatric cardiology at Stanford (Calif.) Medicine.
Everolimus has not been widely used in an antirejection regimen in children following heart transplant in part because of a boxed warning. The warning was added to labeling when this agent was associated with increased infection and increased mortality in adults if given within 3 months of transplant.
In this non-inferiority trial, called TEAMMATE, patients were randomized to the MMF-based or everolimus-based regimen 6 months after transplant.
Everolimus- vs. MMF-based antirejection
The study enrolled 210 children and adolescents 21 years of age or younger. The control arm treatment consisted of MMF (660 mg/m2 every 12 hours) plus standard dose of tacrolimus (initially 7-10 ng/mL followed at 6 months by 5-8 ng/mL).
In the experimental arm, patients received everolimus (3-8 ng/mL) plus a low dose of tacrolimus (initially 3-5 ng/mL followed at 6 months by 2.5-4.5 ng/mL).
The primary endpoint was score on the major adverse transplant event (MATE-6) tool. Based on gradations of severity, this assigns values for cardiac allograft vasculopathy (CAV), chronic kidney disease (CKD), acute cellular rejection (ACR), antibody-mediated rejection, infection, and posttransplant lymphoproliferative disorder (PTLD).
Thirty months after randomization, the MATE-6 scores were 1.96 in the everolimus group and 2.18 in the MMF group, which conferred the everolimus-based regimen with a numerical but not a significant advantage over the MMF-based regimen. For the goal of noninferiority, the everolimus regimen “met the prespecified safety criterion for success,” Dr. Almond said.
Numerical advantage for everolimus on efficacy
The primary efficacy endpoint was the MATE-3 score, which is limited to CAV, CKD, and ACR. Again, the mean score on this metric (0.93 vs. 1.25) was lower on the everolimus-based regimen but not significantly different.
Looking at specific events in the MATE-6 score, the everolimus-based regimen was associated with lower numerical rates of CAV and CKD, but a higher rate of PTLD, Dr. Almond reported.
On the MATE-3 efficacy analysis, the everolimus-based regimen was again associated with lower numerical rates of CAV and CKD but higher rates of ACR.
In terms of adverse events, including those involving the gastrointestinal tract, blood cells, proteinuria, and interstitial lung disease, most did not differ markedly even if many were numerically more common in the MMF-based arm. The exception was aphthous stomatitis, which was more common on everolimus (32% vs. 7%; P < .001). There were more discontinuations for an adverse event in the MMF arm (21% vs. 12%; P < .001).
Other differences included a lower proportion of patients in the everolimus arm with anti-HLA antibodies (17% vs. 30%; P < .05). Total cholesterol levels at the end of the study were lower but not significantly different in the MMF group, while the higher median glomerular filtration rate was higher on everolimus, and this did reach statistical significance (P < .05).
Infection rates overall were similar, but cytomegalovirus (CMV) infection was more common on the MMF-based regimen. The 30% lower rate of CMV infection in the everolimus proved to be potentially clinically meaningful when it was considered in the context of MATE-3. When these two endpoints were combined (MATE-3 and CMV infection as a prespecified secondary endpoint, the difference was statistically significant (P = .03) in favor of the everolimus-based regimen,
Study supports safety of everolimus regimen
The take-home message is that the everolimus-based regimen, which “is safe in children and young adults when initiated at 6 months after transplant,” can be considered as an alternative to MFF, Dr. Almond concluded.
However, one of the coauthors of the study, Joseph Rossano, MD, chief of the division of cardiology, Children’s Hospital of Philadelphia, suggested a stronger message.
“These data provide compelling reasons to consider initiation of the combination of everolimus and tacrolimus at 6 months post transplant in pediatric heart transplant recipients,” Dr. Rossano said.
Even though the everolimus-based regimen met the terms of noninferiority overall, patients who received this combination rather than the MMF-based regimen “were less likely to have the combined endpoints of vasculopathy, CKD, rejection and CMV infection. Additionally, they were less likely to make donor specific antibodies,” he said.
He also said that this study challenges the current boxed warning for everolimus. He pointed out that the warning, based on early use of everolimus in adults, does not appear to be an issue for children treated at 6 months.
Early mortality based on infection “was not observed in our study,” he said.
The AHA-invited discussant, Antonio G. Cabrera, MD, division chief of pediatric cardiology, University of Utah, Salt Lake City, drew the same conclusions. Based on the study, the everolimus-based regimen can only be described as noninferior to the MMF-based regimen, but Dr. Cabrera listed the same relative advantages as Dr. Rossano, including better kidney function.
Overall, either regimen might be more appealing based on several variables, but Dr. Cabrera said these data suggest everolimus-based treatment “should be considered” as one of two evidence-based options,
Dr. Almond reported no potential financial conflicts of interest. Dr. Rossano reports financial relationships with Abiomed, Bayer, Cytokinetics, Merck, and Myokardia. Dr. Cabrera reported no potential financial conflicts of interest.
according to the first phase 3 trial to compare antirejection strategies in the pediatric setting.
Even though MMF and tacrolimus have never been evaluated for pediatric cardiac transplant in a controlled trial, this combination is widely considered a standard based on adult data, said Christopher Almond, MD, a professor of pediatric cardiology at Stanford (Calif.) Medicine.
Everolimus has not been widely used in an antirejection regimen in children following heart transplant in part because of a boxed warning. The warning was added to labeling when this agent was associated with increased infection and increased mortality in adults if given within 3 months of transplant.
In this non-inferiority trial, called TEAMMATE, patients were randomized to the MMF-based or everolimus-based regimen 6 months after transplant.
Everolimus- vs. MMF-based antirejection
The study enrolled 210 children and adolescents 21 years of age or younger. The control arm treatment consisted of MMF (660 mg/m2 every 12 hours) plus standard dose of tacrolimus (initially 7-10 ng/mL followed at 6 months by 5-8 ng/mL).
In the experimental arm, patients received everolimus (3-8 ng/mL) plus a low dose of tacrolimus (initially 3-5 ng/mL followed at 6 months by 2.5-4.5 ng/mL).
The primary endpoint was score on the major adverse transplant event (MATE-6) tool. Based on gradations of severity, this assigns values for cardiac allograft vasculopathy (CAV), chronic kidney disease (CKD), acute cellular rejection (ACR), antibody-mediated rejection, infection, and posttransplant lymphoproliferative disorder (PTLD).
Thirty months after randomization, the MATE-6 scores were 1.96 in the everolimus group and 2.18 in the MMF group, which conferred the everolimus-based regimen with a numerical but not a significant advantage over the MMF-based regimen. For the goal of noninferiority, the everolimus regimen “met the prespecified safety criterion for success,” Dr. Almond said.
Numerical advantage for everolimus on efficacy
The primary efficacy endpoint was the MATE-3 score, which is limited to CAV, CKD, and ACR. Again, the mean score on this metric (0.93 vs. 1.25) was lower on the everolimus-based regimen but not significantly different.
Looking at specific events in the MATE-6 score, the everolimus-based regimen was associated with lower numerical rates of CAV and CKD, but a higher rate of PTLD, Dr. Almond reported.
On the MATE-3 efficacy analysis, the everolimus-based regimen was again associated with lower numerical rates of CAV and CKD but higher rates of ACR.
In terms of adverse events, including those involving the gastrointestinal tract, blood cells, proteinuria, and interstitial lung disease, most did not differ markedly even if many were numerically more common in the MMF-based arm. The exception was aphthous stomatitis, which was more common on everolimus (32% vs. 7%; P < .001). There were more discontinuations for an adverse event in the MMF arm (21% vs. 12%; P < .001).
Other differences included a lower proportion of patients in the everolimus arm with anti-HLA antibodies (17% vs. 30%; P < .05). Total cholesterol levels at the end of the study were lower but not significantly different in the MMF group, while the higher median glomerular filtration rate was higher on everolimus, and this did reach statistical significance (P < .05).
Infection rates overall were similar, but cytomegalovirus (CMV) infection was more common on the MMF-based regimen. The 30% lower rate of CMV infection in the everolimus proved to be potentially clinically meaningful when it was considered in the context of MATE-3. When these two endpoints were combined (MATE-3 and CMV infection as a prespecified secondary endpoint, the difference was statistically significant (P = .03) in favor of the everolimus-based regimen,
Study supports safety of everolimus regimen
The take-home message is that the everolimus-based regimen, which “is safe in children and young adults when initiated at 6 months after transplant,” can be considered as an alternative to MFF, Dr. Almond concluded.
However, one of the coauthors of the study, Joseph Rossano, MD, chief of the division of cardiology, Children’s Hospital of Philadelphia, suggested a stronger message.
“These data provide compelling reasons to consider initiation of the combination of everolimus and tacrolimus at 6 months post transplant in pediatric heart transplant recipients,” Dr. Rossano said.
Even though the everolimus-based regimen met the terms of noninferiority overall, patients who received this combination rather than the MMF-based regimen “were less likely to have the combined endpoints of vasculopathy, CKD, rejection and CMV infection. Additionally, they were less likely to make donor specific antibodies,” he said.
He also said that this study challenges the current boxed warning for everolimus. He pointed out that the warning, based on early use of everolimus in adults, does not appear to be an issue for children treated at 6 months.
Early mortality based on infection “was not observed in our study,” he said.
The AHA-invited discussant, Antonio G. Cabrera, MD, division chief of pediatric cardiology, University of Utah, Salt Lake City, drew the same conclusions. Based on the study, the everolimus-based regimen can only be described as noninferior to the MMF-based regimen, but Dr. Cabrera listed the same relative advantages as Dr. Rossano, including better kidney function.
Overall, either regimen might be more appealing based on several variables, but Dr. Cabrera said these data suggest everolimus-based treatment “should be considered” as one of two evidence-based options,
Dr. Almond reported no potential financial conflicts of interest. Dr. Rossano reports financial relationships with Abiomed, Bayer, Cytokinetics, Merck, and Myokardia. Dr. Cabrera reported no potential financial conflicts of interest.
FROM AHA 2023
Revisiting the role of hydrocortisone, fludrocortisone in septic shock
Earlier this year, I stumbled across a podcast in a content update email from the Journal of the American Medical Association. The moderator was interviewing the first author of a study comparing hydrocortisone and fludrocortisone (hydro/fludro) to hydrocortisone alone for treatment of septic shock. In the introduction,
I thought this issue had been settled with publication of the COIITSS trial in 2010. This study randomly assigned 509 patients with septic shock to hydro/fludro versus hydrocortisone alone. There was a nonsignificant reduction in mortality with hydro/fludro and everyone I knew stopped adding fludrocortisone for septic shock. It wasn’t included in guidelines (and still isn›t). I figured the only docs still using it were also prescribing ivermectin and vitamin C – another treatment touted to work in an apocryphal podcast.
It wasn’t just COIITSS that killed fludrocortisone for me. Back in 2002, I was a loyal adherent. That year, a randomized controlled trial (RCT) published by “the lord of corticosteroids for critical illness” doctor, Djillali Annane, found benefit to hydro/fludro in septic shock . Everyone in that study had a cosyntropin stim test and only certain subgroups had better outcomes. As a medical resident paying obeisance to all things evidence-based medicine, I rigidly adopted their protocol for all septic patients. I also kept their insulin between 80 and 110 mg/dL, prescribed drotrecogin alfa, and made sure they were floating in crystalloid. But those are topics for another time.
Subsequent trials and meta-analyses cast doubt on the need for the stim test, and a consensus around hydrocortisone at moderate doses for patients with septic shock emerged. Because one part of the Annane protocol was already deemed unnecessary (the cosyntropin stim test), it was easy to dismiss fludrocortisone after COIITTS was published. Yes, I read Annane’s 2018 APROCCHSS trial, and I’m aware that it found that hydro/fludro reduced 90-day mortality. Like others, I rationalized this finding by framing it as a function of baseline mortality. The two Annane RCTs that found that hydro/fludro reduced mortality in enrolled patients who were considerably more likely to die than those enrolled in RCTs of hydrocortisone alone were negative. It was the target population mortality rate and not the addition of fludrocortisone that made the difference, right?
Rethinking hydro/fludro
The author interviewed for the recent JAMA podcast forced me to rethink my blithe dismissal of fludrocortisone. He contended that the COIITTS trial was underpowered and the two Annane RCTs that used fludrocortisone supply the evidence that shows corticosteroids reduce septic shock mortality. As discussed earlier, he found clinical equipoise among his colleagues. Last, he invoked pleiotropic mineralocorticoid effects, such as activation of innate immunity and clearance of alveolar fluid, to support the need to reexamine hydro/fludro.
In his study, he used Big Data to compare hospital records from 2016 to 2020. He analyzed a total of 88,275 patients with septic shock. Most were prescribed hydrocortisone alone (85,995 [97.4%] vs. only 2.6% hydro/fludro). After a number of statistical adjustments and sensitivity analyses, the authors concluded that the addition of fludrocortisone to hydrocortisone for patients with septic shock provides a 3.7% absolute risk reduction in mortality (or discharge to hospice) when compared with hydrocortisone alone. That’s a number needed to treat of 28 to prevent one death (or discharge to hospice).
Key takeaways
The study isn’t perfect. In their methods section they use terms like “ensemble machine learner (super learner)” and “immortal time bias.” The first is a fancy way of saying they did a form of propensity scoring, which in turn is a fancy way of saying they tried to control for confounding. The second is a way to adjust for time delays between drug administration. Both are attempts to compensate for the observational design, as is their argument for biologic plausibility. Here they’re on particularly thin ice when trying to prove causal inference. Biologic plausibility is never hard to find; after all, what compound doesn’t have pleiotropic effects? Furthermore, the analysis lacks any data to support their biologic plausibility hypothesis that fludrocortisone’s effect on mortality is mediated via activation of innate immunity and/or clearance of alveolar fluid.
The editorial accompanying this Big Data study endorsed adding fludrocortisone. We have very little that reduces ICU mortality so the low number needed to treat is enticing, especially in light of the low risk from adverse events, so I’m going to start using it. Do I think I’ll save one life for every 28 patients with septic shock to whom I give hydro/fludro instead of hydrocortisone alone? I sure don’t. No way an oral mineralocorticoid at that dose has that type of impact on top of hydrocortisone alone. I still believe that the Annane studies are positive because of the mortality rate in the population enrolled and not because fludrocortisone was added. It all comes full circle, though – 20 years after I abandoned hydro/fludro, I’m going back to it.
Aaron B. Holley, MD, is a professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/critical care and sleep medicine physician at MedStar Washington Hospital Center in Washington, D.C.
A version of this article first appeared on Medscape.com.
Earlier this year, I stumbled across a podcast in a content update email from the Journal of the American Medical Association. The moderator was interviewing the first author of a study comparing hydrocortisone and fludrocortisone (hydro/fludro) to hydrocortisone alone for treatment of septic shock. In the introduction,
I thought this issue had been settled with publication of the COIITSS trial in 2010. This study randomly assigned 509 patients with septic shock to hydro/fludro versus hydrocortisone alone. There was a nonsignificant reduction in mortality with hydro/fludro and everyone I knew stopped adding fludrocortisone for septic shock. It wasn’t included in guidelines (and still isn›t). I figured the only docs still using it were also prescribing ivermectin and vitamin C – another treatment touted to work in an apocryphal podcast.
It wasn’t just COIITSS that killed fludrocortisone for me. Back in 2002, I was a loyal adherent. That year, a randomized controlled trial (RCT) published by “the lord of corticosteroids for critical illness” doctor, Djillali Annane, found benefit to hydro/fludro in septic shock . Everyone in that study had a cosyntropin stim test and only certain subgroups had better outcomes. As a medical resident paying obeisance to all things evidence-based medicine, I rigidly adopted their protocol for all septic patients. I also kept their insulin between 80 and 110 mg/dL, prescribed drotrecogin alfa, and made sure they were floating in crystalloid. But those are topics for another time.
Subsequent trials and meta-analyses cast doubt on the need for the stim test, and a consensus around hydrocortisone at moderate doses for patients with septic shock emerged. Because one part of the Annane protocol was already deemed unnecessary (the cosyntropin stim test), it was easy to dismiss fludrocortisone after COIITTS was published. Yes, I read Annane’s 2018 APROCCHSS trial, and I’m aware that it found that hydro/fludro reduced 90-day mortality. Like others, I rationalized this finding by framing it as a function of baseline mortality. The two Annane RCTs that found that hydro/fludro reduced mortality in enrolled patients who were considerably more likely to die than those enrolled in RCTs of hydrocortisone alone were negative. It was the target population mortality rate and not the addition of fludrocortisone that made the difference, right?
Rethinking hydro/fludro
The author interviewed for the recent JAMA podcast forced me to rethink my blithe dismissal of fludrocortisone. He contended that the COIITTS trial was underpowered and the two Annane RCTs that used fludrocortisone supply the evidence that shows corticosteroids reduce septic shock mortality. As discussed earlier, he found clinical equipoise among his colleagues. Last, he invoked pleiotropic mineralocorticoid effects, such as activation of innate immunity and clearance of alveolar fluid, to support the need to reexamine hydro/fludro.
In his study, he used Big Data to compare hospital records from 2016 to 2020. He analyzed a total of 88,275 patients with septic shock. Most were prescribed hydrocortisone alone (85,995 [97.4%] vs. only 2.6% hydro/fludro). After a number of statistical adjustments and sensitivity analyses, the authors concluded that the addition of fludrocortisone to hydrocortisone for patients with septic shock provides a 3.7% absolute risk reduction in mortality (or discharge to hospice) when compared with hydrocortisone alone. That’s a number needed to treat of 28 to prevent one death (or discharge to hospice).
Key takeaways
The study isn’t perfect. In their methods section they use terms like “ensemble machine learner (super learner)” and “immortal time bias.” The first is a fancy way of saying they did a form of propensity scoring, which in turn is a fancy way of saying they tried to control for confounding. The second is a way to adjust for time delays between drug administration. Both are attempts to compensate for the observational design, as is their argument for biologic plausibility. Here they’re on particularly thin ice when trying to prove causal inference. Biologic plausibility is never hard to find; after all, what compound doesn’t have pleiotropic effects? Furthermore, the analysis lacks any data to support their biologic plausibility hypothesis that fludrocortisone’s effect on mortality is mediated via activation of innate immunity and/or clearance of alveolar fluid.
The editorial accompanying this Big Data study endorsed adding fludrocortisone. We have very little that reduces ICU mortality so the low number needed to treat is enticing, especially in light of the low risk from adverse events, so I’m going to start using it. Do I think I’ll save one life for every 28 patients with septic shock to whom I give hydro/fludro instead of hydrocortisone alone? I sure don’t. No way an oral mineralocorticoid at that dose has that type of impact on top of hydrocortisone alone. I still believe that the Annane studies are positive because of the mortality rate in the population enrolled and not because fludrocortisone was added. It all comes full circle, though – 20 years after I abandoned hydro/fludro, I’m going back to it.
Aaron B. Holley, MD, is a professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/critical care and sleep medicine physician at MedStar Washington Hospital Center in Washington, D.C.
A version of this article first appeared on Medscape.com.
Earlier this year, I stumbled across a podcast in a content update email from the Journal of the American Medical Association. The moderator was interviewing the first author of a study comparing hydrocortisone and fludrocortisone (hydro/fludro) to hydrocortisone alone for treatment of septic shock. In the introduction,
I thought this issue had been settled with publication of the COIITSS trial in 2010. This study randomly assigned 509 patients with septic shock to hydro/fludro versus hydrocortisone alone. There was a nonsignificant reduction in mortality with hydro/fludro and everyone I knew stopped adding fludrocortisone for septic shock. It wasn’t included in guidelines (and still isn›t). I figured the only docs still using it were also prescribing ivermectin and vitamin C – another treatment touted to work in an apocryphal podcast.
It wasn’t just COIITSS that killed fludrocortisone for me. Back in 2002, I was a loyal adherent. That year, a randomized controlled trial (RCT) published by “the lord of corticosteroids for critical illness” doctor, Djillali Annane, found benefit to hydro/fludro in septic shock . Everyone in that study had a cosyntropin stim test and only certain subgroups had better outcomes. As a medical resident paying obeisance to all things evidence-based medicine, I rigidly adopted their protocol for all septic patients. I also kept their insulin between 80 and 110 mg/dL, prescribed drotrecogin alfa, and made sure they were floating in crystalloid. But those are topics for another time.
Subsequent trials and meta-analyses cast doubt on the need for the stim test, and a consensus around hydrocortisone at moderate doses for patients with septic shock emerged. Because one part of the Annane protocol was already deemed unnecessary (the cosyntropin stim test), it was easy to dismiss fludrocortisone after COIITTS was published. Yes, I read Annane’s 2018 APROCCHSS trial, and I’m aware that it found that hydro/fludro reduced 90-day mortality. Like others, I rationalized this finding by framing it as a function of baseline mortality. The two Annane RCTs that found that hydro/fludro reduced mortality in enrolled patients who were considerably more likely to die than those enrolled in RCTs of hydrocortisone alone were negative. It was the target population mortality rate and not the addition of fludrocortisone that made the difference, right?
Rethinking hydro/fludro
The author interviewed for the recent JAMA podcast forced me to rethink my blithe dismissal of fludrocortisone. He contended that the COIITTS trial was underpowered and the two Annane RCTs that used fludrocortisone supply the evidence that shows corticosteroids reduce septic shock mortality. As discussed earlier, he found clinical equipoise among his colleagues. Last, he invoked pleiotropic mineralocorticoid effects, such as activation of innate immunity and clearance of alveolar fluid, to support the need to reexamine hydro/fludro.
In his study, he used Big Data to compare hospital records from 2016 to 2020. He analyzed a total of 88,275 patients with septic shock. Most were prescribed hydrocortisone alone (85,995 [97.4%] vs. only 2.6% hydro/fludro). After a number of statistical adjustments and sensitivity analyses, the authors concluded that the addition of fludrocortisone to hydrocortisone for patients with septic shock provides a 3.7% absolute risk reduction in mortality (or discharge to hospice) when compared with hydrocortisone alone. That’s a number needed to treat of 28 to prevent one death (or discharge to hospice).
Key takeaways
The study isn’t perfect. In their methods section they use terms like “ensemble machine learner (super learner)” and “immortal time bias.” The first is a fancy way of saying they did a form of propensity scoring, which in turn is a fancy way of saying they tried to control for confounding. The second is a way to adjust for time delays between drug administration. Both are attempts to compensate for the observational design, as is their argument for biologic plausibility. Here they’re on particularly thin ice when trying to prove causal inference. Biologic plausibility is never hard to find; after all, what compound doesn’t have pleiotropic effects? Furthermore, the analysis lacks any data to support their biologic plausibility hypothesis that fludrocortisone’s effect on mortality is mediated via activation of innate immunity and/or clearance of alveolar fluid.
The editorial accompanying this Big Data study endorsed adding fludrocortisone. We have very little that reduces ICU mortality so the low number needed to treat is enticing, especially in light of the low risk from adverse events, so I’m going to start using it. Do I think I’ll save one life for every 28 patients with septic shock to whom I give hydro/fludro instead of hydrocortisone alone? I sure don’t. No way an oral mineralocorticoid at that dose has that type of impact on top of hydrocortisone alone. I still believe that the Annane studies are positive because of the mortality rate in the population enrolled and not because fludrocortisone was added. It all comes full circle, though – 20 years after I abandoned hydro/fludro, I’m going back to it.
Aaron B. Holley, MD, is a professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/critical care and sleep medicine physician at MedStar Washington Hospital Center in Washington, D.C.
A version of this article first appeared on Medscape.com.
Switching Patients From a Triptan to a Gepant for Acute Migraine Care and Effective Preventives
Dr. Rapoport: Most patients who come into my office today, even those whom I have
treated for the last 30 years for acute care of migraine attacks, are taking 1 of the 7
triptan medications available. They might be taking triptans as a tablet—the most
common form—as a nasal spray, or by injection; however, not all patients are suited for
triptans, and sometimes, the need arises to switch to a different class of medication for
treating migraine acutely.
What are the reasons patients switch from a triptan to a gepant?
For some patients, triptans are not working well enough or are causing adverse events.
Other patients have developed cardiac risk factors such as elevated blood pressure,
obesity, smoking, and/or lack of exercise. I am always concerned about constriction of
the coronary blood vessels. Patients who already have some cardiac risk factors and
those who have some actual cardiac disease or have had a previous heart attack
already have constriction of their blood vessels and are not candidates for triptans, as
they are contraindicated.
How do you switch a patient from a triptan to a gepant?
It is important to have some discussion with the patient before the switch. For example,
if a patient with no cardiac risk factors comes into the office asking about this new
medicine, I will ask them several questions about their triptan to ensure it works well
enough (ie, to ascertain if the patient’s migraines improve within 30 to 60 minutes and
are much better within 2 hours of taking the medication). I want to be sure that they do
not have any adverse events related to the triptan, such as chest pain, drowsiness, or
dizziness. I like to ensure that whatever they are taking works long enough—at least 24
hours, preferably 48 hours—so they no longer have a headache, especially the next
day. If the headache comes back the next day, they must re-treat. If I determine the
triptan is not working well for them or they have significant adverse events, I will move
on.
Gepants are small-molecule calcitonin gene-related peptide (CGRP) receptor
antagonists, which are pills that only last for 2 to 3 days in the body. There are 2
gepants for acute care and 2 for the prevention of migraine. The first gepant approved
by the US Food and Drug Administration (FDA) for acute care was ubrogepant
(Ubrelvy), which comes in 2 sizes, 50 mg or 100 mg tablets. I sometimes start with 50
mg, but for the more difficult migraine patient, I will start with 100 mg. If the medicine is
not doing a complete job within 2 hours, the patient may take a second dose, up to 200
mg. Some adverse events may include nausea or slight drowsiness. The patient should
avoid certain medicines such as antifungal medicines (eg, ketoconazole, itraconazole)
and certain antibiotics like clarithromycin.
Another gepant, rimegepant (Nurtec), comes in only 1 size, a 75-mg oral disintegrating
tablet, which can be used both for acute care of migraine and for prevention. Patients
can take a tablet as soon as their migraine attack begins, and they are not to repeat it
that day. If the headache does not go away in 2 hours, I want them to then take a triptan
and an anti-inflammatory drug (there is no contraindication to mix these drugs). I want
them to try it at least 1 more time, encouraging patients to take it early, right at the start
of the headache. If the medicine is still not working by the second or third time, they
should stop using it. Preventively, patients take 75 mg every other day, which can be
quite effective. Side effects are slight nausea and some abdominal pain or dyspepsia.
A third gepant is atogepant (Qulipta), which is only for migraine prevention. It comes in
10 mg, 30 mg, and 60 mg and is taken once every day as a preventive. It can cause
some drowsiness, constipation, and nausea.
Are there any other acute care drugs you recommend if triptans are not working?
Yes, there is another drug class called the ditans. These medications work very well but
have more adverse events associated with them than I like. A higher percentage of
patients seem to be pain-free in 2 hours when using a ditan; however, the only one
available, lasmiditan (Reyvow), has never been studied against a gepant, so I cannot
say if one is better than the other. Lasmitidan works similarly to a triptan by stimulating
serotonin 1F receptors but does not constrict blood vessels. Up to 15% of patients have
dizziness and up to 7% have drowsiness, so patients should not drive within 8 hours
after taking lasmiditan. This medication is available in 2 sizes, 100 mg and 200 mg. I
usually give patients a 200-mg dose, which is good enough for 24 hours. Ditans are a
Schedule V drug, meaning some patients might take more than they should because it
makes them feel good. It can be a challenging drug to get, but it is an excellent acute
care drug when none of the mentioned adverse events occur.
Which preventive drugs do you tend to prescribe your patients for migraine since
triptans are not preventive?
For many years, we have used some of the older preventives. Antidepressants can be
an option for preventive treatment of migraine. Amitriptyline, a tricyclic antidepressant, is
a pretty good medicine. However, it has a lot of adverse events associated with it,
including dry mouth, weight gain, and drowsiness, so patients who take this at night
often sleep better. The dose is 10 mg to 50 mg taken before bed. This drug is often
used, but I would not say I like to prescribe it as much as other medications, even
though amitriptyline is effective and likely to work by affecting the level of serotonin and
other chemicals in the brain. There is little evidence that other classes of
antidepressants, such as selective serotonin reuptake inhibitors and serotonin and
norepinephrine reuptake inhibitors, are effective for migraine prevention. Adverse
effects may include weight gain, fatigue, constipation, and dry mouth, making it difficult
for a patient to stick with treatment.
Beta blockers are another preventive medication option for migraine. Beta blockers are
best known as a medical treatment for cardiovascular conditions, such as hypertension,
stable or unstable angina, and congestive heart failure. Beta blockers prevent the stress
hormone adrenaline (epinephrine) from binding to beta receptors, slowing heart rate
and lowering blood pressure. A commonly used beta blocker is propranolol (Inderal),
which also comes in a long-acting preparation. Doses range from 60 mg to 180
mg. Other beta blockers effective for migraine prevention include metoprolol, nadolol,
and atenolol.
Many of my patients are young, healthy females who like to exercise. Most report that
their heart rate is slow, they get short of breath, and they cannot exercise as effectively
while on a beta blocker. It also takes about 2 months until this medication starts
working. Patients may feel as if they are having too many adverse events, so I start
them on a very low dose and build it up gradually for a month and see how they are
feeling.
Epilepsy medicines can also be used to prevent migraine. There are 2 common
epilepsy medications. Topiramate (Topamax) doses can range from 75 mg to 100 mg
and are sometimes higher. Topiramate is a good medicine, but there are many potential
adverse events: tingling in the extremities, difficulty finding words when speaking,
confusion, raised eye pressure, and others. Divalproex sodium (Depakote) is another
popular medication, available in 500 mg to 1000 mg doses. This medicine can cause
some endocrine problems in women and can also damage the spinal cords of a fetus,
so this drug should not be taken during early pregnancy.
Monoclonal antibodies against CGRP are a strong preventive medication and a new
class of drugs that were first approved by the FDA in 2018. They are designed to
prevent episodic migraine (up to 14 headache days per month), chronic migraine (15 or
more headache days per month) and seem to work when a patient has medication
overuse headaches. CGRP is a neuropeptide involved in many body processes,
including blood pressure regulation, tissue repair, wound healing, and inflammation, and
is a potent vasodilator. When CGRP is released in the brain, it affects the trigeminal
nerve, increasing pain transmission and sensitivities to touch and temperature. CGRP
also causes inflammation and pain that happen during a migraine; it makes headache
pain worse and causes headaches to last longer.
Some CGRP inhibitors block CGRP from binding to CGRP receptors, a key contributor
to the trigeminal nerve pain and inflammation of migraine, while some grab the CGRP
and prevent it from activating the receptor.
The 2 classes of these drugs are monoclonal antibodies against CGRP and small
molecule CGRP antagonists. Fortunately, CGRPs have long half-lives and work for 1 to
3 months. The CGRP monoclonal antibodies are large molecule drugs. There are 4
different types, and 2 of them are injected by the patient at home once a month. One
can be injected at home once a month or every 3 months. For the latter option, patients
need to triple up with 3 injections in one day, so they do not have to inject for 3 months.
The fourth CGRP is an intravenous infusion that can be administered in an infusion
center or at home. This one is more inconvenient, but it is a strong drug. The small
molecule CGRP antagonists are taken by mouth in pill form. All CGRPs have been
shown to decrease the number of headaches per month.
The main goal of preventive therapy is to lessen the impact of migraines on patients’
lives by reducing how often they occur, how severe they are, and how long they last.
Preventive therapy also decreases disability and improves patients’ functioning over
time. Preventive therapy can help keep the costs for migraine care down by reducing
the need for acute treatments and allowing the patient to keep working or taking care of
their kids. Furthermore, preventive medications can make acute migraine treatments
more effective and help avoid the overuse of acute medications.
Dr. Rapoport: Most patients who come into my office today, even those whom I have
treated for the last 30 years for acute care of migraine attacks, are taking 1 of the 7
triptan medications available. They might be taking triptans as a tablet—the most
common form—as a nasal spray, or by injection; however, not all patients are suited for
triptans, and sometimes, the need arises to switch to a different class of medication for
treating migraine acutely.
What are the reasons patients switch from a triptan to a gepant?
For some patients, triptans are not working well enough or are causing adverse events.
Other patients have developed cardiac risk factors such as elevated blood pressure,
obesity, smoking, and/or lack of exercise. I am always concerned about constriction of
the coronary blood vessels. Patients who already have some cardiac risk factors and
those who have some actual cardiac disease or have had a previous heart attack
already have constriction of their blood vessels and are not candidates for triptans, as
they are contraindicated.
How do you switch a patient from a triptan to a gepant?
It is important to have some discussion with the patient before the switch. For example,
if a patient with no cardiac risk factors comes into the office asking about this new
medicine, I will ask them several questions about their triptan to ensure it works well
enough (ie, to ascertain if the patient’s migraines improve within 30 to 60 minutes and
are much better within 2 hours of taking the medication). I want to be sure that they do
not have any adverse events related to the triptan, such as chest pain, drowsiness, or
dizziness. I like to ensure that whatever they are taking works long enough—at least 24
hours, preferably 48 hours—so they no longer have a headache, especially the next
day. If the headache comes back the next day, they must re-treat. If I determine the
triptan is not working well for them or they have significant adverse events, I will move
on.
Gepants are small-molecule calcitonin gene-related peptide (CGRP) receptor
antagonists, which are pills that only last for 2 to 3 days in the body. There are 2
gepants for acute care and 2 for the prevention of migraine. The first gepant approved
by the US Food and Drug Administration (FDA) for acute care was ubrogepant
(Ubrelvy), which comes in 2 sizes, 50 mg or 100 mg tablets. I sometimes start with 50
mg, but for the more difficult migraine patient, I will start with 100 mg. If the medicine is
not doing a complete job within 2 hours, the patient may take a second dose, up to 200
mg. Some adverse events may include nausea or slight drowsiness. The patient should
avoid certain medicines such as antifungal medicines (eg, ketoconazole, itraconazole)
and certain antibiotics like clarithromycin.
Another gepant, rimegepant (Nurtec), comes in only 1 size, a 75-mg oral disintegrating
tablet, which can be used both for acute care of migraine and for prevention. Patients
can take a tablet as soon as their migraine attack begins, and they are not to repeat it
that day. If the headache does not go away in 2 hours, I want them to then take a triptan
and an anti-inflammatory drug (there is no contraindication to mix these drugs). I want
them to try it at least 1 more time, encouraging patients to take it early, right at the start
of the headache. If the medicine is still not working by the second or third time, they
should stop using it. Preventively, patients take 75 mg every other day, which can be
quite effective. Side effects are slight nausea and some abdominal pain or dyspepsia.
A third gepant is atogepant (Qulipta), which is only for migraine prevention. It comes in
10 mg, 30 mg, and 60 mg and is taken once every day as a preventive. It can cause
some drowsiness, constipation, and nausea.
Are there any other acute care drugs you recommend if triptans are not working?
Yes, there is another drug class called the ditans. These medications work very well but
have more adverse events associated with them than I like. A higher percentage of
patients seem to be pain-free in 2 hours when using a ditan; however, the only one
available, lasmiditan (Reyvow), has never been studied against a gepant, so I cannot
say if one is better than the other. Lasmitidan works similarly to a triptan by stimulating
serotonin 1F receptors but does not constrict blood vessels. Up to 15% of patients have
dizziness and up to 7% have drowsiness, so patients should not drive within 8 hours
after taking lasmiditan. This medication is available in 2 sizes, 100 mg and 200 mg. I
usually give patients a 200-mg dose, which is good enough for 24 hours. Ditans are a
Schedule V drug, meaning some patients might take more than they should because it
makes them feel good. It can be a challenging drug to get, but it is an excellent acute
care drug when none of the mentioned adverse events occur.
Which preventive drugs do you tend to prescribe your patients for migraine since
triptans are not preventive?
For many years, we have used some of the older preventives. Antidepressants can be
an option for preventive treatment of migraine. Amitriptyline, a tricyclic antidepressant, is
a pretty good medicine. However, it has a lot of adverse events associated with it,
including dry mouth, weight gain, and drowsiness, so patients who take this at night
often sleep better. The dose is 10 mg to 50 mg taken before bed. This drug is often
used, but I would not say I like to prescribe it as much as other medications, even
though amitriptyline is effective and likely to work by affecting the level of serotonin and
other chemicals in the brain. There is little evidence that other classes of
antidepressants, such as selective serotonin reuptake inhibitors and serotonin and
norepinephrine reuptake inhibitors, are effective for migraine prevention. Adverse
effects may include weight gain, fatigue, constipation, and dry mouth, making it difficult
for a patient to stick with treatment.
Beta blockers are another preventive medication option for migraine. Beta blockers are
best known as a medical treatment for cardiovascular conditions, such as hypertension,
stable or unstable angina, and congestive heart failure. Beta blockers prevent the stress
hormone adrenaline (epinephrine) from binding to beta receptors, slowing heart rate
and lowering blood pressure. A commonly used beta blocker is propranolol (Inderal),
which also comes in a long-acting preparation. Doses range from 60 mg to 180
mg. Other beta blockers effective for migraine prevention include metoprolol, nadolol,
and atenolol.
Many of my patients are young, healthy females who like to exercise. Most report that
their heart rate is slow, they get short of breath, and they cannot exercise as effectively
while on a beta blocker. It also takes about 2 months until this medication starts
working. Patients may feel as if they are having too many adverse events, so I start
them on a very low dose and build it up gradually for a month and see how they are
feeling.
Epilepsy medicines can also be used to prevent migraine. There are 2 common
epilepsy medications. Topiramate (Topamax) doses can range from 75 mg to 100 mg
and are sometimes higher. Topiramate is a good medicine, but there are many potential
adverse events: tingling in the extremities, difficulty finding words when speaking,
confusion, raised eye pressure, and others. Divalproex sodium (Depakote) is another
popular medication, available in 500 mg to 1000 mg doses. This medicine can cause
some endocrine problems in women and can also damage the spinal cords of a fetus,
so this drug should not be taken during early pregnancy.
Monoclonal antibodies against CGRP are a strong preventive medication and a new
class of drugs that were first approved by the FDA in 2018. They are designed to
prevent episodic migraine (up to 14 headache days per month), chronic migraine (15 or
more headache days per month) and seem to work when a patient has medication
overuse headaches. CGRP is a neuropeptide involved in many body processes,
including blood pressure regulation, tissue repair, wound healing, and inflammation, and
is a potent vasodilator. When CGRP is released in the brain, it affects the trigeminal
nerve, increasing pain transmission and sensitivities to touch and temperature. CGRP
also causes inflammation and pain that happen during a migraine; it makes headache
pain worse and causes headaches to last longer.
Some CGRP inhibitors block CGRP from binding to CGRP receptors, a key contributor
to the trigeminal nerve pain and inflammation of migraine, while some grab the CGRP
and prevent it from activating the receptor.
The 2 classes of these drugs are monoclonal antibodies against CGRP and small
molecule CGRP antagonists. Fortunately, CGRPs have long half-lives and work for 1 to
3 months. The CGRP monoclonal antibodies are large molecule drugs. There are 4
different types, and 2 of them are injected by the patient at home once a month. One
can be injected at home once a month or every 3 months. For the latter option, patients
need to triple up with 3 injections in one day, so they do not have to inject for 3 months.
The fourth CGRP is an intravenous infusion that can be administered in an infusion
center or at home. This one is more inconvenient, but it is a strong drug. The small
molecule CGRP antagonists are taken by mouth in pill form. All CGRPs have been
shown to decrease the number of headaches per month.
The main goal of preventive therapy is to lessen the impact of migraines on patients’
lives by reducing how often they occur, how severe they are, and how long they last.
Preventive therapy also decreases disability and improves patients’ functioning over
time. Preventive therapy can help keep the costs for migraine care down by reducing
the need for acute treatments and allowing the patient to keep working or taking care of
their kids. Furthermore, preventive medications can make acute migraine treatments
more effective and help avoid the overuse of acute medications.
Dr. Rapoport: Most patients who come into my office today, even those whom I have
treated for the last 30 years for acute care of migraine attacks, are taking 1 of the 7
triptan medications available. They might be taking triptans as a tablet—the most
common form—as a nasal spray, or by injection; however, not all patients are suited for
triptans, and sometimes, the need arises to switch to a different class of medication for
treating migraine acutely.
What are the reasons patients switch from a triptan to a gepant?
For some patients, triptans are not working well enough or are causing adverse events.
Other patients have developed cardiac risk factors such as elevated blood pressure,
obesity, smoking, and/or lack of exercise. I am always concerned about constriction of
the coronary blood vessels. Patients who already have some cardiac risk factors and
those who have some actual cardiac disease or have had a previous heart attack
already have constriction of their blood vessels and are not candidates for triptans, as
they are contraindicated.
How do you switch a patient from a triptan to a gepant?
It is important to have some discussion with the patient before the switch. For example,
if a patient with no cardiac risk factors comes into the office asking about this new
medicine, I will ask them several questions about their triptan to ensure it works well
enough (ie, to ascertain if the patient’s migraines improve within 30 to 60 minutes and
are much better within 2 hours of taking the medication). I want to be sure that they do
not have any adverse events related to the triptan, such as chest pain, drowsiness, or
dizziness. I like to ensure that whatever they are taking works long enough—at least 24
hours, preferably 48 hours—so they no longer have a headache, especially the next
day. If the headache comes back the next day, they must re-treat. If I determine the
triptan is not working well for them or they have significant adverse events, I will move
on.
Gepants are small-molecule calcitonin gene-related peptide (CGRP) receptor
antagonists, which are pills that only last for 2 to 3 days in the body. There are 2
gepants for acute care and 2 for the prevention of migraine. The first gepant approved
by the US Food and Drug Administration (FDA) for acute care was ubrogepant
(Ubrelvy), which comes in 2 sizes, 50 mg or 100 mg tablets. I sometimes start with 50
mg, but for the more difficult migraine patient, I will start with 100 mg. If the medicine is
not doing a complete job within 2 hours, the patient may take a second dose, up to 200
mg. Some adverse events may include nausea or slight drowsiness. The patient should
avoid certain medicines such as antifungal medicines (eg, ketoconazole, itraconazole)
and certain antibiotics like clarithromycin.
Another gepant, rimegepant (Nurtec), comes in only 1 size, a 75-mg oral disintegrating
tablet, which can be used both for acute care of migraine and for prevention. Patients
can take a tablet as soon as their migraine attack begins, and they are not to repeat it
that day. If the headache does not go away in 2 hours, I want them to then take a triptan
and an anti-inflammatory drug (there is no contraindication to mix these drugs). I want
them to try it at least 1 more time, encouraging patients to take it early, right at the start
of the headache. If the medicine is still not working by the second or third time, they
should stop using it. Preventively, patients take 75 mg every other day, which can be
quite effective. Side effects are slight nausea and some abdominal pain or dyspepsia.
A third gepant is atogepant (Qulipta), which is only for migraine prevention. It comes in
10 mg, 30 mg, and 60 mg and is taken once every day as a preventive. It can cause
some drowsiness, constipation, and nausea.
Are there any other acute care drugs you recommend if triptans are not working?
Yes, there is another drug class called the ditans. These medications work very well but
have more adverse events associated with them than I like. A higher percentage of
patients seem to be pain-free in 2 hours when using a ditan; however, the only one
available, lasmiditan (Reyvow), has never been studied against a gepant, so I cannot
say if one is better than the other. Lasmitidan works similarly to a triptan by stimulating
serotonin 1F receptors but does not constrict blood vessels. Up to 15% of patients have
dizziness and up to 7% have drowsiness, so patients should not drive within 8 hours
after taking lasmiditan. This medication is available in 2 sizes, 100 mg and 200 mg. I
usually give patients a 200-mg dose, which is good enough for 24 hours. Ditans are a
Schedule V drug, meaning some patients might take more than they should because it
makes them feel good. It can be a challenging drug to get, but it is an excellent acute
care drug when none of the mentioned adverse events occur.
Which preventive drugs do you tend to prescribe your patients for migraine since
triptans are not preventive?
For many years, we have used some of the older preventives. Antidepressants can be
an option for preventive treatment of migraine. Amitriptyline, a tricyclic antidepressant, is
a pretty good medicine. However, it has a lot of adverse events associated with it,
including dry mouth, weight gain, and drowsiness, so patients who take this at night
often sleep better. The dose is 10 mg to 50 mg taken before bed. This drug is often
used, but I would not say I like to prescribe it as much as other medications, even
though amitriptyline is effective and likely to work by affecting the level of serotonin and
other chemicals in the brain. There is little evidence that other classes of
antidepressants, such as selective serotonin reuptake inhibitors and serotonin and
norepinephrine reuptake inhibitors, are effective for migraine prevention. Adverse
effects may include weight gain, fatigue, constipation, and dry mouth, making it difficult
for a patient to stick with treatment.
Beta blockers are another preventive medication option for migraine. Beta blockers are
best known as a medical treatment for cardiovascular conditions, such as hypertension,
stable or unstable angina, and congestive heart failure. Beta blockers prevent the stress
hormone adrenaline (epinephrine) from binding to beta receptors, slowing heart rate
and lowering blood pressure. A commonly used beta blocker is propranolol (Inderal),
which also comes in a long-acting preparation. Doses range from 60 mg to 180
mg. Other beta blockers effective for migraine prevention include metoprolol, nadolol,
and atenolol.
Many of my patients are young, healthy females who like to exercise. Most report that
their heart rate is slow, they get short of breath, and they cannot exercise as effectively
while on a beta blocker. It also takes about 2 months until this medication starts
working. Patients may feel as if they are having too many adverse events, so I start
them on a very low dose and build it up gradually for a month and see how they are
feeling.
Epilepsy medicines can also be used to prevent migraine. There are 2 common
epilepsy medications. Topiramate (Topamax) doses can range from 75 mg to 100 mg
and are sometimes higher. Topiramate is a good medicine, but there are many potential
adverse events: tingling in the extremities, difficulty finding words when speaking,
confusion, raised eye pressure, and others. Divalproex sodium (Depakote) is another
popular medication, available in 500 mg to 1000 mg doses. This medicine can cause
some endocrine problems in women and can also damage the spinal cords of a fetus,
so this drug should not be taken during early pregnancy.
Monoclonal antibodies against CGRP are a strong preventive medication and a new
class of drugs that were first approved by the FDA in 2018. They are designed to
prevent episodic migraine (up to 14 headache days per month), chronic migraine (15 or
more headache days per month) and seem to work when a patient has medication
overuse headaches. CGRP is a neuropeptide involved in many body processes,
including blood pressure regulation, tissue repair, wound healing, and inflammation, and
is a potent vasodilator. When CGRP is released in the brain, it affects the trigeminal
nerve, increasing pain transmission and sensitivities to touch and temperature. CGRP
also causes inflammation and pain that happen during a migraine; it makes headache
pain worse and causes headaches to last longer.
Some CGRP inhibitors block CGRP from binding to CGRP receptors, a key contributor
to the trigeminal nerve pain and inflammation of migraine, while some grab the CGRP
and prevent it from activating the receptor.
The 2 classes of these drugs are monoclonal antibodies against CGRP and small
molecule CGRP antagonists. Fortunately, CGRPs have long half-lives and work for 1 to
3 months. The CGRP monoclonal antibodies are large molecule drugs. There are 4
different types, and 2 of them are injected by the patient at home once a month. One
can be injected at home once a month or every 3 months. For the latter option, patients
need to triple up with 3 injections in one day, so they do not have to inject for 3 months.
The fourth CGRP is an intravenous infusion that can be administered in an infusion
center or at home. This one is more inconvenient, but it is a strong drug. The small
molecule CGRP antagonists are taken by mouth in pill form. All CGRPs have been
shown to decrease the number of headaches per month.
The main goal of preventive therapy is to lessen the impact of migraines on patients’
lives by reducing how often they occur, how severe they are, and how long they last.
Preventive therapy also decreases disability and improves patients’ functioning over
time. Preventive therapy can help keep the costs for migraine care down by reducing
the need for acute treatments and allowing the patient to keep working or taking care of
their kids. Furthermore, preventive medications can make acute migraine treatments
more effective and help avoid the overuse of acute medications.
Infographic: Careers that tempt doctors to leave medicine
In a recently published Medscape report, 26% of American physicians said they were considering a career away from practicing medicine, for various reasons. Becoming a teacher was one of the nonclinical careers that most enthused them. What were the others?
For more details, check out the Medscape Physicians and Nonclinical Careers Report 2023.
A version of this article first appeared on Medscape.com.
In a recently published Medscape report, 26% of American physicians said they were considering a career away from practicing medicine, for various reasons. Becoming a teacher was one of the nonclinical careers that most enthused them. What were the others?
For more details, check out the Medscape Physicians and Nonclinical Careers Report 2023.
A version of this article first appeared on Medscape.com.
In a recently published Medscape report, 26% of American physicians said they were considering a career away from practicing medicine, for various reasons. Becoming a teacher was one of the nonclinical careers that most enthused them. What were the others?
For more details, check out the Medscape Physicians and Nonclinical Careers Report 2023.
A version of this article first appeared on Medscape.com.
Memory-enhancing intervention may help boost confidence, not necessarily memory, in older adults, study suggests
A novel approach aimed at enhancing everyday memory may lead older adults to feel more confident that they can accurately recollect phone numbers, names, and other information, according to findings from a small randomized controlled trial that were presented at the annual meeting of the Gerontological Society of America.
The tool, called Everyday Memory and Metacognitive Intervention (EMMI), trains people to be more mindful of memories, like where they parked their car, by repeating information at increasing intervals and self-testing.
EMMI “is a very important approach, focused on everyday memory,” said George W. Rebok, PhD, professor emeritus in the department of mental health at Johns Hopkins University, Baltimore, who was not involved with the study. “Many times, when we do memory interventions, we only focus on improving objective memories,” such as recalling major life events or one-time occurrences.
Everyday memory was defined as recalling basic facts including names, phone numbers, and daily appointments. The research, led by Ann Pearman, MD, associate director of adult psychology at Case Western Reserve University School of Medicine at MetroHealth Medical Center, Cleveland, Ohio, expanded on previous work she conducted with colleagues. That study found that EMMI may help improve confidence in the ability to recollect information and functional independence among older adults.
The current study was of 62 of the same participants in the earlier research, with one group that received EMMI (n = 30) and another that underwent traditional memory strategy training ([MSC]; n = 32). Both groups underwent four 3-hour virtual training sessions in their designated intervention over 2 weeks.
“One of the most important parts of the study is the [training] period,” when participants build new habits to help recall their everyday memories, Dr. Pearman said.
For 7 weeks, participants reported errors in everyday memories on a smartphone and submitted diary entries for each. Dr. Rebok that said tracking can help identify patterns or circumstances under which a person is likely to experience a memory lapse.
The study found mixed results when comparing EMMI with MSC, with the latter group demonstrating greater improvements in associative memory, such as pairing of a name to a face, highlighting the effectiveness of traditional MCS.
However, participants who underwent EMMI reported an increase in self-confidence that they were able to remember things, compared with those in the MSC group (4.92, confidence interval 95%, P = .30).
The EMMI intervention also was not uniformly effective in reducing memory errors across all participants in the group, which is to be expected, experts note. “In memory training, as with any kind of cognitive training, one size doesn’t fit all,” Dr. Rebok said.
“The mixed findings may highlight the need for a holistic approach to memory improvement and brain health, especially in older adults,” said Krystal L. Culler, DBH, founder of the Virtual Brain Health Center in Cleveland, who was not involved with the study.
EMMI could potentially be part of a broader strategy that includes lifestyle factors like sleep hygiene, physical exercise, diet, and social engagement to support optimal memory care, Dr. Culler said.
Patients who noticed some change in their memory and who are interested in making some positive changes in their daily cognitive functioning may benefit most from EMMI, according to Dr. Pearman.
“Making proactive decisions about memory challenges [patients] in their thinking and doing in everyday life,” she said.
Dr. Pearman shared that she and her colleagues are now looking into a combined EMMI and traditional memory strategy training to maximize the benefits of both interventions.
The study was supported by the Retirement Research Foundation (2018-2019); and the National Institute of Diabetes and Digestive and Kidney Diseases (P30DK111024) from the Georgia Center for Diabetes Translation Research. The study authors report no relevant conflicts. Dr. Culler and Dr. Rebok report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A novel approach aimed at enhancing everyday memory may lead older adults to feel more confident that they can accurately recollect phone numbers, names, and other information, according to findings from a small randomized controlled trial that were presented at the annual meeting of the Gerontological Society of America.
The tool, called Everyday Memory and Metacognitive Intervention (EMMI), trains people to be more mindful of memories, like where they parked their car, by repeating information at increasing intervals and self-testing.
EMMI “is a very important approach, focused on everyday memory,” said George W. Rebok, PhD, professor emeritus in the department of mental health at Johns Hopkins University, Baltimore, who was not involved with the study. “Many times, when we do memory interventions, we only focus on improving objective memories,” such as recalling major life events or one-time occurrences.
Everyday memory was defined as recalling basic facts including names, phone numbers, and daily appointments. The research, led by Ann Pearman, MD, associate director of adult psychology at Case Western Reserve University School of Medicine at MetroHealth Medical Center, Cleveland, Ohio, expanded on previous work she conducted with colleagues. That study found that EMMI may help improve confidence in the ability to recollect information and functional independence among older adults.
The current study was of 62 of the same participants in the earlier research, with one group that received EMMI (n = 30) and another that underwent traditional memory strategy training ([MSC]; n = 32). Both groups underwent four 3-hour virtual training sessions in their designated intervention over 2 weeks.
“One of the most important parts of the study is the [training] period,” when participants build new habits to help recall their everyday memories, Dr. Pearman said.
For 7 weeks, participants reported errors in everyday memories on a smartphone and submitted diary entries for each. Dr. Rebok that said tracking can help identify patterns or circumstances under which a person is likely to experience a memory lapse.
The study found mixed results when comparing EMMI with MSC, with the latter group demonstrating greater improvements in associative memory, such as pairing of a name to a face, highlighting the effectiveness of traditional MCS.
However, participants who underwent EMMI reported an increase in self-confidence that they were able to remember things, compared with those in the MSC group (4.92, confidence interval 95%, P = .30).
The EMMI intervention also was not uniformly effective in reducing memory errors across all participants in the group, which is to be expected, experts note. “In memory training, as with any kind of cognitive training, one size doesn’t fit all,” Dr. Rebok said.
“The mixed findings may highlight the need for a holistic approach to memory improvement and brain health, especially in older adults,” said Krystal L. Culler, DBH, founder of the Virtual Brain Health Center in Cleveland, who was not involved with the study.
EMMI could potentially be part of a broader strategy that includes lifestyle factors like sleep hygiene, physical exercise, diet, and social engagement to support optimal memory care, Dr. Culler said.
Patients who noticed some change in their memory and who are interested in making some positive changes in their daily cognitive functioning may benefit most from EMMI, according to Dr. Pearman.
“Making proactive decisions about memory challenges [patients] in their thinking and doing in everyday life,” she said.
Dr. Pearman shared that she and her colleagues are now looking into a combined EMMI and traditional memory strategy training to maximize the benefits of both interventions.
The study was supported by the Retirement Research Foundation (2018-2019); and the National Institute of Diabetes and Digestive and Kidney Diseases (P30DK111024) from the Georgia Center for Diabetes Translation Research. The study authors report no relevant conflicts. Dr. Culler and Dr. Rebok report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A novel approach aimed at enhancing everyday memory may lead older adults to feel more confident that they can accurately recollect phone numbers, names, and other information, according to findings from a small randomized controlled trial that were presented at the annual meeting of the Gerontological Society of America.
The tool, called Everyday Memory and Metacognitive Intervention (EMMI), trains people to be more mindful of memories, like where they parked their car, by repeating information at increasing intervals and self-testing.
EMMI “is a very important approach, focused on everyday memory,” said George W. Rebok, PhD, professor emeritus in the department of mental health at Johns Hopkins University, Baltimore, who was not involved with the study. “Many times, when we do memory interventions, we only focus on improving objective memories,” such as recalling major life events or one-time occurrences.
Everyday memory was defined as recalling basic facts including names, phone numbers, and daily appointments. The research, led by Ann Pearman, MD, associate director of adult psychology at Case Western Reserve University School of Medicine at MetroHealth Medical Center, Cleveland, Ohio, expanded on previous work she conducted with colleagues. That study found that EMMI may help improve confidence in the ability to recollect information and functional independence among older adults.
The current study was of 62 of the same participants in the earlier research, with one group that received EMMI (n = 30) and another that underwent traditional memory strategy training ([MSC]; n = 32). Both groups underwent four 3-hour virtual training sessions in their designated intervention over 2 weeks.
“One of the most important parts of the study is the [training] period,” when participants build new habits to help recall their everyday memories, Dr. Pearman said.
For 7 weeks, participants reported errors in everyday memories on a smartphone and submitted diary entries for each. Dr. Rebok that said tracking can help identify patterns or circumstances under which a person is likely to experience a memory lapse.
The study found mixed results when comparing EMMI with MSC, with the latter group demonstrating greater improvements in associative memory, such as pairing of a name to a face, highlighting the effectiveness of traditional MCS.
However, participants who underwent EMMI reported an increase in self-confidence that they were able to remember things, compared with those in the MSC group (4.92, confidence interval 95%, P = .30).
The EMMI intervention also was not uniformly effective in reducing memory errors across all participants in the group, which is to be expected, experts note. “In memory training, as with any kind of cognitive training, one size doesn’t fit all,” Dr. Rebok said.
“The mixed findings may highlight the need for a holistic approach to memory improvement and brain health, especially in older adults,” said Krystal L. Culler, DBH, founder of the Virtual Brain Health Center in Cleveland, who was not involved with the study.
EMMI could potentially be part of a broader strategy that includes lifestyle factors like sleep hygiene, physical exercise, diet, and social engagement to support optimal memory care, Dr. Culler said.
Patients who noticed some change in their memory and who are interested in making some positive changes in their daily cognitive functioning may benefit most from EMMI, according to Dr. Pearman.
“Making proactive decisions about memory challenges [patients] in their thinking and doing in everyday life,” she said.
Dr. Pearman shared that she and her colleagues are now looking into a combined EMMI and traditional memory strategy training to maximize the benefits of both interventions.
The study was supported by the Retirement Research Foundation (2018-2019); and the National Institute of Diabetes and Digestive and Kidney Diseases (P30DK111024) from the Georgia Center for Diabetes Translation Research. The study authors report no relevant conflicts. Dr. Culler and Dr. Rebok report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM GSA 2023
Use the stool! Fecal microbiota transplants help kids with diarrheal infection
(AAP).
However, fecal microbiota transplants (FMTs) should not be used to treat other gastrointestinal ailments such as Crohn’s disease or ulcerative colitis, because scientific evidence falls short on effectiveness in treating these conditions, the group said.
C. difficile infections (CDIs) are major contributors to hospital-associated diarrhea and diarrhea caused by antibiotics. An FMT involves introducing the feces of a healthy person into the gastrointestinal tract, usually through a nasogastric tube but sometimes in capsules containing healthy stool. Serious adverse reactions associated with an FMT, such as hospitalization, are rare, occuring in roughly 2% of case, the AAP said.
An FMT “does have a place for treatment of recurrent CDIs in children,” said Maria Oliva-Hemker, MD, a pediatric gastroenterologist at Johns Hopkins University School of Medicine in Baltimore and the lead author of the report, which was online in Pediatrics.
The AAP strongly encourages people not to perform an FMT at home, although caregivers may be tempted due to a lack of medical facilities located nearby to deliver this care.
“People might see a video on YouTube and think they can do this themselves,” Dr. Oliva-Hemker said.
An FMT requires screening of donors for any infections, which involves administering questionnaires and analyzing donor blood and stool, which are tasks better suited for medical facilities than for a living room.
No controlled or prospective clinical trials on the efficacy of FMT for children exist, according to the AAP. But a retrospective study published in 2020 showed that one or two courses of FMT prevented CDI recurrence in children 87% of the time. Researchers defined the eradication of CDIs as no recurrence for at least 2 months after an FMT and noted the success rates in children were comaparable to those reported in adults.
Unlike pediatric data, adult data come from a randomized clinical trial.
“Sometimes, kids are the last people to be enrolled in these trials,” said Maribeth Nicholson, MD, MPH, a pediatric gastroenterologist at Vanderbilt University Medical Center in Nashville, Tenn., an author of the 2020 study.
Dr. Nicholson, who was not involved in the AAP report, said that the retrospective data are strong enough to justify using FMT to eradicate CDIs in children. But researchers are unclear about the biologic mechanisms that make FMTs work.
Dr. Nicholson said that many therapeutics meant to produce a healthier microbiome are being studied in clinical trials. Any clinical trials of such products should include children, Dr. Nicholson said. A child’s gastrointestinal microbiome is actively developing, Dr. Nicholson added, compared with the relatively stable microbiome of an adult.
“When we think about the microbiome it makes sense to target kids, because they’re more apt to respond to these therapies. I worry that somebody will say ‘this doesn’t work in adults,’ and it just stops there,” Dr. Nicholson said.
Though the AAP said that the benefits of FMT for treating CDIs are clear, the data available for treating other conditions such as ulcerative colitis or Crohn’s disease are less convincing. Any child receiving an FMT for these ailments should only do so as part of a clinical trial, the group said.
The AAP report endorses a joint position paper, published in 2019, about the benefits of FMTs for CDIs from North American and European pediatric gastroenterology societies. Dr. Nicholson was an author of this joint statement and hopes that the AAP report raises further awareness among pediatricians that FMTs are a safe and effective treatment for recurrent CDIs.
“This is something that maybe is not as discussed in pediatric circles. Kids need FMTs sometimes,” Dr. Nicholson said.
Dr. Oliva-Hemker and Dr. Nicholson report no relevant financial relationships.
A version of this article appeared on Medscape.com.
(AAP).
However, fecal microbiota transplants (FMTs) should not be used to treat other gastrointestinal ailments such as Crohn’s disease or ulcerative colitis, because scientific evidence falls short on effectiveness in treating these conditions, the group said.
C. difficile infections (CDIs) are major contributors to hospital-associated diarrhea and diarrhea caused by antibiotics. An FMT involves introducing the feces of a healthy person into the gastrointestinal tract, usually through a nasogastric tube but sometimes in capsules containing healthy stool. Serious adverse reactions associated with an FMT, such as hospitalization, are rare, occuring in roughly 2% of case, the AAP said.
An FMT “does have a place for treatment of recurrent CDIs in children,” said Maria Oliva-Hemker, MD, a pediatric gastroenterologist at Johns Hopkins University School of Medicine in Baltimore and the lead author of the report, which was online in Pediatrics.
The AAP strongly encourages people not to perform an FMT at home, although caregivers may be tempted due to a lack of medical facilities located nearby to deliver this care.
“People might see a video on YouTube and think they can do this themselves,” Dr. Oliva-Hemker said.
An FMT requires screening of donors for any infections, which involves administering questionnaires and analyzing donor blood and stool, which are tasks better suited for medical facilities than for a living room.
No controlled or prospective clinical trials on the efficacy of FMT for children exist, according to the AAP. But a retrospective study published in 2020 showed that one or two courses of FMT prevented CDI recurrence in children 87% of the time. Researchers defined the eradication of CDIs as no recurrence for at least 2 months after an FMT and noted the success rates in children were comaparable to those reported in adults.
Unlike pediatric data, adult data come from a randomized clinical trial.
“Sometimes, kids are the last people to be enrolled in these trials,” said Maribeth Nicholson, MD, MPH, a pediatric gastroenterologist at Vanderbilt University Medical Center in Nashville, Tenn., an author of the 2020 study.
Dr. Nicholson, who was not involved in the AAP report, said that the retrospective data are strong enough to justify using FMT to eradicate CDIs in children. But researchers are unclear about the biologic mechanisms that make FMTs work.
Dr. Nicholson said that many therapeutics meant to produce a healthier microbiome are being studied in clinical trials. Any clinical trials of such products should include children, Dr. Nicholson said. A child’s gastrointestinal microbiome is actively developing, Dr. Nicholson added, compared with the relatively stable microbiome of an adult.
“When we think about the microbiome it makes sense to target kids, because they’re more apt to respond to these therapies. I worry that somebody will say ‘this doesn’t work in adults,’ and it just stops there,” Dr. Nicholson said.
Though the AAP said that the benefits of FMT for treating CDIs are clear, the data available for treating other conditions such as ulcerative colitis or Crohn’s disease are less convincing. Any child receiving an FMT for these ailments should only do so as part of a clinical trial, the group said.
The AAP report endorses a joint position paper, published in 2019, about the benefits of FMTs for CDIs from North American and European pediatric gastroenterology societies. Dr. Nicholson was an author of this joint statement and hopes that the AAP report raises further awareness among pediatricians that FMTs are a safe and effective treatment for recurrent CDIs.
“This is something that maybe is not as discussed in pediatric circles. Kids need FMTs sometimes,” Dr. Nicholson said.
Dr. Oliva-Hemker and Dr. Nicholson report no relevant financial relationships.
A version of this article appeared on Medscape.com.
(AAP).
However, fecal microbiota transplants (FMTs) should not be used to treat other gastrointestinal ailments such as Crohn’s disease or ulcerative colitis, because scientific evidence falls short on effectiveness in treating these conditions, the group said.
C. difficile infections (CDIs) are major contributors to hospital-associated diarrhea and diarrhea caused by antibiotics. An FMT involves introducing the feces of a healthy person into the gastrointestinal tract, usually through a nasogastric tube but sometimes in capsules containing healthy stool. Serious adverse reactions associated with an FMT, such as hospitalization, are rare, occuring in roughly 2% of case, the AAP said.
An FMT “does have a place for treatment of recurrent CDIs in children,” said Maria Oliva-Hemker, MD, a pediatric gastroenterologist at Johns Hopkins University School of Medicine in Baltimore and the lead author of the report, which was online in Pediatrics.
The AAP strongly encourages people not to perform an FMT at home, although caregivers may be tempted due to a lack of medical facilities located nearby to deliver this care.
“People might see a video on YouTube and think they can do this themselves,” Dr. Oliva-Hemker said.
An FMT requires screening of donors for any infections, which involves administering questionnaires and analyzing donor blood and stool, which are tasks better suited for medical facilities than for a living room.
No controlled or prospective clinical trials on the efficacy of FMT for children exist, according to the AAP. But a retrospective study published in 2020 showed that one or two courses of FMT prevented CDI recurrence in children 87% of the time. Researchers defined the eradication of CDIs as no recurrence for at least 2 months after an FMT and noted the success rates in children were comaparable to those reported in adults.
Unlike pediatric data, adult data come from a randomized clinical trial.
“Sometimes, kids are the last people to be enrolled in these trials,” said Maribeth Nicholson, MD, MPH, a pediatric gastroenterologist at Vanderbilt University Medical Center in Nashville, Tenn., an author of the 2020 study.
Dr. Nicholson, who was not involved in the AAP report, said that the retrospective data are strong enough to justify using FMT to eradicate CDIs in children. But researchers are unclear about the biologic mechanisms that make FMTs work.
Dr. Nicholson said that many therapeutics meant to produce a healthier microbiome are being studied in clinical trials. Any clinical trials of such products should include children, Dr. Nicholson said. A child’s gastrointestinal microbiome is actively developing, Dr. Nicholson added, compared with the relatively stable microbiome of an adult.
“When we think about the microbiome it makes sense to target kids, because they’re more apt to respond to these therapies. I worry that somebody will say ‘this doesn’t work in adults,’ and it just stops there,” Dr. Nicholson said.
Though the AAP said that the benefits of FMT for treating CDIs are clear, the data available for treating other conditions such as ulcerative colitis or Crohn’s disease are less convincing. Any child receiving an FMT for these ailments should only do so as part of a clinical trial, the group said.
The AAP report endorses a joint position paper, published in 2019, about the benefits of FMTs for CDIs from North American and European pediatric gastroenterology societies. Dr. Nicholson was an author of this joint statement and hopes that the AAP report raises further awareness among pediatricians that FMTs are a safe and effective treatment for recurrent CDIs.
“This is something that maybe is not as discussed in pediatric circles. Kids need FMTs sometimes,” Dr. Nicholson said.
Dr. Oliva-Hemker and Dr. Nicholson report no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM PEDIATRICS
WHO: Smoking cessation reduces risk of type 2 diabetes up to 40%
TOPLINE:
, and quitting even after one has developed type 2 diabetes is important in preventing a worsening of the disease’s many serious comorbidities, according to a new policy brief jointly issued by the World Health Organization, the International Diabetes Federation (IDF), and the University of Newcastle, Callaghan, Australia.
With type 2 diabetes representing one of the most prevalent chronic diseases worldwide and the ninth cause of death globally, the potential to reduce the risk and worsening of the disease by quitting smoking adds to the urgency of smoking cessation as a public health interest.
METHODOLOGY:
- The policy brief summarizes the evidence on the health impacts of type 2 diabetes, tobacco smoking, and the pathophysiology of tobacco use and its role in the development of type 2 diabetes.
- The brief also describes the latest data on newer products that target smokers or potential smokers, including smokeless tobacco, new nicotine and tobacco products, and their relationship with type 2 diabetes. For instance, evidence suggests that even with smokeless tobacco, heavy use or high consumption increases the risk of developing type 2 diabetes, as the products often contain nicotine, known to contribute to the development of type 2 diabetes and related health conditions.
- Evidence on the effectiveness of tobacco control interventions among those with type 2 diabetes is also summarized, including discussion of a systematic review of six studies suggesting that interventions focusing on education and the involvement of health care professionals and pharmacists can be beneficial for people with type 2 diabetes.
TAKEAWAY:
- Smoking exacerbates the known serious complications of diabetic neuropathy and foot ulcers with type 2 diabetes, while further impeding wound healing.
- Smoking also causes damage to retinal blood vessels already at risk with type 2 diabetes, increasing the risk of diabetic retinopathy and vision loss.
- Quitting tobacco use can help prevent those and other major health complications already linked to diabetes, including kidney failure and cardiovascular events.
- Studies show that key misconceptions among smokers with type 2 diabetes that can prevent cessation include concerns about post-cessation weight gain, the influence of peers who smoke, and the psychological aspect of addiction.
- Clinicians are urged to provide advice on how to stop smoking to all tobacco users during the course of a routine consultation or interaction, which can be accomplished in only a few minutes.
IN PRACTICE:
“Health professionals play a vital role in motivating and guiding individuals with type 2 diabetes in their journey to quit tobacco,” Ruediger Krech, MD, director of the Department of Health Promotion at the World Health Organization in Geneva, Switzerland, said in a press statement on the policy brief.
“Simultaneously, governments must take the crucial step of ensuring all indoor public places, workplaces, and public transport are completely smoke-free. These interventions are essential safeguards against the onset and progression of this and many other chronic diseases,” he emphasized.
SOURCE:
The policy brief was jointly developed by the World Health Organization, the International Diabetes Federation, and the University of Newcastle.
The detailed policy brief can be downloaded on the IDF website.
LIMITATIONS:
Research remains limited on some issues, including the effectiveness of tobacco control interventions and smoking cessation methods for people with type 2 diabetes.
Likewise, specific guidelines for smoking cessation in the type 2 diabetes population are lacking. However, the general approaches of building patient motivation, behavioral interventions, and pharmacological treatments are advised.
“These interventions should be at least as intensive as those for the general population, while considering the unique characteristics of the disease and the individual,” the authors asserted.
DISCLOSURES:
The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
, and quitting even after one has developed type 2 diabetes is important in preventing a worsening of the disease’s many serious comorbidities, according to a new policy brief jointly issued by the World Health Organization, the International Diabetes Federation (IDF), and the University of Newcastle, Callaghan, Australia.
With type 2 diabetes representing one of the most prevalent chronic diseases worldwide and the ninth cause of death globally, the potential to reduce the risk and worsening of the disease by quitting smoking adds to the urgency of smoking cessation as a public health interest.
METHODOLOGY:
- The policy brief summarizes the evidence on the health impacts of type 2 diabetes, tobacco smoking, and the pathophysiology of tobacco use and its role in the development of type 2 diabetes.
- The brief also describes the latest data on newer products that target smokers or potential smokers, including smokeless tobacco, new nicotine and tobacco products, and their relationship with type 2 diabetes. For instance, evidence suggests that even with smokeless tobacco, heavy use or high consumption increases the risk of developing type 2 diabetes, as the products often contain nicotine, known to contribute to the development of type 2 diabetes and related health conditions.
- Evidence on the effectiveness of tobacco control interventions among those with type 2 diabetes is also summarized, including discussion of a systematic review of six studies suggesting that interventions focusing on education and the involvement of health care professionals and pharmacists can be beneficial for people with type 2 diabetes.
TAKEAWAY:
- Smoking exacerbates the known serious complications of diabetic neuropathy and foot ulcers with type 2 diabetes, while further impeding wound healing.
- Smoking also causes damage to retinal blood vessels already at risk with type 2 diabetes, increasing the risk of diabetic retinopathy and vision loss.
- Quitting tobacco use can help prevent those and other major health complications already linked to diabetes, including kidney failure and cardiovascular events.
- Studies show that key misconceptions among smokers with type 2 diabetes that can prevent cessation include concerns about post-cessation weight gain, the influence of peers who smoke, and the psychological aspect of addiction.
- Clinicians are urged to provide advice on how to stop smoking to all tobacco users during the course of a routine consultation or interaction, which can be accomplished in only a few minutes.
IN PRACTICE:
“Health professionals play a vital role in motivating and guiding individuals with type 2 diabetes in their journey to quit tobacco,” Ruediger Krech, MD, director of the Department of Health Promotion at the World Health Organization in Geneva, Switzerland, said in a press statement on the policy brief.
“Simultaneously, governments must take the crucial step of ensuring all indoor public places, workplaces, and public transport are completely smoke-free. These interventions are essential safeguards against the onset and progression of this and many other chronic diseases,” he emphasized.
SOURCE:
The policy brief was jointly developed by the World Health Organization, the International Diabetes Federation, and the University of Newcastle.
The detailed policy brief can be downloaded on the IDF website.
LIMITATIONS:
Research remains limited on some issues, including the effectiveness of tobacco control interventions and smoking cessation methods for people with type 2 diabetes.
Likewise, specific guidelines for smoking cessation in the type 2 diabetes population are lacking. However, the general approaches of building patient motivation, behavioral interventions, and pharmacological treatments are advised.
“These interventions should be at least as intensive as those for the general population, while considering the unique characteristics of the disease and the individual,” the authors asserted.
DISCLOSURES:
The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
, and quitting even after one has developed type 2 diabetes is important in preventing a worsening of the disease’s many serious comorbidities, according to a new policy brief jointly issued by the World Health Organization, the International Diabetes Federation (IDF), and the University of Newcastle, Callaghan, Australia.
With type 2 diabetes representing one of the most prevalent chronic diseases worldwide and the ninth cause of death globally, the potential to reduce the risk and worsening of the disease by quitting smoking adds to the urgency of smoking cessation as a public health interest.
METHODOLOGY:
- The policy brief summarizes the evidence on the health impacts of type 2 diabetes, tobacco smoking, and the pathophysiology of tobacco use and its role in the development of type 2 diabetes.
- The brief also describes the latest data on newer products that target smokers or potential smokers, including smokeless tobacco, new nicotine and tobacco products, and their relationship with type 2 diabetes. For instance, evidence suggests that even with smokeless tobacco, heavy use or high consumption increases the risk of developing type 2 diabetes, as the products often contain nicotine, known to contribute to the development of type 2 diabetes and related health conditions.
- Evidence on the effectiveness of tobacco control interventions among those with type 2 diabetes is also summarized, including discussion of a systematic review of six studies suggesting that interventions focusing on education and the involvement of health care professionals and pharmacists can be beneficial for people with type 2 diabetes.
TAKEAWAY:
- Smoking exacerbates the known serious complications of diabetic neuropathy and foot ulcers with type 2 diabetes, while further impeding wound healing.
- Smoking also causes damage to retinal blood vessels already at risk with type 2 diabetes, increasing the risk of diabetic retinopathy and vision loss.
- Quitting tobacco use can help prevent those and other major health complications already linked to diabetes, including kidney failure and cardiovascular events.
- Studies show that key misconceptions among smokers with type 2 diabetes that can prevent cessation include concerns about post-cessation weight gain, the influence of peers who smoke, and the psychological aspect of addiction.
- Clinicians are urged to provide advice on how to stop smoking to all tobacco users during the course of a routine consultation or interaction, which can be accomplished in only a few minutes.
IN PRACTICE:
“Health professionals play a vital role in motivating and guiding individuals with type 2 diabetes in their journey to quit tobacco,” Ruediger Krech, MD, director of the Department of Health Promotion at the World Health Organization in Geneva, Switzerland, said in a press statement on the policy brief.
“Simultaneously, governments must take the crucial step of ensuring all indoor public places, workplaces, and public transport are completely smoke-free. These interventions are essential safeguards against the onset and progression of this and many other chronic diseases,” he emphasized.
SOURCE:
The policy brief was jointly developed by the World Health Organization, the International Diabetes Federation, and the University of Newcastle.
The detailed policy brief can be downloaded on the IDF website.
LIMITATIONS:
Research remains limited on some issues, including the effectiveness of tobacco control interventions and smoking cessation methods for people with type 2 diabetes.
Likewise, specific guidelines for smoking cessation in the type 2 diabetes population are lacking. However, the general approaches of building patient motivation, behavioral interventions, and pharmacological treatments are advised.
“These interventions should be at least as intensive as those for the general population, while considering the unique characteristics of the disease and the individual,” the authors asserted.
DISCLOSURES:
The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A better way to control blood pressure
My Bing AI engine, when prompted, tells me that there are about 87 journals, 45 conferences, and 53 workshops presently dedicated exclusively to hypertension. All of that attention, and yet ...
What is going on?
The top killers of Americans remain coronary artery heart disease (26%), cancer (22%), and stroke (6%). The precursors and attributable risk factors for coronary artery heart disease include hypertension (40%), obesity (20%), diabetes (15%), and combustible tobacco use (15%). The key precursors and attributable risk factors for stroke are hypertension (53%), obesity (37%), diabetes (9%), and combustible tobacco use (11%). Obviously, these are estimates, with substantial overlap.
It’s pretty obvious that
We have addressed improving tobacco control and preventing obesity and diabetes on these pages many times, and lamented the medical, public health, and societal failings. Today we turn our attention to the control of hypertension. That is much easier and far less expensive.
All physicians and medical organizations know that hypertension is a major attributable cause of many serious, expensive, and fatal illnesses. As many as 119 million (48%) of American adults have hypertension. The American Heart Association (AHA), American Medical Association (AMA), American College of Cardiology (ACC), and hundreds of other organizations have set a new target of 130/80 (revised from 140/90) for blood pressure control and have launched a major initiative, Target: BP, to reach it.
That is just great. We all wish this massive effort to succeed where few others have. But do AHA, AMA, ACC, and others understand why most efforts to this point have failed? The blame is typically aimed at patients failing to adhere to their instructions. Maybe, but why? And how does Target: BP intend to convert chronic failure into success if it just continues to do everything they have been trying to do that doesn’t work?
At this point, the Centers for Disease Control and Prevention reports that fewer than 48% of American patients with hypertension meet even the less stringent historical 140/90 goal.
A group practice in Ohio, PriMed Physicians, has consistently exceeded 90% or even 95% blood pressure control for its patients with hypertension for more than 10 years. Exemplary. How do they do it? This video of the 13th annual Lundberg Institute lecture describes this unique and successful program.
PriMed’s clinicians use the MedsEngine AI tool from MediSync and the NICaS (noninvasive cardiac system with impedance cardiography) to determine each patient’s unique blood pressure pathophysiology. Clinicians and patients understand that the simplest explanation of this pathophysiology encompasses three factors: (1) the volume of “water” (blood) in the system; (2) the strength of the pumping (pulsatile) process; and (3) the tightness (resistance) of the tubes that carry the blood. Patients “get it” when it is explained this way, and they cooperate.
At the first patient encounter, the Food and Drug Administration–approved PhysioFlow is employed to assess those three vital hemodynamic factors. The individual patient’s data are loaded into a tightly programed EHR-based algorithm with 37 clinical factors and five classes of drugs, providing multiple ways to influence the three key pathophysiologic processes. In this way, they arrive at the precise drug(s) and dosages for that patient. During the second visit, most patients are already showing improvement. By the third visit, the blood pressures of most patients have reached target control. After that, it is maintenance and tweaking.
These factors summarize why it works:
- Senior management belief, commitment, and leadership
- Informed buy-in from clinicians and patients
- A test that determines root causes of too much fluid, too strong pump action, or too tight pipes, and their proportionality
- An AI tool that matches those three pathophysiologic factors and 35 other clinical factors with the best drug or drugs (of many, not just a few) and dosages
- Persistent clinician-patient follow-up
- Refusal to accept failure
Since this approach is so successful, why is its use not everywhere?
It is not as if nobody noticed, even if you and many organizations have not. The American Medical Group Association recognized the program’s success by giving its top award to PriMed in 2015.
Klepper and Rodis wrote about this approach for managing multiple chronic conditions in 2021. Here’s a background article and an explainer, Clinical use of impedance cardiography for hemodynamic assessment of early cardiovascular disease and management of hypertension.
I found one pragmatic controlled clinical trial of impedance cardiography with a decision-support system from Beijing that did demonstrate clinical and statistical significance.
Frankly, we do need more rigorous, unbiased, large, controlled clinical trials assessing the MedsEngine and NICaS approach to managing blood pressure to facilitate a massive switch from the old and established (but failing) approach to a starkly better way.
Almost no one ever “completes a database.” All decision makers must act based upon the best data to which they have access. Data are often incomplete. The difference between success and mediocrity is often the ability of an individual or system to decide when enough information is enough and act accordingly.
Cost-effectiveness studies in three countries (United Kingdom, United States, and China) confirm sharply lower lifelong costs when blood pressure is well controlled. Of course.
For the American medical-industrial complex, lowered costs for managing common serious diseases may be an undesired rather than a good thing. In money-driven medicine, lower costs to the payer and purchaser translate to less revenue for the providers. Imagine all of those invasive and noninvasive diagnostic and therapeutic procedures forgone by prevention of hypertension. Is it possible that such an underlying truth is the real reason why American medicine is habitually unsuccessful at controlling blood pressure?
Right now, if my blood pressure were not well controlled (it is), I would find my way to Cincinnati, to give PriMed physicians, MediSync, and MedsEngine a crack at prolonging my useful life.
Dr. Lundberg is editor in chief of Cancer Commons. He disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
My Bing AI engine, when prompted, tells me that there are about 87 journals, 45 conferences, and 53 workshops presently dedicated exclusively to hypertension. All of that attention, and yet ...
What is going on?
The top killers of Americans remain coronary artery heart disease (26%), cancer (22%), and stroke (6%). The precursors and attributable risk factors for coronary artery heart disease include hypertension (40%), obesity (20%), diabetes (15%), and combustible tobacco use (15%). The key precursors and attributable risk factors for stroke are hypertension (53%), obesity (37%), diabetes (9%), and combustible tobacco use (11%). Obviously, these are estimates, with substantial overlap.
It’s pretty obvious that
We have addressed improving tobacco control and preventing obesity and diabetes on these pages many times, and lamented the medical, public health, and societal failings. Today we turn our attention to the control of hypertension. That is much easier and far less expensive.
All physicians and medical organizations know that hypertension is a major attributable cause of many serious, expensive, and fatal illnesses. As many as 119 million (48%) of American adults have hypertension. The American Heart Association (AHA), American Medical Association (AMA), American College of Cardiology (ACC), and hundreds of other organizations have set a new target of 130/80 (revised from 140/90) for blood pressure control and have launched a major initiative, Target: BP, to reach it.
That is just great. We all wish this massive effort to succeed where few others have. But do AHA, AMA, ACC, and others understand why most efforts to this point have failed? The blame is typically aimed at patients failing to adhere to their instructions. Maybe, but why? And how does Target: BP intend to convert chronic failure into success if it just continues to do everything they have been trying to do that doesn’t work?
At this point, the Centers for Disease Control and Prevention reports that fewer than 48% of American patients with hypertension meet even the less stringent historical 140/90 goal.
A group practice in Ohio, PriMed Physicians, has consistently exceeded 90% or even 95% blood pressure control for its patients with hypertension for more than 10 years. Exemplary. How do they do it? This video of the 13th annual Lundberg Institute lecture describes this unique and successful program.
PriMed’s clinicians use the MedsEngine AI tool from MediSync and the NICaS (noninvasive cardiac system with impedance cardiography) to determine each patient’s unique blood pressure pathophysiology. Clinicians and patients understand that the simplest explanation of this pathophysiology encompasses three factors: (1) the volume of “water” (blood) in the system; (2) the strength of the pumping (pulsatile) process; and (3) the tightness (resistance) of the tubes that carry the blood. Patients “get it” when it is explained this way, and they cooperate.
At the first patient encounter, the Food and Drug Administration–approved PhysioFlow is employed to assess those three vital hemodynamic factors. The individual patient’s data are loaded into a tightly programed EHR-based algorithm with 37 clinical factors and five classes of drugs, providing multiple ways to influence the three key pathophysiologic processes. In this way, they arrive at the precise drug(s) and dosages for that patient. During the second visit, most patients are already showing improvement. By the third visit, the blood pressures of most patients have reached target control. After that, it is maintenance and tweaking.
These factors summarize why it works:
- Senior management belief, commitment, and leadership
- Informed buy-in from clinicians and patients
- A test that determines root causes of too much fluid, too strong pump action, or too tight pipes, and their proportionality
- An AI tool that matches those three pathophysiologic factors and 35 other clinical factors with the best drug or drugs (of many, not just a few) and dosages
- Persistent clinician-patient follow-up
- Refusal to accept failure
Since this approach is so successful, why is its use not everywhere?
It is not as if nobody noticed, even if you and many organizations have not. The American Medical Group Association recognized the program’s success by giving its top award to PriMed in 2015.
Klepper and Rodis wrote about this approach for managing multiple chronic conditions in 2021. Here’s a background article and an explainer, Clinical use of impedance cardiography for hemodynamic assessment of early cardiovascular disease and management of hypertension.
I found one pragmatic controlled clinical trial of impedance cardiography with a decision-support system from Beijing that did demonstrate clinical and statistical significance.
Frankly, we do need more rigorous, unbiased, large, controlled clinical trials assessing the MedsEngine and NICaS approach to managing blood pressure to facilitate a massive switch from the old and established (but failing) approach to a starkly better way.
Almost no one ever “completes a database.” All decision makers must act based upon the best data to which they have access. Data are often incomplete. The difference between success and mediocrity is often the ability of an individual or system to decide when enough information is enough and act accordingly.
Cost-effectiveness studies in three countries (United Kingdom, United States, and China) confirm sharply lower lifelong costs when blood pressure is well controlled. Of course.
For the American medical-industrial complex, lowered costs for managing common serious diseases may be an undesired rather than a good thing. In money-driven medicine, lower costs to the payer and purchaser translate to less revenue for the providers. Imagine all of those invasive and noninvasive diagnostic and therapeutic procedures forgone by prevention of hypertension. Is it possible that such an underlying truth is the real reason why American medicine is habitually unsuccessful at controlling blood pressure?
Right now, if my blood pressure were not well controlled (it is), I would find my way to Cincinnati, to give PriMed physicians, MediSync, and MedsEngine a crack at prolonging my useful life.
Dr. Lundberg is editor in chief of Cancer Commons. He disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
My Bing AI engine, when prompted, tells me that there are about 87 journals, 45 conferences, and 53 workshops presently dedicated exclusively to hypertension. All of that attention, and yet ...
What is going on?
The top killers of Americans remain coronary artery heart disease (26%), cancer (22%), and stroke (6%). The precursors and attributable risk factors for coronary artery heart disease include hypertension (40%), obesity (20%), diabetes (15%), and combustible tobacco use (15%). The key precursors and attributable risk factors for stroke are hypertension (53%), obesity (37%), diabetes (9%), and combustible tobacco use (11%). Obviously, these are estimates, with substantial overlap.
It’s pretty obvious that
We have addressed improving tobacco control and preventing obesity and diabetes on these pages many times, and lamented the medical, public health, and societal failings. Today we turn our attention to the control of hypertension. That is much easier and far less expensive.
All physicians and medical organizations know that hypertension is a major attributable cause of many serious, expensive, and fatal illnesses. As many as 119 million (48%) of American adults have hypertension. The American Heart Association (AHA), American Medical Association (AMA), American College of Cardiology (ACC), and hundreds of other organizations have set a new target of 130/80 (revised from 140/90) for blood pressure control and have launched a major initiative, Target: BP, to reach it.
That is just great. We all wish this massive effort to succeed where few others have. But do AHA, AMA, ACC, and others understand why most efforts to this point have failed? The blame is typically aimed at patients failing to adhere to their instructions. Maybe, but why? And how does Target: BP intend to convert chronic failure into success if it just continues to do everything they have been trying to do that doesn’t work?
At this point, the Centers for Disease Control and Prevention reports that fewer than 48% of American patients with hypertension meet even the less stringent historical 140/90 goal.
A group practice in Ohio, PriMed Physicians, has consistently exceeded 90% or even 95% blood pressure control for its patients with hypertension for more than 10 years. Exemplary. How do they do it? This video of the 13th annual Lundberg Institute lecture describes this unique and successful program.
PriMed’s clinicians use the MedsEngine AI tool from MediSync and the NICaS (noninvasive cardiac system with impedance cardiography) to determine each patient’s unique blood pressure pathophysiology. Clinicians and patients understand that the simplest explanation of this pathophysiology encompasses three factors: (1) the volume of “water” (blood) in the system; (2) the strength of the pumping (pulsatile) process; and (3) the tightness (resistance) of the tubes that carry the blood. Patients “get it” when it is explained this way, and they cooperate.
At the first patient encounter, the Food and Drug Administration–approved PhysioFlow is employed to assess those three vital hemodynamic factors. The individual patient’s data are loaded into a tightly programed EHR-based algorithm with 37 clinical factors and five classes of drugs, providing multiple ways to influence the three key pathophysiologic processes. In this way, they arrive at the precise drug(s) and dosages for that patient. During the second visit, most patients are already showing improvement. By the third visit, the blood pressures of most patients have reached target control. After that, it is maintenance and tweaking.
These factors summarize why it works:
- Senior management belief, commitment, and leadership
- Informed buy-in from clinicians and patients
- A test that determines root causes of too much fluid, too strong pump action, or too tight pipes, and their proportionality
- An AI tool that matches those three pathophysiologic factors and 35 other clinical factors with the best drug or drugs (of many, not just a few) and dosages
- Persistent clinician-patient follow-up
- Refusal to accept failure
Since this approach is so successful, why is its use not everywhere?
It is not as if nobody noticed, even if you and many organizations have not. The American Medical Group Association recognized the program’s success by giving its top award to PriMed in 2015.
Klepper and Rodis wrote about this approach for managing multiple chronic conditions in 2021. Here’s a background article and an explainer, Clinical use of impedance cardiography for hemodynamic assessment of early cardiovascular disease and management of hypertension.
I found one pragmatic controlled clinical trial of impedance cardiography with a decision-support system from Beijing that did demonstrate clinical and statistical significance.
Frankly, we do need more rigorous, unbiased, large, controlled clinical trials assessing the MedsEngine and NICaS approach to managing blood pressure to facilitate a massive switch from the old and established (but failing) approach to a starkly better way.
Almost no one ever “completes a database.” All decision makers must act based upon the best data to which they have access. Data are often incomplete. The difference between success and mediocrity is often the ability of an individual or system to decide when enough information is enough and act accordingly.
Cost-effectiveness studies in three countries (United Kingdom, United States, and China) confirm sharply lower lifelong costs when blood pressure is well controlled. Of course.
For the American medical-industrial complex, lowered costs for managing common serious diseases may be an undesired rather than a good thing. In money-driven medicine, lower costs to the payer and purchaser translate to less revenue for the providers. Imagine all of those invasive and noninvasive diagnostic and therapeutic procedures forgone by prevention of hypertension. Is it possible that such an underlying truth is the real reason why American medicine is habitually unsuccessful at controlling blood pressure?
Right now, if my blood pressure were not well controlled (it is), I would find my way to Cincinnati, to give PriMed physicians, MediSync, and MedsEngine a crack at prolonging my useful life.
Dr. Lundberg is editor in chief of Cancer Commons. He disclosed no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Cold-water swimming for your health? These docs say jump in
Adam Boggon, MBChB, was working at the Royal Free Hospital in North London during the city’s second wave of COVID-19. “I was effectively living in the hospital,” he recalled. “It felt like I was going 10,000 miles per hour, trying to corral hundreds of medical students and doctors.”
During a national lockdown, there were few places Dr. Boggon could escape to, but the Hampstead Heath swimming ponds mostly remained open. He swam there regularly to exercise and recharge even in winter.
“Swimming in cold water takes you out of yourself,” Dr. Boggon said. “It was such a release for someone who grew up in a rural place and had access to green space, even though the water is murky.” It also hovers around 50 °F (10 °C).
Jumping into cold water, well, kind of stinks. So why do it? It’s not only for bragging rights. , specifically to improve depression symptoms and even ease inflammatory conditions.
And a lot of that research is driven by medical pros who love to do it themselves.
For Dr. Boggon, swimming in frigid water is uncomfortable, but he feels that a sensation of calmness follows that makes the plunge more than worth it. Now a Fulbright Scholar at Harvard, where he studies public health and health management, Dr. Boggon is able to frequent the fabled Walden Pond just outside of Boston.
As Thoreau himself said, “You can never have enough of nature.”
Yes, even if it’s really, really cold.
Taking a deeper dive
Heather Massey, PhD, a senior lecturer in Sport, Health, and Exercise Science at University of Portsmouth, blames her father, a dinghy sailor, for her affinity for cold-water swimming.
And she’s done more than most, including an epic 16-hour crossing of the English Channel. The water temperature was in the upper-50s °F, and she swam without a wetsuit. “Time just seemed to collapse,” she has shared about the experience.
While working on her PhD and studying the effects of environmental physiology, in particular what happens to the body when it gets hot or cold, Dr. Massey’s hobby and studies seemed to coalesce.
Her research initially focused on the hazards around being in cold open water. But she also noticed a growing trend of people claiming health benefits from the practice. “People started to talk about experiencing improved symptoms of depression or improved mental health from their activities in the water,” she said.
She partnered with another outdoor swimming enthusiast, Hannah Denton, a counseling psychologist working for the National Health Service in the United Kingdom. Ms. Denton was publishing papers on the potential impact that outdoor swimming may have on people with depression and how it could improve mental health in general. She also regularly engages in cold-water swims to boost feelings of mindfulness and peace.
“Having the experience of being so close to nature, as well as the strong sensory experience of being in cold water, does really encourage you to be in the moment,” Ms. Denton wrote in an article for the Sussex Mindfulness Centre. “My experiences of sea swimming and mindfulness support each other. Both have made me feel more comfortable with my body, to have more of a present moment focus, to pay attention to my breathing, and to gain distance from difficult thoughts.”
Over the past few years, Dr. Massey and Ms. Denton have moved from fairly small-scale studies with no real controls to today, completing a randomized controlled trial and looking at the impact that outdoor swimming may have on people living with mild to moderate depression.
“At first, people sort of thought our idea was a bit wacky,” said Dr. Massey. “Now, the popularity of open-water swimming has really blossomed, and so has this area of research. We’re starting to build more rigor into the work.”
Like all the researchers and physicians interviewed for this article, Dr. Massey hesitates to claim that cold-water swimming is a “cure” that should be medicalized.
“It’s not about prescribing it or forcing people to do it,” said Dr. Massey. “This is not something that a doctor should write on a prescription and say you should go and have eight 1-hour sessions of swimming.”
(Not yet) a common cure
Enter into the conversation Mark Harper, MD, PhD, consultant anesthetist at Sussex University Hospitals in the United Kingdom and Kristiansand, Norway. Dr. Harper is the author of the 2022 book, Chill: The Cold Water Swim Cure – A Transformative Guide to Renew Your Body and Mind.
Dr. Harper grew up swimming in pools, and it wasn’t until his pool closed for 2 weeks that he ventured into the sea. He recalled walking up the beach afterward, thinking, God, this feels good, and from that moment on, he became hooked on outdoor swimming and curious about its therapeutic potential.
The “cure” in the book’s title, Dr. Harper explained, is being used in the historical sense of “treatment,” as in the first medical book about sea-bathing written over 250 years ago. Dr. Harper acknowledged that the connection to health is still speculative. “However, the circumstantial evidence, the feedback from participants and early study data for its benefits are now very strong,” he said.
In a small study published in 2022, Dr. Harper and colleagues took 59 people with anxiety and depression and put them through a sea-swimming course. Afterward, 80% showed a clinically significant improvement in their mental health.
More recently, Dr. Harper and his team of researchers released a survey to determine how many people were using cold-water swimming as a treatment for a mental or physical ailment. “We thought 30 or 40 people would respond, but we ended up with over 700,” he said. “The majority were using it for mental health but also included inflammation-related conditions.”
Over 2 decades, Dr. Harper has seen dramatic success stories. In his book, he recalled a good friend who, in his early 20s, suffered from Crohn’s disease so badly he couldn’t walk up the steps to his parents’ house. The friend turned to outdoor cold swimming as a low-impact workout and began noticing the symptoms of his disease were improving. Within months, he was able to go off his medications. In 2022, he completed 52 triathlons: one per week for the entire year.
How cold exposure may play with your brain
Vaibhav Diwadkar, PhD, professor of psychiatry and behavioral neurosciences at Wayne State University, in Detroit, is studying how human brain networks respond to cold exposure. Dr. Diwadkar and his colleague, Otto Muzik, PhD, began by putting volunteers in a rubber suit with thin tubing and infusing the tubing with temperature-controlled water. Meanwhile, they collected functional brain imaging data to analyze which parts of the brain were responding as body temperature changed.
The data showed that the cold exposure made certain areas of the brain very active, including some that have been associated with the regulation of mood.
Dr. Diwadkar posits that controlled exposure to cold serves as a low-level stressor that knocks different systems within the brain and body out of homeostasis. Once the stress is removed, the brain responds by releasing neurotransmitters that enhance mood, frequently leading to feelings of euphoria in participants.
“We don’t have direct evidence of such a mechanism, but it’s a reasonable speculation,” said Dr. Diwadkar.
However, he pointed out that science writers in the media often portray topics such as this one in black and white, which is “oversimplifying the scientific complexity of biology.”
Clearly, more research needs to be done on the potential therapeutic benefits of cold-water swimming. But for those suffering from anxiety, depression, or chronic illness, if taking a cold dip makes you feel better, the why and how might be beside the point.
Plus, as Dr. Harper pointed out, it’s an easy and accessible therapy.
“All you need is some water – enough to submerge your entire body in – that’s less than 68 °F (20 °C),” he said. “If you stay long enough to get over that initial shock, which is just 2 or 3 minutes, then you’ve got the effect. If you get out and want to go back in again, then you’ve done it right.”
A version of this article first appeared on Medscape.com.
Adam Boggon, MBChB, was working at the Royal Free Hospital in North London during the city’s second wave of COVID-19. “I was effectively living in the hospital,” he recalled. “It felt like I was going 10,000 miles per hour, trying to corral hundreds of medical students and doctors.”
During a national lockdown, there were few places Dr. Boggon could escape to, but the Hampstead Heath swimming ponds mostly remained open. He swam there regularly to exercise and recharge even in winter.
“Swimming in cold water takes you out of yourself,” Dr. Boggon said. “It was such a release for someone who grew up in a rural place and had access to green space, even though the water is murky.” It also hovers around 50 °F (10 °C).
Jumping into cold water, well, kind of stinks. So why do it? It’s not only for bragging rights. , specifically to improve depression symptoms and even ease inflammatory conditions.
And a lot of that research is driven by medical pros who love to do it themselves.
For Dr. Boggon, swimming in frigid water is uncomfortable, but he feels that a sensation of calmness follows that makes the plunge more than worth it. Now a Fulbright Scholar at Harvard, where he studies public health and health management, Dr. Boggon is able to frequent the fabled Walden Pond just outside of Boston.
As Thoreau himself said, “You can never have enough of nature.”
Yes, even if it’s really, really cold.
Taking a deeper dive
Heather Massey, PhD, a senior lecturer in Sport, Health, and Exercise Science at University of Portsmouth, blames her father, a dinghy sailor, for her affinity for cold-water swimming.
And she’s done more than most, including an epic 16-hour crossing of the English Channel. The water temperature was in the upper-50s °F, and she swam without a wetsuit. “Time just seemed to collapse,” she has shared about the experience.
While working on her PhD and studying the effects of environmental physiology, in particular what happens to the body when it gets hot or cold, Dr. Massey’s hobby and studies seemed to coalesce.
Her research initially focused on the hazards around being in cold open water. But she also noticed a growing trend of people claiming health benefits from the practice. “People started to talk about experiencing improved symptoms of depression or improved mental health from their activities in the water,” she said.
She partnered with another outdoor swimming enthusiast, Hannah Denton, a counseling psychologist working for the National Health Service in the United Kingdom. Ms. Denton was publishing papers on the potential impact that outdoor swimming may have on people with depression and how it could improve mental health in general. She also regularly engages in cold-water swims to boost feelings of mindfulness and peace.
“Having the experience of being so close to nature, as well as the strong sensory experience of being in cold water, does really encourage you to be in the moment,” Ms. Denton wrote in an article for the Sussex Mindfulness Centre. “My experiences of sea swimming and mindfulness support each other. Both have made me feel more comfortable with my body, to have more of a present moment focus, to pay attention to my breathing, and to gain distance from difficult thoughts.”
Over the past few years, Dr. Massey and Ms. Denton have moved from fairly small-scale studies with no real controls to today, completing a randomized controlled trial and looking at the impact that outdoor swimming may have on people living with mild to moderate depression.
“At first, people sort of thought our idea was a bit wacky,” said Dr. Massey. “Now, the popularity of open-water swimming has really blossomed, and so has this area of research. We’re starting to build more rigor into the work.”
Like all the researchers and physicians interviewed for this article, Dr. Massey hesitates to claim that cold-water swimming is a “cure” that should be medicalized.
“It’s not about prescribing it or forcing people to do it,” said Dr. Massey. “This is not something that a doctor should write on a prescription and say you should go and have eight 1-hour sessions of swimming.”
(Not yet) a common cure
Enter into the conversation Mark Harper, MD, PhD, consultant anesthetist at Sussex University Hospitals in the United Kingdom and Kristiansand, Norway. Dr. Harper is the author of the 2022 book, Chill: The Cold Water Swim Cure – A Transformative Guide to Renew Your Body and Mind.
Dr. Harper grew up swimming in pools, and it wasn’t until his pool closed for 2 weeks that he ventured into the sea. He recalled walking up the beach afterward, thinking, God, this feels good, and from that moment on, he became hooked on outdoor swimming and curious about its therapeutic potential.
The “cure” in the book’s title, Dr. Harper explained, is being used in the historical sense of “treatment,” as in the first medical book about sea-bathing written over 250 years ago. Dr. Harper acknowledged that the connection to health is still speculative. “However, the circumstantial evidence, the feedback from participants and early study data for its benefits are now very strong,” he said.
In a small study published in 2022, Dr. Harper and colleagues took 59 people with anxiety and depression and put them through a sea-swimming course. Afterward, 80% showed a clinically significant improvement in their mental health.
More recently, Dr. Harper and his team of researchers released a survey to determine how many people were using cold-water swimming as a treatment for a mental or physical ailment. “We thought 30 or 40 people would respond, but we ended up with over 700,” he said. “The majority were using it for mental health but also included inflammation-related conditions.”
Over 2 decades, Dr. Harper has seen dramatic success stories. In his book, he recalled a good friend who, in his early 20s, suffered from Crohn’s disease so badly he couldn’t walk up the steps to his parents’ house. The friend turned to outdoor cold swimming as a low-impact workout and began noticing the symptoms of his disease were improving. Within months, he was able to go off his medications. In 2022, he completed 52 triathlons: one per week for the entire year.
How cold exposure may play with your brain
Vaibhav Diwadkar, PhD, professor of psychiatry and behavioral neurosciences at Wayne State University, in Detroit, is studying how human brain networks respond to cold exposure. Dr. Diwadkar and his colleague, Otto Muzik, PhD, began by putting volunteers in a rubber suit with thin tubing and infusing the tubing with temperature-controlled water. Meanwhile, they collected functional brain imaging data to analyze which parts of the brain were responding as body temperature changed.
The data showed that the cold exposure made certain areas of the brain very active, including some that have been associated with the regulation of mood.
Dr. Diwadkar posits that controlled exposure to cold serves as a low-level stressor that knocks different systems within the brain and body out of homeostasis. Once the stress is removed, the brain responds by releasing neurotransmitters that enhance mood, frequently leading to feelings of euphoria in participants.
“We don’t have direct evidence of such a mechanism, but it’s a reasonable speculation,” said Dr. Diwadkar.
However, he pointed out that science writers in the media often portray topics such as this one in black and white, which is “oversimplifying the scientific complexity of biology.”
Clearly, more research needs to be done on the potential therapeutic benefits of cold-water swimming. But for those suffering from anxiety, depression, or chronic illness, if taking a cold dip makes you feel better, the why and how might be beside the point.
Plus, as Dr. Harper pointed out, it’s an easy and accessible therapy.
“All you need is some water – enough to submerge your entire body in – that’s less than 68 °F (20 °C),” he said. “If you stay long enough to get over that initial shock, which is just 2 or 3 minutes, then you’ve got the effect. If you get out and want to go back in again, then you’ve done it right.”
A version of this article first appeared on Medscape.com.
Adam Boggon, MBChB, was working at the Royal Free Hospital in North London during the city’s second wave of COVID-19. “I was effectively living in the hospital,” he recalled. “It felt like I was going 10,000 miles per hour, trying to corral hundreds of medical students and doctors.”
During a national lockdown, there were few places Dr. Boggon could escape to, but the Hampstead Heath swimming ponds mostly remained open. He swam there regularly to exercise and recharge even in winter.
“Swimming in cold water takes you out of yourself,” Dr. Boggon said. “It was such a release for someone who grew up in a rural place and had access to green space, even though the water is murky.” It also hovers around 50 °F (10 °C).
Jumping into cold water, well, kind of stinks. So why do it? It’s not only for bragging rights. , specifically to improve depression symptoms and even ease inflammatory conditions.
And a lot of that research is driven by medical pros who love to do it themselves.
For Dr. Boggon, swimming in frigid water is uncomfortable, but he feels that a sensation of calmness follows that makes the plunge more than worth it. Now a Fulbright Scholar at Harvard, where he studies public health and health management, Dr. Boggon is able to frequent the fabled Walden Pond just outside of Boston.
As Thoreau himself said, “You can never have enough of nature.”
Yes, even if it’s really, really cold.
Taking a deeper dive
Heather Massey, PhD, a senior lecturer in Sport, Health, and Exercise Science at University of Portsmouth, blames her father, a dinghy sailor, for her affinity for cold-water swimming.
And she’s done more than most, including an epic 16-hour crossing of the English Channel. The water temperature was in the upper-50s °F, and she swam without a wetsuit. “Time just seemed to collapse,” she has shared about the experience.
While working on her PhD and studying the effects of environmental physiology, in particular what happens to the body when it gets hot or cold, Dr. Massey’s hobby and studies seemed to coalesce.
Her research initially focused on the hazards around being in cold open water. But she also noticed a growing trend of people claiming health benefits from the practice. “People started to talk about experiencing improved symptoms of depression or improved mental health from their activities in the water,” she said.
She partnered with another outdoor swimming enthusiast, Hannah Denton, a counseling psychologist working for the National Health Service in the United Kingdom. Ms. Denton was publishing papers on the potential impact that outdoor swimming may have on people with depression and how it could improve mental health in general. She also regularly engages in cold-water swims to boost feelings of mindfulness and peace.
“Having the experience of being so close to nature, as well as the strong sensory experience of being in cold water, does really encourage you to be in the moment,” Ms. Denton wrote in an article for the Sussex Mindfulness Centre. “My experiences of sea swimming and mindfulness support each other. Both have made me feel more comfortable with my body, to have more of a present moment focus, to pay attention to my breathing, and to gain distance from difficult thoughts.”
Over the past few years, Dr. Massey and Ms. Denton have moved from fairly small-scale studies with no real controls to today, completing a randomized controlled trial and looking at the impact that outdoor swimming may have on people living with mild to moderate depression.
“At first, people sort of thought our idea was a bit wacky,” said Dr. Massey. “Now, the popularity of open-water swimming has really blossomed, and so has this area of research. We’re starting to build more rigor into the work.”
Like all the researchers and physicians interviewed for this article, Dr. Massey hesitates to claim that cold-water swimming is a “cure” that should be medicalized.
“It’s not about prescribing it or forcing people to do it,” said Dr. Massey. “This is not something that a doctor should write on a prescription and say you should go and have eight 1-hour sessions of swimming.”
(Not yet) a common cure
Enter into the conversation Mark Harper, MD, PhD, consultant anesthetist at Sussex University Hospitals in the United Kingdom and Kristiansand, Norway. Dr. Harper is the author of the 2022 book, Chill: The Cold Water Swim Cure – A Transformative Guide to Renew Your Body and Mind.
Dr. Harper grew up swimming in pools, and it wasn’t until his pool closed for 2 weeks that he ventured into the sea. He recalled walking up the beach afterward, thinking, God, this feels good, and from that moment on, he became hooked on outdoor swimming and curious about its therapeutic potential.
The “cure” in the book’s title, Dr. Harper explained, is being used in the historical sense of “treatment,” as in the first medical book about sea-bathing written over 250 years ago. Dr. Harper acknowledged that the connection to health is still speculative. “However, the circumstantial evidence, the feedback from participants and early study data for its benefits are now very strong,” he said.
In a small study published in 2022, Dr. Harper and colleagues took 59 people with anxiety and depression and put them through a sea-swimming course. Afterward, 80% showed a clinically significant improvement in their mental health.
More recently, Dr. Harper and his team of researchers released a survey to determine how many people were using cold-water swimming as a treatment for a mental or physical ailment. “We thought 30 or 40 people would respond, but we ended up with over 700,” he said. “The majority were using it for mental health but also included inflammation-related conditions.”
Over 2 decades, Dr. Harper has seen dramatic success stories. In his book, he recalled a good friend who, in his early 20s, suffered from Crohn’s disease so badly he couldn’t walk up the steps to his parents’ house. The friend turned to outdoor cold swimming as a low-impact workout and began noticing the symptoms of his disease were improving. Within months, he was able to go off his medications. In 2022, he completed 52 triathlons: one per week for the entire year.
How cold exposure may play with your brain
Vaibhav Diwadkar, PhD, professor of psychiatry and behavioral neurosciences at Wayne State University, in Detroit, is studying how human brain networks respond to cold exposure. Dr. Diwadkar and his colleague, Otto Muzik, PhD, began by putting volunteers in a rubber suit with thin tubing and infusing the tubing with temperature-controlled water. Meanwhile, they collected functional brain imaging data to analyze which parts of the brain were responding as body temperature changed.
The data showed that the cold exposure made certain areas of the brain very active, including some that have been associated with the regulation of mood.
Dr. Diwadkar posits that controlled exposure to cold serves as a low-level stressor that knocks different systems within the brain and body out of homeostasis. Once the stress is removed, the brain responds by releasing neurotransmitters that enhance mood, frequently leading to feelings of euphoria in participants.
“We don’t have direct evidence of such a mechanism, but it’s a reasonable speculation,” said Dr. Diwadkar.
However, he pointed out that science writers in the media often portray topics such as this one in black and white, which is “oversimplifying the scientific complexity of biology.”
Clearly, more research needs to be done on the potential therapeutic benefits of cold-water swimming. But for those suffering from anxiety, depression, or chronic illness, if taking a cold dip makes you feel better, the why and how might be beside the point.
Plus, as Dr. Harper pointed out, it’s an easy and accessible therapy.
“All you need is some water – enough to submerge your entire body in – that’s less than 68 °F (20 °C),” he said. “If you stay long enough to get over that initial shock, which is just 2 or 3 minutes, then you’ve got the effect. If you get out and want to go back in again, then you’ve done it right.”
A version of this article first appeared on Medscape.com.
A mid-marathon cardiac arrest, an MD’s crisis of confidence
I was running my 25th New York City Marathon. It was 2018, and I almost pulled out of running that year. I wasn’t myself, and maybe that’s an understatement.
A month earlier, I had been involved in a malpractice case. I was found liable for $10 million. My colleagues didn’t think I had done anything wrong, but the jury did. And the local newspapers made me look like a villain.
I was devastated. But my priest, my friends, and my family all told me, “You can’t quit.” So, I decided to run for them.
I started on the Verrazzano-Narrows Bridge that morning with some friends from work. I usually listen to music as I’m running, but I didn’t that year. I was just in my zone, enjoying the crowds. They’re huge. Millions of people on the streets.
I was running well. I did half the race in an hour and 57 minutes. My family always meets me at mile 17, and I was almost there. I had reached 59th Street and was about to make the turn onto First Avenue.
That’s one of the noisiest places in the marathon. There’s a kind of tunnel, and with the crowd and the throng of runners, it’s incredibly loud. But somehow, I heard somebody yell, “Help!”
Now, how I heard that, I don’t know. And if I’d been listening to music like I always do, no way I would’ve heard it. I could swear it was an angel on my shoulder that said, “Turn around, dummy. You’ve got a person that needs your help to your left.”
I turned around and about 30 feet behind me, I saw a woman waving her hands and a runner on the ground. I thought, Somebody fainted. I pushed through the crowd to get to them. The woman was crying, saying, “My friend went down to tie her shoe and she fell back. I think she’s seizing or something.”
I got down and tried to wake the other woman up. I lifted her legs up. But I quickly realized there was more to the story.
Some volunteers and police started coming toward us. The police officers looked at me like, What’s this guy doing? I explained that I was a physician, and one of them began helping me with the CPR. As we did that, someone brought a defibrillator.
Meanwhile, runners were going past, almost over us. The police officers were trying to create a barrier.
The machine gave the woman a shock, but we didn’t get a response, so we resumed CPR. At that point, my legs began to cramp so badly I couldn’t go on. So the police officer took over, and I yelled, “I need an ambu bag!” Somebody brought one, and I started giving her oxygen.
At that point, a paramedic team arrived with a bigger defibrillator. We shocked her again. And again. That time we got results, but she quickly went out again. The fourth time, we got her heart back and she started breathing on her own.
We finally got her into an ambulance. I wanted to go with them, but the woman’s friend needed to get in, so there wasn’t enough room.
And then they were gone, and I was just standing there.
A police officer put his arm around me. He said, “Doc, you’re amazing. What do you need? Where can I take you?”
I said, “Take me? My wife is waiting for me at mile 17.”
I took off and ran. When I got to my wife and kids, they were so worried. We all wear tracking devices, and they could see that I had stopped for more than 20 minutes.
I fell into my wife’s arms and told her what had happened. I was crying. “I don’t know what to do. I need to get to the hospital.”
And she said, “No, you need to go finish the race.”
So, I did. It was painful because of the cramps, but I was numb at that point. I was thinking about the woman the whole way. My time was 5 hours and 20 minutes.
As soon as I finished, I went to every police officer I could find, but nobody knew anything. Suddenly, I remembered my cousin. He had previously been the head of EMS for New York City. I called him. “Abdo, it’s Ted, you’ve got to do me a favor.”
“What?” he said. “Are you delirious from running the marathon?”
I told him what I needed. He called me back 5 minutes later and said, “Ted, what’d you do? Everybody wants to know who you are and where you are! The woman just went out again at New York Cornell. But they got her back, and they’re bringing her up to the cath lab.”
After every marathon that I run, we host a big party at our house. My family and friends and neighbors all celebrate while I’m dying on the couch. That night, my daughter told everyone the story of what happened.
But I was still not right. Still thinking about the malpractice suit.
Yes, I just did something great. But I’d recently been called the worst physician in the world. The distraction of the marathon was gone, and I was back to thinking, What am I going to do with my life? Who’s ever going to want to see me again? I’m a pariah.
Everybody said, “Ted, what happened a month ago isn’t you. What happened today was you.”
I told them to leave it alone, but my daughter and my neighbor started calling people anyway. The next day I got a call from the local newspaper. It was the same journalist who had written about me from the trial. I told him I didn’t want to talk. I was actually pretty nasty.
But my wife said, “Ted, what are you doing? That guy was trying to help you.” So, I called back and apologized.
“Dr. Strange, we knew that story wasn’t right,” he said. “We have to write this story.”
After the article came out, I started getting more calls from the media. Channel 7 News and CBS News did segments. The New York Knicks invited us to a game and presented me with a watch. It was incredible. But I was also really embarrassed by it.
People started calling me a hero. I’m not a hero. I just did what I’m supposed to do, what I’m trained to do. Shame on me if I don’t do that. Good guy and hopefully good physician, sure, but not a hero.
I also give credit to the City of New York Police Department, the FDNY, and the volunteers. Without them, I couldn’t have done what I did. It was a true team effort.
A few weeks later, the woman went home to Minnesota. She’ll never run a marathon again, but she’s still alive to this day. It turned out she had a single lesion called the “widow-maker” lesion. She was in perfect health and had just completed an ultramarathon a few months before; but she had a genetic predisposition. She still calls me every December to thank me for another Christmas.
There’s more.
One year after this whole thing, almost to the date, I got a call from my attorney. “The court just threw out the malpractice verdict,” he said. “You didn’t do anything wrong.”
I’m a man of faith. And I believe all this happened for a reason. Maybe God was sending me a message, and that’s why I heard a call for help on 59th Street in my 25th marathon among millions of people in a crowd.
I ran the marathon the next year. And when I got to that spot, I stopped and reflected. Nobody knew why I was standing there, but I knew. To this day, I could take you to that spot.
I turn 65 next July, and I plan to keep on running the race.
Dr. Strange is chair of medicine at Staten Island University Hospital, associate ambulatory physician executive of the Staten Island Region, and an internal medicine and geriatric medicine physician with Northwell Health.
A version of this article first appeared on Medscape.com.
I was running my 25th New York City Marathon. It was 2018, and I almost pulled out of running that year. I wasn’t myself, and maybe that’s an understatement.
A month earlier, I had been involved in a malpractice case. I was found liable for $10 million. My colleagues didn’t think I had done anything wrong, but the jury did. And the local newspapers made me look like a villain.
I was devastated. But my priest, my friends, and my family all told me, “You can’t quit.” So, I decided to run for them.
I started on the Verrazzano-Narrows Bridge that morning with some friends from work. I usually listen to music as I’m running, but I didn’t that year. I was just in my zone, enjoying the crowds. They’re huge. Millions of people on the streets.
I was running well. I did half the race in an hour and 57 minutes. My family always meets me at mile 17, and I was almost there. I had reached 59th Street and was about to make the turn onto First Avenue.
That’s one of the noisiest places in the marathon. There’s a kind of tunnel, and with the crowd and the throng of runners, it’s incredibly loud. But somehow, I heard somebody yell, “Help!”
Now, how I heard that, I don’t know. And if I’d been listening to music like I always do, no way I would’ve heard it. I could swear it was an angel on my shoulder that said, “Turn around, dummy. You’ve got a person that needs your help to your left.”
I turned around and about 30 feet behind me, I saw a woman waving her hands and a runner on the ground. I thought, Somebody fainted. I pushed through the crowd to get to them. The woman was crying, saying, “My friend went down to tie her shoe and she fell back. I think she’s seizing or something.”
I got down and tried to wake the other woman up. I lifted her legs up. But I quickly realized there was more to the story.
Some volunteers and police started coming toward us. The police officers looked at me like, What’s this guy doing? I explained that I was a physician, and one of them began helping me with the CPR. As we did that, someone brought a defibrillator.
Meanwhile, runners were going past, almost over us. The police officers were trying to create a barrier.
The machine gave the woman a shock, but we didn’t get a response, so we resumed CPR. At that point, my legs began to cramp so badly I couldn’t go on. So the police officer took over, and I yelled, “I need an ambu bag!” Somebody brought one, and I started giving her oxygen.
At that point, a paramedic team arrived with a bigger defibrillator. We shocked her again. And again. That time we got results, but she quickly went out again. The fourth time, we got her heart back and she started breathing on her own.
We finally got her into an ambulance. I wanted to go with them, but the woman’s friend needed to get in, so there wasn’t enough room.
And then they were gone, and I was just standing there.
A police officer put his arm around me. He said, “Doc, you’re amazing. What do you need? Where can I take you?”
I said, “Take me? My wife is waiting for me at mile 17.”
I took off and ran. When I got to my wife and kids, they were so worried. We all wear tracking devices, and they could see that I had stopped for more than 20 minutes.
I fell into my wife’s arms and told her what had happened. I was crying. “I don’t know what to do. I need to get to the hospital.”
And she said, “No, you need to go finish the race.”
So, I did. It was painful because of the cramps, but I was numb at that point. I was thinking about the woman the whole way. My time was 5 hours and 20 minutes.
As soon as I finished, I went to every police officer I could find, but nobody knew anything. Suddenly, I remembered my cousin. He had previously been the head of EMS for New York City. I called him. “Abdo, it’s Ted, you’ve got to do me a favor.”
“What?” he said. “Are you delirious from running the marathon?”
I told him what I needed. He called me back 5 minutes later and said, “Ted, what’d you do? Everybody wants to know who you are and where you are! The woman just went out again at New York Cornell. But they got her back, and they’re bringing her up to the cath lab.”
After every marathon that I run, we host a big party at our house. My family and friends and neighbors all celebrate while I’m dying on the couch. That night, my daughter told everyone the story of what happened.
But I was still not right. Still thinking about the malpractice suit.
Yes, I just did something great. But I’d recently been called the worst physician in the world. The distraction of the marathon was gone, and I was back to thinking, What am I going to do with my life? Who’s ever going to want to see me again? I’m a pariah.
Everybody said, “Ted, what happened a month ago isn’t you. What happened today was you.”
I told them to leave it alone, but my daughter and my neighbor started calling people anyway. The next day I got a call from the local newspaper. It was the same journalist who had written about me from the trial. I told him I didn’t want to talk. I was actually pretty nasty.
But my wife said, “Ted, what are you doing? That guy was trying to help you.” So, I called back and apologized.
“Dr. Strange, we knew that story wasn’t right,” he said. “We have to write this story.”
After the article came out, I started getting more calls from the media. Channel 7 News and CBS News did segments. The New York Knicks invited us to a game and presented me with a watch. It was incredible. But I was also really embarrassed by it.
People started calling me a hero. I’m not a hero. I just did what I’m supposed to do, what I’m trained to do. Shame on me if I don’t do that. Good guy and hopefully good physician, sure, but not a hero.
I also give credit to the City of New York Police Department, the FDNY, and the volunteers. Without them, I couldn’t have done what I did. It was a true team effort.
A few weeks later, the woman went home to Minnesota. She’ll never run a marathon again, but she’s still alive to this day. It turned out she had a single lesion called the “widow-maker” lesion. She was in perfect health and had just completed an ultramarathon a few months before; but she had a genetic predisposition. She still calls me every December to thank me for another Christmas.
There’s more.
One year after this whole thing, almost to the date, I got a call from my attorney. “The court just threw out the malpractice verdict,” he said. “You didn’t do anything wrong.”
I’m a man of faith. And I believe all this happened for a reason. Maybe God was sending me a message, and that’s why I heard a call for help on 59th Street in my 25th marathon among millions of people in a crowd.
I ran the marathon the next year. And when I got to that spot, I stopped and reflected. Nobody knew why I was standing there, but I knew. To this day, I could take you to that spot.
I turn 65 next July, and I plan to keep on running the race.
Dr. Strange is chair of medicine at Staten Island University Hospital, associate ambulatory physician executive of the Staten Island Region, and an internal medicine and geriatric medicine physician with Northwell Health.
A version of this article first appeared on Medscape.com.
I was running my 25th New York City Marathon. It was 2018, and I almost pulled out of running that year. I wasn’t myself, and maybe that’s an understatement.
A month earlier, I had been involved in a malpractice case. I was found liable for $10 million. My colleagues didn’t think I had done anything wrong, but the jury did. And the local newspapers made me look like a villain.
I was devastated. But my priest, my friends, and my family all told me, “You can’t quit.” So, I decided to run for them.
I started on the Verrazzano-Narrows Bridge that morning with some friends from work. I usually listen to music as I’m running, but I didn’t that year. I was just in my zone, enjoying the crowds. They’re huge. Millions of people on the streets.
I was running well. I did half the race in an hour and 57 minutes. My family always meets me at mile 17, and I was almost there. I had reached 59th Street and was about to make the turn onto First Avenue.
That’s one of the noisiest places in the marathon. There’s a kind of tunnel, and with the crowd and the throng of runners, it’s incredibly loud. But somehow, I heard somebody yell, “Help!”
Now, how I heard that, I don’t know. And if I’d been listening to music like I always do, no way I would’ve heard it. I could swear it was an angel on my shoulder that said, “Turn around, dummy. You’ve got a person that needs your help to your left.”
I turned around and about 30 feet behind me, I saw a woman waving her hands and a runner on the ground. I thought, Somebody fainted. I pushed through the crowd to get to them. The woman was crying, saying, “My friend went down to tie her shoe and she fell back. I think she’s seizing or something.”
I got down and tried to wake the other woman up. I lifted her legs up. But I quickly realized there was more to the story.
Some volunteers and police started coming toward us. The police officers looked at me like, What’s this guy doing? I explained that I was a physician, and one of them began helping me with the CPR. As we did that, someone brought a defibrillator.
Meanwhile, runners were going past, almost over us. The police officers were trying to create a barrier.
The machine gave the woman a shock, but we didn’t get a response, so we resumed CPR. At that point, my legs began to cramp so badly I couldn’t go on. So the police officer took over, and I yelled, “I need an ambu bag!” Somebody brought one, and I started giving her oxygen.
At that point, a paramedic team arrived with a bigger defibrillator. We shocked her again. And again. That time we got results, but she quickly went out again. The fourth time, we got her heart back and she started breathing on her own.
We finally got her into an ambulance. I wanted to go with them, but the woman’s friend needed to get in, so there wasn’t enough room.
And then they were gone, and I was just standing there.
A police officer put his arm around me. He said, “Doc, you’re amazing. What do you need? Where can I take you?”
I said, “Take me? My wife is waiting for me at mile 17.”
I took off and ran. When I got to my wife and kids, they were so worried. We all wear tracking devices, and they could see that I had stopped for more than 20 minutes.
I fell into my wife’s arms and told her what had happened. I was crying. “I don’t know what to do. I need to get to the hospital.”
And she said, “No, you need to go finish the race.”
So, I did. It was painful because of the cramps, but I was numb at that point. I was thinking about the woman the whole way. My time was 5 hours and 20 minutes.
As soon as I finished, I went to every police officer I could find, but nobody knew anything. Suddenly, I remembered my cousin. He had previously been the head of EMS for New York City. I called him. “Abdo, it’s Ted, you’ve got to do me a favor.”
“What?” he said. “Are you delirious from running the marathon?”
I told him what I needed. He called me back 5 minutes later and said, “Ted, what’d you do? Everybody wants to know who you are and where you are! The woman just went out again at New York Cornell. But they got her back, and they’re bringing her up to the cath lab.”
After every marathon that I run, we host a big party at our house. My family and friends and neighbors all celebrate while I’m dying on the couch. That night, my daughter told everyone the story of what happened.
But I was still not right. Still thinking about the malpractice suit.
Yes, I just did something great. But I’d recently been called the worst physician in the world. The distraction of the marathon was gone, and I was back to thinking, What am I going to do with my life? Who’s ever going to want to see me again? I’m a pariah.
Everybody said, “Ted, what happened a month ago isn’t you. What happened today was you.”
I told them to leave it alone, but my daughter and my neighbor started calling people anyway. The next day I got a call from the local newspaper. It was the same journalist who had written about me from the trial. I told him I didn’t want to talk. I was actually pretty nasty.
But my wife said, “Ted, what are you doing? That guy was trying to help you.” So, I called back and apologized.
“Dr. Strange, we knew that story wasn’t right,” he said. “We have to write this story.”
After the article came out, I started getting more calls from the media. Channel 7 News and CBS News did segments. The New York Knicks invited us to a game and presented me with a watch. It was incredible. But I was also really embarrassed by it.
People started calling me a hero. I’m not a hero. I just did what I’m supposed to do, what I’m trained to do. Shame on me if I don’t do that. Good guy and hopefully good physician, sure, but not a hero.
I also give credit to the City of New York Police Department, the FDNY, and the volunteers. Without them, I couldn’t have done what I did. It was a true team effort.
A few weeks later, the woman went home to Minnesota. She’ll never run a marathon again, but she’s still alive to this day. It turned out she had a single lesion called the “widow-maker” lesion. She was in perfect health and had just completed an ultramarathon a few months before; but she had a genetic predisposition. She still calls me every December to thank me for another Christmas.
There’s more.
One year after this whole thing, almost to the date, I got a call from my attorney. “The court just threw out the malpractice verdict,” he said. “You didn’t do anything wrong.”
I’m a man of faith. And I believe all this happened for a reason. Maybe God was sending me a message, and that’s why I heard a call for help on 59th Street in my 25th marathon among millions of people in a crowd.
I ran the marathon the next year. And when I got to that spot, I stopped and reflected. Nobody knew why I was standing there, but I knew. To this day, I could take you to that spot.
I turn 65 next July, and I plan to keep on running the race.
Dr. Strange is chair of medicine at Staten Island University Hospital, associate ambulatory physician executive of the Staten Island Region, and an internal medicine and geriatric medicine physician with Northwell Health.
A version of this article first appeared on Medscape.com.