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It Sure Looks Like Cannabis Is Bad for the Heart, Doesn’t It?
This transcript has been edited for clarity.
If you’re an epidemiologist trying to explore whether some exposure is a risk factor for a disease, you can run into a tough problem when your exposure of interest is highly correlated with another risk factor for the disease. For decades, this stymied investigations into the link, if any, between marijuana use and cardiovascular disease because, for decades, most people who used marijuana in some way also smoked cigarettes — which is a very clear risk factor for heart disease.
But the times they are a-changing.
Thanks to the legalization of marijuana for recreational use in many states, and even broader social trends, there is now a large population of people who use marijuana but do not use cigarettes. That means we can start to determine whether marijuana use is an independent risk factor for heart disease.
And this week, we have the largest study yet to attempt to answer that question, though, as I’ll explain momentarily, the smoke hasn’t entirely cleared yet.
The centerpiece of the study we are discussing this week, “Association of Cannabis Use With Cardiovascular Outcomes Among US Adults,” which appeared in the Journal of the American Heart Association, is the Behavioral Risk Factor Surveillance System, an annual telephone survey conducted by the Centers for Disease Control and Prevention since 1984 that gathers data on all sorts of stuff that we do to ourselves: our drinking habits, our smoking habits, and, more recently, our marijuana habits.
The paper combines annual data from 2016 to 2020 representing 27 states and two US territories for a total sample size of more than 430,000 individuals. The key exposure? Marijuana use, which was coded as the number of days of marijuana use in the past 30 days. The key outcome? Coronary heart disease, collected through questions such as “Has a doctor, nurse, or other health professional ever told you that you had a heart attack?”
Right away you might detect a couple of problems here. But let me show you the results before we worry about what they mean.
You can see the rates of the major cardiovascular outcomes here, stratified by daily use of marijuana, nondaily use, and no use. Broadly speaking, the risk was highest for daily users, lowest for occasional users, and in the middle for non-users.
Of course, non-users and users are different in lots of other ways; non-users were quite a bit older, for example. Adjusting for all those factors showed that, independent of age, smoking status, the presence of diabetes, and so on, there was an independently increased risk for cardiovascular outcomes in people who used marijuana.
Importantly, 60% of people in this study were never smokers, and the results in that group looked pretty similar to the results overall.
But I said there were a couple of problems, so let’s dig into those a bit.
First, like most survey studies, this one requires honest and accurate reporting from its subjects. There was no verification of heart disease using electronic health records or of marijuana usage based on biosamples. Broadly, miscategorization of exposure and outcomes in surveys tends to bias the results toward the null hypothesis, toward concluding that there is no link between exposure and outcome, so perhaps this is okay.
The bigger problem is the fact that this is a cross-sectional design. If you really wanted to know whether marijuana led to heart disease, you’d do a longitudinal study following users and non-users for some number of decades and see who developed heart disease and who didn’t. (For the pedants out there, I suppose you’d actually want to randomize people to use marijuana or not and then see who had a heart attack, but the IRB keeps rejecting my protocol when I submit it.)
Here, though, we literally can’t tell whether people who use marijuana have more heart attacks or whether people who have heart attacks use more marijuana. The authors argue that there are no data that show that people are more likely to use marijuana after a heart attack or stroke, but at the time the survey was conducted, they had already had their heart attack or stroke.
The authors also imply that they found a dose-response relationship between marijuana use and these cardiovascular outcomes. This is an important statement because dose response is one factor that we use to determine whether a risk factor may actually be causative as opposed to just correlative.
But I take issue with the dose-response language here. The model used to make these graphs classifies marijuana use as a single continuous variable ranging from 0 (no days of use in the past 30 days) to 1 (30 days of use in the past 30 days). The model is thus constrained to monotonically increase or decrease with respect to the outcome. To prove a dose response, you have to give the model the option to find something that isn’t a dose response — for example, by classifying marijuana use into discrete, independent categories rather than a single continuous number.
Am I arguing here that marijuana use is good for you? Of course not. Nor am I even arguing that it has no effect on the cardiovascular system. There are endocannabinoid receptors all over your vasculature. But a cross-sectional survey study, while a good start, is not quite the right way to answer the question. So, while the jury is still out, it’s high time for more research.
Dr. F. Perry Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Connecticut. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
If you’re an epidemiologist trying to explore whether some exposure is a risk factor for a disease, you can run into a tough problem when your exposure of interest is highly correlated with another risk factor for the disease. For decades, this stymied investigations into the link, if any, between marijuana use and cardiovascular disease because, for decades, most people who used marijuana in some way also smoked cigarettes — which is a very clear risk factor for heart disease.
But the times they are a-changing.
Thanks to the legalization of marijuana for recreational use in many states, and even broader social trends, there is now a large population of people who use marijuana but do not use cigarettes. That means we can start to determine whether marijuana use is an independent risk factor for heart disease.
And this week, we have the largest study yet to attempt to answer that question, though, as I’ll explain momentarily, the smoke hasn’t entirely cleared yet.
The centerpiece of the study we are discussing this week, “Association of Cannabis Use With Cardiovascular Outcomes Among US Adults,” which appeared in the Journal of the American Heart Association, is the Behavioral Risk Factor Surveillance System, an annual telephone survey conducted by the Centers for Disease Control and Prevention since 1984 that gathers data on all sorts of stuff that we do to ourselves: our drinking habits, our smoking habits, and, more recently, our marijuana habits.
The paper combines annual data from 2016 to 2020 representing 27 states and two US territories for a total sample size of more than 430,000 individuals. The key exposure? Marijuana use, which was coded as the number of days of marijuana use in the past 30 days. The key outcome? Coronary heart disease, collected through questions such as “Has a doctor, nurse, or other health professional ever told you that you had a heart attack?”
Right away you might detect a couple of problems here. But let me show you the results before we worry about what they mean.
You can see the rates of the major cardiovascular outcomes here, stratified by daily use of marijuana, nondaily use, and no use. Broadly speaking, the risk was highest for daily users, lowest for occasional users, and in the middle for non-users.
Of course, non-users and users are different in lots of other ways; non-users were quite a bit older, for example. Adjusting for all those factors showed that, independent of age, smoking status, the presence of diabetes, and so on, there was an independently increased risk for cardiovascular outcomes in people who used marijuana.
Importantly, 60% of people in this study were never smokers, and the results in that group looked pretty similar to the results overall.
But I said there were a couple of problems, so let’s dig into those a bit.
First, like most survey studies, this one requires honest and accurate reporting from its subjects. There was no verification of heart disease using electronic health records or of marijuana usage based on biosamples. Broadly, miscategorization of exposure and outcomes in surveys tends to bias the results toward the null hypothesis, toward concluding that there is no link between exposure and outcome, so perhaps this is okay.
The bigger problem is the fact that this is a cross-sectional design. If you really wanted to know whether marijuana led to heart disease, you’d do a longitudinal study following users and non-users for some number of decades and see who developed heart disease and who didn’t. (For the pedants out there, I suppose you’d actually want to randomize people to use marijuana or not and then see who had a heart attack, but the IRB keeps rejecting my protocol when I submit it.)
Here, though, we literally can’t tell whether people who use marijuana have more heart attacks or whether people who have heart attacks use more marijuana. The authors argue that there are no data that show that people are more likely to use marijuana after a heart attack or stroke, but at the time the survey was conducted, they had already had their heart attack or stroke.
The authors also imply that they found a dose-response relationship between marijuana use and these cardiovascular outcomes. This is an important statement because dose response is one factor that we use to determine whether a risk factor may actually be causative as opposed to just correlative.
But I take issue with the dose-response language here. The model used to make these graphs classifies marijuana use as a single continuous variable ranging from 0 (no days of use in the past 30 days) to 1 (30 days of use in the past 30 days). The model is thus constrained to monotonically increase or decrease with respect to the outcome. To prove a dose response, you have to give the model the option to find something that isn’t a dose response — for example, by classifying marijuana use into discrete, independent categories rather than a single continuous number.
Am I arguing here that marijuana use is good for you? Of course not. Nor am I even arguing that it has no effect on the cardiovascular system. There are endocannabinoid receptors all over your vasculature. But a cross-sectional survey study, while a good start, is not quite the right way to answer the question. So, while the jury is still out, it’s high time for more research.
Dr. F. Perry Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Connecticut. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
If you’re an epidemiologist trying to explore whether some exposure is a risk factor for a disease, you can run into a tough problem when your exposure of interest is highly correlated with another risk factor for the disease. For decades, this stymied investigations into the link, if any, between marijuana use and cardiovascular disease because, for decades, most people who used marijuana in some way also smoked cigarettes — which is a very clear risk factor for heart disease.
But the times they are a-changing.
Thanks to the legalization of marijuana for recreational use in many states, and even broader social trends, there is now a large population of people who use marijuana but do not use cigarettes. That means we can start to determine whether marijuana use is an independent risk factor for heart disease.
And this week, we have the largest study yet to attempt to answer that question, though, as I’ll explain momentarily, the smoke hasn’t entirely cleared yet.
The centerpiece of the study we are discussing this week, “Association of Cannabis Use With Cardiovascular Outcomes Among US Adults,” which appeared in the Journal of the American Heart Association, is the Behavioral Risk Factor Surveillance System, an annual telephone survey conducted by the Centers for Disease Control and Prevention since 1984 that gathers data on all sorts of stuff that we do to ourselves: our drinking habits, our smoking habits, and, more recently, our marijuana habits.
The paper combines annual data from 2016 to 2020 representing 27 states and two US territories for a total sample size of more than 430,000 individuals. The key exposure? Marijuana use, which was coded as the number of days of marijuana use in the past 30 days. The key outcome? Coronary heart disease, collected through questions such as “Has a doctor, nurse, or other health professional ever told you that you had a heart attack?”
Right away you might detect a couple of problems here. But let me show you the results before we worry about what they mean.
You can see the rates of the major cardiovascular outcomes here, stratified by daily use of marijuana, nondaily use, and no use. Broadly speaking, the risk was highest for daily users, lowest for occasional users, and in the middle for non-users.
Of course, non-users and users are different in lots of other ways; non-users were quite a bit older, for example. Adjusting for all those factors showed that, independent of age, smoking status, the presence of diabetes, and so on, there was an independently increased risk for cardiovascular outcomes in people who used marijuana.
Importantly, 60% of people in this study were never smokers, and the results in that group looked pretty similar to the results overall.
But I said there were a couple of problems, so let’s dig into those a bit.
First, like most survey studies, this one requires honest and accurate reporting from its subjects. There was no verification of heart disease using electronic health records or of marijuana usage based on biosamples. Broadly, miscategorization of exposure and outcomes in surveys tends to bias the results toward the null hypothesis, toward concluding that there is no link between exposure and outcome, so perhaps this is okay.
The bigger problem is the fact that this is a cross-sectional design. If you really wanted to know whether marijuana led to heart disease, you’d do a longitudinal study following users and non-users for some number of decades and see who developed heart disease and who didn’t. (For the pedants out there, I suppose you’d actually want to randomize people to use marijuana or not and then see who had a heart attack, but the IRB keeps rejecting my protocol when I submit it.)
Here, though, we literally can’t tell whether people who use marijuana have more heart attacks or whether people who have heart attacks use more marijuana. The authors argue that there are no data that show that people are more likely to use marijuana after a heart attack or stroke, but at the time the survey was conducted, they had already had their heart attack or stroke.
The authors also imply that they found a dose-response relationship between marijuana use and these cardiovascular outcomes. This is an important statement because dose response is one factor that we use to determine whether a risk factor may actually be causative as opposed to just correlative.
But I take issue with the dose-response language here. The model used to make these graphs classifies marijuana use as a single continuous variable ranging from 0 (no days of use in the past 30 days) to 1 (30 days of use in the past 30 days). The model is thus constrained to monotonically increase or decrease with respect to the outcome. To prove a dose response, you have to give the model the option to find something that isn’t a dose response — for example, by classifying marijuana use into discrete, independent categories rather than a single continuous number.
Am I arguing here that marijuana use is good for you? Of course not. Nor am I even arguing that it has no effect on the cardiovascular system. There are endocannabinoid receptors all over your vasculature. But a cross-sectional survey study, while a good start, is not quite the right way to answer the question. So, while the jury is still out, it’s high time for more research.
Dr. F. Perry Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Connecticut. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Oxaliplatin in Older Adults With Resected Colorectal Cancer: Is There a Benefit?
This transcript has been edited for clarity.
Our group, the QUASAR Group, made a very significant contribution in terms of trials and knowledge in this field. One of the things that we still need to discuss and think about in our wider community is the impact of adjuvant chemotherapy in older patients.
Colorectal cancer is a disease of the elderly, with the median age of presentation around 72. We know that, at presentation, more than 50% of patients are aged 65 or over and one third of patients are 75 or over. It’s a disease predominantly of the elderly. Are we justified in giving combination chemotherapy with oxaliplatin to high-risk resected colorectal cancer patients?
There’s a very nice report of a meta-analysis by Dottorini and colleagues that came out recently in the Journal of Clinical Oncology. It’s an excellent group. They did their meta-analytical work according to a strict, rational protocol. Their statistical analyses were on point, and they collected data from all the relevant trials.
According to the results of their study, it could be concluded that the addition of oxaliplatin to adjuvant therapy for resected high-risk colorectal cancer in older patients — patients older than 70 — doesn’t result in any statistically significant gain in terms of preventing recurrences or saving lives.
When we did our QUASAR trials, initially we were looking at control vs fluoropyrimidine chemotherapy. Although there was an overall impact on survival of the whole trial group (the 5000 patients in our study), when we looked by decile, there was a significant diminution of benefit even to fluoropyrimidine therapy in our trial in patients aged 70 or above. I think this careful meta-analysis must make us question the use of oxaliplatin in elderly patients.
What could the explanation be? Why could the well-known and described benefits of oxaliplatin, particularly for stage III disease, attenuate in older people? It may be to do with reduction in dose intensity. Older people have more side effects; therefore, the chemotherapy isn’t completed as planned. Although, increasingly these days, we tend only to be giving 3 months of treatment.
Is there something biologically in terms of the biology or the somatic mutational landscape of the tumor in older people? I don’t think so. Certainly, in terms of their capacity, in terms of stem cell reserve to be as resistant to the side effects of chemotherapy as younger people, we know that does attenuate with age.
Food for thought: The majority of patients I see in the clinic for the adjuvant treatment are elderly. The majority are coming these days with high-risk stage II or stage III disease. There is a real question mark about whether we should be using oxaliplatin at all.
Clearly, one would say that we need more trials of chemotherapy in older folk to see if the addition of drugs like oxaliplatin to a fluoropyrimidine backbone really does make a difference. I’ve said many times before that we, the medical community recommending adjuvant treatment, need to have better risk stratifiers. We need to have better prognostic markers. We need to have better indices that would allow us to perhaps consider these combination treatments in a more focused group of patients who may have a higher risk for recurrence.
Have a look at the paper and see what you think. I think it’s well done. It’s certainly given me pause for thought about the treatment that we will offer our elderly patients.
Have a think about it. Let me know if there are any comments that you’d like to make. For the time being, over and out.
Dr. Kerr is Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom. He disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer HealthCare Pharmaceuticals, Genomic Health, Merck Serono, and Roche.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Our group, the QUASAR Group, made a very significant contribution in terms of trials and knowledge in this field. One of the things that we still need to discuss and think about in our wider community is the impact of adjuvant chemotherapy in older patients.
Colorectal cancer is a disease of the elderly, with the median age of presentation around 72. We know that, at presentation, more than 50% of patients are aged 65 or over and one third of patients are 75 or over. It’s a disease predominantly of the elderly. Are we justified in giving combination chemotherapy with oxaliplatin to high-risk resected colorectal cancer patients?
There’s a very nice report of a meta-analysis by Dottorini and colleagues that came out recently in the Journal of Clinical Oncology. It’s an excellent group. They did their meta-analytical work according to a strict, rational protocol. Their statistical analyses were on point, and they collected data from all the relevant trials.
According to the results of their study, it could be concluded that the addition of oxaliplatin to adjuvant therapy for resected high-risk colorectal cancer in older patients — patients older than 70 — doesn’t result in any statistically significant gain in terms of preventing recurrences or saving lives.
When we did our QUASAR trials, initially we were looking at control vs fluoropyrimidine chemotherapy. Although there was an overall impact on survival of the whole trial group (the 5000 patients in our study), when we looked by decile, there was a significant diminution of benefit even to fluoropyrimidine therapy in our trial in patients aged 70 or above. I think this careful meta-analysis must make us question the use of oxaliplatin in elderly patients.
What could the explanation be? Why could the well-known and described benefits of oxaliplatin, particularly for stage III disease, attenuate in older people? It may be to do with reduction in dose intensity. Older people have more side effects; therefore, the chemotherapy isn’t completed as planned. Although, increasingly these days, we tend only to be giving 3 months of treatment.
Is there something biologically in terms of the biology or the somatic mutational landscape of the tumor in older people? I don’t think so. Certainly, in terms of their capacity, in terms of stem cell reserve to be as resistant to the side effects of chemotherapy as younger people, we know that does attenuate with age.
Food for thought: The majority of patients I see in the clinic for the adjuvant treatment are elderly. The majority are coming these days with high-risk stage II or stage III disease. There is a real question mark about whether we should be using oxaliplatin at all.
Clearly, one would say that we need more trials of chemotherapy in older folk to see if the addition of drugs like oxaliplatin to a fluoropyrimidine backbone really does make a difference. I’ve said many times before that we, the medical community recommending adjuvant treatment, need to have better risk stratifiers. We need to have better prognostic markers. We need to have better indices that would allow us to perhaps consider these combination treatments in a more focused group of patients who may have a higher risk for recurrence.
Have a look at the paper and see what you think. I think it’s well done. It’s certainly given me pause for thought about the treatment that we will offer our elderly patients.
Have a think about it. Let me know if there are any comments that you’d like to make. For the time being, over and out.
Dr. Kerr is Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom. He disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer HealthCare Pharmaceuticals, Genomic Health, Merck Serono, and Roche.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Our group, the QUASAR Group, made a very significant contribution in terms of trials and knowledge in this field. One of the things that we still need to discuss and think about in our wider community is the impact of adjuvant chemotherapy in older patients.
Colorectal cancer is a disease of the elderly, with the median age of presentation around 72. We know that, at presentation, more than 50% of patients are aged 65 or over and one third of patients are 75 or over. It’s a disease predominantly of the elderly. Are we justified in giving combination chemotherapy with oxaliplatin to high-risk resected colorectal cancer patients?
There’s a very nice report of a meta-analysis by Dottorini and colleagues that came out recently in the Journal of Clinical Oncology. It’s an excellent group. They did their meta-analytical work according to a strict, rational protocol. Their statistical analyses were on point, and they collected data from all the relevant trials.
According to the results of their study, it could be concluded that the addition of oxaliplatin to adjuvant therapy for resected high-risk colorectal cancer in older patients — patients older than 70 — doesn’t result in any statistically significant gain in terms of preventing recurrences or saving lives.
When we did our QUASAR trials, initially we were looking at control vs fluoropyrimidine chemotherapy. Although there was an overall impact on survival of the whole trial group (the 5000 patients in our study), when we looked by decile, there was a significant diminution of benefit even to fluoropyrimidine therapy in our trial in patients aged 70 or above. I think this careful meta-analysis must make us question the use of oxaliplatin in elderly patients.
What could the explanation be? Why could the well-known and described benefits of oxaliplatin, particularly for stage III disease, attenuate in older people? It may be to do with reduction in dose intensity. Older people have more side effects; therefore, the chemotherapy isn’t completed as planned. Although, increasingly these days, we tend only to be giving 3 months of treatment.
Is there something biologically in terms of the biology or the somatic mutational landscape of the tumor in older people? I don’t think so. Certainly, in terms of their capacity, in terms of stem cell reserve to be as resistant to the side effects of chemotherapy as younger people, we know that does attenuate with age.
Food for thought: The majority of patients I see in the clinic for the adjuvant treatment are elderly. The majority are coming these days with high-risk stage II or stage III disease. There is a real question mark about whether we should be using oxaliplatin at all.
Clearly, one would say that we need more trials of chemotherapy in older folk to see if the addition of drugs like oxaliplatin to a fluoropyrimidine backbone really does make a difference. I’ve said many times before that we, the medical community recommending adjuvant treatment, need to have better risk stratifiers. We need to have better prognostic markers. We need to have better indices that would allow us to perhaps consider these combination treatments in a more focused group of patients who may have a higher risk for recurrence.
Have a look at the paper and see what you think. I think it’s well done. It’s certainly given me pause for thought about the treatment that we will offer our elderly patients.
Have a think about it. Let me know if there are any comments that you’d like to make. For the time being, over and out.
Dr. Kerr is Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom. He disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer HealthCare Pharmaceuticals, Genomic Health, Merck Serono, and Roche.
A version of this article appeared on Medscape.com.
Poor Quality of Cancer Content on Social Media
This transcript has been edited for clarity.
I’m delighted to talk about a very interesting topic in this commentary. This is an area that we generally don’t discuss, but it’s one that’s obviously very topical, which includes the question of social media.
The paper I’m referring to is entitled, “More Than a Song and Dance”: Exploration of Patient Perspectives and Educational Quality of Gynecologic Cancer Content on TikTok. The paper was published in Gynecologic Oncology in 2023.
They had a total of 466.7 million views. They looked at 430 of the 500 top posts that were eligible, looked at 11 central themes, did an objective analysis of educational content based on published strategy for looking at this.
What they found, unfortunately but not surprisingly, overall was that the educational quality and reliability were quite poor. They also noticed considerable differences in disparities based on racial background and really emphasized in their analysis not only how common it is for individuals to look at this content on TikTok but also concerns about what it is that the public, patients, and their families are actually seeing.
This, of course, specifically relates to gynecologic cancers, but almost certainly relates to other cancers as well. Clearly, this is a topic that needs to be discussed widely. It’s very complex and very controversial, but when you think about the information that might be provided to our patients and their families going to social media, it’s important that we understand what they’re seeing, what they’re hearing, what they’re viewing, and the impact this might have on their care and outcomes.
I encourage you to read this very interesting paper if you have an interest in this topic. Again, it was recently published in Gynecologic Oncology. I thank you for your attention.
Dr. Markman is professor, Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, California; president of Medicine & Science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed ties with GlaxoSmithKline and AstraZeneca.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I’m delighted to talk about a very interesting topic in this commentary. This is an area that we generally don’t discuss, but it’s one that’s obviously very topical, which includes the question of social media.
The paper I’m referring to is entitled, “More Than a Song and Dance”: Exploration of Patient Perspectives and Educational Quality of Gynecologic Cancer Content on TikTok. The paper was published in Gynecologic Oncology in 2023.
They had a total of 466.7 million views. They looked at 430 of the 500 top posts that were eligible, looked at 11 central themes, did an objective analysis of educational content based on published strategy for looking at this.
What they found, unfortunately but not surprisingly, overall was that the educational quality and reliability were quite poor. They also noticed considerable differences in disparities based on racial background and really emphasized in their analysis not only how common it is for individuals to look at this content on TikTok but also concerns about what it is that the public, patients, and their families are actually seeing.
This, of course, specifically relates to gynecologic cancers, but almost certainly relates to other cancers as well. Clearly, this is a topic that needs to be discussed widely. It’s very complex and very controversial, but when you think about the information that might be provided to our patients and their families going to social media, it’s important that we understand what they’re seeing, what they’re hearing, what they’re viewing, and the impact this might have on their care and outcomes.
I encourage you to read this very interesting paper if you have an interest in this topic. Again, it was recently published in Gynecologic Oncology. I thank you for your attention.
Dr. Markman is professor, Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, California; president of Medicine & Science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed ties with GlaxoSmithKline and AstraZeneca.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I’m delighted to talk about a very interesting topic in this commentary. This is an area that we generally don’t discuss, but it’s one that’s obviously very topical, which includes the question of social media.
The paper I’m referring to is entitled, “More Than a Song and Dance”: Exploration of Patient Perspectives and Educational Quality of Gynecologic Cancer Content on TikTok. The paper was published in Gynecologic Oncology in 2023.
They had a total of 466.7 million views. They looked at 430 of the 500 top posts that were eligible, looked at 11 central themes, did an objective analysis of educational content based on published strategy for looking at this.
What they found, unfortunately but not surprisingly, overall was that the educational quality and reliability were quite poor. They also noticed considerable differences in disparities based on racial background and really emphasized in their analysis not only how common it is for individuals to look at this content on TikTok but also concerns about what it is that the public, patients, and their families are actually seeing.
This, of course, specifically relates to gynecologic cancers, but almost certainly relates to other cancers as well. Clearly, this is a topic that needs to be discussed widely. It’s very complex and very controversial, but when you think about the information that might be provided to our patients and their families going to social media, it’s important that we understand what they’re seeing, what they’re hearing, what they’re viewing, and the impact this might have on their care and outcomes.
I encourage you to read this very interesting paper if you have an interest in this topic. Again, it was recently published in Gynecologic Oncology. I thank you for your attention.
Dr. Markman is professor, Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, California; president of Medicine & Science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed ties with GlaxoSmithKline and AstraZeneca.
A version of this article appeared on Medscape.com.
Bent but Not Broken: The Truth About Penile Curvature
This transcript has been edited for clarity.
Rachel S. Rubin, MD: I’m Dr Rachel Rubin, urologist and sexual medicine specialist in the Washington, DC, area. This is Sex Matters, and I’m here today with my friend and colleague, Dr. Matt Ziegelmann, who is the sexual medicine expert at the Mayo Clinic and who does all things men’s health, including penile curvature, testosterone, and sexual function.
Matthew J. Ziegelmann, MD: Penile curvature (often due to Peyronie’s disease) is actually incredibly common; as many as 10% of men have this condition. We need to normalize it and let men know that this is something we see often, and we have treatments for it. One of the biggest concerns these men have is cancer, but I have yet to see this as an indicator of cancer.
Penile curvature has a significant impact on affected men — their relationships, psychological well-being, sexual functioning, and overall health. We can provide treatment if they are interested. A small subset of men are born with natural penile curvature, which is different from Peyronie’s disease. Natural curvature can still affect their mental health, and we have treatment options.
Rubin: What happens when a patient is referred to urology? We want to tell our patients what to expect. What’s in our toolbox to help patients with penile curvature?
Dr. Ziegelmann: Many patient resources are available. For example, the Sexual Medicine Society of North America (SMSNA) has a patient-facing website on sexual health with lots of information about Peyronie’s disease and other aspects of sexual health.
Patients who are bothered by their penile curvature can be referred to us to find out about treatment options, or even just to get reassurance. It might be as simple as a conversation and a physical exam — that’s all we need to make the diagnosis. We can provide reassurance and get an idea of how bothered they are by this condition without doing anything invasive.
If they are considering definitive treatment, we would need to do more invasive testing. Sometimes we have the patient bring in photos of their erection to help establish the change they see in the shape of their penis.
Dr. Rubin: What about the patient who asks, “Doc, did I do this to myself? Did I break my penis? What do I do?”
Dr. Ziegelmann: That’s a common question — “How the heck did this happen?” No, you didn’t do this to yourself. We still have much to understand about why this happens to some men. Our approach is to acknowledge what we do and don’t know, and partner with the patient to discuss treatment.
Dr. Rubin: It’s very important to support your patient’s mental health, because this can be really devastating. So, what are the treatment options from conservative to invasive? What do you recommend for patients?
Dr. Ziegelmann: It can be as simple as observation if the patient is just seeking reassurance that it’s not cancer. This is a benign condition, but for men who are more bothered by their curvature, we’ll talk about options. We have oral medications that help improved the rigidity of the penis. Many men are also suffering from inadequate functioning. We can use devices called traction or vacuum to stretch the area of the penis that’s curved. We can use injections of medications, including FDA-approved agents that are injected into the penis in the outpatient setting. For men who are either later in the treatment protocol or want to resolve the problem right away, we can offer surgical intervention. We have a host of options, and a very individualized approach and a shared decision-making model. It’s not a one-size-fits-all problem.
Dr. Rubin: The real takeaway is that there is a lot of hope for this condition. Many doctors care deeply about these issues and are ready to partner with specialists to figure out the right treatment strategy. The SMSNA is a great place to find a provider like Dr Ziegelmann or myself, or any of our incredible colleagues throughout North America and the world. Thank you for joining us today.
Dr. Rubin is Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC; Private practice, North Bethesda, Maryland. She disclosed ties with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Rachel S. Rubin, MD: I’m Dr Rachel Rubin, urologist and sexual medicine specialist in the Washington, DC, area. This is Sex Matters, and I’m here today with my friend and colleague, Dr. Matt Ziegelmann, who is the sexual medicine expert at the Mayo Clinic and who does all things men’s health, including penile curvature, testosterone, and sexual function.
Matthew J. Ziegelmann, MD: Penile curvature (often due to Peyronie’s disease) is actually incredibly common; as many as 10% of men have this condition. We need to normalize it and let men know that this is something we see often, and we have treatments for it. One of the biggest concerns these men have is cancer, but I have yet to see this as an indicator of cancer.
Penile curvature has a significant impact on affected men — their relationships, psychological well-being, sexual functioning, and overall health. We can provide treatment if they are interested. A small subset of men are born with natural penile curvature, which is different from Peyronie’s disease. Natural curvature can still affect their mental health, and we have treatment options.
Rubin: What happens when a patient is referred to urology? We want to tell our patients what to expect. What’s in our toolbox to help patients with penile curvature?
Dr. Ziegelmann: Many patient resources are available. For example, the Sexual Medicine Society of North America (SMSNA) has a patient-facing website on sexual health with lots of information about Peyronie’s disease and other aspects of sexual health.
Patients who are bothered by their penile curvature can be referred to us to find out about treatment options, or even just to get reassurance. It might be as simple as a conversation and a physical exam — that’s all we need to make the diagnosis. We can provide reassurance and get an idea of how bothered they are by this condition without doing anything invasive.
If they are considering definitive treatment, we would need to do more invasive testing. Sometimes we have the patient bring in photos of their erection to help establish the change they see in the shape of their penis.
Dr. Rubin: What about the patient who asks, “Doc, did I do this to myself? Did I break my penis? What do I do?”
Dr. Ziegelmann: That’s a common question — “How the heck did this happen?” No, you didn’t do this to yourself. We still have much to understand about why this happens to some men. Our approach is to acknowledge what we do and don’t know, and partner with the patient to discuss treatment.
Dr. Rubin: It’s very important to support your patient’s mental health, because this can be really devastating. So, what are the treatment options from conservative to invasive? What do you recommend for patients?
Dr. Ziegelmann: It can be as simple as observation if the patient is just seeking reassurance that it’s not cancer. This is a benign condition, but for men who are more bothered by their curvature, we’ll talk about options. We have oral medications that help improved the rigidity of the penis. Many men are also suffering from inadequate functioning. We can use devices called traction or vacuum to stretch the area of the penis that’s curved. We can use injections of medications, including FDA-approved agents that are injected into the penis in the outpatient setting. For men who are either later in the treatment protocol or want to resolve the problem right away, we can offer surgical intervention. We have a host of options, and a very individualized approach and a shared decision-making model. It’s not a one-size-fits-all problem.
Dr. Rubin: The real takeaway is that there is a lot of hope for this condition. Many doctors care deeply about these issues and are ready to partner with specialists to figure out the right treatment strategy. The SMSNA is a great place to find a provider like Dr Ziegelmann or myself, or any of our incredible colleagues throughout North America and the world. Thank you for joining us today.
Dr. Rubin is Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC; Private practice, North Bethesda, Maryland. She disclosed ties with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Rachel S. Rubin, MD: I’m Dr Rachel Rubin, urologist and sexual medicine specialist in the Washington, DC, area. This is Sex Matters, and I’m here today with my friend and colleague, Dr. Matt Ziegelmann, who is the sexual medicine expert at the Mayo Clinic and who does all things men’s health, including penile curvature, testosterone, and sexual function.
Matthew J. Ziegelmann, MD: Penile curvature (often due to Peyronie’s disease) is actually incredibly common; as many as 10% of men have this condition. We need to normalize it and let men know that this is something we see often, and we have treatments for it. One of the biggest concerns these men have is cancer, but I have yet to see this as an indicator of cancer.
Penile curvature has a significant impact on affected men — their relationships, psychological well-being, sexual functioning, and overall health. We can provide treatment if they are interested. A small subset of men are born with natural penile curvature, which is different from Peyronie’s disease. Natural curvature can still affect their mental health, and we have treatment options.
Rubin: What happens when a patient is referred to urology? We want to tell our patients what to expect. What’s in our toolbox to help patients with penile curvature?
Dr. Ziegelmann: Many patient resources are available. For example, the Sexual Medicine Society of North America (SMSNA) has a patient-facing website on sexual health with lots of information about Peyronie’s disease and other aspects of sexual health.
Patients who are bothered by their penile curvature can be referred to us to find out about treatment options, or even just to get reassurance. It might be as simple as a conversation and a physical exam — that’s all we need to make the diagnosis. We can provide reassurance and get an idea of how bothered they are by this condition without doing anything invasive.
If they are considering definitive treatment, we would need to do more invasive testing. Sometimes we have the patient bring in photos of their erection to help establish the change they see in the shape of their penis.
Dr. Rubin: What about the patient who asks, “Doc, did I do this to myself? Did I break my penis? What do I do?”
Dr. Ziegelmann: That’s a common question — “How the heck did this happen?” No, you didn’t do this to yourself. We still have much to understand about why this happens to some men. Our approach is to acknowledge what we do and don’t know, and partner with the patient to discuss treatment.
Dr. Rubin: It’s very important to support your patient’s mental health, because this can be really devastating. So, what are the treatment options from conservative to invasive? What do you recommend for patients?
Dr. Ziegelmann: It can be as simple as observation if the patient is just seeking reassurance that it’s not cancer. This is a benign condition, but for men who are more bothered by their curvature, we’ll talk about options. We have oral medications that help improved the rigidity of the penis. Many men are also suffering from inadequate functioning. We can use devices called traction or vacuum to stretch the area of the penis that’s curved. We can use injections of medications, including FDA-approved agents that are injected into the penis in the outpatient setting. For men who are either later in the treatment protocol or want to resolve the problem right away, we can offer surgical intervention. We have a host of options, and a very individualized approach and a shared decision-making model. It’s not a one-size-fits-all problem.
Dr. Rubin: The real takeaway is that there is a lot of hope for this condition. Many doctors care deeply about these issues and are ready to partner with specialists to figure out the right treatment strategy. The SMSNA is a great place to find a provider like Dr Ziegelmann or myself, or any of our incredible colleagues throughout North America and the world. Thank you for joining us today.
Dr. Rubin is Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC; Private practice, North Bethesda, Maryland. She disclosed ties with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.
A version of this article appeared on Medscape.com.
CRC: Troubling Mortality Rates for a Preventable Cancer
This transcript has been edited for clarity.
The American Cancer Society has just published its cancer statistics for 2024. This is an annual report, the latest version of which has some alarming news for gastroenterologists. Usually, we think of being “number one” as a positive thing, but that’s not the case this year when it comes to the projections for colorectal cancer.
But first, let’s discuss the report’s overall findings. That decline over the past four decades is due to reductions in smoking, earlier detection, and improved screening and treatments for localized or metastatic disease. But these gains are now threatened by some offsets that we’re seeing, with increasing rates of six of the top 10 cancers in the past several years.
Increasing Rates of Gastrointestinal Cancers
The incidence rate of pancreas cancer has increased from 0.6% to 1% annually.
Pancreas cancer has a 5-year relative survival rate of 13%, which ranks as one of the three worst rates for cancers. This cancer represents a real screening challenge for us, as it typically presents asymptomatically.
Women have experienced a 2%-3% annual increase in incidence rates for liver cancer.
I suspect that this is due to cases of fibrotic liver disease resulting from viral hepatitis and metabolic liver diseases with nonalcoholic fatty liver and advanced fibrosis (F3 and F4). These cases may be carried over from before, thereby contributing to the increasing incremental cancer risk.
We can’t overlook the need for risk reduction here and should focus on applying regular screening efforts in our female patients. However, it’s also true that we require better liver cancer screening tests to accomplish that goal.
In Those Under 50, CRC the Leading Cause of Cancer Death in Men, Second in Women
I really want to focus on the news around colorectal cancer.
To put this in perspective, in the late 1990s, colorectal cancer was the fourth leading cause of death in men and women. The current report extrapolated 2024 projections using the Surveillance, Epidemiology, and End Results (SEER) database ending in 2020, which was necessary given the incremental time it takes to develop cancers. The SEER database suggests that in 2024, colorectal cancer in those younger than 50 years of age will become the number-one leading cause of cancer death in men and number-two in women. The increasing incidence of colorectal cancer in younger people is probably the result of a number of epidemiologic and other reasons.
The current report offers evidence of racial disparities in cancer mortality rates in general, which are twofold higher in Black people compared with White people, particularly for gastric cancer. There is also an evident disparity in Native Americans, who have higher rates of gastric and liver cancer. This is a reminder of the increasing need for equity to address racial disparities across these populations.
But returning to colon cancer, it’s a marked change to go from being the fourth-leading cause of cancer death in those younger than 50 years of age to being number one for men and number two for women.
Being “number one” is supposed to make you famous. This “number one,” however, should in fact be infamous. It’s a travesty, because colorectal cancer is a potentially preventable disease.
As we move into March, which happens to be Colorectal Cancer Awareness Month, hopefully this fires up some of the conversations you have with your younger at-risk population, who may be reticent or resistant to colorectal cancer screening.
We have to do better at getting this message out to that population at large. “Number one” is not where we want to be for this potentially preventable problem.
Dr. Johnson is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He has disclosed ties with ISOTHRIVE and Johnson & Johnson.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
The American Cancer Society has just published its cancer statistics for 2024. This is an annual report, the latest version of which has some alarming news for gastroenterologists. Usually, we think of being “number one” as a positive thing, but that’s not the case this year when it comes to the projections for colorectal cancer.
But first, let’s discuss the report’s overall findings. That decline over the past four decades is due to reductions in smoking, earlier detection, and improved screening and treatments for localized or metastatic disease. But these gains are now threatened by some offsets that we’re seeing, with increasing rates of six of the top 10 cancers in the past several years.
Increasing Rates of Gastrointestinal Cancers
The incidence rate of pancreas cancer has increased from 0.6% to 1% annually.
Pancreas cancer has a 5-year relative survival rate of 13%, which ranks as one of the three worst rates for cancers. This cancer represents a real screening challenge for us, as it typically presents asymptomatically.
Women have experienced a 2%-3% annual increase in incidence rates for liver cancer.
I suspect that this is due to cases of fibrotic liver disease resulting from viral hepatitis and metabolic liver diseases with nonalcoholic fatty liver and advanced fibrosis (F3 and F4). These cases may be carried over from before, thereby contributing to the increasing incremental cancer risk.
We can’t overlook the need for risk reduction here and should focus on applying regular screening efforts in our female patients. However, it’s also true that we require better liver cancer screening tests to accomplish that goal.
In Those Under 50, CRC the Leading Cause of Cancer Death in Men, Second in Women
I really want to focus on the news around colorectal cancer.
To put this in perspective, in the late 1990s, colorectal cancer was the fourth leading cause of death in men and women. The current report extrapolated 2024 projections using the Surveillance, Epidemiology, and End Results (SEER) database ending in 2020, which was necessary given the incremental time it takes to develop cancers. The SEER database suggests that in 2024, colorectal cancer in those younger than 50 years of age will become the number-one leading cause of cancer death in men and number-two in women. The increasing incidence of colorectal cancer in younger people is probably the result of a number of epidemiologic and other reasons.
The current report offers evidence of racial disparities in cancer mortality rates in general, which are twofold higher in Black people compared with White people, particularly for gastric cancer. There is also an evident disparity in Native Americans, who have higher rates of gastric and liver cancer. This is a reminder of the increasing need for equity to address racial disparities across these populations.
But returning to colon cancer, it’s a marked change to go from being the fourth-leading cause of cancer death in those younger than 50 years of age to being number one for men and number two for women.
Being “number one” is supposed to make you famous. This “number one,” however, should in fact be infamous. It’s a travesty, because colorectal cancer is a potentially preventable disease.
As we move into March, which happens to be Colorectal Cancer Awareness Month, hopefully this fires up some of the conversations you have with your younger at-risk population, who may be reticent or resistant to colorectal cancer screening.
We have to do better at getting this message out to that population at large. “Number one” is not where we want to be for this potentially preventable problem.
Dr. Johnson is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He has disclosed ties with ISOTHRIVE and Johnson & Johnson.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
The American Cancer Society has just published its cancer statistics for 2024. This is an annual report, the latest version of which has some alarming news for gastroenterologists. Usually, we think of being “number one” as a positive thing, but that’s not the case this year when it comes to the projections for colorectal cancer.
But first, let’s discuss the report’s overall findings. That decline over the past four decades is due to reductions in smoking, earlier detection, and improved screening and treatments for localized or metastatic disease. But these gains are now threatened by some offsets that we’re seeing, with increasing rates of six of the top 10 cancers in the past several years.
Increasing Rates of Gastrointestinal Cancers
The incidence rate of pancreas cancer has increased from 0.6% to 1% annually.
Pancreas cancer has a 5-year relative survival rate of 13%, which ranks as one of the three worst rates for cancers. This cancer represents a real screening challenge for us, as it typically presents asymptomatically.
Women have experienced a 2%-3% annual increase in incidence rates for liver cancer.
I suspect that this is due to cases of fibrotic liver disease resulting from viral hepatitis and metabolic liver diseases with nonalcoholic fatty liver and advanced fibrosis (F3 and F4). These cases may be carried over from before, thereby contributing to the increasing incremental cancer risk.
We can’t overlook the need for risk reduction here and should focus on applying regular screening efforts in our female patients. However, it’s also true that we require better liver cancer screening tests to accomplish that goal.
In Those Under 50, CRC the Leading Cause of Cancer Death in Men, Second in Women
I really want to focus on the news around colorectal cancer.
To put this in perspective, in the late 1990s, colorectal cancer was the fourth leading cause of death in men and women. The current report extrapolated 2024 projections using the Surveillance, Epidemiology, and End Results (SEER) database ending in 2020, which was necessary given the incremental time it takes to develop cancers. The SEER database suggests that in 2024, colorectal cancer in those younger than 50 years of age will become the number-one leading cause of cancer death in men and number-two in women. The increasing incidence of colorectal cancer in younger people is probably the result of a number of epidemiologic and other reasons.
The current report offers evidence of racial disparities in cancer mortality rates in general, which are twofold higher in Black people compared with White people, particularly for gastric cancer. There is also an evident disparity in Native Americans, who have higher rates of gastric and liver cancer. This is a reminder of the increasing need for equity to address racial disparities across these populations.
But returning to colon cancer, it’s a marked change to go from being the fourth-leading cause of cancer death in those younger than 50 years of age to being number one for men and number two for women.
Being “number one” is supposed to make you famous. This “number one,” however, should in fact be infamous. It’s a travesty, because colorectal cancer is a potentially preventable disease.
As we move into March, which happens to be Colorectal Cancer Awareness Month, hopefully this fires up some of the conversations you have with your younger at-risk population, who may be reticent or resistant to colorectal cancer screening.
We have to do better at getting this message out to that population at large. “Number one” is not where we want to be for this potentially preventable problem.
Dr. Johnson is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease. He has disclosed ties with ISOTHRIVE and Johnson & Johnson.
A version of this article appeared on Medscape.com.
Unleashing Our Immune Response to Quash Cancer
This article was originally published on February 10 in Eric Topol’s substack “Ground Truths.”
It’s astounding how devious cancer cells and tumor tissue can be. This week in Science we learned how certain lung cancer cells can function like “Catch Me If You Can” — changing their driver mutation and cell identity to escape targeted therapy. This histologic transformation, as seen in an experimental model, is just one of so many cancer tricks that we are learning about.
Recently, as shown by single-cell sequencing, cancer cells can steal the mitochondria from T cells, a double whammy that turbocharges cancer cells with the hijacked fuel supply and, at the same time, dismantles the immune response.
Last week, we saw how tumor cells can release a virus-like protein that unleashes a vicious autoimmune response.
And then there’s the finding that cancer cell spread predominantly is occurring while we sleep.
As I previously reviewed, the ability for cancer cells to hijack neurons and neural circuits is now well established, no less their ability to reprogram neurons to become adrenergic and stimulate tumor progression, and interfere with the immune response. Stay tuned on that for a new Ground Truths podcast with Prof Michelle Monje, a leader in cancer neuroscience, which will post soon.
Add advancing age’s immunosenescence as yet another challenge to the long and growing list of formidable ways that cancer cells, and the tumor microenvironment, evade our immune response.
An Ever-Expanding Armamentarium
Immune Checkpoint Inhibitors
The field of immunotherapies took off with the immune checkpoint inhibitors, first approved by the FDA in 2011, that take the brakes off of T cells, with the programmed death-1 (PD-1), PD-ligand1, and anti-CTLA-4 monoclonal antibodies.
But we’re clearly learning they are not enough to prevail over cancer with common recurrences, only short term success in most patients, with some notable exceptions. Adding other immune response strategies, such as a vaccine, or antibody-drug conjugates, or engineered T cells, are showing improved chances for success.
Therapeutic Cancer Vaccines
There are many therapeutic cancer vaccines in the works, as reviewed in depth here.
Here’s a list of ongoing clinical trials of cancer vaccines. You’ll note most of these are on top of a checkpoint inhibitor and use personalized neoantigens (cancer cell surface proteins) derived from sequencing (whole-exome or whole genome, RNA-sequencing and HLA-profiling) the patient’s tumor.
An example of positive findings is with the combination of an mRNA-nanoparticle vaccine with up to 34 personalized neoantigens and pembrolizumab (Keytruda) vs pembrolizumab alone in advanced melanoma after resection, with improved outcomes at 3-year follow-up, cutting death or relapse rate in half.
Antibody-Drug Conjugates (ADC)
There is considerable excitement about antibody-drug conjugates (ADC) whereby a linker is used to attach a chemotherapy agent to the checkpoint inhibitor antibody, specifically targeting the cancer cell and facilitating entry of the chemotherapy into the cell. Akin to these are bispecific antibodies (BiTEs, binding to a tumor antigen and T cell receptor simultaneously), both of these conjugates acting as “biologic” or “guided” missiles.
A very good example of the potency of an ADC was seen in a “HER2-low” breast cancer randomized trial. The absence or very low expression or amplification of the HER2 receptor is common in breast cancer and successful treatment has been elusive. A randomized trial of an ADC (trastuzumab deruxtecan) compared to physician’s choice therapy demonstrated a marked success for progression-free survival in HER2-low patients, which was characterized as “unheard-of success” by media coverage.
This strategy is being used to target some of the most difficult cancer driver mutations such as TP53 and KRAS.
Oncolytic Viruses
Modifying viruses to infect the tumor and make it more visible to the immune system, potentiating anti-tumor responses, known as oncolytic viruses, have been proposed as a way to rev up the immune response for a long time but without positive Phase 3 clinical trials.
After decades of failure, a recent trial in refractory bladder cancer showed marked success, along with others, summarized here, now providing very encouraging results. It looks like oncolytic viruses are on a comeback path.
Engineering T Cells (Chimeric Antigen Receptor [CAR-T])
As I recently reviewed, there are over 500 ongoing clinical trials to build on the success of the first CAR-T approval for leukemia 7 years ago. I won’t go through that all again here, but to reiterate most of the success to date has been in “liquid” blood (leukemia and lymphoma) cancer tumors. This week in Nature is the discovery of a T cell cancer mutation, a gene fusion CARD11-PIK3R3, from a T cell lymphoma that can potentially be used to augment CAR-T efficacy. It has pronounced and prolonged effects in the experimental model. Instead of 1 million cells needed for treatment, even 20,000 were enough to melt the tumor. This is a noteworthy discovery since CAR-T work to date has largely not exploited such naturally occurring mutations, while instead concentrating on those seen in the patient’s set of key tumor mutations.
As currently conceived, CAR-T, and what is being referred to more broadly as adoptive cell therapies, involves removing T cells from the patient’s body and engineering their activation, then reintroducing them back to the patient. This is laborious, technically difficult, and very expensive. Recently, the idea of achieving all of this via an injection of virus that specifically infects T cells and inserts the genes needed, was advanced by two biotech companies with preclinical results, one in non-human primates.
Gearing up to meet the challenge of solid tumor CAR-T intervention, there’s more work using CRISPR genome editing of T cell receptors. A.I. is increasingly being exploited to process the data from sequencing and identify optimal neoantigens.
Instead of just CAR-T, we’re seeing the emergence of CAR-macrophage and CAR-natural killer (NK) cells strategies, and rapidly expanding potential combinations of all the strategies I’ve mentioned. No less, there’s been maturation of on-off suicide switches programmed in, to limit cytokine release and promote safety of these interventions. Overall, major side effects of immunotherapies are not only cytokine release syndromes, but also include interstitial pneumonitis and neurotoxicity.
Summary
Given the multitude of ways cancer cells and tumor tissue can evade our immune response, durably successful treatment remains a daunting challenge. But the ingenuity of so many different approaches to unleash our immune response, and their combinations, provides considerable hope that we’ll increasingly meet the challenge in the years ahead. We have clearly learned that combining different immunotherapy strategies will be essential for many patients with the most resilient solid tumors.
Of concern, as noted by a recent editorial in The Lancet, entitled “Cancer Research Equity: Innovations For The Many, Not The Few,” is that these individualized, sophisticated strategies are not scalable; they will have limited reach and benefit. The movement towards “off the shelf” CAR-T and inexpensive, orally active checkpoint inhibitors may help mitigate this issue.
Notwithstanding this important concern, we’re seeing an array of diverse and potent immunotherapy strategies that are providing highly encouraging results, engendering more excitement than we’ve seen in this space for some time. These should propel substantial improvements in outcomes for patients in the years ahead. It can’t happen soon enough.
Thanks for reading this edition of Ground Truths. If you found it informative, please share it with your colleagues.
Dr. Topol has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for Dexcom; Illumina; Molecular Stethoscope; Quest Diagnostics; Blue Cross Blue Shield Association. Received research grant from National Institutes of Health.
A version of this article appeared on Medscape.com.
This article was originally published on February 10 in Eric Topol’s substack “Ground Truths.”
It’s astounding how devious cancer cells and tumor tissue can be. This week in Science we learned how certain lung cancer cells can function like “Catch Me If You Can” — changing their driver mutation and cell identity to escape targeted therapy. This histologic transformation, as seen in an experimental model, is just one of so many cancer tricks that we are learning about.
Recently, as shown by single-cell sequencing, cancer cells can steal the mitochondria from T cells, a double whammy that turbocharges cancer cells with the hijacked fuel supply and, at the same time, dismantles the immune response.
Last week, we saw how tumor cells can release a virus-like protein that unleashes a vicious autoimmune response.
And then there’s the finding that cancer cell spread predominantly is occurring while we sleep.
As I previously reviewed, the ability for cancer cells to hijack neurons and neural circuits is now well established, no less their ability to reprogram neurons to become adrenergic and stimulate tumor progression, and interfere with the immune response. Stay tuned on that for a new Ground Truths podcast with Prof Michelle Monje, a leader in cancer neuroscience, which will post soon.
Add advancing age’s immunosenescence as yet another challenge to the long and growing list of formidable ways that cancer cells, and the tumor microenvironment, evade our immune response.
An Ever-Expanding Armamentarium
Immune Checkpoint Inhibitors
The field of immunotherapies took off with the immune checkpoint inhibitors, first approved by the FDA in 2011, that take the brakes off of T cells, with the programmed death-1 (PD-1), PD-ligand1, and anti-CTLA-4 monoclonal antibodies.
But we’re clearly learning they are not enough to prevail over cancer with common recurrences, only short term success in most patients, with some notable exceptions. Adding other immune response strategies, such as a vaccine, or antibody-drug conjugates, or engineered T cells, are showing improved chances for success.
Therapeutic Cancer Vaccines
There are many therapeutic cancer vaccines in the works, as reviewed in depth here.
Here’s a list of ongoing clinical trials of cancer vaccines. You’ll note most of these are on top of a checkpoint inhibitor and use personalized neoantigens (cancer cell surface proteins) derived from sequencing (whole-exome or whole genome, RNA-sequencing and HLA-profiling) the patient’s tumor.
An example of positive findings is with the combination of an mRNA-nanoparticle vaccine with up to 34 personalized neoantigens and pembrolizumab (Keytruda) vs pembrolizumab alone in advanced melanoma after resection, with improved outcomes at 3-year follow-up, cutting death or relapse rate in half.
Antibody-Drug Conjugates (ADC)
There is considerable excitement about antibody-drug conjugates (ADC) whereby a linker is used to attach a chemotherapy agent to the checkpoint inhibitor antibody, specifically targeting the cancer cell and facilitating entry of the chemotherapy into the cell. Akin to these are bispecific antibodies (BiTEs, binding to a tumor antigen and T cell receptor simultaneously), both of these conjugates acting as “biologic” or “guided” missiles.
A very good example of the potency of an ADC was seen in a “HER2-low” breast cancer randomized trial. The absence or very low expression or amplification of the HER2 receptor is common in breast cancer and successful treatment has been elusive. A randomized trial of an ADC (trastuzumab deruxtecan) compared to physician’s choice therapy demonstrated a marked success for progression-free survival in HER2-low patients, which was characterized as “unheard-of success” by media coverage.
This strategy is being used to target some of the most difficult cancer driver mutations such as TP53 and KRAS.
Oncolytic Viruses
Modifying viruses to infect the tumor and make it more visible to the immune system, potentiating anti-tumor responses, known as oncolytic viruses, have been proposed as a way to rev up the immune response for a long time but without positive Phase 3 clinical trials.
After decades of failure, a recent trial in refractory bladder cancer showed marked success, along with others, summarized here, now providing very encouraging results. It looks like oncolytic viruses are on a comeback path.
Engineering T Cells (Chimeric Antigen Receptor [CAR-T])
As I recently reviewed, there are over 500 ongoing clinical trials to build on the success of the first CAR-T approval for leukemia 7 years ago. I won’t go through that all again here, but to reiterate most of the success to date has been in “liquid” blood (leukemia and lymphoma) cancer tumors. This week in Nature is the discovery of a T cell cancer mutation, a gene fusion CARD11-PIK3R3, from a T cell lymphoma that can potentially be used to augment CAR-T efficacy. It has pronounced and prolonged effects in the experimental model. Instead of 1 million cells needed for treatment, even 20,000 were enough to melt the tumor. This is a noteworthy discovery since CAR-T work to date has largely not exploited such naturally occurring mutations, while instead concentrating on those seen in the patient’s set of key tumor mutations.
As currently conceived, CAR-T, and what is being referred to more broadly as adoptive cell therapies, involves removing T cells from the patient’s body and engineering their activation, then reintroducing them back to the patient. This is laborious, technically difficult, and very expensive. Recently, the idea of achieving all of this via an injection of virus that specifically infects T cells and inserts the genes needed, was advanced by two biotech companies with preclinical results, one in non-human primates.
Gearing up to meet the challenge of solid tumor CAR-T intervention, there’s more work using CRISPR genome editing of T cell receptors. A.I. is increasingly being exploited to process the data from sequencing and identify optimal neoantigens.
Instead of just CAR-T, we’re seeing the emergence of CAR-macrophage and CAR-natural killer (NK) cells strategies, and rapidly expanding potential combinations of all the strategies I’ve mentioned. No less, there’s been maturation of on-off suicide switches programmed in, to limit cytokine release and promote safety of these interventions. Overall, major side effects of immunotherapies are not only cytokine release syndromes, but also include interstitial pneumonitis and neurotoxicity.
Summary
Given the multitude of ways cancer cells and tumor tissue can evade our immune response, durably successful treatment remains a daunting challenge. But the ingenuity of so many different approaches to unleash our immune response, and their combinations, provides considerable hope that we’ll increasingly meet the challenge in the years ahead. We have clearly learned that combining different immunotherapy strategies will be essential for many patients with the most resilient solid tumors.
Of concern, as noted by a recent editorial in The Lancet, entitled “Cancer Research Equity: Innovations For The Many, Not The Few,” is that these individualized, sophisticated strategies are not scalable; they will have limited reach and benefit. The movement towards “off the shelf” CAR-T and inexpensive, orally active checkpoint inhibitors may help mitigate this issue.
Notwithstanding this important concern, we’re seeing an array of diverse and potent immunotherapy strategies that are providing highly encouraging results, engendering more excitement than we’ve seen in this space for some time. These should propel substantial improvements in outcomes for patients in the years ahead. It can’t happen soon enough.
Thanks for reading this edition of Ground Truths. If you found it informative, please share it with your colleagues.
Dr. Topol has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for Dexcom; Illumina; Molecular Stethoscope; Quest Diagnostics; Blue Cross Blue Shield Association. Received research grant from National Institutes of Health.
A version of this article appeared on Medscape.com.
This article was originally published on February 10 in Eric Topol’s substack “Ground Truths.”
It’s astounding how devious cancer cells and tumor tissue can be. This week in Science we learned how certain lung cancer cells can function like “Catch Me If You Can” — changing their driver mutation and cell identity to escape targeted therapy. This histologic transformation, as seen in an experimental model, is just one of so many cancer tricks that we are learning about.
Recently, as shown by single-cell sequencing, cancer cells can steal the mitochondria from T cells, a double whammy that turbocharges cancer cells with the hijacked fuel supply and, at the same time, dismantles the immune response.
Last week, we saw how tumor cells can release a virus-like protein that unleashes a vicious autoimmune response.
And then there’s the finding that cancer cell spread predominantly is occurring while we sleep.
As I previously reviewed, the ability for cancer cells to hijack neurons and neural circuits is now well established, no less their ability to reprogram neurons to become adrenergic and stimulate tumor progression, and interfere with the immune response. Stay tuned on that for a new Ground Truths podcast with Prof Michelle Monje, a leader in cancer neuroscience, which will post soon.
Add advancing age’s immunosenescence as yet another challenge to the long and growing list of formidable ways that cancer cells, and the tumor microenvironment, evade our immune response.
An Ever-Expanding Armamentarium
Immune Checkpoint Inhibitors
The field of immunotherapies took off with the immune checkpoint inhibitors, first approved by the FDA in 2011, that take the brakes off of T cells, with the programmed death-1 (PD-1), PD-ligand1, and anti-CTLA-4 monoclonal antibodies.
But we’re clearly learning they are not enough to prevail over cancer with common recurrences, only short term success in most patients, with some notable exceptions. Adding other immune response strategies, such as a vaccine, or antibody-drug conjugates, or engineered T cells, are showing improved chances for success.
Therapeutic Cancer Vaccines
There are many therapeutic cancer vaccines in the works, as reviewed in depth here.
Here’s a list of ongoing clinical trials of cancer vaccines. You’ll note most of these are on top of a checkpoint inhibitor and use personalized neoantigens (cancer cell surface proteins) derived from sequencing (whole-exome or whole genome, RNA-sequencing and HLA-profiling) the patient’s tumor.
An example of positive findings is with the combination of an mRNA-nanoparticle vaccine with up to 34 personalized neoantigens and pembrolizumab (Keytruda) vs pembrolizumab alone in advanced melanoma after resection, with improved outcomes at 3-year follow-up, cutting death or relapse rate in half.
Antibody-Drug Conjugates (ADC)
There is considerable excitement about antibody-drug conjugates (ADC) whereby a linker is used to attach a chemotherapy agent to the checkpoint inhibitor antibody, specifically targeting the cancer cell and facilitating entry of the chemotherapy into the cell. Akin to these are bispecific antibodies (BiTEs, binding to a tumor antigen and T cell receptor simultaneously), both of these conjugates acting as “biologic” or “guided” missiles.
A very good example of the potency of an ADC was seen in a “HER2-low” breast cancer randomized trial. The absence or very low expression or amplification of the HER2 receptor is common in breast cancer and successful treatment has been elusive. A randomized trial of an ADC (trastuzumab deruxtecan) compared to physician’s choice therapy demonstrated a marked success for progression-free survival in HER2-low patients, which was characterized as “unheard-of success” by media coverage.
This strategy is being used to target some of the most difficult cancer driver mutations such as TP53 and KRAS.
Oncolytic Viruses
Modifying viruses to infect the tumor and make it more visible to the immune system, potentiating anti-tumor responses, known as oncolytic viruses, have been proposed as a way to rev up the immune response for a long time but without positive Phase 3 clinical trials.
After decades of failure, a recent trial in refractory bladder cancer showed marked success, along with others, summarized here, now providing very encouraging results. It looks like oncolytic viruses are on a comeback path.
Engineering T Cells (Chimeric Antigen Receptor [CAR-T])
As I recently reviewed, there are over 500 ongoing clinical trials to build on the success of the first CAR-T approval for leukemia 7 years ago. I won’t go through that all again here, but to reiterate most of the success to date has been in “liquid” blood (leukemia and lymphoma) cancer tumors. This week in Nature is the discovery of a T cell cancer mutation, a gene fusion CARD11-PIK3R3, from a T cell lymphoma that can potentially be used to augment CAR-T efficacy. It has pronounced and prolonged effects in the experimental model. Instead of 1 million cells needed for treatment, even 20,000 were enough to melt the tumor. This is a noteworthy discovery since CAR-T work to date has largely not exploited such naturally occurring mutations, while instead concentrating on those seen in the patient’s set of key tumor mutations.
As currently conceived, CAR-T, and what is being referred to more broadly as adoptive cell therapies, involves removing T cells from the patient’s body and engineering their activation, then reintroducing them back to the patient. This is laborious, technically difficult, and very expensive. Recently, the idea of achieving all of this via an injection of virus that specifically infects T cells and inserts the genes needed, was advanced by two biotech companies with preclinical results, one in non-human primates.
Gearing up to meet the challenge of solid tumor CAR-T intervention, there’s more work using CRISPR genome editing of T cell receptors. A.I. is increasingly being exploited to process the data from sequencing and identify optimal neoantigens.
Instead of just CAR-T, we’re seeing the emergence of CAR-macrophage and CAR-natural killer (NK) cells strategies, and rapidly expanding potential combinations of all the strategies I’ve mentioned. No less, there’s been maturation of on-off suicide switches programmed in, to limit cytokine release and promote safety of these interventions. Overall, major side effects of immunotherapies are not only cytokine release syndromes, but also include interstitial pneumonitis and neurotoxicity.
Summary
Given the multitude of ways cancer cells and tumor tissue can evade our immune response, durably successful treatment remains a daunting challenge. But the ingenuity of so many different approaches to unleash our immune response, and their combinations, provides considerable hope that we’ll increasingly meet the challenge in the years ahead. We have clearly learned that combining different immunotherapy strategies will be essential for many patients with the most resilient solid tumors.
Of concern, as noted by a recent editorial in The Lancet, entitled “Cancer Research Equity: Innovations For The Many, Not The Few,” is that these individualized, sophisticated strategies are not scalable; they will have limited reach and benefit. The movement towards “off the shelf” CAR-T and inexpensive, orally active checkpoint inhibitors may help mitigate this issue.
Notwithstanding this important concern, we’re seeing an array of diverse and potent immunotherapy strategies that are providing highly encouraging results, engendering more excitement than we’ve seen in this space for some time. These should propel substantial improvements in outcomes for patients in the years ahead. It can’t happen soon enough.
Thanks for reading this edition of Ground Truths. If you found it informative, please share it with your colleagues.
Dr. Topol has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for Dexcom; Illumina; Molecular Stethoscope; Quest Diagnostics; Blue Cross Blue Shield Association. Received research grant from National Institutes of Health.
A version of this article appeared on Medscape.com.
Kimchi: Not Magically Protective Against Weight Gain
How much of societal diet-related scientific illiteracy can be blamed on the publication decisions of medical journals around food studies?
That was the question I pondered when reading “Association between kimchi consumption and obesity based on BMI and abdominal obesity in Korean adults: a cross-sectional analysis of the Health Examinees study,” recently published in BMJ Open. Although I will get to the study particulars momentarily, that it’s 2024 and journals are still publishing cross-sectional studies of the impact of a single food’s subjectively reported consumption on health outcomes is mind boggling.
You might wonder why I wasn’t mind boggled by the authors rather than the journal — but the authors’ interest in publishing a study on kimchi’s supposed impact on obesity is an easy thing to explain, in that the study was funded by the World Institute of Kimchi, where two of its four authors are employed.
You might also wonder why I wasn’t mind boggled by media running with this story — but the media’s job is to capture eyeballs, and who doesn’t love a good magic food story, doubly so for one involving obesity and one with a study backing it up?
Back to this World Institute of Kimchi project looking at kimchi intake on obesity rates. No doubt if I worked for the World Institute of Kimchi, I would want kimchi to be shown to be somehow magically protective against weight gain. So how might I go about exploring that?
Well, I could look to the data from the Health Examinees (HEXA) Study. The HEXA study was a cross-sectional look at South Koreans; included in their data collection was a 106-item food frequency questionnaire (FFQ).
That questionnaire looked at 106 food items — yep, you guessed it, explicitly including kimchi. Not included in this FFQ, though, were prepared foods, meaning that it was unable to measure seasonings, spices, or cooking oils. Also perhaps problematic is that no doubt most of us consume more than 106 total food items in our diets. Perhaps this is why the validation study of HEXA’s food item–based FFQ found that it had “relatively low validity” when compared against 12-day food diaries and why its creators themselves report it to be in their study’s conclusion only “reasonably acceptable” to apply to a population. But yes, kimchi!
So for the sake of this exercise, though, let’s assume that instead of only a reasonably acceptable FFQ with low validity, the FFQ was fantastic and its data robust. How great then is kimchi at preventing obesity? Certainly, the media report it’s pretty darn good. Here’s a smattering from the literal dozens of headlines of stories covering this paper:
Eating kimchi every day could help stave off weight gain, new study says — NBC News
Eating kimchi every day may prevent weight gain, research suggests — Sky News
Want to avoid piling on the pounds? Try kimchi for breakfast — The Telegraph
But when we turn to the paper itself, suddenly things aren’t so clear.
According to the paper, men who reported eating two to three servings of kimchi per day were found to have lower rates of obesity, whereas men who reported eating three to five servings of kimchi per day were not. But these are overlapping groups! Also found was that men consuming more than five servings of kimchi per day have higher rates of obesity. When taken together, these findings do not demonstrate a statistically significant trend of kimchi intake on obesity in men. Whereas in women, things are worse in that the more kimchi reportedly consumed, the more obesity, in a trend that did (just) reach statistical significance.
So even if we pretend the FFQs were robust enough to make conclusions about a single food’s impact on obesity, and we pretend there was a well-described, plausible mechanistic reason to believe same (there isn’t), and we pretend that this particular FFQ had better than “relatively low validity,” there is no conclusion here to be drawn about kimchi’s impact on obesity.
What we can conclude is that when it comes to publishing papers purporting to find the impact of single foods on obesity, journals will still happily publish them and their publication will lead to hyperbolic headlines and stories, which in turn reinforce the scientifically illiterate notion that the highly complex multifactorial problem of obesity boils down to simple food choices, which in turn keeps weight loss grifters everywhere in business while fueling societal weight bias.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, and Novo Nordisk.
A version of this article appeared on Medscape.com.
How much of societal diet-related scientific illiteracy can be blamed on the publication decisions of medical journals around food studies?
That was the question I pondered when reading “Association between kimchi consumption and obesity based on BMI and abdominal obesity in Korean adults: a cross-sectional analysis of the Health Examinees study,” recently published in BMJ Open. Although I will get to the study particulars momentarily, that it’s 2024 and journals are still publishing cross-sectional studies of the impact of a single food’s subjectively reported consumption on health outcomes is mind boggling.
You might wonder why I wasn’t mind boggled by the authors rather than the journal — but the authors’ interest in publishing a study on kimchi’s supposed impact on obesity is an easy thing to explain, in that the study was funded by the World Institute of Kimchi, where two of its four authors are employed.
You might also wonder why I wasn’t mind boggled by media running with this story — but the media’s job is to capture eyeballs, and who doesn’t love a good magic food story, doubly so for one involving obesity and one with a study backing it up?
Back to this World Institute of Kimchi project looking at kimchi intake on obesity rates. No doubt if I worked for the World Institute of Kimchi, I would want kimchi to be shown to be somehow magically protective against weight gain. So how might I go about exploring that?
Well, I could look to the data from the Health Examinees (HEXA) Study. The HEXA study was a cross-sectional look at South Koreans; included in their data collection was a 106-item food frequency questionnaire (FFQ).
That questionnaire looked at 106 food items — yep, you guessed it, explicitly including kimchi. Not included in this FFQ, though, were prepared foods, meaning that it was unable to measure seasonings, spices, or cooking oils. Also perhaps problematic is that no doubt most of us consume more than 106 total food items in our diets. Perhaps this is why the validation study of HEXA’s food item–based FFQ found that it had “relatively low validity” when compared against 12-day food diaries and why its creators themselves report it to be in their study’s conclusion only “reasonably acceptable” to apply to a population. But yes, kimchi!
So for the sake of this exercise, though, let’s assume that instead of only a reasonably acceptable FFQ with low validity, the FFQ was fantastic and its data robust. How great then is kimchi at preventing obesity? Certainly, the media report it’s pretty darn good. Here’s a smattering from the literal dozens of headlines of stories covering this paper:
Eating kimchi every day could help stave off weight gain, new study says — NBC News
Eating kimchi every day may prevent weight gain, research suggests — Sky News
Want to avoid piling on the pounds? Try kimchi for breakfast — The Telegraph
But when we turn to the paper itself, suddenly things aren’t so clear.
According to the paper, men who reported eating two to three servings of kimchi per day were found to have lower rates of obesity, whereas men who reported eating three to five servings of kimchi per day were not. But these are overlapping groups! Also found was that men consuming more than five servings of kimchi per day have higher rates of obesity. When taken together, these findings do not demonstrate a statistically significant trend of kimchi intake on obesity in men. Whereas in women, things are worse in that the more kimchi reportedly consumed, the more obesity, in a trend that did (just) reach statistical significance.
So even if we pretend the FFQs were robust enough to make conclusions about a single food’s impact on obesity, and we pretend there was a well-described, plausible mechanistic reason to believe same (there isn’t), and we pretend that this particular FFQ had better than “relatively low validity,” there is no conclusion here to be drawn about kimchi’s impact on obesity.
What we can conclude is that when it comes to publishing papers purporting to find the impact of single foods on obesity, journals will still happily publish them and their publication will lead to hyperbolic headlines and stories, which in turn reinforce the scientifically illiterate notion that the highly complex multifactorial problem of obesity boils down to simple food choices, which in turn keeps weight loss grifters everywhere in business while fueling societal weight bias.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, and Novo Nordisk.
A version of this article appeared on Medscape.com.
How much of societal diet-related scientific illiteracy can be blamed on the publication decisions of medical journals around food studies?
That was the question I pondered when reading “Association between kimchi consumption and obesity based on BMI and abdominal obesity in Korean adults: a cross-sectional analysis of the Health Examinees study,” recently published in BMJ Open. Although I will get to the study particulars momentarily, that it’s 2024 and journals are still publishing cross-sectional studies of the impact of a single food’s subjectively reported consumption on health outcomes is mind boggling.
You might wonder why I wasn’t mind boggled by the authors rather than the journal — but the authors’ interest in publishing a study on kimchi’s supposed impact on obesity is an easy thing to explain, in that the study was funded by the World Institute of Kimchi, where two of its four authors are employed.
You might also wonder why I wasn’t mind boggled by media running with this story — but the media’s job is to capture eyeballs, and who doesn’t love a good magic food story, doubly so for one involving obesity and one with a study backing it up?
Back to this World Institute of Kimchi project looking at kimchi intake on obesity rates. No doubt if I worked for the World Institute of Kimchi, I would want kimchi to be shown to be somehow magically protective against weight gain. So how might I go about exploring that?
Well, I could look to the data from the Health Examinees (HEXA) Study. The HEXA study was a cross-sectional look at South Koreans; included in their data collection was a 106-item food frequency questionnaire (FFQ).
That questionnaire looked at 106 food items — yep, you guessed it, explicitly including kimchi. Not included in this FFQ, though, were prepared foods, meaning that it was unable to measure seasonings, spices, or cooking oils. Also perhaps problematic is that no doubt most of us consume more than 106 total food items in our diets. Perhaps this is why the validation study of HEXA’s food item–based FFQ found that it had “relatively low validity” when compared against 12-day food diaries and why its creators themselves report it to be in their study’s conclusion only “reasonably acceptable” to apply to a population. But yes, kimchi!
So for the sake of this exercise, though, let’s assume that instead of only a reasonably acceptable FFQ with low validity, the FFQ was fantastic and its data robust. How great then is kimchi at preventing obesity? Certainly, the media report it’s pretty darn good. Here’s a smattering from the literal dozens of headlines of stories covering this paper:
Eating kimchi every day could help stave off weight gain, new study says — NBC News
Eating kimchi every day may prevent weight gain, research suggests — Sky News
Want to avoid piling on the pounds? Try kimchi for breakfast — The Telegraph
But when we turn to the paper itself, suddenly things aren’t so clear.
According to the paper, men who reported eating two to three servings of kimchi per day were found to have lower rates of obesity, whereas men who reported eating three to five servings of kimchi per day were not. But these are overlapping groups! Also found was that men consuming more than five servings of kimchi per day have higher rates of obesity. When taken together, these findings do not demonstrate a statistically significant trend of kimchi intake on obesity in men. Whereas in women, things are worse in that the more kimchi reportedly consumed, the more obesity, in a trend that did (just) reach statistical significance.
So even if we pretend the FFQs were robust enough to make conclusions about a single food’s impact on obesity, and we pretend there was a well-described, plausible mechanistic reason to believe same (there isn’t), and we pretend that this particular FFQ had better than “relatively low validity,” there is no conclusion here to be drawn about kimchi’s impact on obesity.
What we can conclude is that when it comes to publishing papers purporting to find the impact of single foods on obesity, journals will still happily publish them and their publication will lead to hyperbolic headlines and stories, which in turn reinforce the scientifically illiterate notion that the highly complex multifactorial problem of obesity boils down to simple food choices, which in turn keeps weight loss grifters everywhere in business while fueling societal weight bias.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, and Novo Nordisk.
A version of this article appeared on Medscape.com.
Beware the Letter of Intent
I recently received an email from a distraught physician. Several months previously, He could continue running his office any way he wished, set his own hours and fees, and keep his employees. All his overhead expenses would disappear. His income would remain the same, maybe even increase. He signed it eagerly.
When he received the actual sale and employment contracts, none of the details promised in the LOI were included; but he figured that since they were spelled out in the LOI, which both he and the buyer had signed, he was covered. His attorney — a family friend with no experience in medical practice transactions — approved the documents.
The deal seemed too good to be true, and it was. The day after the sale closed, all his employees received termination notices. The group offered to rehire some of them, but at lower salaries and reduced benefits. (Most declined.) The new staffers he received were inadequately trained and unfamiliar with his standard office procedures. Patients complained that fees had increased substantially. His own compensation was contingent on meeting strict billing and performance goals. Malpractice premiums remained his responsibility. His office hours were lengthened to include evenings and Saturday mornings.
When he complained to the group that none of the things promised in the LOI had been delivered, he was informed that the LOI was not legally binding. In fact, the sale and employment contracts both clearly specified that they “replaced any previous written or oral agreements between the parties.”
There are some valuable lessons to be learned here. First, whether you are a young physician seeking a new job with a hospital or large practice, or an older one looking to sell an established practice, retain an attorney experienced in medical transactions early, before you sign anything, binding or not. Second, recognize that any promises made in an LOI must be spelled out in the employment and/or sale contract as well.
You might ask, if the terms in an LOI are not binding, why bother with one at all? For one thing, you want to make sure that you and your potential employer or buyer are on the same page with respect to major terms before you get down to details in the employment agreement and/or the medical practice sale agreement. For another, in most states certain LOI provisions are legally binding. For example, the document will most likely provide that each party is responsible for its own attorneys’ fees and for maintaining confidentiality during the negotiations, and that you will not negotiate with any other parties for some specified period of time. In most cases, such provisions are binding whether you go on to sign a formal contract or not.
When you receive an LOI, go through it carefully and identify areas of concern. The offering party will likely be in a rush to sign you up; but once you sign, you won’t be able to negotiate with anyone else for a while, which weakens your negotiating position. Regardless of what is said about time being “of the essence,” proceed slowly and with caution.
Bear in mind that employers and buyers never begin with their best offer. Unless you have been through this before, it is unlikely that you will know your value as an employee or the value of your practice, or what exactly you are entitled to ask for. Rather than signing something you don’t completely understand, explain to the offering party that you need time to consider and evaluate their offer.
This is the time to hire a competent medical attorney to do some due diligence on the offering party and review their offer, and to educate yourself about practice value and compensation benchmarks in your area. You and your counsel should assemble a list of things that you want changed in the LOI, then present them to the other side. They should be amenable to negotiation. If they are not (as was the case in the example presented earlier), you should reconsider whether you really want to be associated with that particular buyer or employer.
Once you have signed the LOI, experts say speed then works to your advantage. “Time kills all deals,” as one lawyer put it. “The longer it takes to close the transaction, the more that can go wrong.” The prospective employer or buyer could uncover information about you or your practice that decreases their perception of value, or economic conditions might change.
While speed is now important, and most of the core issues should already have been resolved in the LOI, don’t be afraid to ask for everything you want, whether it’s a better sale price, higher compensation, a favorable call schedule, more vacation time, or anything else. You won’t know what you can get if you don’t ask for it.
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.
I recently received an email from a distraught physician. Several months previously, He could continue running his office any way he wished, set his own hours and fees, and keep his employees. All his overhead expenses would disappear. His income would remain the same, maybe even increase. He signed it eagerly.
When he received the actual sale and employment contracts, none of the details promised in the LOI were included; but he figured that since they were spelled out in the LOI, which both he and the buyer had signed, he was covered. His attorney — a family friend with no experience in medical practice transactions — approved the documents.
The deal seemed too good to be true, and it was. The day after the sale closed, all his employees received termination notices. The group offered to rehire some of them, but at lower salaries and reduced benefits. (Most declined.) The new staffers he received were inadequately trained and unfamiliar with his standard office procedures. Patients complained that fees had increased substantially. His own compensation was contingent on meeting strict billing and performance goals. Malpractice premiums remained his responsibility. His office hours were lengthened to include evenings and Saturday mornings.
When he complained to the group that none of the things promised in the LOI had been delivered, he was informed that the LOI was not legally binding. In fact, the sale and employment contracts both clearly specified that they “replaced any previous written or oral agreements between the parties.”
There are some valuable lessons to be learned here. First, whether you are a young physician seeking a new job with a hospital or large practice, or an older one looking to sell an established practice, retain an attorney experienced in medical transactions early, before you sign anything, binding or not. Second, recognize that any promises made in an LOI must be spelled out in the employment and/or sale contract as well.
You might ask, if the terms in an LOI are not binding, why bother with one at all? For one thing, you want to make sure that you and your potential employer or buyer are on the same page with respect to major terms before you get down to details in the employment agreement and/or the medical practice sale agreement. For another, in most states certain LOI provisions are legally binding. For example, the document will most likely provide that each party is responsible for its own attorneys’ fees and for maintaining confidentiality during the negotiations, and that you will not negotiate with any other parties for some specified period of time. In most cases, such provisions are binding whether you go on to sign a formal contract or not.
When you receive an LOI, go through it carefully and identify areas of concern. The offering party will likely be in a rush to sign you up; but once you sign, you won’t be able to negotiate with anyone else for a while, which weakens your negotiating position. Regardless of what is said about time being “of the essence,” proceed slowly and with caution.
Bear in mind that employers and buyers never begin with their best offer. Unless you have been through this before, it is unlikely that you will know your value as an employee or the value of your practice, or what exactly you are entitled to ask for. Rather than signing something you don’t completely understand, explain to the offering party that you need time to consider and evaluate their offer.
This is the time to hire a competent medical attorney to do some due diligence on the offering party and review their offer, and to educate yourself about practice value and compensation benchmarks in your area. You and your counsel should assemble a list of things that you want changed in the LOI, then present them to the other side. They should be amenable to negotiation. If they are not (as was the case in the example presented earlier), you should reconsider whether you really want to be associated with that particular buyer or employer.
Once you have signed the LOI, experts say speed then works to your advantage. “Time kills all deals,” as one lawyer put it. “The longer it takes to close the transaction, the more that can go wrong.” The prospective employer or buyer could uncover information about you or your practice that decreases their perception of value, or economic conditions might change.
While speed is now important, and most of the core issues should already have been resolved in the LOI, don’t be afraid to ask for everything you want, whether it’s a better sale price, higher compensation, a favorable call schedule, more vacation time, or anything else. You won’t know what you can get if you don’t ask for it.
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.
I recently received an email from a distraught physician. Several months previously, He could continue running his office any way he wished, set his own hours and fees, and keep his employees. All his overhead expenses would disappear. His income would remain the same, maybe even increase. He signed it eagerly.
When he received the actual sale and employment contracts, none of the details promised in the LOI were included; but he figured that since they were spelled out in the LOI, which both he and the buyer had signed, he was covered. His attorney — a family friend with no experience in medical practice transactions — approved the documents.
The deal seemed too good to be true, and it was. The day after the sale closed, all his employees received termination notices. The group offered to rehire some of them, but at lower salaries and reduced benefits. (Most declined.) The new staffers he received were inadequately trained and unfamiliar with his standard office procedures. Patients complained that fees had increased substantially. His own compensation was contingent on meeting strict billing and performance goals. Malpractice premiums remained his responsibility. His office hours were lengthened to include evenings and Saturday mornings.
When he complained to the group that none of the things promised in the LOI had been delivered, he was informed that the LOI was not legally binding. In fact, the sale and employment contracts both clearly specified that they “replaced any previous written or oral agreements between the parties.”
There are some valuable lessons to be learned here. First, whether you are a young physician seeking a new job with a hospital or large practice, or an older one looking to sell an established practice, retain an attorney experienced in medical transactions early, before you sign anything, binding or not. Second, recognize that any promises made in an LOI must be spelled out in the employment and/or sale contract as well.
You might ask, if the terms in an LOI are not binding, why bother with one at all? For one thing, you want to make sure that you and your potential employer or buyer are on the same page with respect to major terms before you get down to details in the employment agreement and/or the medical practice sale agreement. For another, in most states certain LOI provisions are legally binding. For example, the document will most likely provide that each party is responsible for its own attorneys’ fees and for maintaining confidentiality during the negotiations, and that you will not negotiate with any other parties for some specified period of time. In most cases, such provisions are binding whether you go on to sign a formal contract or not.
When you receive an LOI, go through it carefully and identify areas of concern. The offering party will likely be in a rush to sign you up; but once you sign, you won’t be able to negotiate with anyone else for a while, which weakens your negotiating position. Regardless of what is said about time being “of the essence,” proceed slowly and with caution.
Bear in mind that employers and buyers never begin with their best offer. Unless you have been through this before, it is unlikely that you will know your value as an employee or the value of your practice, or what exactly you are entitled to ask for. Rather than signing something you don’t completely understand, explain to the offering party that you need time to consider and evaluate their offer.
This is the time to hire a competent medical attorney to do some due diligence on the offering party and review their offer, and to educate yourself about practice value and compensation benchmarks in your area. You and your counsel should assemble a list of things that you want changed in the LOI, then present them to the other side. They should be amenable to negotiation. If they are not (as was the case in the example presented earlier), you should reconsider whether you really want to be associated with that particular buyer or employer.
Once you have signed the LOI, experts say speed then works to your advantage. “Time kills all deals,” as one lawyer put it. “The longer it takes to close the transaction, the more that can go wrong.” The prospective employer or buyer could uncover information about you or your practice that decreases their perception of value, or economic conditions might change.
While speed is now important, and most of the core issues should already have been resolved in the LOI, don’t be afraid to ask for everything you want, whether it’s a better sale price, higher compensation, a favorable call schedule, more vacation time, or anything else. You won’t know what you can get if you don’t ask for it.
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.
Long-Term Follow-Up Emphasizes HPV Vaccination Importance
This transcript has been edited for clarity.
I want to briefly discuss a critically important topic that cannot be overly emphasized. It is the relevance, the importance, the benefits, and the outcome of HPV vaccination.
The paper I’m referring to was published in Pediatrics in October 2023. It’s titled, “Ten-Year Follow-up of 9-Valent Human Papillomavirus Vaccine: Immunogenicity, Effectiveness, and Safety.”
Let me emphasize that we’re talking about a 10-year follow-up. In this particular paper and analysis, 301 boys — I emphasize boys — were included and 971 girls at 40 different sites in 13 countries, who received the 9-valent vaccine, which includes HPV 16, 18, and seven other types.
Most importantly, there was not a single case. Not one. Let me repeat this: There was not a single case of high-grade intraepithelial neoplasia, or worse, or condyloma in either males or females. There was not a single case in over 1000 individuals with a follow-up of more than 10 years.
It is difficult to overstate the magnitude of the benefit associated with HPV vaccination for our children and young adults on their risk of developing highly relevant, life-changing, potentially deadly cancers.
For those of you who are interested in this topic — which should include almost all of you, if not all of you — I encourage you to read this very important follow-up paper, again, demonstrating the simple, overwhelming magnitude of the benefit of HPV vaccination. I thank you for your attention.
Dr. Markman is a professor in the department of medical oncology and therapeutics research, City of Hope, Duarte, California, and president of medicine and science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed ties with GlaxoSmithKline; AstraZeneca.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I want to briefly discuss a critically important topic that cannot be overly emphasized. It is the relevance, the importance, the benefits, and the outcome of HPV vaccination.
The paper I’m referring to was published in Pediatrics in October 2023. It’s titled, “Ten-Year Follow-up of 9-Valent Human Papillomavirus Vaccine: Immunogenicity, Effectiveness, and Safety.”
Let me emphasize that we’re talking about a 10-year follow-up. In this particular paper and analysis, 301 boys — I emphasize boys — were included and 971 girls at 40 different sites in 13 countries, who received the 9-valent vaccine, which includes HPV 16, 18, and seven other types.
Most importantly, there was not a single case. Not one. Let me repeat this: There was not a single case of high-grade intraepithelial neoplasia, or worse, or condyloma in either males or females. There was not a single case in over 1000 individuals with a follow-up of more than 10 years.
It is difficult to overstate the magnitude of the benefit associated with HPV vaccination for our children and young adults on their risk of developing highly relevant, life-changing, potentially deadly cancers.
For those of you who are interested in this topic — which should include almost all of you, if not all of you — I encourage you to read this very important follow-up paper, again, demonstrating the simple, overwhelming magnitude of the benefit of HPV vaccination. I thank you for your attention.
Dr. Markman is a professor in the department of medical oncology and therapeutics research, City of Hope, Duarte, California, and president of medicine and science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed ties with GlaxoSmithKline; AstraZeneca.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I want to briefly discuss a critically important topic that cannot be overly emphasized. It is the relevance, the importance, the benefits, and the outcome of HPV vaccination.
The paper I’m referring to was published in Pediatrics in October 2023. It’s titled, “Ten-Year Follow-up of 9-Valent Human Papillomavirus Vaccine: Immunogenicity, Effectiveness, and Safety.”
Let me emphasize that we’re talking about a 10-year follow-up. In this particular paper and analysis, 301 boys — I emphasize boys — were included and 971 girls at 40 different sites in 13 countries, who received the 9-valent vaccine, which includes HPV 16, 18, and seven other types.
Most importantly, there was not a single case. Not one. Let me repeat this: There was not a single case of high-grade intraepithelial neoplasia, or worse, or condyloma in either males or females. There was not a single case in over 1000 individuals with a follow-up of more than 10 years.
It is difficult to overstate the magnitude of the benefit associated with HPV vaccination for our children and young adults on their risk of developing highly relevant, life-changing, potentially deadly cancers.
For those of you who are interested in this topic — which should include almost all of you, if not all of you — I encourage you to read this very important follow-up paper, again, demonstrating the simple, overwhelming magnitude of the benefit of HPV vaccination. I thank you for your attention.
Dr. Markman is a professor in the department of medical oncology and therapeutics research, City of Hope, Duarte, California, and president of medicine and science, City of Hope Atlanta, Chicago, and Phoenix. He disclosed ties with GlaxoSmithKline; AstraZeneca.
A version of this article appeared on Medscape.com.
Healing From Trauma
“You’ll never walk alone.” — Nettie Fowler, Carousel
A few winters ago, a young man and his fiancée were driving on the 91 freeway in southern California during a torrential downpour when their Honda Civic hydroplaned, slamming into the jersey barrier. They were both unhurt. Unsure what to do next, they made the catastrophic decision to exit the vehicle. As the man walked around the back of the car he was nearly hit by a black sedan sliding out of control trying to avoid them. When he came around the car, his fiancé was nowhere to be found. She had been struck at highway speed and lay crushed under the sedan hundreds of feet away.
I know this poor man because he was referred to me. Not as a dermatologist, but as a fellow human healing from trauma. On January 1, 2019, at about 9:30 PM, while we were home together, my beloved wife of 24 years took her own life. Even 5 years on it is difficult to believe that she isn’t proofing this paragraph like she had done for every one of my Derm News columns for years. We had been together since teenagers and had lived a joy-filled life. There isn’t any medical reason to share. But that day I joined the community of those who have carried unbearable heaviness of grief and survived. Sometimes others seek me out for help.
At first, my instinct was to guide them, to give advice, to tell them what to do and where to go. But I’ve learned that people in this dark valley don’t need a guide. They need someone to accompany them. To walk with them for a few minutes on their lonely journey. I recently read David Brooks’s new book, How to Know a Person. I’ve been a fan of his since he joined the New York Times in 2003 and have read almost everything he’s written. I sometimes even imagine how he might approach a column whenever I’m stuck (thank you, David). His The Road to Character book is in my canon of literature for self-growth. This latest book is an interesting digression from that central theme. He argues that our society is in acute need of forming better connections and that an important way we can be moral is to learn, and to practice, how to know each other. He shares an emotional experience of losing a close friend to suicide and writes a poignant explanation of what it means to accompany someone in need. It particularly resonated with me. We are doctors and are wired to find the source of a problem, like quickly rotating through the 4X, 10X, 40X on a microscope. Once identified, we spend most of our time creating and explaining treatments. I see how this makes me a great dermatologist but just an average human.
Brooks tells the story of a woman with a brain tumor who often finds herself on the ground surrounded by well-meaning people trying to help. She explains later that what she really needs in those moments is just for someone to get on the ground and lie with her. To accompany her.
Having crossed the midpoint of life, I see with the benefit of perspective how suffering has afforded me wisdom: I am more sensitive and attuned to others. It also gave me credibility: I know how it feels to walk life’s loneliest journey. I’ve also learned to make myself vulnerable for someone to share their story with me. I won’t be afraid to hear the details. I won’t judge them for weeping too little or for sobbing too much. I don’t answer whys. I won’t say what they should do next. But for a few minutes I can walk beside them as a person who cares.
I do not try to remember the hours and days after Susan’s death, but one moment stands out and makes my eyes well when I think of it. That following day my dear brother flew across the country on the next flight out. I was sitting in a psychiatry waiting room when he came down the hall with his luggage in tow. He hugged me as only a brother could, then looked me in my eyes, which were bloodshot from tears just as his were, and he said, “We’re going to be OK.” And with that he walked with me into the office.
We physicians are blessed to have so many intimate human interactions. This book reminded me that sometimes my most important job is not to be the optimized doctor, but just a good human walking alongside.
I have no conflict of interest and purchased these books.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at dermnews@mdedge.com.
“You’ll never walk alone.” — Nettie Fowler, Carousel
A few winters ago, a young man and his fiancée were driving on the 91 freeway in southern California during a torrential downpour when their Honda Civic hydroplaned, slamming into the jersey barrier. They were both unhurt. Unsure what to do next, they made the catastrophic decision to exit the vehicle. As the man walked around the back of the car he was nearly hit by a black sedan sliding out of control trying to avoid them. When he came around the car, his fiancé was nowhere to be found. She had been struck at highway speed and lay crushed under the sedan hundreds of feet away.
I know this poor man because he was referred to me. Not as a dermatologist, but as a fellow human healing from trauma. On January 1, 2019, at about 9:30 PM, while we were home together, my beloved wife of 24 years took her own life. Even 5 years on it is difficult to believe that she isn’t proofing this paragraph like she had done for every one of my Derm News columns for years. We had been together since teenagers and had lived a joy-filled life. There isn’t any medical reason to share. But that day I joined the community of those who have carried unbearable heaviness of grief and survived. Sometimes others seek me out for help.
At first, my instinct was to guide them, to give advice, to tell them what to do and where to go. But I’ve learned that people in this dark valley don’t need a guide. They need someone to accompany them. To walk with them for a few minutes on their lonely journey. I recently read David Brooks’s new book, How to Know a Person. I’ve been a fan of his since he joined the New York Times in 2003 and have read almost everything he’s written. I sometimes even imagine how he might approach a column whenever I’m stuck (thank you, David). His The Road to Character book is in my canon of literature for self-growth. This latest book is an interesting digression from that central theme. He argues that our society is in acute need of forming better connections and that an important way we can be moral is to learn, and to practice, how to know each other. He shares an emotional experience of losing a close friend to suicide and writes a poignant explanation of what it means to accompany someone in need. It particularly resonated with me. We are doctors and are wired to find the source of a problem, like quickly rotating through the 4X, 10X, 40X on a microscope. Once identified, we spend most of our time creating and explaining treatments. I see how this makes me a great dermatologist but just an average human.
Brooks tells the story of a woman with a brain tumor who often finds herself on the ground surrounded by well-meaning people trying to help. She explains later that what she really needs in those moments is just for someone to get on the ground and lie with her. To accompany her.
Having crossed the midpoint of life, I see with the benefit of perspective how suffering has afforded me wisdom: I am more sensitive and attuned to others. It also gave me credibility: I know how it feels to walk life’s loneliest journey. I’ve also learned to make myself vulnerable for someone to share their story with me. I won’t be afraid to hear the details. I won’t judge them for weeping too little or for sobbing too much. I don’t answer whys. I won’t say what they should do next. But for a few minutes I can walk beside them as a person who cares.
I do not try to remember the hours and days after Susan’s death, but one moment stands out and makes my eyes well when I think of it. That following day my dear brother flew across the country on the next flight out. I was sitting in a psychiatry waiting room when he came down the hall with his luggage in tow. He hugged me as only a brother could, then looked me in my eyes, which were bloodshot from tears just as his were, and he said, “We’re going to be OK.” And with that he walked with me into the office.
We physicians are blessed to have so many intimate human interactions. This book reminded me that sometimes my most important job is not to be the optimized doctor, but just a good human walking alongside.
I have no conflict of interest and purchased these books.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at dermnews@mdedge.com.
“You’ll never walk alone.” — Nettie Fowler, Carousel
A few winters ago, a young man and his fiancée were driving on the 91 freeway in southern California during a torrential downpour when their Honda Civic hydroplaned, slamming into the jersey barrier. They were both unhurt. Unsure what to do next, they made the catastrophic decision to exit the vehicle. As the man walked around the back of the car he was nearly hit by a black sedan sliding out of control trying to avoid them. When he came around the car, his fiancé was nowhere to be found. She had been struck at highway speed and lay crushed under the sedan hundreds of feet away.
I know this poor man because he was referred to me. Not as a dermatologist, but as a fellow human healing from trauma. On January 1, 2019, at about 9:30 PM, while we were home together, my beloved wife of 24 years took her own life. Even 5 years on it is difficult to believe that she isn’t proofing this paragraph like she had done for every one of my Derm News columns for years. We had been together since teenagers and had lived a joy-filled life. There isn’t any medical reason to share. But that day I joined the community of those who have carried unbearable heaviness of grief and survived. Sometimes others seek me out for help.
At first, my instinct was to guide them, to give advice, to tell them what to do and where to go. But I’ve learned that people in this dark valley don’t need a guide. They need someone to accompany them. To walk with them for a few minutes on their lonely journey. I recently read David Brooks’s new book, How to Know a Person. I’ve been a fan of his since he joined the New York Times in 2003 and have read almost everything he’s written. I sometimes even imagine how he might approach a column whenever I’m stuck (thank you, David). His The Road to Character book is in my canon of literature for self-growth. This latest book is an interesting digression from that central theme. He argues that our society is in acute need of forming better connections and that an important way we can be moral is to learn, and to practice, how to know each other. He shares an emotional experience of losing a close friend to suicide and writes a poignant explanation of what it means to accompany someone in need. It particularly resonated with me. We are doctors and are wired to find the source of a problem, like quickly rotating through the 4X, 10X, 40X on a microscope. Once identified, we spend most of our time creating and explaining treatments. I see how this makes me a great dermatologist but just an average human.
Brooks tells the story of a woman with a brain tumor who often finds herself on the ground surrounded by well-meaning people trying to help. She explains later that what she really needs in those moments is just for someone to get on the ground and lie with her. To accompany her.
Having crossed the midpoint of life, I see with the benefit of perspective how suffering has afforded me wisdom: I am more sensitive and attuned to others. It also gave me credibility: I know how it feels to walk life’s loneliest journey. I’ve also learned to make myself vulnerable for someone to share their story with me. I won’t be afraid to hear the details. I won’t judge them for weeping too little or for sobbing too much. I don’t answer whys. I won’t say what they should do next. But for a few minutes I can walk beside them as a person who cares.
I do not try to remember the hours and days after Susan’s death, but one moment stands out and makes my eyes well when I think of it. That following day my dear brother flew across the country on the next flight out. I was sitting in a psychiatry waiting room when he came down the hall with his luggage in tow. He hugged me as only a brother could, then looked me in my eyes, which were bloodshot from tears just as his were, and he said, “We’re going to be OK.” And with that he walked with me into the office.
We physicians are blessed to have so many intimate human interactions. This book reminded me that sometimes my most important job is not to be the optimized doctor, but just a good human walking alongside.
I have no conflict of interest and purchased these books.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at dermnews@mdedge.com.