Opinion

Dear Friends,

The prevailing theme of this issue is “Success.” I have learned that “success” is personal and personalized. What “success” looked like 10, or even 5, years ago to me is very different from how I perceive it now; and I know it may be different 5 years from now. My definition of success should not look like another’s — that was the best advice I have gotten over the years and it has kept me constantly redefining what is important to me and placing value on where I want to allocate my time and efforts, at work and at home.

This issue of The New Gastroenterologist highlights topics from successful GIs within their own realms of expertise, offering insights on advancing in academic medicine, navigating financial wellness with a financial adviser, and becoming a future leader in GI.

Yours truly,

Judy A. Trieu, MD, MPH

Editor-in-Chief
Interventional Endoscopy, Division of Gastroenterology
Washington University in St. Louis

Dear Friends,

The prevailing theme of this issue is “Success.” I have learned that “success” is personal and personalized. What “success” looked like 10, or even 5, years ago to me is very different from how I perceive it now; and I know it may be different 5 years from now. My definition of success should not look like another’s — that was the best advice I have gotten over the years and it has kept me constantly redefining what is important to me and placing value on where I want to allocate my time and efforts, at work and at home.

This issue of The New Gastroenterologist highlights topics from successful GIs within their own realms of expertise, offering insights on advancing in academic medicine, navigating financial wellness with a financial adviser, and becoming a future leader in GI.

Yours truly,

Judy A. Trieu, MD, MPH

Editor-in-Chief
Interventional Endoscopy, Division of Gastroenterology
Washington University in St. Louis

Dear Friends,

The prevailing theme of this issue is “Success.” I have learned that “success” is personal and personalized. What “success” looked like 10, or even 5, years ago to me is very different from how I perceive it now; and I know it may be different 5 years from now. My definition of success should not look like another’s — that was the best advice I have gotten over the years and it has kept me constantly redefining what is important to me and placing value on where I want to allocate my time and efforts, at work and at home.

This issue of The New Gastroenterologist highlights topics from successful GIs within their own realms of expertise, offering insights on advancing in academic medicine, navigating financial wellness with a financial adviser, and becoming a future leader in GI.

Yours truly,

Judy A. Trieu, MD, MPH

Editor-in-Chief
Interventional Endoscopy, Division of Gastroenterology
Washington University in St. Louis

Release of our May issue coincides with our annual pilgrimage to Digestive Disease Week^® (DDW), this year held in our nation’s capital of Washington, D.C.

As we peruse the preliminary program in planning our meeting coverage, I am always amazed at the breadth and depth of programming offered as part of a relatively brief, 4-day meeting — this is a testament to the hard work of the AGA Council and DDW organizing committees, who have the gargantuan task of ensuring an engaging, seamless meeting each year.

University of Michigan

This year’s conference features over 400 original scientific sessions and 4,300 oral abstract and poster presentations, in addition to the always well-attended AGA Postgraduate Course. This year’s AGA Presidential Plenary, which will feature a series of thought-provoking panel discussions on the future of GI healthcare and innovations in how we treat, disseminate, and teach, also is not to be missed. Beyond DDW, I hope you will join me in taking advantage of some of D.C.’s amazing cultural offerings, including the Smithsonian museums, National Gallery, Kennedy Center for the Performing Arts, and many others.

In this month’s issue of GIHN, we highlight an important AGA expert consensus commentary published in Clinical Gastroenterology and Hepatology examining the role of blood-based tests (“liquid biopsy”) in colorectal cancer screening. This guidance, which recognizes the promise of such tests but also urges caution in their adoption, is particularly important considering recently published data from the ECLIPSE study (also covered in this issue) evaluating the performance of Guardant’s ctDNA liquid biopsy compared to a screening colonoscopy. Also relevant to CRC screening, we highlight data on the performance of the “next gen” Cologuard test compared with FIT, which was recently published in NEJM. In our May Member Spotlight, we feature gastroenterologist Adjoa Anyane-Yeboa, MD, MPH, who shares her passion for addressing barriers to CRC screening for Black patients. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column highlighting emerging applications of AI in GI endoscopy and hepatology. We hope you enjoy all the exciting content featured in this issue and look forward to seeing you in Washington, D.C. (or virtually) for DDW.
 

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Release of our May issue coincides with our annual pilgrimage to Digestive Disease Week^® (DDW), this year held in our nation’s capital of Washington, D.C.

As we peruse the preliminary program in planning our meeting coverage, I am always amazed at the breadth and depth of programming offered as part of a relatively brief, 4-day meeting — this is a testament to the hard work of the AGA Council and DDW organizing committees, who have the gargantuan task of ensuring an engaging, seamless meeting each year.

University of Michigan

This year’s conference features over 400 original scientific sessions and 4,300 oral abstract and poster presentations, in addition to the always well-attended AGA Postgraduate Course. This year’s AGA Presidential Plenary, which will feature a series of thought-provoking panel discussions on the future of GI healthcare and innovations in how we treat, disseminate, and teach, also is not to be missed. Beyond DDW, I hope you will join me in taking advantage of some of D.C.’s amazing cultural offerings, including the Smithsonian museums, National Gallery, Kennedy Center for the Performing Arts, and many others.

In this month’s issue of GIHN, we highlight an important AGA expert consensus commentary published in Clinical Gastroenterology and Hepatology examining the role of blood-based tests (“liquid biopsy”) in colorectal cancer screening. This guidance, which recognizes the promise of such tests but also urges caution in their adoption, is particularly important considering recently published data from the ECLIPSE study (also covered in this issue) evaluating the performance of Guardant’s ctDNA liquid biopsy compared to a screening colonoscopy. Also relevant to CRC screening, we highlight data on the performance of the “next gen” Cologuard test compared with FIT, which was recently published in NEJM. In our May Member Spotlight, we feature gastroenterologist Adjoa Anyane-Yeboa, MD, MPH, who shares her passion for addressing barriers to CRC screening for Black patients. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column highlighting emerging applications of AI in GI endoscopy and hepatology. We hope you enjoy all the exciting content featured in this issue and look forward to seeing you in Washington, D.C. (or virtually) for DDW.
 

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Release of our May issue coincides with our annual pilgrimage to Digestive Disease Week^® (DDW), this year held in our nation’s capital of Washington, D.C.

As we peruse the preliminary program in planning our meeting coverage, I am always amazed at the breadth and depth of programming offered as part of a relatively brief, 4-day meeting — this is a testament to the hard work of the AGA Council and DDW organizing committees, who have the gargantuan task of ensuring an engaging, seamless meeting each year.

University of Michigan

This year’s conference features over 400 original scientific sessions and 4,300 oral abstract and poster presentations, in addition to the always well-attended AGA Postgraduate Course. This year’s AGA Presidential Plenary, which will feature a series of thought-provoking panel discussions on the future of GI healthcare and innovations in how we treat, disseminate, and teach, also is not to be missed. Beyond DDW, I hope you will join me in taking advantage of some of D.C.’s amazing cultural offerings, including the Smithsonian museums, National Gallery, Kennedy Center for the Performing Arts, and many others.

In this month’s issue of GIHN, we highlight an important AGA expert consensus commentary published in Clinical Gastroenterology and Hepatology examining the role of blood-based tests (“liquid biopsy”) in colorectal cancer screening. This guidance, which recognizes the promise of such tests but also urges caution in their adoption, is particularly important considering recently published data from the ECLIPSE study (also covered in this issue) evaluating the performance of Guardant’s ctDNA liquid biopsy compared to a screening colonoscopy. Also relevant to CRC screening, we highlight data on the performance of the “next gen” Cologuard test compared with FIT, which was recently published in NEJM. In our May Member Spotlight, we feature gastroenterologist Adjoa Anyane-Yeboa, MD, MPH, who shares her passion for addressing barriers to CRC screening for Black patients. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column highlighting emerging applications of AI in GI endoscopy and hepatology. We hope you enjoy all the exciting content featured in this issue and look forward to seeing you in Washington, D.C. (or virtually) for DDW.
 

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Smoldering multiple myeloma (SMM), a potential precursor to multiple myeloma (MM), has become a controversial topic. Some people diagnosed with SMM will live their whole lives without ever developing MM, while others will develop it quickly.

My approach to treating SMM takes into account what its history can teach us about 1) how advancements in imaging and diagnostic reclassifications can revise the entire natural history of a disease, and 2) how evidence generated by even the best of studies may have an expiration date.

Huntsman Cancer Institute

Much of what we know about SMM today dates to a pivotal study by Robert A. Kyle, MD, and colleagues, published in 2007. That inspirational team of investigators followed people diagnosed with SMM from 1970 to 1995 and established the first natural history of the condition. Their monumental effort and the data and conclusions it generated (eg,10% risk annually of SMM becoming MM for the first 5 years) are still cited today in references, papers, and slide sets.

Despite the seminal importance of this work, from today’s perspective the 2007 study might just as well have been describing a different disease. Back then people were diagnosed with SMM if their blood work detected a monoclonal protein and a follow-up bone marrow biopsy found at least 10% plasma cells (or a monoclonal protein exceeding 3g/dL). If there were no signs of end-organ damage (ie, no anemia or kidney problems) and an x-ray showed no fractures or lesions in the bones, the diagnosis was determined to be SMM.

What’s different in 2024? First and foremost: advanced, highly sensitive imaging techniques. MRIs can pick up small lytic lesions (and even the precursor to lytic lesions) that would not appear on an x-ray. In fact, relying solely on x-rays risks missing half of the lytic lesions.

Therefore, using the same criteria, many people who in the past were diagnosed with SMM would today be diagnosed with MM. Furthermore, in 2014 a diagnostic change reclassified people’s diagnosis from the highest risk category of SMM to the category of active MM.

Due to these scientific advances and classification changes, I believe that the natural history of SMM is unknown. Risk stratification models for SMM derived from data sets of people who had not undergone rigorous advanced imaging likely are skewed by data from people who had MM. In addition, current risk stratification models have very poor concordance with each other. I routinely see people whose 2-year risk according to different models varies by more than 30%-40%.

All this information tells us that SMM today is more indolent than the SMM of the past. Paradoxically, however, our therapies keep getting more and more aggressive, exposing this vulnerable group of people to intense treatment regimens that they may not require. Therapies tested on people diagnosed with SMM include an aggressive three-drug regimen, autologous stem cell transplant, and 2 years of additional therapy, as well as, more recently CAR T-cell therapy which so far has at least a 4%-5% treatment-related mortality risk in people with myeloma and a strong signal for secondary cancer risk. Other trials are testing bispecific therapies such as talquetamab, a drug which in my experience causes horrendous skin toxicity, profound weight loss, and one’s nails to fall off.

Doctors routinely keep showing slides from Kyle’s pivotal work to describe the natural history of SMM and to justify the need for treatment, and trials continue to use outdated progression prediction models. In my opinion, as people with MM keep living longer and treatments for MM keep getting better, the threshold for intervening with asymptomatic, healthy people with SMM should be getting higher, not lower.

I strongly believe that the current landscape of SMM treatment exemplifies good intentions leading to bad outcomes. A routine blood test in a completely healthy person that finds elevated total protein in the blood could culminate in well-intentioned but aggressive therapies that can lead to many serious side effects. (I repeat: Secondary cancers and deaths from infections have all occurred in SMM trials.)

With no control arm, we simply don’t know how well these people might have fared without any therapy. For all we know, treatment may have shortened their lives due to complications up to and including death — all because of a blood test often conducted for reasons that have no evidentiary basis.

For example, plasma cell diseases are not linked to low bone density or auto-immune diseases, yet these labs are sent routinely as part of a workup for those conditions, leading to increasing anxiety and costs.

So, what is my approach? When treating people with SMM, I hold nuanced discussions of this data to help prioritize and reach informed decisions. After our honest conversation about the limitations of SMM models, older data, and the limitations of prospective data studying pharmacological treatment, almost no one signs up for treatment.

I want these people to stay safe, and I’m proud to be a part of a trial (SPOTLIGHT, NCT06212323) that aims to show prospectively that these people can be watched off treatment with monitoring via advanced imaging modalities.

In conclusion: SMM teaches us how, even in the absence of pharmacological interventions, the natural history of a disease can change over time, simply via better imaging techniques and changes in diagnostic classifications. Unfortunately, SMM also illustrates how good intentions can lead to harm.
 

Dr. Mohyuddin is assistant professor in the multiple myeloma program at the Huntsman Cancer Institute at the University of Utah in Salt Lake City.

Smoldering multiple myeloma (SMM), a potential precursor to multiple myeloma (MM), has become a controversial topic. Some people diagnosed with SMM will live their whole lives without ever developing MM, while others will develop it quickly.

My approach to treating SMM takes into account what its history can teach us about 1) how advancements in imaging and diagnostic reclassifications can revise the entire natural history of a disease, and 2) how evidence generated by even the best of studies may have an expiration date.

Huntsman Cancer Institute

Much of what we know about SMM today dates to a pivotal study by Robert A. Kyle, MD, and colleagues, published in 2007. That inspirational team of investigators followed people diagnosed with SMM from 1970 to 1995 and established the first natural history of the condition. Their monumental effort and the data and conclusions it generated (eg,10% risk annually of SMM becoming MM for the first 5 years) are still cited today in references, papers, and slide sets.

Despite the seminal importance of this work, from today’s perspective the 2007 study might just as well have been describing a different disease. Back then people were diagnosed with SMM if their blood work detected a monoclonal protein and a follow-up bone marrow biopsy found at least 10% plasma cells (or a monoclonal protein exceeding 3g/dL). If there were no signs of end-organ damage (ie, no anemia or kidney problems) and an x-ray showed no fractures or lesions in the bones, the diagnosis was determined to be SMM.

What’s different in 2024? First and foremost: advanced, highly sensitive imaging techniques. MRIs can pick up small lytic lesions (and even the precursor to lytic lesions) that would not appear on an x-ray. In fact, relying solely on x-rays risks missing half of the lytic lesions.

Therefore, using the same criteria, many people who in the past were diagnosed with SMM would today be diagnosed with MM. Furthermore, in 2014 a diagnostic change reclassified people’s diagnosis from the highest risk category of SMM to the category of active MM.

Due to these scientific advances and classification changes, I believe that the natural history of SMM is unknown. Risk stratification models for SMM derived from data sets of people who had not undergone rigorous advanced imaging likely are skewed by data from people who had MM. In addition, current risk stratification models have very poor concordance with each other. I routinely see people whose 2-year risk according to different models varies by more than 30%-40%.

All this information tells us that SMM today is more indolent than the SMM of the past. Paradoxically, however, our therapies keep getting more and more aggressive, exposing this vulnerable group of people to intense treatment regimens that they may not require. Therapies tested on people diagnosed with SMM include an aggressive three-drug regimen, autologous stem cell transplant, and 2 years of additional therapy, as well as, more recently CAR T-cell therapy which so far has at least a 4%-5% treatment-related mortality risk in people with myeloma and a strong signal for secondary cancer risk. Other trials are testing bispecific therapies such as talquetamab, a drug which in my experience causes horrendous skin toxicity, profound weight loss, and one’s nails to fall off.

Doctors routinely keep showing slides from Kyle’s pivotal work to describe the natural history of SMM and to justify the need for treatment, and trials continue to use outdated progression prediction models. In my opinion, as people with MM keep living longer and treatments for MM keep getting better, the threshold for intervening with asymptomatic, healthy people with SMM should be getting higher, not lower.

I strongly believe that the current landscape of SMM treatment exemplifies good intentions leading to bad outcomes. A routine blood test in a completely healthy person that finds elevated total protein in the blood could culminate in well-intentioned but aggressive therapies that can lead to many serious side effects. (I repeat: Secondary cancers and deaths from infections have all occurred in SMM trials.)

With no control arm, we simply don’t know how well these people might have fared without any therapy. For all we know, treatment may have shortened their lives due to complications up to and including death — all because of a blood test often conducted for reasons that have no evidentiary basis.

For example, plasma cell diseases are not linked to low bone density or auto-immune diseases, yet these labs are sent routinely as part of a workup for those conditions, leading to increasing anxiety and costs.

So, what is my approach? When treating people with SMM, I hold nuanced discussions of this data to help prioritize and reach informed decisions. After our honest conversation about the limitations of SMM models, older data, and the limitations of prospective data studying pharmacological treatment, almost no one signs up for treatment.

I want these people to stay safe, and I’m proud to be a part of a trial (SPOTLIGHT, NCT06212323) that aims to show prospectively that these people can be watched off treatment with monitoring via advanced imaging modalities.

In conclusion: SMM teaches us how, even in the absence of pharmacological interventions, the natural history of a disease can change over time, simply via better imaging techniques and changes in diagnostic classifications. Unfortunately, SMM also illustrates how good intentions can lead to harm.
 

Dr. Mohyuddin is assistant professor in the multiple myeloma program at the Huntsman Cancer Institute at the University of Utah in Salt Lake City.

Smoldering multiple myeloma (SMM), a potential precursor to multiple myeloma (MM), has become a controversial topic. Some people diagnosed with SMM will live their whole lives without ever developing MM, while others will develop it quickly.

My approach to treating SMM takes into account what its history can teach us about 1) how advancements in imaging and diagnostic reclassifications can revise the entire natural history of a disease, and 2) how evidence generated by even the best of studies may have an expiration date.

Huntsman Cancer Institute

Much of what we know about SMM today dates to a pivotal study by Robert A. Kyle, MD, and colleagues, published in 2007. That inspirational team of investigators followed people diagnosed with SMM from 1970 to 1995 and established the first natural history of the condition. Their monumental effort and the data and conclusions it generated (eg,10% risk annually of SMM becoming MM for the first 5 years) are still cited today in references, papers, and slide sets.

Despite the seminal importance of this work, from today’s perspective the 2007 study might just as well have been describing a different disease. Back then people were diagnosed with SMM if their blood work detected a monoclonal protein and a follow-up bone marrow biopsy found at least 10% plasma cells (or a monoclonal protein exceeding 3g/dL). If there were no signs of end-organ damage (ie, no anemia or kidney problems) and an x-ray showed no fractures or lesions in the bones, the diagnosis was determined to be SMM.

What’s different in 2024? First and foremost: advanced, highly sensitive imaging techniques. MRIs can pick up small lytic lesions (and even the precursor to lytic lesions) that would not appear on an x-ray. In fact, relying solely on x-rays risks missing half of the lytic lesions.

Therefore, using the same criteria, many people who in the past were diagnosed with SMM would today be diagnosed with MM. Furthermore, in 2014 a diagnostic change reclassified people’s diagnosis from the highest risk category of SMM to the category of active MM.

Due to these scientific advances and classification changes, I believe that the natural history of SMM is unknown. Risk stratification models for SMM derived from data sets of people who had not undergone rigorous advanced imaging likely are skewed by data from people who had MM. In addition, current risk stratification models have very poor concordance with each other. I routinely see people whose 2-year risk according to different models varies by more than 30%-40%.

All this information tells us that SMM today is more indolent than the SMM of the past. Paradoxically, however, our therapies keep getting more and more aggressive, exposing this vulnerable group of people to intense treatment regimens that they may not require. Therapies tested on people diagnosed with SMM include an aggressive three-drug regimen, autologous stem cell transplant, and 2 years of additional therapy, as well as, more recently CAR T-cell therapy which so far has at least a 4%-5% treatment-related mortality risk in people with myeloma and a strong signal for secondary cancer risk. Other trials are testing bispecific therapies such as talquetamab, a drug which in my experience causes horrendous skin toxicity, profound weight loss, and one’s nails to fall off.

Doctors routinely keep showing slides from Kyle’s pivotal work to describe the natural history of SMM and to justify the need for treatment, and trials continue to use outdated progression prediction models. In my opinion, as people with MM keep living longer and treatments for MM keep getting better, the threshold for intervening with asymptomatic, healthy people with SMM should be getting higher, not lower.

I strongly believe that the current landscape of SMM treatment exemplifies good intentions leading to bad outcomes. A routine blood test in a completely healthy person that finds elevated total protein in the blood could culminate in well-intentioned but aggressive therapies that can lead to many serious side effects. (I repeat: Secondary cancers and deaths from infections have all occurred in SMM trials.)

With no control arm, we simply don’t know how well these people might have fared without any therapy. For all we know, treatment may have shortened their lives due to complications up to and including death — all because of a blood test often conducted for reasons that have no evidentiary basis.

For example, plasma cell diseases are not linked to low bone density or auto-immune diseases, yet these labs are sent routinely as part of a workup for those conditions, leading to increasing anxiety and costs.

So, what is my approach? When treating people with SMM, I hold nuanced discussions of this data to help prioritize and reach informed decisions. After our honest conversation about the limitations of SMM models, older data, and the limitations of prospective data studying pharmacological treatment, almost no one signs up for treatment.

I want these people to stay safe, and I’m proud to be a part of a trial (SPOTLIGHT, NCT06212323) that aims to show prospectively that these people can be watched off treatment with monitoring via advanced imaging modalities.

In conclusion: SMM teaches us how, even in the absence of pharmacological interventions, the natural history of a disease can change over time, simply via better imaging techniques and changes in diagnostic classifications. Unfortunately, SMM also illustrates how good intentions can lead to harm.
 

Dr. Mohyuddin is assistant professor in the multiple myeloma program at the Huntsman Cancer Institute at the University of Utah in Salt Lake City.

I recently read an op-ed piece in which the author wondered if any young people entering the practice of medicine felt that they were answering a “calling.” I suspect that there will continue to be, and will always be, idealists whose primary motivation for choosing medicine is that they will be healing the sick or at least providing comfort to the suffering. I occasionally hear that about a former patient who has been inspired by a personal or familial experience with a serious illness.

Unfortunately, I suspect those who feel called are the providers most likely to feel discouraged and frustrated by the current state of primary care. Luckily, I never felt a calling. For me, primary care pediatrics was a job. One that l felt obligated to perform to the best of my ability. Mine was not a calling but an inherited philosophy that work in itself was virtuous. A work ethic, if you will. Pediatrics offered the additional reward that, if well done, it might help some parents and their children feel a little better.

Fifty years ago I was not alone in treating medicine as a job. Most physicians were self-employed. Although there were exceptions like Albert Schweitzer, even those of us with a calling had to obey the basic rules of business as it applied to medicine. We were employer and employee and had to understand the critical factors of overhead, profit, and loss.

I have burdened you with this little history recitation not to suggest that things were better in the good old days, but to provide a stepping stone into the murky and uncomfortable topic of primary care physician (PCP) compensation. Because almost three quarters of you work for a hospital, health system, or corporate entity, I am going to illuminate our journey by leaning on the advice of an international company with 7000 employees and revenue of 2.5 billion dollars that considers itself a “global leader” in management consulting. Your employer is listening to some management consultant and it may help us to view your compensation from someone on their side of the table.

First, you should be aware that “most health systems lose money on their primary care operations — up to $200,000 or more per primary care physician.” This may help explain why despite being in short supply, you and most PCPs feel undervalued. However, if we are such losers, we must provide something(s) that the systems are seeking. It is likely that the system is looking to tout its ability to provide comprehensive care and demonstrate that it has a patient base broad enough to warrant attention and provide bargaining leverage on volume discounts.

The system also may want to minimize competition by absorbing the remaining PCPs in the community into their system. With you outside of the system, it had less control over your compensation than it does when you are under its umbrella.

Your employer may want to grow and feed its specialty care network, and it sees PCPs as having the fuel stored in their patient volume to do just that. In simplest and most cynical terms, the systems are willing to take a loss on us less profitable high-volume grunts in order to reap the profits of the lower-volume high-profitability specialties and subspecialties.

So that’s why you as a PCP have any value at all to a large healthcare system. But, it means that to maintain your value to the system you must continue to provide the volume it anticipates and needs. While the system may have been willing to accept some degrees of unprofitability when it hired you, there are limits. And, we shouldn’t be surprised if they continue to urge or demand that we narrow the gap between the revenue we generate and the costs that we incur, ie, our overhead.

In Part 2 of this series, I’m going to discuss the collateral damage that occurs when volume and overhead collide in an environment that claims to be committed to patient care.

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

I recently read an op-ed piece in which the author wondered if any young people entering the practice of medicine felt that they were answering a “calling.” I suspect that there will continue to be, and will always be, idealists whose primary motivation for choosing medicine is that they will be healing the sick or at least providing comfort to the suffering. I occasionally hear that about a former patient who has been inspired by a personal or familial experience with a serious illness.

Unfortunately, I suspect those who feel called are the providers most likely to feel discouraged and frustrated by the current state of primary care. Luckily, I never felt a calling. For me, primary care pediatrics was a job. One that l felt obligated to perform to the best of my ability. Mine was not a calling but an inherited philosophy that work in itself was virtuous. A work ethic, if you will. Pediatrics offered the additional reward that, if well done, it might help some parents and their children feel a little better.

Fifty years ago I was not alone in treating medicine as a job. Most physicians were self-employed. Although there were exceptions like Albert Schweitzer, even those of us with a calling had to obey the basic rules of business as it applied to medicine. We were employer and employee and had to understand the critical factors of overhead, profit, and loss.

I have burdened you with this little history recitation not to suggest that things were better in the good old days, but to provide a stepping stone into the murky and uncomfortable topic of primary care physician (PCP) compensation. Because almost three quarters of you work for a hospital, health system, or corporate entity, I am going to illuminate our journey by leaning on the advice of an international company with 7000 employees and revenue of 2.5 billion dollars that considers itself a “global leader” in management consulting. Your employer is listening to some management consultant and it may help us to view your compensation from someone on their side of the table.

First, you should be aware that “most health systems lose money on their primary care operations — up to $200,000 or more per primary care physician.” This may help explain why despite being in short supply, you and most PCPs feel undervalued. However, if we are such losers, we must provide something(s) that the systems are seeking. It is likely that the system is looking to tout its ability to provide comprehensive care and demonstrate that it has a patient base broad enough to warrant attention and provide bargaining leverage on volume discounts.

The system also may want to minimize competition by absorbing the remaining PCPs in the community into their system. With you outside of the system, it had less control over your compensation than it does when you are under its umbrella.

Your employer may want to grow and feed its specialty care network, and it sees PCPs as having the fuel stored in their patient volume to do just that. In simplest and most cynical terms, the systems are willing to take a loss on us less profitable high-volume grunts in order to reap the profits of the lower-volume high-profitability specialties and subspecialties.

So that’s why you as a PCP have any value at all to a large healthcare system. But, it means that to maintain your value to the system you must continue to provide the volume it anticipates and needs. While the system may have been willing to accept some degrees of unprofitability when it hired you, there are limits. And, we shouldn’t be surprised if they continue to urge or demand that we narrow the gap between the revenue we generate and the costs that we incur, ie, our overhead.

In Part 2 of this series, I’m going to discuss the collateral damage that occurs when volume and overhead collide in an environment that claims to be committed to patient care.

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

I recently read an op-ed piece in which the author wondered if any young people entering the practice of medicine felt that they were answering a “calling.” I suspect that there will continue to be, and will always be, idealists whose primary motivation for choosing medicine is that they will be healing the sick or at least providing comfort to the suffering. I occasionally hear that about a former patient who has been inspired by a personal or familial experience with a serious illness.

Unfortunately, I suspect those who feel called are the providers most likely to feel discouraged and frustrated by the current state of primary care. Luckily, I never felt a calling. For me, primary care pediatrics was a job. One that l felt obligated to perform to the best of my ability. Mine was not a calling but an inherited philosophy that work in itself was virtuous. A work ethic, if you will. Pediatrics offered the additional reward that, if well done, it might help some parents and their children feel a little better.

Fifty years ago I was not alone in treating medicine as a job. Most physicians were self-employed. Although there were exceptions like Albert Schweitzer, even those of us with a calling had to obey the basic rules of business as it applied to medicine. We were employer and employee and had to understand the critical factors of overhead, profit, and loss.

I have burdened you with this little history recitation not to suggest that things were better in the good old days, but to provide a stepping stone into the murky and uncomfortable topic of primary care physician (PCP) compensation. Because almost three quarters of you work for a hospital, health system, or corporate entity, I am going to illuminate our journey by leaning on the advice of an international company with 7000 employees and revenue of 2.5 billion dollars that considers itself a “global leader” in management consulting. Your employer is listening to some management consultant and it may help us to view your compensation from someone on their side of the table.

First, you should be aware that “most health systems lose money on their primary care operations — up to $200,000 or more per primary care physician.” This may help explain why despite being in short supply, you and most PCPs feel undervalued. However, if we are such losers, we must provide something(s) that the systems are seeking. It is likely that the system is looking to tout its ability to provide comprehensive care and demonstrate that it has a patient base broad enough to warrant attention and provide bargaining leverage on volume discounts.

The system also may want to minimize competition by absorbing the remaining PCPs in the community into their system. With you outside of the system, it had less control over your compensation than it does when you are under its umbrella.

Your employer may want to grow and feed its specialty care network, and it sees PCPs as having the fuel stored in their patient volume to do just that. In simplest and most cynical terms, the systems are willing to take a loss on us less profitable high-volume grunts in order to reap the profits of the lower-volume high-profitability specialties and subspecialties.

So that’s why you as a PCP have any value at all to a large healthcare system. But, it means that to maintain your value to the system you must continue to provide the volume it anticipates and needs. While the system may have been willing to accept some degrees of unprofitability when it hired you, there are limits. And, we shouldn’t be surprised if they continue to urge or demand that we narrow the gap between the revenue we generate and the costs that we incur, ie, our overhead.

In Part 2 of this series, I’m going to discuss the collateral damage that occurs when volume and overhead collide in an environment that claims to be committed to patient care.

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

This transcript has been edited for clarity.

Hello. It’s Mark Kris reporting back after attending the New York Lung Cancer Foundation Summit here in New York. A large amount of discussion went on, but as usual, I was most interested in the perioperative space.

In previous videos, I’ve talked about this ongoing discussion of whether you should operate and give adjuvant therapy or give neoadjuvant therapy, and I’ve addressed that already. One thing I want to bring up – and as we move off of that argument, which frankly doesn’t have an answer today, with neoadjuvant therapy, having all the data to support it – is what are the patterns of recurrence now that we have more successful systemic therapies, both targeted therapies and checkpoint inhibitors?

I was taught early on by my surgical mentors that the issue here was systemic control. While they could do very successful surgery to get high levels of local control, they could not control systemic disease. Sadly, the tools we had early on with chemotherapy were just not good enough. Suddenly, we have better tools to control systemic spread. In the past, the vast majority of occurrences were systemic; they’re now local.

What I think we need to do as a group of practitioners trying to deal with the problems getting in the way of curing our patients is look at what the issue is now. Frankly, the big issue now, as systemic therapy has controlled metastatic disease, is recurrence in the chest.

We give adjuvant osimertinib. Please remember what the numbers are. In the osimertinib arm, of the 11 recurrences reported in the European Society for Medical Oncology presentation a few years back, nine of them were in the chest or mediastinal nodes. In the arm that got no osimertinib afterward, there were 46 recurrences, and 32 of those 46 recurrences were in the chest, either the lung or mediastinal nodes. Therefore, 74% of the recurrences are suddenly in the chest. What’s the issue here?

The issue is we need to find strategies to give better disease control in the chest, as we have made inroads in controlling systemic disease with the targeted therapies in the endothelial growth factor receptor space, and very likely the checkpoint inhibitors, too, as that data kind of filters out. We need to think about how better to get local control.

I think rather than continue to get into this argument of neoadjuvant vs adjuvant, we should move to what’s really hurting our patients. Again, the data I quoted you was from the ADAURA trial, which was adjuvant therapy, and I’m sure the neoadjuvant is going to show the same thing. It’s better systemic therapy but now, more trouble in the chest.

How are we going to deal with that? I’d like to throw out one strategy, and that is to rethink the role of radiation in these patients. Again, if the problem is local in the chest, lung, and lymph nodes, we have to think about local therapy. Yes, we’re not recommending it routinely for everybody, but now that we have better systemic control, we need to rethink our options. The obvious one to rethink is about giving radiotherapy.

We should also use what we learned in the earlier trials, which is that there is harm in giving excessive radiation to the heart. If you avoid the heart, you avoid the harm. We have better planning strategies for stereotactic body radiotherapy and more traditional radiation, and of course, we have proton therapy as well.

As we continue to struggle with the idea of that patient with stage II or III disease, whether to give adjuvant vs neoadjuvant therapy, please remember to consider their risk in 2024. Their risk for first recurrence is in the chest.

What are we going to do to better control disease in the chest? We have a challenge. I’m sure we can meet it if we put our heads together.

Dr. Kris is professor of medicine at Weill Cornell Medical College, and attending physician, Thoracic Oncology Service, Memorial Sloan Kettering Cancer Center, New York. He disclosed ties with AstraZeneca, Roche/Genentech, Ariad Pharmaceuticals, Pfizer, and PUMA.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hello. It’s Mark Kris reporting back after attending the New York Lung Cancer Foundation Summit here in New York. A large amount of discussion went on, but as usual, I was most interested in the perioperative space.

In previous videos, I’ve talked about this ongoing discussion of whether you should operate and give adjuvant therapy or give neoadjuvant therapy, and I’ve addressed that already. One thing I want to bring up – and as we move off of that argument, which frankly doesn’t have an answer today, with neoadjuvant therapy, having all the data to support it – is what are the patterns of recurrence now that we have more successful systemic therapies, both targeted therapies and checkpoint inhibitors?

I was taught early on by my surgical mentors that the issue here was systemic control. While they could do very successful surgery to get high levels of local control, they could not control systemic disease. Sadly, the tools we had early on with chemotherapy were just not good enough. Suddenly, we have better tools to control systemic spread. In the past, the vast majority of occurrences were systemic; they’re now local.

What I think we need to do as a group of practitioners trying to deal with the problems getting in the way of curing our patients is look at what the issue is now. Frankly, the big issue now, as systemic therapy has controlled metastatic disease, is recurrence in the chest.

We give adjuvant osimertinib. Please remember what the numbers are. In the osimertinib arm, of the 11 recurrences reported in the European Society for Medical Oncology presentation a few years back, nine of them were in the chest or mediastinal nodes. In the arm that got no osimertinib afterward, there were 46 recurrences, and 32 of those 46 recurrences were in the chest, either the lung or mediastinal nodes. Therefore, 74% of the recurrences are suddenly in the chest. What’s the issue here?

The issue is we need to find strategies to give better disease control in the chest, as we have made inroads in controlling systemic disease with the targeted therapies in the endothelial growth factor receptor space, and very likely the checkpoint inhibitors, too, as that data kind of filters out. We need to think about how better to get local control.

I think rather than continue to get into this argument of neoadjuvant vs adjuvant, we should move to what’s really hurting our patients. Again, the data I quoted you was from the ADAURA trial, which was adjuvant therapy, and I’m sure the neoadjuvant is going to show the same thing. It’s better systemic therapy but now, more trouble in the chest.

How are we going to deal with that? I’d like to throw out one strategy, and that is to rethink the role of radiation in these patients. Again, if the problem is local in the chest, lung, and lymph nodes, we have to think about local therapy. Yes, we’re not recommending it routinely for everybody, but now that we have better systemic control, we need to rethink our options. The obvious one to rethink is about giving radiotherapy.

We should also use what we learned in the earlier trials, which is that there is harm in giving excessive radiation to the heart. If you avoid the heart, you avoid the harm. We have better planning strategies for stereotactic body radiotherapy and more traditional radiation, and of course, we have proton therapy as well.

As we continue to struggle with the idea of that patient with stage II or III disease, whether to give adjuvant vs neoadjuvant therapy, please remember to consider their risk in 2024. Their risk for first recurrence is in the chest.

What are we going to do to better control disease in the chest? We have a challenge. I’m sure we can meet it if we put our heads together.

Dr. Kris is professor of medicine at Weill Cornell Medical College, and attending physician, Thoracic Oncology Service, Memorial Sloan Kettering Cancer Center, New York. He disclosed ties with AstraZeneca, Roche/Genentech, Ariad Pharmaceuticals, Pfizer, and PUMA.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hello. It’s Mark Kris reporting back after attending the New York Lung Cancer Foundation Summit here in New York. A large amount of discussion went on, but as usual, I was most interested in the perioperative space.

In previous videos, I’ve talked about this ongoing discussion of whether you should operate and give adjuvant therapy or give neoadjuvant therapy, and I’ve addressed that already. One thing I want to bring up – and as we move off of that argument, which frankly doesn’t have an answer today, with neoadjuvant therapy, having all the data to support it – is what are the patterns of recurrence now that we have more successful systemic therapies, both targeted therapies and checkpoint inhibitors?

I was taught early on by my surgical mentors that the issue here was systemic control. While they could do very successful surgery to get high levels of local control, they could not control systemic disease. Sadly, the tools we had early on with chemotherapy were just not good enough. Suddenly, we have better tools to control systemic spread. In the past, the vast majority of occurrences were systemic; they’re now local.

What I think we need to do as a group of practitioners trying to deal with the problems getting in the way of curing our patients is look at what the issue is now. Frankly, the big issue now, as systemic therapy has controlled metastatic disease, is recurrence in the chest.

We give adjuvant osimertinib. Please remember what the numbers are. In the osimertinib arm, of the 11 recurrences reported in the European Society for Medical Oncology presentation a few years back, nine of them were in the chest or mediastinal nodes. In the arm that got no osimertinib afterward, there were 46 recurrences, and 32 of those 46 recurrences were in the chest, either the lung or mediastinal nodes. Therefore, 74% of the recurrences are suddenly in the chest. What’s the issue here?

The issue is we need to find strategies to give better disease control in the chest, as we have made inroads in controlling systemic disease with the targeted therapies in the endothelial growth factor receptor space, and very likely the checkpoint inhibitors, too, as that data kind of filters out. We need to think about how better to get local control.

I think rather than continue to get into this argument of neoadjuvant vs adjuvant, we should move to what’s really hurting our patients. Again, the data I quoted you was from the ADAURA trial, which was adjuvant therapy, and I’m sure the neoadjuvant is going to show the same thing. It’s better systemic therapy but now, more trouble in the chest.

How are we going to deal with that? I’d like to throw out one strategy, and that is to rethink the role of radiation in these patients. Again, if the problem is local in the chest, lung, and lymph nodes, we have to think about local therapy. Yes, we’re not recommending it routinely for everybody, but now that we have better systemic control, we need to rethink our options. The obvious one to rethink is about giving radiotherapy.

We should also use what we learned in the earlier trials, which is that there is harm in giving excessive radiation to the heart. If you avoid the heart, you avoid the harm. We have better planning strategies for stereotactic body radiotherapy and more traditional radiation, and of course, we have proton therapy as well.

As we continue to struggle with the idea of that patient with stage II or III disease, whether to give adjuvant vs neoadjuvant therapy, please remember to consider their risk in 2024. Their risk for first recurrence is in the chest.

What are we going to do to better control disease in the chest? We have a challenge. I’m sure we can meet it if we put our heads together.

Dr. Kris is professor of medicine at Weill Cornell Medical College, and attending physician, Thoracic Oncology Service, Memorial Sloan Kettering Cancer Center, New York. He disclosed ties with AstraZeneca, Roche/Genentech, Ariad Pharmaceuticals, Pfizer, and PUMA.

A version of this article appeared on Medscape.com.

At the end of March, in an anniversary no one but I noticed, I passed 4 years since I’d last rounded at the hospital.

It’s hard to comprehend that. I was at the hospital regularly for the first 22 years of my career, though admittedly it had dwindled from daily (1998-2011) to 1-2 weekends a month at the end.

Looking back, I still don’t miss it, and have no desire to go back. That’s not to say I don’t keep up on inpatient neurology, in case circumstances change, but at this point, honestly, I don’t want to. I’ve become accustomed to my non-hospital world, no late-night consults, no weekends spent rounding, no taking separate cars to restaurants or family events in case I get called in.

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

At the end of March, in an anniversary no one but I noticed, I passed 4 years since I’d last rounded at the hospital.

It’s hard to comprehend that. I was at the hospital regularly for the first 22 years of my career, though admittedly it had dwindled from daily (1998-2011) to 1-2 weekends a month at the end.

Looking back, I still don’t miss it, and have no desire to go back. That’s not to say I don’t keep up on inpatient neurology, in case circumstances change, but at this point, honestly, I don’t want to. I’ve become accustomed to my non-hospital world, no late-night consults, no weekends spent rounding, no taking separate cars to restaurants or family events in case I get called in.

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

At the end of March, in an anniversary no one but I noticed, I passed 4 years since I’d last rounded at the hospital.

It’s hard to comprehend that. I was at the hospital regularly for the first 22 years of my career, though admittedly it had dwindled from daily (1998-2011) to 1-2 weekends a month at the end.

Looking back, I still don’t miss it, and have no desire to go back. That’s not to say I don’t keep up on inpatient neurology, in case circumstances change, but at this point, honestly, I don’t want to. I’ve become accustomed to my non-hospital world, no late-night consults, no weekends spent rounding, no taking separate cars to restaurants or family events in case I get called in.

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

With all the excitement about GLP-1 agonists, I get many questions from providers about which antiobesity drug they should prescribe. I’ll tell you the methods that I use to determine which drug is best for which patient.

Of course, we want to make sure that we’re treating the right condition. If the patient has type 2 diabetes, we tend to give them medication that is indicated for type 2 diabetes. Many GLP-1 agonists are available in a diabetes version and a chronic weight management or obesity version. If a patient has diabetes and obesity, they can receive either one. If a patient has only diabetes but not obesity, they should be prescribed the diabetes version. For obesity without diabetes, we tend to stick with the drugs that are indicated for chronic weight management.

Let’s go through them.

Exenatide. In chronological order of approval, the first GLP-1 drug that was used for diabetes dates back to exenatide (Bydureon). Bydureon had a partner called Byetta (also exenatide), both of which are still on the market but infrequently used. Some patients reported that these medications were inconvenient because they required twice-daily injections and caused painful injection-site nodules.

Diabetes drugs in more common use include liraglutide (Victoza) for type 2 diabetes. It is a daily injection and has various doses. We always start low and increase with tolerance and desired effect for A1c.

Liraglutide. Victoza has an antiobesity counterpart called Saxenda. The Saxenda pen looks very similar to the Victoza pen. It is a daily GLP-1 agonist for chronic weight management. The SCALE trial demonstrated 8%-12% weight loss with Saxenda.

Those are the daily injections: Victoza for diabetes and Saxenda for weight loss.

Our patients are very excited about the advent of weekly injections for diabetes and weight management. Ozempic is very popular. It is a weekly GLP-1 agonist for type 2 diabetes. Many patients come in asking for Ozempic, and we must make sure that we’re moving them in the right direction depending on their condition.

Semaglutide. Ozempic has a few different doses. It is a weekly injection and has been found to be quite efficacious for treating diabetes. The drug’s weight loss counterpart is called Wegovy, which comes in a different pen. Both forms contain the compound semaglutide. While all of these GLP-1 agonists are indicated to treat type 2 diabetes or for weight management, Wegovy has a special indication that none of the others have. In March 2024, Wegovy acquired an indication to decrease cardiac risk in those with a BMI ≥ 27 and a previous cardiac history. This will really change the accessibility of this medication because patients with heart conditions who are on Medicare are expected to have access to Wegovy.

Tirzepatide. Another weekly injection for treatment of type 2 diabetes is called Mounjaro. Its counterpart for weight management is called Zepbound, which was found to have about 20.9% weight loss over 72 weeks. These medications have similar side effects in differing degrees, but the most-often reported are nausea, stool changes, abdominal pain, and reflux. There are some other potential side effects; I recommend that you read the individual prescribing information available for each drug to have more clarity about that.

It is important that we stay on label for using the GLP-1 receptor agonists, for many reasons. One, it increases our patients’ accessibility to the right medication for them, and we can also make sure that we’re treating the patient with the right drug according to the clinical trials. When the clinical trials are done, the study populations demonstrate safety and efficacy for that population. But if we’re prescribing a GLP-1 for a different population, it is considered off-label use.
 

Dr. Lofton, an obesity medicine specialist, is clinical associate professor of surgery and medicine at NYU Grossman School of Medicine, and director of the medical weight management program at NYU Langone Weight Management Center, New York. She disclosed ties to Novo Nordisk and Eli Lilly. This transcript has been edited for clarity.

A version of this article appeared on Medscape.com.

With all the excitement about GLP-1 agonists, I get many questions from providers about which antiobesity drug they should prescribe. I’ll tell you the methods that I use to determine which drug is best for which patient.

Of course, we want to make sure that we’re treating the right condition. If the patient has type 2 diabetes, we tend to give them medication that is indicated for type 2 diabetes. Many GLP-1 agonists are available in a diabetes version and a chronic weight management or obesity version. If a patient has diabetes and obesity, they can receive either one. If a patient has only diabetes but not obesity, they should be prescribed the diabetes version. For obesity without diabetes, we tend to stick with the drugs that are indicated for chronic weight management.

Let’s go through them.

Exenatide. In chronological order of approval, the first GLP-1 drug that was used for diabetes dates back to exenatide (Bydureon). Bydureon had a partner called Byetta (also exenatide), both of which are still on the market but infrequently used. Some patients reported that these medications were inconvenient because they required twice-daily injections and caused painful injection-site nodules.

Diabetes drugs in more common use include liraglutide (Victoza) for type 2 diabetes. It is a daily injection and has various doses. We always start low and increase with tolerance and desired effect for A1c.

Liraglutide. Victoza has an antiobesity counterpart called Saxenda. The Saxenda pen looks very similar to the Victoza pen. It is a daily GLP-1 agonist for chronic weight management. The SCALE trial demonstrated 8%-12% weight loss with Saxenda.

Those are the daily injections: Victoza for diabetes and Saxenda for weight loss.

Our patients are very excited about the advent of weekly injections for diabetes and weight management. Ozempic is very popular. It is a weekly GLP-1 agonist for type 2 diabetes. Many patients come in asking for Ozempic, and we must make sure that we’re moving them in the right direction depending on their condition.

Semaglutide. Ozempic has a few different doses. It is a weekly injection and has been found to be quite efficacious for treating diabetes. The drug’s weight loss counterpart is called Wegovy, which comes in a different pen. Both forms contain the compound semaglutide. While all of these GLP-1 agonists are indicated to treat type 2 diabetes or for weight management, Wegovy has a special indication that none of the others have. In March 2024, Wegovy acquired an indication to decrease cardiac risk in those with a BMI ≥ 27 and a previous cardiac history. This will really change the accessibility of this medication because patients with heart conditions who are on Medicare are expected to have access to Wegovy.

Tirzepatide. Another weekly injection for treatment of type 2 diabetes is called Mounjaro. Its counterpart for weight management is called Zepbound, which was found to have about 20.9% weight loss over 72 weeks. These medications have similar side effects in differing degrees, but the most-often reported are nausea, stool changes, abdominal pain, and reflux. There are some other potential side effects; I recommend that you read the individual prescribing information available for each drug to have more clarity about that.

It is important that we stay on label for using the GLP-1 receptor agonists, for many reasons. One, it increases our patients’ accessibility to the right medication for them, and we can also make sure that we’re treating the patient with the right drug according to the clinical trials. When the clinical trials are done, the study populations demonstrate safety and efficacy for that population. But if we’re prescribing a GLP-1 for a different population, it is considered off-label use.
 

Dr. Lofton, an obesity medicine specialist, is clinical associate professor of surgery and medicine at NYU Grossman School of Medicine, and director of the medical weight management program at NYU Langone Weight Management Center, New York. She disclosed ties to Novo Nordisk and Eli Lilly. This transcript has been edited for clarity.

A version of this article appeared on Medscape.com.

With all the excitement about GLP-1 agonists, I get many questions from providers about which antiobesity drug they should prescribe. I’ll tell you the methods that I use to determine which drug is best for which patient.

Of course, we want to make sure that we’re treating the right condition. If the patient has type 2 diabetes, we tend to give them medication that is indicated for type 2 diabetes. Many GLP-1 agonists are available in a diabetes version and a chronic weight management or obesity version. If a patient has diabetes and obesity, they can receive either one. If a patient has only diabetes but not obesity, they should be prescribed the diabetes version. For obesity without diabetes, we tend to stick with the drugs that are indicated for chronic weight management.

Let’s go through them.

Exenatide. In chronological order of approval, the first GLP-1 drug that was used for diabetes dates back to exenatide (Bydureon). Bydureon had a partner called Byetta (also exenatide), both of which are still on the market but infrequently used. Some patients reported that these medications were inconvenient because they required twice-daily injections and caused painful injection-site nodules.

Diabetes drugs in more common use include liraglutide (Victoza) for type 2 diabetes. It is a daily injection and has various doses. We always start low and increase with tolerance and desired effect for A1c.

Liraglutide. Victoza has an antiobesity counterpart called Saxenda. The Saxenda pen looks very similar to the Victoza pen. It is a daily GLP-1 agonist for chronic weight management. The SCALE trial demonstrated 8%-12% weight loss with Saxenda.

Those are the daily injections: Victoza for diabetes and Saxenda for weight loss.

Our patients are very excited about the advent of weekly injections for diabetes and weight management. Ozempic is very popular. It is a weekly GLP-1 agonist for type 2 diabetes. Many patients come in asking for Ozempic, and we must make sure that we’re moving them in the right direction depending on their condition.

Semaglutide. Ozempic has a few different doses. It is a weekly injection and has been found to be quite efficacious for treating diabetes. The drug’s weight loss counterpart is called Wegovy, which comes in a different pen. Both forms contain the compound semaglutide. While all of these GLP-1 agonists are indicated to treat type 2 diabetes or for weight management, Wegovy has a special indication that none of the others have. In March 2024, Wegovy acquired an indication to decrease cardiac risk in those with a BMI ≥ 27 and a previous cardiac history. This will really change the accessibility of this medication because patients with heart conditions who are on Medicare are expected to have access to Wegovy.

Tirzepatide. Another weekly injection for treatment of type 2 diabetes is called Mounjaro. Its counterpart for weight management is called Zepbound, which was found to have about 20.9% weight loss over 72 weeks. These medications have similar side effects in differing degrees, but the most-often reported are nausea, stool changes, abdominal pain, and reflux. There are some other potential side effects; I recommend that you read the individual prescribing information available for each drug to have more clarity about that.

It is important that we stay on label for using the GLP-1 receptor agonists, for many reasons. One, it increases our patients’ accessibility to the right medication for them, and we can also make sure that we’re treating the patient with the right drug according to the clinical trials. When the clinical trials are done, the study populations demonstrate safety and efficacy for that population. But if we’re prescribing a GLP-1 for a different population, it is considered off-label use.
 

Dr. Lofton, an obesity medicine specialist, is clinical associate professor of surgery and medicine at NYU Grossman School of Medicine, and director of the medical weight management program at NYU Langone Weight Management Center, New York. She disclosed ties to Novo Nordisk and Eli Lilly. This transcript has been edited for clarity.

A version of this article appeared on Medscape.com.

Thirty years ago I had an experience in the office that influenced my approach to obesity for the rest of my career. The patient was a 4-year-old whom I had been seeing since her birth. At her annual well-child visit her weight had jumped up significantly from the previous year’s visit. She appeared well, but the change in her growth trajectory prompted a bit more in-depth history taking.

It turned out that finances had forced the family to employ one of the child’s grandmothers as the day care provider. Unfortunately, this grandmother’s passion was cooking and she was particularly adept at baking. She had no other hobbies and a sore hip limited her mobility, so she seldom went outside. When I eventually met her she was a cheerful, overweight, and delightful woman.

Deconstructing this obesogenic environment without disrupting this otherwise healthy family was an exercise that required tact, patience, and creativity. Fortunately, the young girl’s mother had already harbored some concerns about her child’s weight and was more than willing to participate in this environmental re-engineering project. It’s a long story, but she and I achieved our goals and the child eventually coasted back toward her previous growth curve.

I have always suspected that this scenario is being replayed hundreds of thousands of time across this country. But, sadly most don’t share this one’s happy ending. Parents don’t alway perceive the seriousness of the problem. The economic hurdles are often too steep to overcome, even when the most creative minds are involved.

How prevalent are obesogenic day care environments? We certainly know childhood obesity is a problem and the statistics in the preschool age group are particularly concerning. More than 14 million children are in non-parental early care and education programs; these environments would seem to be a logical place to target our prevention strategies. Understandably, there seems to be a hesitancy to point fingers, but how many day care providers are similar to the well-intentioned grandmother in the scenario I described? We must at least suspect that the example set by the adults in the preschool and day care environment might be having some influence on the children under their care.

There has been some research that sheds some light on this question. A paper from the University of Oklahoma has looked at the predictors of overweight and obesity in early care and education (ECE) teachers in hopes of “finding modifiable opportunities to enhance the health of this critical workforce.” In their paper, the investigators refer to other research that has found the prevalence of overweight and obesity among ECE teachers is higher than our national average and their waist circumference is significantly greater than the standard recommendation for women.

A study from Norway has looked at the association between preschool staff’s activity level and that of the children under their care using accelerometers. This particular investigation couldn’t determine whether it was the staff’s activity level that influenced the children or vice versa because it wasn’t an observational study. Common sense would lead one to believe it was the staff’s relative inactivity that was being reflected in the children’s.

It is interesting that in this Norwegian study when the teachers were asked about their attitudes toward activity and their self-perception of their own activity, there was no relationship between the staff’s and the children’s level of activity. In other words, the educators and caregivers bought into the importance of activity but had difficulty translating this philosophy into own behavior.

So where does this leave us? It turns out my experience decades ago was not a one-off event, but instead represents the tip of very large iceberg. Should we immediately create a system of day care provider boot camps? Let’s remember that each educator and caregiver is one of us. They may be slight outliers but not a group of individuals deserving of forced marches and half-rations to get them in shape.

ECEs have listened to the same message we have all heard about diet and activity and their importance for a child’s health. Our challenge is to create effective, yet sensitive, strategies to help the educators and caregivers modify their dietary habits behaviors in a way that helps them be a more positive influence on their students. It’s for their own health and that of their charges. This could be as simple as providing accelerometers or step-counting smartwatches. Or, by having physical educators perform on-site audits that could then be used to create site-specific plans for increasing both teacher and student activity.

Modifying the educators’ diet is a more complex procedure and can quickly become entangled in the socio-economic background of each individual teacher. A healthy diet is not always equally available to everyone. The solution may involve providing the teachers with food to be eaten at work and to be prepared at home. But, creative answers can be found if we look for them.

Before we get too far down the obesity-is-a-disease pathway, we must take a closer look at the role the early care and early school milieu are playing in the obesity problem. A little common sense behavior modification when children are in the controlled environment of school/day care may allow us to be less reliant on the those new wonder drugs in the long run.

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

Thirty years ago I had an experience in the office that influenced my approach to obesity for the rest of my career. The patient was a 4-year-old whom I had been seeing since her birth. At her annual well-child visit her weight had jumped up significantly from the previous year’s visit. She appeared well, but the change in her growth trajectory prompted a bit more in-depth history taking.

It turned out that finances had forced the family to employ one of the child’s grandmothers as the day care provider. Unfortunately, this grandmother’s passion was cooking and she was particularly adept at baking. She had no other hobbies and a sore hip limited her mobility, so she seldom went outside. When I eventually met her she was a cheerful, overweight, and delightful woman.

Deconstructing this obesogenic environment without disrupting this otherwise healthy family was an exercise that required tact, patience, and creativity. Fortunately, the young girl’s mother had already harbored some concerns about her child’s weight and was more than willing to participate in this environmental re-engineering project. It’s a long story, but she and I achieved our goals and the child eventually coasted back toward her previous growth curve.

I have always suspected that this scenario is being replayed hundreds of thousands of time across this country. But, sadly most don’t share this one’s happy ending. Parents don’t alway perceive the seriousness of the problem. The economic hurdles are often too steep to overcome, even when the most creative minds are involved.

How prevalent are obesogenic day care environments? We certainly know childhood obesity is a problem and the statistics in the preschool age group are particularly concerning. More than 14 million children are in non-parental early care and education programs; these environments would seem to be a logical place to target our prevention strategies. Understandably, there seems to be a hesitancy to point fingers, but how many day care providers are similar to the well-intentioned grandmother in the scenario I described? We must at least suspect that the example set by the adults in the preschool and day care environment might be having some influence on the children under their care.

There has been some research that sheds some light on this question. A paper from the University of Oklahoma has looked at the predictors of overweight and obesity in early care and education (ECE) teachers in hopes of “finding modifiable opportunities to enhance the health of this critical workforce.” In their paper, the investigators refer to other research that has found the prevalence of overweight and obesity among ECE teachers is higher than our national average and their waist circumference is significantly greater than the standard recommendation for women.

A study from Norway has looked at the association between preschool staff’s activity level and that of the children under their care using accelerometers. This particular investigation couldn’t determine whether it was the staff’s activity level that influenced the children or vice versa because it wasn’t an observational study. Common sense would lead one to believe it was the staff’s relative inactivity that was being reflected in the children’s.

It is interesting that in this Norwegian study when the teachers were asked about their attitudes toward activity and their self-perception of their own activity, there was no relationship between the staff’s and the children’s level of activity. In other words, the educators and caregivers bought into the importance of activity but had difficulty translating this philosophy into own behavior.

So where does this leave us? It turns out my experience decades ago was not a one-off event, but instead represents the tip of very large iceberg. Should we immediately create a system of day care provider boot camps? Let’s remember that each educator and caregiver is one of us. They may be slight outliers but not a group of individuals deserving of forced marches and half-rations to get them in shape.

ECEs have listened to the same message we have all heard about diet and activity and their importance for a child’s health. Our challenge is to create effective, yet sensitive, strategies to help the educators and caregivers modify their dietary habits behaviors in a way that helps them be a more positive influence on their students. It’s for their own health and that of their charges. This could be as simple as providing accelerometers or step-counting smartwatches. Or, by having physical educators perform on-site audits that could then be used to create site-specific plans for increasing both teacher and student activity.

Modifying the educators’ diet is a more complex procedure and can quickly become entangled in the socio-economic background of each individual teacher. A healthy diet is not always equally available to everyone. The solution may involve providing the teachers with food to be eaten at work and to be prepared at home. But, creative answers can be found if we look for them.

Before we get too far down the obesity-is-a-disease pathway, we must take a closer look at the role the early care and early school milieu are playing in the obesity problem. A little common sense behavior modification when children are in the controlled environment of school/day care may allow us to be less reliant on the those new wonder drugs in the long run.

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

Thirty years ago I had an experience in the office that influenced my approach to obesity for the rest of my career. The patient was a 4-year-old whom I had been seeing since her birth. At her annual well-child visit her weight had jumped up significantly from the previous year’s visit. She appeared well, but the change in her growth trajectory prompted a bit more in-depth history taking.

It turned out that finances had forced the family to employ one of the child’s grandmothers as the day care provider. Unfortunately, this grandmother’s passion was cooking and she was particularly adept at baking. She had no other hobbies and a sore hip limited her mobility, so she seldom went outside. When I eventually met her she was a cheerful, overweight, and delightful woman.

Deconstructing this obesogenic environment without disrupting this otherwise healthy family was an exercise that required tact, patience, and creativity. Fortunately, the young girl’s mother had already harbored some concerns about her child’s weight and was more than willing to participate in this environmental re-engineering project. It’s a long story, but she and I achieved our goals and the child eventually coasted back toward her previous growth curve.

I have always suspected that this scenario is being replayed hundreds of thousands of time across this country. But, sadly most don’t share this one’s happy ending. Parents don’t alway perceive the seriousness of the problem. The economic hurdles are often too steep to overcome, even when the most creative minds are involved.

How prevalent are obesogenic day care environments? We certainly know childhood obesity is a problem and the statistics in the preschool age group are particularly concerning. More than 14 million children are in non-parental early care and education programs; these environments would seem to be a logical place to target our prevention strategies. Understandably, there seems to be a hesitancy to point fingers, but how many day care providers are similar to the well-intentioned grandmother in the scenario I described? We must at least suspect that the example set by the adults in the preschool and day care environment might be having some influence on the children under their care.

There has been some research that sheds some light on this question. A paper from the University of Oklahoma has looked at the predictors of overweight and obesity in early care and education (ECE) teachers in hopes of “finding modifiable opportunities to enhance the health of this critical workforce.” In their paper, the investigators refer to other research that has found the prevalence of overweight and obesity among ECE teachers is higher than our national average and their waist circumference is significantly greater than the standard recommendation for women.

A study from Norway has looked at the association between preschool staff’s activity level and that of the children under their care using accelerometers. This particular investigation couldn’t determine whether it was the staff’s activity level that influenced the children or vice versa because it wasn’t an observational study. Common sense would lead one to believe it was the staff’s relative inactivity that was being reflected in the children’s.

It is interesting that in this Norwegian study when the teachers were asked about their attitudes toward activity and their self-perception of their own activity, there was no relationship between the staff’s and the children’s level of activity. In other words, the educators and caregivers bought into the importance of activity but had difficulty translating this philosophy into own behavior.

So where does this leave us? It turns out my experience decades ago was not a one-off event, but instead represents the tip of very large iceberg. Should we immediately create a system of day care provider boot camps? Let’s remember that each educator and caregiver is one of us. They may be slight outliers but not a group of individuals deserving of forced marches and half-rations to get them in shape.

ECEs have listened to the same message we have all heard about diet and activity and their importance for a child’s health. Our challenge is to create effective, yet sensitive, strategies to help the educators and caregivers modify their dietary habits behaviors in a way that helps them be a more positive influence on their students. It’s for their own health and that of their charges. This could be as simple as providing accelerometers or step-counting smartwatches. Or, by having physical educators perform on-site audits that could then be used to create site-specific plans for increasing both teacher and student activity.

Modifying the educators’ diet is a more complex procedure and can quickly become entangled in the socio-economic background of each individual teacher. A healthy diet is not always equally available to everyone. The solution may involve providing the teachers with food to be eaten at work and to be prepared at home. But, creative answers can be found if we look for them.

Before we get too far down the obesity-is-a-disease pathway, we must take a closer look at the role the early care and early school milieu are playing in the obesity problem. A little common sense behavior modification when children are in the controlled environment of school/day care may allow us to be less reliant on the those new wonder drugs in the long run.

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

Last year, I concluded a commentary for this news organization on colorectal cancer (CRC) screening guidelines by stating that between stool-based tests, flexible sigmoidoscopy, and colonoscopy, “the best screening test is the test that gets done.” But should that maxim apply to the new blood-based screening test, Guardant Health Shield? This proprietary test, which costs $895 and is not generally covered by insurance, identifies alterations in cell-free DNA that are characteristic of CRC.

Shield’s test characteristics were recently evaluated in a prospective study of more than 10,000 adults aged 45-84 at average risk for CRC. The test had an 87.5% sensitivity for stage I, II, or III colorectal cancer but only a 13% sensitivity for advanced precancerous lesions. Test specificity was 89.6%, meaning that about 1 in 10 participants without CRC or advanced precancerous lesions on colonoscopy had a false-positive result.

Although the Shield blood test has a higher rate of false positives than the traditional fecal immunochemical test (FIT) and lower sensitivity and specificity than a multitarget stool DNA (FIT-DNA) test designed to improve on Cologuard, it meets the previously established criteria set forth by the Centers for Medicare & Medicaid Services (CMS) to be covered for Medicare beneficiaries at 3-year intervals, pending FDA approval. If public and private payers start covering Shield alongside other CRC screening tests, it presents an opportunity for primary care physicians to reach the approximately 3 in 10 adults between ages 45 and 75 who are not being routinely screened.

A big concern, however, is that the availability of a blood test may cause patients who would have otherwise been screened with colonoscopy or stool tests to switch to the blood test. A cost-effectiveness analysis found that offering a blood test to patients who decline screening colonoscopy saves additional lives, but at the cost of more than $377,000 per life-year gained. Another study relying on three microsimulation models previously utilized by the US Preventive Services Task Force (USPSTF) found that annual FIT results in more life-years gained at substantially lower cost than blood-based screening every 3 years “even when uptake of blood-based screening was 20 percentage points higher than uptake of FIT.” As a result, a multidisciplinary expert panel concluded that blood-based screening should not substitute for established CRC screening tests, but instead be offered only to patients who decline those tests.

In practice, this will increase the complexity of the CRC screening conversations we have with patients. We will need to be clear that the blood test is not yet endorsed by the USPSTF or any major guideline group and is a second-line test that will miss most precancerous polyps. As with the stool tests, it is essential to emphasize that a positive result must be followed by diagnostic colonoscopy. To addend the cancer screening maxim I mentioned before, the blood test is not the best test for CRC, but it’s probably better than no test at all.

Dr. Lin is a family physician and associate director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania. He blogs at Common Sense Family Doctor.

A version of this article appeared on Medscape.com.

Last year, I concluded a commentary for this news organization on colorectal cancer (CRC) screening guidelines by stating that between stool-based tests, flexible sigmoidoscopy, and colonoscopy, “the best screening test is the test that gets done.” But should that maxim apply to the new blood-based screening test, Guardant Health Shield? This proprietary test, which costs $895 and is not generally covered by insurance, identifies alterations in cell-free DNA that are characteristic of CRC.

Shield’s test characteristics were recently evaluated in a prospective study of more than 10,000 adults aged 45-84 at average risk for CRC. The test had an 87.5% sensitivity for stage I, II, or III colorectal cancer but only a 13% sensitivity for advanced precancerous lesions. Test specificity was 89.6%, meaning that about 1 in 10 participants without CRC or advanced precancerous lesions on colonoscopy had a false-positive result.

Although the Shield blood test has a higher rate of false positives than the traditional fecal immunochemical test (FIT) and lower sensitivity and specificity than a multitarget stool DNA (FIT-DNA) test designed to improve on Cologuard, it meets the previously established criteria set forth by the Centers for Medicare & Medicaid Services (CMS) to be covered for Medicare beneficiaries at 3-year intervals, pending FDA approval. If public and private payers start covering Shield alongside other CRC screening tests, it presents an opportunity for primary care physicians to reach the approximately 3 in 10 adults between ages 45 and 75 who are not being routinely screened.

A big concern, however, is that the availability of a blood test may cause patients who would have otherwise been screened with colonoscopy or stool tests to switch to the blood test. A cost-effectiveness analysis found that offering a blood test to patients who decline screening colonoscopy saves additional lives, but at the cost of more than $377,000 per life-year gained. Another study relying on three microsimulation models previously utilized by the US Preventive Services Task Force (USPSTF) found that annual FIT results in more life-years gained at substantially lower cost than blood-based screening every 3 years “even when uptake of blood-based screening was 20 percentage points higher than uptake of FIT.” As a result, a multidisciplinary expert panel concluded that blood-based screening should not substitute for established CRC screening tests, but instead be offered only to patients who decline those tests.

In practice, this will increase the complexity of the CRC screening conversations we have with patients. We will need to be clear that the blood test is not yet endorsed by the USPSTF or any major guideline group and is a second-line test that will miss most precancerous polyps. As with the stool tests, it is essential to emphasize that a positive result must be followed by diagnostic colonoscopy. To addend the cancer screening maxim I mentioned before, the blood test is not the best test for CRC, but it’s probably better than no test at all.

Dr. Lin is a family physician and associate director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania. He blogs at Common Sense Family Doctor.

A version of this article appeared on Medscape.com.

Last year, I concluded a commentary for this news organization on colorectal cancer (CRC) screening guidelines by stating that between stool-based tests, flexible sigmoidoscopy, and colonoscopy, “the best screening test is the test that gets done.” But should that maxim apply to the new blood-based screening test, Guardant Health Shield? This proprietary test, which costs $895 and is not generally covered by insurance, identifies alterations in cell-free DNA that are characteristic of CRC.

Shield’s test characteristics were recently evaluated in a prospective study of more than 10,000 adults aged 45-84 at average risk for CRC. The test had an 87.5% sensitivity for stage I, II, or III colorectal cancer but only a 13% sensitivity for advanced precancerous lesions. Test specificity was 89.6%, meaning that about 1 in 10 participants without CRC or advanced precancerous lesions on colonoscopy had a false-positive result.

Although the Shield blood test has a higher rate of false positives than the traditional fecal immunochemical test (FIT) and lower sensitivity and specificity than a multitarget stool DNA (FIT-DNA) test designed to improve on Cologuard, it meets the previously established criteria set forth by the Centers for Medicare & Medicaid Services (CMS) to be covered for Medicare beneficiaries at 3-year intervals, pending FDA approval. If public and private payers start covering Shield alongside other CRC screening tests, it presents an opportunity for primary care physicians to reach the approximately 3 in 10 adults between ages 45 and 75 who are not being routinely screened.

A big concern, however, is that the availability of a blood test may cause patients who would have otherwise been screened with colonoscopy or stool tests to switch to the blood test. A cost-effectiveness analysis found that offering a blood test to patients who decline screening colonoscopy saves additional lives, but at the cost of more than $377,000 per life-year gained. Another study relying on three microsimulation models previously utilized by the US Preventive Services Task Force (USPSTF) found that annual FIT results in more life-years gained at substantially lower cost than blood-based screening every 3 years “even when uptake of blood-based screening was 20 percentage points higher than uptake of FIT.” As a result, a multidisciplinary expert panel concluded that blood-based screening should not substitute for established CRC screening tests, but instead be offered only to patients who decline those tests.

In practice, this will increase the complexity of the CRC screening conversations we have with patients. We will need to be clear that the blood test is not yet endorsed by the USPSTF or any major guideline group and is a second-line test that will miss most precancerous polyps. As with the stool tests, it is essential to emphasize that a positive result must be followed by diagnostic colonoscopy. To addend the cancer screening maxim I mentioned before, the blood test is not the best test for CRC, but it’s probably better than no test at all.

Dr. Lin is a family physician and associate director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania. He blogs at Common Sense Family Doctor.

A version of this article appeared on Medscape.com.

Recent headlines scream that we have an obesity problem and that carbs are the culprit for the problem. That leads me to ask: How did we get to blaming carbs as the enemy in the war against obesity?

First, a quick review of the history of diet and macronutrient content.

A long time ago, prehistoric humans foraged and hunted for food. Protein and fat were procured from animal meat, which was very important for encephalization, or evolutionary increase in the complexity or relative size of the brain. Most of the requirements for protein and iron were satisfied by hunting and eating land animals as well as consuming marine life that washed up on shore.

Carbohydrates in the form of plant foods served as the only sources of energy available to prehistoric hunter-gatherers, which offset the high protein content of the rest of their diet. These were only available during spring and summer.

Then, about 10,000 years ago, plant and animal agriculture began, and humans saw a permanent shift in the macronutrient content of our daily intake so that it was more consistent and stable. Initially, the nutrient characteristic changes were subtle, going from wild food to cultivated food with the Agricultural Revolution in the mid-17th century. Then, it changed even more rapidly less than 200 years ago with the Industrial Revolution, resulting in semiprocessed and ultraprocessed foods.

This change in food intake altered human physiology, with major changes in our digestive, immune, and neural physiology and an increase in chronic disease prevalence. The last 50 years has seen an increase in obesity in the United States, along with increases in chronic disease such as type 2 diabetes, which leads cardiovascular disease and certain cancers. 
 

Back to Carbohydrates: Do We Need Them? How Much? What Kind?

The increase in the macronutrient content of the food we eat containing saturated fat and refined carbohydrates and sugars represents a major change and is arguably the smoking gun of the obesity epidemic. Unfortunately, ultraprocessed foods have become a staple of the standard American or Western diet. 

Ultraprocessed foods such as cakes, cookies, crackers, sugary breakfast cereals, pizza, potato chips, soft drinks, and ice cream are eons away from our prehistoric diet of wild game, nuts, fruits, and berries, at which time, our digestive immune and nervous systems evolved. The pace at which ultraprocessed foods have entered our diet outpaces the time necessary for adaptation of our digestive systems and genes to these foods. They are indeed pathogenic in this context. 

So when was the time when humans consumed an “optimal” diet? This is hard to say because during the time of brain evolution, we needed protein and iron and succumbed to infections and trauma. In the early 1900s, we continued to succumb to infection until the discovery of antibiotics. Soon thereafter, industrialization and processed foods led to weight gain and the chronic diseases of the cardiovascular system and type 2 diabetes. 

Carbohydrates provide calories and fiber and some micronutrients, which are needed for energy, metabolism, and bowel and immune health. But how much do we need? 

Currently in the United States, the percentage of total food energy derived from the three major macronutrients is: carbohydrates, 51.8%; fat, 32.8%; and protein, 15.4%. Current advice for a healthy diet to lower risk for cardiovascular disease is to limit fat intake to 30% of total energy, protein to 15%, and to increase complex carbohydrates to 55%-60% of total energy. But we also need to qualify this in terms of the quality of the macronutrient, particularly carbohydrates. 

In addition to the quality, the macronutrient content of the diet has varied considerably from our prehistoric times when dietary protein intakes were high at 19%-35% of energy at the expense of carbohydrate (22%-40% of energy). 

If our genes haven’t kept up with industrialization, then why do we need so many carbohydrates to equate to 55%-60% of energy? Is it possible that we are confusing what is available with what we actually need? What do I mean by this?

We certainly have changed the landscape of the world due to agriculture, which has allowed us to procreate and feed ourselves, and certainly, industrialization has increased the availability of accessible cheap food. Protein in the form of meat, fish, and fowl are harder to get in industrialized nations as are fruits and vegetables. These macronutrients were the foods of our ancestors. It may be that a healthy diet is considered the one that is available. 

For instance, the Mediterranean diet is somewhat higher in fat content, 40%-50% fat (mostly mono and unsaturated), and similar in protein content but lower in carbohydrate content than the typical Western diet. The Dietary Approaches to Stop Hypertension (DASH) diet is lower in fat at 25% total calories, is higher in carbohydrates at 55%, and is lower in protein, but this diet was generated in the United States, therefore it is more Western. 

We need high-quality protein for organ and muscle function, high-quality unsaturated and monounsaturated fats for brain function and cellular functions, and high-quality complex carbohydrates for energy and gut health as well as micronutrients for many cellular functions. A ketogenic diet is not sustainable in the long-term for these reasons: chiefly the need for some carbohydrates for gut health and micronutrients. 

How much carbohydrate content is needed should take into consideration energy expenditure as well as micronutrients and fiber intake. Protein and fat can contribute to energy production but not as readily as carbohydrates that can quickly restore glycogen in the muscle and liver. What’s interesting is that our ancestors were able to hunt and run away from danger with the small amounts of carbohydrates from plants and berries plus the protein and fat intake from animals and fish — but the Olympics weren’t a thing then!

It may be another 200,000 years before our genes catch up to ultraprocessed foods and the simple carbohydrates and sugars contained in these products. Evidence suggests that ultraprocessed foods cause inflammation in organs like the liver, adipose tissue, the heart, and even the brain. In the brain, this inflammation may be what’s causing us to defend a higher body weight set point in this environment of easily obtained highly palatable ultraprocessed foods. 

Let’s not wait until our genes catch up and our bodies tolerate junk food without disease progression. It could be like waiting for Godot!

Dr. Apovian is professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, Boston, Massachusetts. She disclosed ties to Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, and L-Nutra.

A version of this article appeared on Medscape.com.

Recent headlines scream that we have an obesity problem and that carbs are the culprit for the problem. That leads me to ask: How did we get to blaming carbs as the enemy in the war against obesity?

First, a quick review of the history of diet and macronutrient content.

A long time ago, prehistoric humans foraged and hunted for food. Protein and fat were procured from animal meat, which was very important for encephalization, or evolutionary increase in the complexity or relative size of the brain. Most of the requirements for protein and iron were satisfied by hunting and eating land animals as well as consuming marine life that washed up on shore.

Carbohydrates in the form of plant foods served as the only sources of energy available to prehistoric hunter-gatherers, which offset the high protein content of the rest of their diet. These were only available during spring and summer.

Then, about 10,000 years ago, plant and animal agriculture began, and humans saw a permanent shift in the macronutrient content of our daily intake so that it was more consistent and stable. Initially, the nutrient characteristic changes were subtle, going from wild food to cultivated food with the Agricultural Revolution in the mid-17th century. Then, it changed even more rapidly less than 200 years ago with the Industrial Revolution, resulting in semiprocessed and ultraprocessed foods.

This change in food intake altered human physiology, with major changes in our digestive, immune, and neural physiology and an increase in chronic disease prevalence. The last 50 years has seen an increase in obesity in the United States, along with increases in chronic disease such as type 2 diabetes, which leads cardiovascular disease and certain cancers. 
 

Back to Carbohydrates: Do We Need Them? How Much? What Kind?

The increase in the macronutrient content of the food we eat containing saturated fat and refined carbohydrates and sugars represents a major change and is arguably the smoking gun of the obesity epidemic. Unfortunately, ultraprocessed foods have become a staple of the standard American or Western diet. 

Ultraprocessed foods such as cakes, cookies, crackers, sugary breakfast cereals, pizza, potato chips, soft drinks, and ice cream are eons away from our prehistoric diet of wild game, nuts, fruits, and berries, at which time, our digestive immune and nervous systems evolved. The pace at which ultraprocessed foods have entered our diet outpaces the time necessary for adaptation of our digestive systems and genes to these foods. They are indeed pathogenic in this context. 

So when was the time when humans consumed an “optimal” diet? This is hard to say because during the time of brain evolution, we needed protein and iron and succumbed to infections and trauma. In the early 1900s, we continued to succumb to infection until the discovery of antibiotics. Soon thereafter, industrialization and processed foods led to weight gain and the chronic diseases of the cardiovascular system and type 2 diabetes. 

Carbohydrates provide calories and fiber and some micronutrients, which are needed for energy, metabolism, and bowel and immune health. But how much do we need? 

Currently in the United States, the percentage of total food energy derived from the three major macronutrients is: carbohydrates, 51.8%; fat, 32.8%; and protein, 15.4%. Current advice for a healthy diet to lower risk for cardiovascular disease is to limit fat intake to 30% of total energy, protein to 15%, and to increase complex carbohydrates to 55%-60% of total energy. But we also need to qualify this in terms of the quality of the macronutrient, particularly carbohydrates. 

In addition to the quality, the macronutrient content of the diet has varied considerably from our prehistoric times when dietary protein intakes were high at 19%-35% of energy at the expense of carbohydrate (22%-40% of energy). 

If our genes haven’t kept up with industrialization, then why do we need so many carbohydrates to equate to 55%-60% of energy? Is it possible that we are confusing what is available with what we actually need? What do I mean by this?

We certainly have changed the landscape of the world due to agriculture, which has allowed us to procreate and feed ourselves, and certainly, industrialization has increased the availability of accessible cheap food. Protein in the form of meat, fish, and fowl are harder to get in industrialized nations as are fruits and vegetables. These macronutrients were the foods of our ancestors. It may be that a healthy diet is considered the one that is available. 

For instance, the Mediterranean diet is somewhat higher in fat content, 40%-50% fat (mostly mono and unsaturated), and similar in protein content but lower in carbohydrate content than the typical Western diet. The Dietary Approaches to Stop Hypertension (DASH) diet is lower in fat at 25% total calories, is higher in carbohydrates at 55%, and is lower in protein, but this diet was generated in the United States, therefore it is more Western. 

We need high-quality protein for organ and muscle function, high-quality unsaturated and monounsaturated fats for brain function and cellular functions, and high-quality complex carbohydrates for energy and gut health as well as micronutrients for many cellular functions. A ketogenic diet is not sustainable in the long-term for these reasons: chiefly the need for some carbohydrates for gut health and micronutrients. 

How much carbohydrate content is needed should take into consideration energy expenditure as well as micronutrients and fiber intake. Protein and fat can contribute to energy production but not as readily as carbohydrates that can quickly restore glycogen in the muscle and liver. What’s interesting is that our ancestors were able to hunt and run away from danger with the small amounts of carbohydrates from plants and berries plus the protein and fat intake from animals and fish — but the Olympics weren’t a thing then!

It may be another 200,000 years before our genes catch up to ultraprocessed foods and the simple carbohydrates and sugars contained in these products. Evidence suggests that ultraprocessed foods cause inflammation in organs like the liver, adipose tissue, the heart, and even the brain. In the brain, this inflammation may be what’s causing us to defend a higher body weight set point in this environment of easily obtained highly palatable ultraprocessed foods. 

Let’s not wait until our genes catch up and our bodies tolerate junk food without disease progression. It could be like waiting for Godot!

Dr. Apovian is professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, Boston, Massachusetts. She disclosed ties to Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, and L-Nutra.

A version of this article appeared on Medscape.com.

Recent headlines scream that we have an obesity problem and that carbs are the culprit for the problem. That leads me to ask: How did we get to blaming carbs as the enemy in the war against obesity?

First, a quick review of the history of diet and macronutrient content.

A long time ago, prehistoric humans foraged and hunted for food. Protein and fat were procured from animal meat, which was very important for encephalization, or evolutionary increase in the complexity or relative size of the brain. Most of the requirements for protein and iron were satisfied by hunting and eating land animals as well as consuming marine life that washed up on shore.

Carbohydrates in the form of plant foods served as the only sources of energy available to prehistoric hunter-gatherers, which offset the high protein content of the rest of their diet. These were only available during spring and summer.

Then, about 10,000 years ago, plant and animal agriculture began, and humans saw a permanent shift in the macronutrient content of our daily intake so that it was more consistent and stable. Initially, the nutrient characteristic changes were subtle, going from wild food to cultivated food with the Agricultural Revolution in the mid-17th century. Then, it changed even more rapidly less than 200 years ago with the Industrial Revolution, resulting in semiprocessed and ultraprocessed foods.

This change in food intake altered human physiology, with major changes in our digestive, immune, and neural physiology and an increase in chronic disease prevalence. The last 50 years has seen an increase in obesity in the United States, along with increases in chronic disease such as type 2 diabetes, which leads cardiovascular disease and certain cancers. 
 

Back to Carbohydrates: Do We Need Them? How Much? What Kind?

The increase in the macronutrient content of the food we eat containing saturated fat and refined carbohydrates and sugars represents a major change and is arguably the smoking gun of the obesity epidemic. Unfortunately, ultraprocessed foods have become a staple of the standard American or Western diet. 

Ultraprocessed foods such as cakes, cookies, crackers, sugary breakfast cereals, pizza, potato chips, soft drinks, and ice cream are eons away from our prehistoric diet of wild game, nuts, fruits, and berries, at which time, our digestive immune and nervous systems evolved. The pace at which ultraprocessed foods have entered our diet outpaces the time necessary for adaptation of our digestive systems and genes to these foods. They are indeed pathogenic in this context. 

So when was the time when humans consumed an “optimal” diet? This is hard to say because during the time of brain evolution, we needed protein and iron and succumbed to infections and trauma. In the early 1900s, we continued to succumb to infection until the discovery of antibiotics. Soon thereafter, industrialization and processed foods led to weight gain and the chronic diseases of the cardiovascular system and type 2 diabetes. 

Carbohydrates provide calories and fiber and some micronutrients, which are needed for energy, metabolism, and bowel and immune health. But how much do we need? 

Currently in the United States, the percentage of total food energy derived from the three major macronutrients is: carbohydrates, 51.8%; fat, 32.8%; and protein, 15.4%. Current advice for a healthy diet to lower risk for cardiovascular disease is to limit fat intake to 30% of total energy, protein to 15%, and to increase complex carbohydrates to 55%-60% of total energy. But we also need to qualify this in terms of the quality of the macronutrient, particularly carbohydrates. 

In addition to the quality, the macronutrient content of the diet has varied considerably from our prehistoric times when dietary protein intakes were high at 19%-35% of energy at the expense of carbohydrate (22%-40% of energy). 

If our genes haven’t kept up with industrialization, then why do we need so many carbohydrates to equate to 55%-60% of energy? Is it possible that we are confusing what is available with what we actually need? What do I mean by this?

We certainly have changed the landscape of the world due to agriculture, which has allowed us to procreate and feed ourselves, and certainly, industrialization has increased the availability of accessible cheap food. Protein in the form of meat, fish, and fowl are harder to get in industrialized nations as are fruits and vegetables. These macronutrients were the foods of our ancestors. It may be that a healthy diet is considered the one that is available. 

For instance, the Mediterranean diet is somewhat higher in fat content, 40%-50% fat (mostly mono and unsaturated), and similar in protein content but lower in carbohydrate content than the typical Western diet. The Dietary Approaches to Stop Hypertension (DASH) diet is lower in fat at 25% total calories, is higher in carbohydrates at 55%, and is lower in protein, but this diet was generated in the United States, therefore it is more Western. 

We need high-quality protein for organ and muscle function, high-quality unsaturated and monounsaturated fats for brain function and cellular functions, and high-quality complex carbohydrates for energy and gut health as well as micronutrients for many cellular functions. A ketogenic diet is not sustainable in the long-term for these reasons: chiefly the need for some carbohydrates for gut health and micronutrients. 

How much carbohydrate content is needed should take into consideration energy expenditure as well as micronutrients and fiber intake. Protein and fat can contribute to energy production but not as readily as carbohydrates that can quickly restore glycogen in the muscle and liver. What’s interesting is that our ancestors were able to hunt and run away from danger with the small amounts of carbohydrates from plants and berries plus the protein and fat intake from animals and fish — but the Olympics weren’t a thing then!

It may be another 200,000 years before our genes catch up to ultraprocessed foods and the simple carbohydrates and sugars contained in these products. Evidence suggests that ultraprocessed foods cause inflammation in organs like the liver, adipose tissue, the heart, and even the brain. In the brain, this inflammation may be what’s causing us to defend a higher body weight set point in this environment of easily obtained highly palatable ultraprocessed foods. 

Let’s not wait until our genes catch up and our bodies tolerate junk food without disease progression. It could be like waiting for Godot!

Dr. Apovian is professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, Boston, Massachusetts. She disclosed ties to Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, and L-Nutra.

A version of this article appeared on Medscape.com.