Family Practice News

Three basic truths about ultraprocessed foods: Junk food, available pretty much everywhere, tastes great. Advertising works. And most of us don’t crave green leafy salads when we’re hungry.

Of those three truths, the one that tends to get more public health attention is advertising. More specifically, advertising junk food to kids. 

Back in the days when cable television was king of all free time, study after study tried to quantify junk- and fast-food advertising to kids and speculated about its impact on childhood obesity rates. But as broadcast television use began fading, advertisers — and, of course, studies about advertising — turned their attention first to gaming and now to social media.

The social media numbers are quite staggering. According to a study published — probably not coincidentally — on Halloween, looking at the 40 top brands of junk- and fast food sold in Canada, those 40 brands alone were mentioned over 16 million times by social media users, reaching an estimated 42 billion total users within a 1-year period. 

And unique to the challenge of junk- and fast-food advertising on social media is that it also includes “earned” advertising, the kind not paid for by manufacturers but rather the kind where friends, family, and influencers post about junk food. Occasionally, though, these lines are blurred by initiatives from fast-food manufacturers explicitly encouraging social sharing. Consequently, even were there a desire, there isn’t likely to be a regulatory mechanism to markedly reduce it. 

For years, here in North America, excepting Quebec, the desire has been mainly to just talk about how concerned we are about junk-food advertising to kids. Elsewhere, however, some countries tried to do more, including both Mexico and Chile, which put kid-targeted TV food advertising bans in place in 2014 and 2016, respectively. 

Did they work? It depends on what outcome you’re considering. If the question is, did they work in regard to obesity? — which is how everyone tends to frame the question — by themselves, probably not. No one sandbag stops a flood, and though junk-food advertising is certainly a sandbag, we’re still facing a torrential downpour of obesity contributors. No doubt they did work to reduce kids’ exposure to junk-food advertising on television, but what remains to be seen is whether there is a means to now tackle social media’s generous servings of the same. Moreover, the obesity lens is the wrong one. Ultraprocessed food consumption isn’t good for anyone, regardless of weight, and its reduced marketing and consumption is a worthy goal of its own.

But Chile and Mexico are filling more than single sandbags, as both countries have rolled out a suite of interventions they are hoping will help improve nutrition: from front-of–package labeling reforms and warnings, to the banning of advertising geared specifically to appeal to children (like sugary cereal cartoon mascots), to implementing sugar-sweetened-beverage taxes, to having blanket overall bans on food advertising during the daytime.

Mexico is even taking first steps to start addressing junk food’s ubiquity by banning its sale in schools altogether. Schools found to be selling common Mexican junk food fare, such as sugary fruit drinks; chips; artificial pork rinds; and soy-encased, salty peanuts with chili, will see their administrators facing heavy fines. 

Because therein lies the biggest rub. Going back to those three simple truths, junk food is hyperpalatable and consequently tends to be what we crave when we’re hungry. So even if we miraculously one day do more than just talk about advertising reforms, and especially given that we won’t be able to do anything about social media’s earned product placements, junk food’s ubiquitous availability within arms’ reach or on our Uber Eats apps will see us be likely to continue its excessive consumption. 

That’s not to say we shouldn’t emulate Mexico and Chile’s initiatives, nor that they shouldn’t continue to build upon them, but one thing is certain: Human nature and inconvenient truths around food are incredibly powerful forces that we haven’t yet figured out how to tame.

Dr. Freedhoff, Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada, has disclosed relevant financial relationships with Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.

A version of this article appeared on Medscape.com.

Three basic truths about ultraprocessed foods: Junk food, available pretty much everywhere, tastes great. Advertising works. And most of us don’t crave green leafy salads when we’re hungry.

Of those three truths, the one that tends to get more public health attention is advertising. More specifically, advertising junk food to kids. 

Back in the days when cable television was king of all free time, study after study tried to quantify junk- and fast-food advertising to kids and speculated about its impact on childhood obesity rates. But as broadcast television use began fading, advertisers — and, of course, studies about advertising — turned their attention first to gaming and now to social media.

The social media numbers are quite staggering. According to a study published — probably not coincidentally — on Halloween, looking at the 40 top brands of junk- and fast food sold in Canada, those 40 brands alone were mentioned over 16 million times by social media users, reaching an estimated 42 billion total users within a 1-year period. 

And unique to the challenge of junk- and fast-food advertising on social media is that it also includes “earned” advertising, the kind not paid for by manufacturers but rather the kind where friends, family, and influencers post about junk food. Occasionally, though, these lines are blurred by initiatives from fast-food manufacturers explicitly encouraging social sharing. Consequently, even were there a desire, there isn’t likely to be a regulatory mechanism to markedly reduce it. 

For years, here in North America, excepting Quebec, the desire has been mainly to just talk about how concerned we are about junk-food advertising to kids. Elsewhere, however, some countries tried to do more, including both Mexico and Chile, which put kid-targeted TV food advertising bans in place in 2014 and 2016, respectively. 

Did they work? It depends on what outcome you’re considering. If the question is, did they work in regard to obesity? — which is how everyone tends to frame the question — by themselves, probably not. No one sandbag stops a flood, and though junk-food advertising is certainly a sandbag, we’re still facing a torrential downpour of obesity contributors. No doubt they did work to reduce kids’ exposure to junk-food advertising on television, but what remains to be seen is whether there is a means to now tackle social media’s generous servings of the same. Moreover, the obesity lens is the wrong one. Ultraprocessed food consumption isn’t good for anyone, regardless of weight, and its reduced marketing and consumption is a worthy goal of its own.

But Chile and Mexico are filling more than single sandbags, as both countries have rolled out a suite of interventions they are hoping will help improve nutrition: from front-of–package labeling reforms and warnings, to the banning of advertising geared specifically to appeal to children (like sugary cereal cartoon mascots), to implementing sugar-sweetened-beverage taxes, to having blanket overall bans on food advertising during the daytime.

Mexico is even taking first steps to start addressing junk food’s ubiquity by banning its sale in schools altogether. Schools found to be selling common Mexican junk food fare, such as sugary fruit drinks; chips; artificial pork rinds; and soy-encased, salty peanuts with chili, will see their administrators facing heavy fines. 

Because therein lies the biggest rub. Going back to those three simple truths, junk food is hyperpalatable and consequently tends to be what we crave when we’re hungry. So even if we miraculously one day do more than just talk about advertising reforms, and especially given that we won’t be able to do anything about social media’s earned product placements, junk food’s ubiquitous availability within arms’ reach or on our Uber Eats apps will see us be likely to continue its excessive consumption. 

That’s not to say we shouldn’t emulate Mexico and Chile’s initiatives, nor that they shouldn’t continue to build upon them, but one thing is certain: Human nature and inconvenient truths around food are incredibly powerful forces that we haven’t yet figured out how to tame.

Dr. Freedhoff, Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada, has disclosed relevant financial relationships with Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.

A version of this article appeared on Medscape.com.

Three basic truths about ultraprocessed foods: Junk food, available pretty much everywhere, tastes great. Advertising works. And most of us don’t crave green leafy salads when we’re hungry.

Of those three truths, the one that tends to get more public health attention is advertising. More specifically, advertising junk food to kids. 

Back in the days when cable television was king of all free time, study after study tried to quantify junk- and fast-food advertising to kids and speculated about its impact on childhood obesity rates. But as broadcast television use began fading, advertisers — and, of course, studies about advertising — turned their attention first to gaming and now to social media.

The social media numbers are quite staggering. According to a study published — probably not coincidentally — on Halloween, looking at the 40 top brands of junk- and fast food sold in Canada, those 40 brands alone were mentioned over 16 million times by social media users, reaching an estimated 42 billion total users within a 1-year period. 

And unique to the challenge of junk- and fast-food advertising on social media is that it also includes “earned” advertising, the kind not paid for by manufacturers but rather the kind where friends, family, and influencers post about junk food. Occasionally, though, these lines are blurred by initiatives from fast-food manufacturers explicitly encouraging social sharing. Consequently, even were there a desire, there isn’t likely to be a regulatory mechanism to markedly reduce it. 

For years, here in North America, excepting Quebec, the desire has been mainly to just talk about how concerned we are about junk-food advertising to kids. Elsewhere, however, some countries tried to do more, including both Mexico and Chile, which put kid-targeted TV food advertising bans in place in 2014 and 2016, respectively. 

Did they work? It depends on what outcome you’re considering. If the question is, did they work in regard to obesity? — which is how everyone tends to frame the question — by themselves, probably not. No one sandbag stops a flood, and though junk-food advertising is certainly a sandbag, we’re still facing a torrential downpour of obesity contributors. No doubt they did work to reduce kids’ exposure to junk-food advertising on television, but what remains to be seen is whether there is a means to now tackle social media’s generous servings of the same. Moreover, the obesity lens is the wrong one. Ultraprocessed food consumption isn’t good for anyone, regardless of weight, and its reduced marketing and consumption is a worthy goal of its own.

But Chile and Mexico are filling more than single sandbags, as both countries have rolled out a suite of interventions they are hoping will help improve nutrition: from front-of–package labeling reforms and warnings, to the banning of advertising geared specifically to appeal to children (like sugary cereal cartoon mascots), to implementing sugar-sweetened-beverage taxes, to having blanket overall bans on food advertising during the daytime.

Mexico is even taking first steps to start addressing junk food’s ubiquity by banning its sale in schools altogether. Schools found to be selling common Mexican junk food fare, such as sugary fruit drinks; chips; artificial pork rinds; and soy-encased, salty peanuts with chili, will see their administrators facing heavy fines. 

Because therein lies the biggest rub. Going back to those three simple truths, junk food is hyperpalatable and consequently tends to be what we crave when we’re hungry. So even if we miraculously one day do more than just talk about advertising reforms, and especially given that we won’t be able to do anything about social media’s earned product placements, junk food’s ubiquitous availability within arms’ reach or on our Uber Eats apps will see us be likely to continue its excessive consumption. 

That’s not to say we shouldn’t emulate Mexico and Chile’s initiatives, nor that they shouldn’t continue to build upon them, but one thing is certain: Human nature and inconvenient truths around food are incredibly powerful forces that we haven’t yet figured out how to tame.

Dr. Freedhoff, Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada, has disclosed relevant financial relationships with Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

We have talked often in the past about potassium. Why is potassium so important in heart failure? It’s because many doctors are afraid to give some of the drugs that will raise the potassium, because then you need to deal with it —and everybody is afraid of hyperkalemia causing arrhythmias. 

Calm those nerves. Just remember that arrhythmias only occur when the potassium suddenly goes up. This chronic hyperkalemia, which occurs with many of our drugs, usually — I can’t say every time — does not result in arrhythmias.

 

Patiromer and Zirconium Cyclosilicate

Now, we’ve got potassium binders. You’ve heard me talk about the potassium binders in several of my other chats with you, and they work. We have primarily two of them. The first one that came out was patiromer, and now I’m going to talk to you a little bit about zirconium cyclosilicate, which uses sodium as its exchange ion. Whenever you take out one ion, you have to put another one in, and in this case it’s sodium. Maybe if you use it in the higher doses, you can give the patient more edema or you can make the patient congested with more fluid. 

Years ago we did the DIAMOND study; it was a patiromer study, but in essence we found that you could continue to give the drug, particularly the mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone, as long as you have the patiromer as your safety net, and that the drugs were well tolerated and the adverse events were significantly less.

 

The REALIZE-K Trial

Now, let’s talk about the REALIZE-K trial. The researchers wanted to prove basically the same thing: that the patients could be started or kept on their spironolactone as long as you had that backup of the zirconium cyclosilicate binder.

They picked patients who had HFrEF — so, low ejection fractions, defined as less than 40% — and they were already on guideline-directed medical therapy, but not an MRA. They divided up the patients right from the beginning between those who were already hyperkalemic — in other words, they had potassiums of 5.1-5.9 mEq/L, which is when doctors start getting worried. GFRs had to be better than 30 mL/min per 1.73 m², and if the potassium was not yet okay, they were given the zirconium cyclosilicate to normalize the potassium and then they entered the study. 

The second group had some history of or were at risk for hyperkalemia. Maybe their GFRs were lower, but their potassiums were somewhere between 3.5 and 5 mEq/L.

They started with about 366 patients. These trials have not been huge, certainly not what we normally see in heart failure trials. About 95 patients had hyperkalemia initially and 271 patients were normokalemic. 

Then they were randomized; about 102 patients went on the potassium binder and the other group went on the placebo. They continued the study and they continued to check whether the patient had to come off the drug or had to reduce or remove the spironolactone. 

These were older patients, mostly in their early seventies. This was an international trial. There were not that many patients from North America, but they had quite a few patients from Europe and some patients from Latin America. There were many with diabetes, atrial fibrillation, and all the usual comorbidities that we typically see. 

The proportions of patients classified as New York Heart Association Class III and IV were about 16% to 17% and the rest were Class II, so this is really the ambulatory population. NT-proBNP levels were elevated, at approximately 1000-1200 pg/mL, and the GFRs were either in the high 40s or about 60 mL/min per 1.73 m². The patients were pretty well medicated, including with RAAS inhibition, beta-blockers, and even SGLT2 inhibitors. 

This is a very typical population and they wanted to see what happened. Did the patients remain on the binder and were they able to tolerate the spironolactone? In fact, that was the case.

At the end of the study, more patients had been able to stay on their spironolactone, which is that one drug that we’re not doing so well on when you look at large databases. If they were on the zirconium drug, they were more likely to stay on the spironolactone. They even did a sensitivity analysis, which really showed that it was consistent across the board. 

 

Edema and Hyperkalemia

Now we have two binders that have shown to us that patients can stay on their drugs. There were some interesting findings here, though.

There was more edema — again, everything is based on small numbers — and there seemed to be more heart failure events in the group that received the zirconium cyclosilicate. The first episode of hyperkalemia was delayed or didn’t happen at all. Again, the hyperkalemia was controlled. 

What does that tell you? Well, the exchange is sodium. There had been reports before that if you gave this binder at the higher doses, you would have more retention of sodium. I think we see that in this trial, even though the numbers are very small. 

According to the investigators, these were issues that could be resolved through an increase in diuretics or having the patient remember to be careful with their sodium intake so they don’t retain more fluid. 

My message to you is to use these binders, whichever one of the two you want or whichever your hospital has available for you on their formulary, because it may give you that sense of comfort and self-efficacy so that you can actually start your patients on an MRA and keep them on it.

The MRAs are lifesaving drugs and the patients with HFrEF need to be on them. This is a way to do it without having to sacrifice your true guideline-directed medical therapy.

Dr. Piña, Professor of Medicine/Cardiology/Heart Failure/Transplant; Quality Officer, Cardiovascular Line, Sidney Kimmel College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Clinical Professor of Medicine, Central Michigan University College of Medicine, Mount Pleasant, Michigan; Adjunct Professor of Epidemiology and Biostatistics, Population & Quantitative Health Sciences, Case Western University, Cleveland, Ohio, disclosed ties with the Food and Drug Administration’s Center for Devices and Radiological Health.

A version of this article appeared on Medscape.com

This transcript has been edited for clarity. 

We have talked often in the past about potassium. Why is potassium so important in heart failure? It’s because many doctors are afraid to give some of the drugs that will raise the potassium, because then you need to deal with it —and everybody is afraid of hyperkalemia causing arrhythmias. 

Calm those nerves. Just remember that arrhythmias only occur when the potassium suddenly goes up. This chronic hyperkalemia, which occurs with many of our drugs, usually — I can’t say every time — does not result in arrhythmias.

 

Patiromer and Zirconium Cyclosilicate

Now, we’ve got potassium binders. You’ve heard me talk about the potassium binders in several of my other chats with you, and they work. We have primarily two of them. The first one that came out was patiromer, and now I’m going to talk to you a little bit about zirconium cyclosilicate, which uses sodium as its exchange ion. Whenever you take out one ion, you have to put another one in, and in this case it’s sodium. Maybe if you use it in the higher doses, you can give the patient more edema or you can make the patient congested with more fluid. 

Years ago we did the DIAMOND study; it was a patiromer study, but in essence we found that you could continue to give the drug, particularly the mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone, as long as you have the patiromer as your safety net, and that the drugs were well tolerated and the adverse events were significantly less.

 

The REALIZE-K Trial

Now, let’s talk about the REALIZE-K trial. The researchers wanted to prove basically the same thing: that the patients could be started or kept on their spironolactone as long as you had that backup of the zirconium cyclosilicate binder.

They picked patients who had HFrEF — so, low ejection fractions, defined as less than 40% — and they were already on guideline-directed medical therapy, but not an MRA. They divided up the patients right from the beginning between those who were already hyperkalemic — in other words, they had potassiums of 5.1-5.9 mEq/L, which is when doctors start getting worried. GFRs had to be better than 30 mL/min per 1.73 m², and if the potassium was not yet okay, they were given the zirconium cyclosilicate to normalize the potassium and then they entered the study. 

The second group had some history of or were at risk for hyperkalemia. Maybe their GFRs were lower, but their potassiums were somewhere between 3.5 and 5 mEq/L.

They started with about 366 patients. These trials have not been huge, certainly not what we normally see in heart failure trials. About 95 patients had hyperkalemia initially and 271 patients were normokalemic. 

Then they were randomized; about 102 patients went on the potassium binder and the other group went on the placebo. They continued the study and they continued to check whether the patient had to come off the drug or had to reduce or remove the spironolactone. 

These were older patients, mostly in their early seventies. This was an international trial. There were not that many patients from North America, but they had quite a few patients from Europe and some patients from Latin America. There were many with diabetes, atrial fibrillation, and all the usual comorbidities that we typically see. 

The proportions of patients classified as New York Heart Association Class III and IV were about 16% to 17% and the rest were Class II, so this is really the ambulatory population. NT-proBNP levels were elevated, at approximately 1000-1200 pg/mL, and the GFRs were either in the high 40s or about 60 mL/min per 1.73 m². The patients were pretty well medicated, including with RAAS inhibition, beta-blockers, and even SGLT2 inhibitors. 

This is a very typical population and they wanted to see what happened. Did the patients remain on the binder and were they able to tolerate the spironolactone? In fact, that was the case.

At the end of the study, more patients had been able to stay on their spironolactone, which is that one drug that we’re not doing so well on when you look at large databases. If they were on the zirconium drug, they were more likely to stay on the spironolactone. They even did a sensitivity analysis, which really showed that it was consistent across the board. 

 

Edema and Hyperkalemia

Now we have two binders that have shown to us that patients can stay on their drugs. There were some interesting findings here, though.

There was more edema — again, everything is based on small numbers — and there seemed to be more heart failure events in the group that received the zirconium cyclosilicate. The first episode of hyperkalemia was delayed or didn’t happen at all. Again, the hyperkalemia was controlled. 

What does that tell you? Well, the exchange is sodium. There had been reports before that if you gave this binder at the higher doses, you would have more retention of sodium. I think we see that in this trial, even though the numbers are very small. 

According to the investigators, these were issues that could be resolved through an increase in diuretics or having the patient remember to be careful with their sodium intake so they don’t retain more fluid. 

My message to you is to use these binders, whichever one of the two you want or whichever your hospital has available for you on their formulary, because it may give you that sense of comfort and self-efficacy so that you can actually start your patients on an MRA and keep them on it.

The MRAs are lifesaving drugs and the patients with HFrEF need to be on them. This is a way to do it without having to sacrifice your true guideline-directed medical therapy.

Dr. Piña, Professor of Medicine/Cardiology/Heart Failure/Transplant; Quality Officer, Cardiovascular Line, Sidney Kimmel College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Clinical Professor of Medicine, Central Michigan University College of Medicine, Mount Pleasant, Michigan; Adjunct Professor of Epidemiology and Biostatistics, Population & Quantitative Health Sciences, Case Western University, Cleveland, Ohio, disclosed ties with the Food and Drug Administration’s Center for Devices and Radiological Health.

A version of this article appeared on Medscape.com

This transcript has been edited for clarity. 

We have talked often in the past about potassium. Why is potassium so important in heart failure? It’s because many doctors are afraid to give some of the drugs that will raise the potassium, because then you need to deal with it —and everybody is afraid of hyperkalemia causing arrhythmias. 

Calm those nerves. Just remember that arrhythmias only occur when the potassium suddenly goes up. This chronic hyperkalemia, which occurs with many of our drugs, usually — I can’t say every time — does not result in arrhythmias.

 

Patiromer and Zirconium Cyclosilicate

Now, we’ve got potassium binders. You’ve heard me talk about the potassium binders in several of my other chats with you, and they work. We have primarily two of them. The first one that came out was patiromer, and now I’m going to talk to you a little bit about zirconium cyclosilicate, which uses sodium as its exchange ion. Whenever you take out one ion, you have to put another one in, and in this case it’s sodium. Maybe if you use it in the higher doses, you can give the patient more edema or you can make the patient congested with more fluid. 

Years ago we did the DIAMOND study; it was a patiromer study, but in essence we found that you could continue to give the drug, particularly the mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone, as long as you have the patiromer as your safety net, and that the drugs were well tolerated and the adverse events were significantly less.

 

The REALIZE-K Trial

Now, let’s talk about the REALIZE-K trial. The researchers wanted to prove basically the same thing: that the patients could be started or kept on their spironolactone as long as you had that backup of the zirconium cyclosilicate binder.

They picked patients who had HFrEF — so, low ejection fractions, defined as less than 40% — and they were already on guideline-directed medical therapy, but not an MRA. They divided up the patients right from the beginning between those who were already hyperkalemic — in other words, they had potassiums of 5.1-5.9 mEq/L, which is when doctors start getting worried. GFRs had to be better than 30 mL/min per 1.73 m², and if the potassium was not yet okay, they were given the zirconium cyclosilicate to normalize the potassium and then they entered the study. 

The second group had some history of or were at risk for hyperkalemia. Maybe their GFRs were lower, but their potassiums were somewhere between 3.5 and 5 mEq/L.

They started with about 366 patients. These trials have not been huge, certainly not what we normally see in heart failure trials. About 95 patients had hyperkalemia initially and 271 patients were normokalemic. 

Then they were randomized; about 102 patients went on the potassium binder and the other group went on the placebo. They continued the study and they continued to check whether the patient had to come off the drug or had to reduce or remove the spironolactone. 

These were older patients, mostly in their early seventies. This was an international trial. There were not that many patients from North America, but they had quite a few patients from Europe and some patients from Latin America. There were many with diabetes, atrial fibrillation, and all the usual comorbidities that we typically see. 

The proportions of patients classified as New York Heart Association Class III and IV were about 16% to 17% and the rest were Class II, so this is really the ambulatory population. NT-proBNP levels were elevated, at approximately 1000-1200 pg/mL, and the GFRs were either in the high 40s or about 60 mL/min per 1.73 m². The patients were pretty well medicated, including with RAAS inhibition, beta-blockers, and even SGLT2 inhibitors. 

This is a very typical population and they wanted to see what happened. Did the patients remain on the binder and were they able to tolerate the spironolactone? In fact, that was the case.

At the end of the study, more patients had been able to stay on their spironolactone, which is that one drug that we’re not doing so well on when you look at large databases. If they were on the zirconium drug, they were more likely to stay on the spironolactone. They even did a sensitivity analysis, which really showed that it was consistent across the board. 

 

Edema and Hyperkalemia

Now we have two binders that have shown to us that patients can stay on their drugs. There were some interesting findings here, though.

There was more edema — again, everything is based on small numbers — and there seemed to be more heart failure events in the group that received the zirconium cyclosilicate. The first episode of hyperkalemia was delayed or didn’t happen at all. Again, the hyperkalemia was controlled. 

What does that tell you? Well, the exchange is sodium. There had been reports before that if you gave this binder at the higher doses, you would have more retention of sodium. I think we see that in this trial, even though the numbers are very small. 

According to the investigators, these were issues that could be resolved through an increase in diuretics or having the patient remember to be careful with their sodium intake so they don’t retain more fluid. 

My message to you is to use these binders, whichever one of the two you want or whichever your hospital has available for you on their formulary, because it may give you that sense of comfort and self-efficacy so that you can actually start your patients on an MRA and keep them on it.

The MRAs are lifesaving drugs and the patients with HFrEF need to be on them. This is a way to do it without having to sacrifice your true guideline-directed medical therapy.

Dr. Piña, Professor of Medicine/Cardiology/Heart Failure/Transplant; Quality Officer, Cardiovascular Line, Sidney Kimmel College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Clinical Professor of Medicine, Central Michigan University College of Medicine, Mount Pleasant, Michigan; Adjunct Professor of Epidemiology and Biostatistics, Population & Quantitative Health Sciences, Case Western University, Cleveland, Ohio, disclosed ties with the Food and Drug Administration’s Center for Devices and Radiological Health.

A version of this article appeared on Medscape.com

TOPLINE:

Veterans receiving blood pressure (BP) medication as needed while hospitalized were at a 23% higher risk for acute kidney injury (AKI) and a 1.5-fold greater risk for potentially dangerous rapid reductions in BP.

METHODOLOGY:

• Researchers analyzed the records of 133,760 veterans (90% men; mean age, 71.2 years) hospitalized in Veterans Affairs hospitals between 2015 and 2020.
• The study analyzed as-needed administration of BP drugs to patients who had an elevated BP but were asymptomatic.
• Patients who had at least one systolic BP reading above 140 mm Hg and received scheduled BP medication in the first 24 hours of hospitalization were included; those admitted to intensive care units or those who required surgery were excluded.
• The analysis compared outcomes between 28,526 patients who received as-needed drugs and 105,234 who did not; the primary outcome was time to the first AKI occurrence while hospitalized.
• Secondary outcomes included a reduction of more than 25% in systolic BP within 3 hours of as-needed BP medication, as well as a composite outcome of myocardial infarction, stroke, or death during hospitalization.

TAKEAWAY:

• Researchers found that an AKI was 23% more likely to occur in veterans who received at least one as-needed BP medication (hazard ratio [HR], 1.23; 95% CI, 1.18-1.29).
• Veterans who received BP medication as needed were 50% more likely to experience a rapid drop in BP within 3 hours (HR, 1.50; 95% CI, 1.39-1.62) and more than twice as likely after 1 hour (HR, 2.11; 95% CI, 1.81-2.46) than those who did not receive medication.
• The risk of experiencing the composite outcome was 69% times higher in the as-needed group (rate ratio [RR], 1.69; 95% CI, 1.49-1.92), with individual increased risks for myocardial infarction (RR, 2.92; 95% CI, 2.09-4.07), stroke (RR, 1.99; 95% CI, 1.30-3.03), and death (RR, 1.52; 95% CI, 1.32-1.75).

IN PRACTICE:

“The practical implication of our findings is that there is at least equipoise regarding the utility of as-needed BP medication use for asymptomatic BP elevations in hospitals ... future prospective trials should evaluate the risks and benefits of this common practice,” the study authors wrote.

SOURCE:

The study was led by Muna Thalji Canales, MD, MS, of the North Florida/South Georgia Veterans Health System in Gainesville, Florida. It was published online on November 25 in JAMA Internal Medicine.

LIMITATIONS:

The analysis may have included confounding factors that could have influenced results. The focus on veterans who had not undergone surgery limits generalizability to women, surgical patients, and nonveteran populations. The researchers noted limited data on factors that might influence BP readings in the hospital such as pain, stress, and faulty machinery.

DISCLOSURES:

Study authors reported grants and consulting fees from Merck Sharp & Dohme and BMS, and Teva Pharmaceuticals, among others.

 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Veterans receiving blood pressure (BP) medication as needed while hospitalized were at a 23% higher risk for acute kidney injury (AKI) and a 1.5-fold greater risk for potentially dangerous rapid reductions in BP.

METHODOLOGY:

• Researchers analyzed the records of 133,760 veterans (90% men; mean age, 71.2 years) hospitalized in Veterans Affairs hospitals between 2015 and 2020.
• The study analyzed as-needed administration of BP drugs to patients who had an elevated BP but were asymptomatic.
• Patients who had at least one systolic BP reading above 140 mm Hg and received scheduled BP medication in the first 24 hours of hospitalization were included; those admitted to intensive care units or those who required surgery were excluded.
• The analysis compared outcomes between 28,526 patients who received as-needed drugs and 105,234 who did not; the primary outcome was time to the first AKI occurrence while hospitalized.
• Secondary outcomes included a reduction of more than 25% in systolic BP within 3 hours of as-needed BP medication, as well as a composite outcome of myocardial infarction, stroke, or death during hospitalization.

TAKEAWAY:

• Researchers found that an AKI was 23% more likely to occur in veterans who received at least one as-needed BP medication (hazard ratio [HR], 1.23; 95% CI, 1.18-1.29).
• Veterans who received BP medication as needed were 50% more likely to experience a rapid drop in BP within 3 hours (HR, 1.50; 95% CI, 1.39-1.62) and more than twice as likely after 1 hour (HR, 2.11; 95% CI, 1.81-2.46) than those who did not receive medication.
• The risk of experiencing the composite outcome was 69% times higher in the as-needed group (rate ratio [RR], 1.69; 95% CI, 1.49-1.92), with individual increased risks for myocardial infarction (RR, 2.92; 95% CI, 2.09-4.07), stroke (RR, 1.99; 95% CI, 1.30-3.03), and death (RR, 1.52; 95% CI, 1.32-1.75).

IN PRACTICE:

“The practical implication of our findings is that there is at least equipoise regarding the utility of as-needed BP medication use for asymptomatic BP elevations in hospitals ... future prospective trials should evaluate the risks and benefits of this common practice,” the study authors wrote.

SOURCE:

The study was led by Muna Thalji Canales, MD, MS, of the North Florida/South Georgia Veterans Health System in Gainesville, Florida. It was published online on November 25 in JAMA Internal Medicine.

LIMITATIONS:

The analysis may have included confounding factors that could have influenced results. The focus on veterans who had not undergone surgery limits generalizability to women, surgical patients, and nonveteran populations. The researchers noted limited data on factors that might influence BP readings in the hospital such as pain, stress, and faulty machinery.

DISCLOSURES:

Study authors reported grants and consulting fees from Merck Sharp & Dohme and BMS, and Teva Pharmaceuticals, among others.

 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Veterans receiving blood pressure (BP) medication as needed while hospitalized were at a 23% higher risk for acute kidney injury (AKI) and a 1.5-fold greater risk for potentially dangerous rapid reductions in BP.

METHODOLOGY:

• Researchers analyzed the records of 133,760 veterans (90% men; mean age, 71.2 years) hospitalized in Veterans Affairs hospitals between 2015 and 2020.
• The study analyzed as-needed administration of BP drugs to patients who had an elevated BP but were asymptomatic.
• Patients who had at least one systolic BP reading above 140 mm Hg and received scheduled BP medication in the first 24 hours of hospitalization were included; those admitted to intensive care units or those who required surgery were excluded.
• The analysis compared outcomes between 28,526 patients who received as-needed drugs and 105,234 who did not; the primary outcome was time to the first AKI occurrence while hospitalized.
• Secondary outcomes included a reduction of more than 25% in systolic BP within 3 hours of as-needed BP medication, as well as a composite outcome of myocardial infarction, stroke, or death during hospitalization.

TAKEAWAY:

• Researchers found that an AKI was 23% more likely to occur in veterans who received at least one as-needed BP medication (hazard ratio [HR], 1.23; 95% CI, 1.18-1.29).
• Veterans who received BP medication as needed were 50% more likely to experience a rapid drop in BP within 3 hours (HR, 1.50; 95% CI, 1.39-1.62) and more than twice as likely after 1 hour (HR, 2.11; 95% CI, 1.81-2.46) than those who did not receive medication.
• The risk of experiencing the composite outcome was 69% times higher in the as-needed group (rate ratio [RR], 1.69; 95% CI, 1.49-1.92), with individual increased risks for myocardial infarction (RR, 2.92; 95% CI, 2.09-4.07), stroke (RR, 1.99; 95% CI, 1.30-3.03), and death (RR, 1.52; 95% CI, 1.32-1.75).

IN PRACTICE:

“The practical implication of our findings is that there is at least equipoise regarding the utility of as-needed BP medication use for asymptomatic BP elevations in hospitals ... future prospective trials should evaluate the risks and benefits of this common practice,” the study authors wrote.

SOURCE:

The study was led by Muna Thalji Canales, MD, MS, of the North Florida/South Georgia Veterans Health System in Gainesville, Florida. It was published online on November 25 in JAMA Internal Medicine.

LIMITATIONS:

The analysis may have included confounding factors that could have influenced results. The focus on veterans who had not undergone surgery limits generalizability to women, surgical patients, and nonveteran populations. The researchers noted limited data on factors that might influence BP readings in the hospital such as pain, stress, and faulty machinery.

DISCLOSURES:

Study authors reported grants and consulting fees from Merck Sharp & Dohme and BMS, and Teva Pharmaceuticals, among others.

 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In a new statement, the American Diabetes Association (ADA) has advised against the use of compounded glucagon-like peptide 1 receptor agonist (GLP-1 RA) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA medication classes.

The ADA recommends GLP-1 RA and GIP/GLP-1 RA medications approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes, cardiovascular and kidney disease risk reduction, and weight management. The new ADA statement pertains to the unapproved, unregulated versions that have emerged as the demand for these medications for weight loss increases. These are often marketed directly to consumers.

“Compounded GLP-1 RA and dual GIP/GLP-1 RA products have been associated with clinically important dosing errors and adverse events. More concerning to individuals’ safety are counterfeit products that have made their way into the US drug supply chain and those advertised online and by unregulated sources,” the ADA said in the statement, published online on December 2, 2024, in Diabetes Care.

The statement, authored by Joshua J. Neumiller, PharmD, CDCES, of the Department of Pharmacotherapy, Washington State University, Spokane, and colleagues, states the following:

• Non–FDA-approved compounded incretin products are not recommended for use due to uncertainty about their content and resulting concerns about safety, quality, and effectiveness.
• If an incretin medication is unavailable (eg, in shortage), switching to a different FDA-approved medication is recommended as clinically appropriate to achieve and maintain individualized glucose-lowering, weight management, and/or cardiovascular and kidney risk reduction goals.
• Upon resolution of incretin product unavailability, reassess the appropriateness of resuming the original FDA-approved incretin medication.

The document points out that compounded products are not identical to the FDA-approved versions, may be distributed in nonstandard dosing devices, and may not provide sufficient user instructions.

However, “the ADA also recognizes that individuals and clinicians may still elect to use or recommend compounded products for financial or other reasons,” and therefore offers additional advice for the public, including the following:

• Discuss product use with their usual healthcare providers.
• Only use products that include dosing guidance.
• Verify that the compounding pharmacy is registered with FDA.

In addition, report any adverse events or medication errors to the FDA’s Medwatch.

A version of this article appeared on Medscape.com.

In a new statement, the American Diabetes Association (ADA) has advised against the use of compounded glucagon-like peptide 1 receptor agonist (GLP-1 RA) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA medication classes.

The ADA recommends GLP-1 RA and GIP/GLP-1 RA medications approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes, cardiovascular and kidney disease risk reduction, and weight management. The new ADA statement pertains to the unapproved, unregulated versions that have emerged as the demand for these medications for weight loss increases. These are often marketed directly to consumers.

“Compounded GLP-1 RA and dual GIP/GLP-1 RA products have been associated with clinically important dosing errors and adverse events. More concerning to individuals’ safety are counterfeit products that have made their way into the US drug supply chain and those advertised online and by unregulated sources,” the ADA said in the statement, published online on December 2, 2024, in Diabetes Care.

The statement, authored by Joshua J. Neumiller, PharmD, CDCES, of the Department of Pharmacotherapy, Washington State University, Spokane, and colleagues, states the following:

• Non–FDA-approved compounded incretin products are not recommended for use due to uncertainty about their content and resulting concerns about safety, quality, and effectiveness.
• If an incretin medication is unavailable (eg, in shortage), switching to a different FDA-approved medication is recommended as clinically appropriate to achieve and maintain individualized glucose-lowering, weight management, and/or cardiovascular and kidney risk reduction goals.
• Upon resolution of incretin product unavailability, reassess the appropriateness of resuming the original FDA-approved incretin medication.

The document points out that compounded products are not identical to the FDA-approved versions, may be distributed in nonstandard dosing devices, and may not provide sufficient user instructions.

However, “the ADA also recognizes that individuals and clinicians may still elect to use or recommend compounded products for financial or other reasons,” and therefore offers additional advice for the public, including the following:

• Discuss product use with their usual healthcare providers.
• Only use products that include dosing guidance.
• Verify that the compounding pharmacy is registered with FDA.

In addition, report any adverse events or medication errors to the FDA’s Medwatch.

A version of this article appeared on Medscape.com.

In a new statement, the American Diabetes Association (ADA) has advised against the use of compounded glucagon-like peptide 1 receptor agonist (GLP-1 RA) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA medication classes.

The ADA recommends GLP-1 RA and GIP/GLP-1 RA medications approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes, cardiovascular and kidney disease risk reduction, and weight management. The new ADA statement pertains to the unapproved, unregulated versions that have emerged as the demand for these medications for weight loss increases. These are often marketed directly to consumers.

“Compounded GLP-1 RA and dual GIP/GLP-1 RA products have been associated with clinically important dosing errors and adverse events. More concerning to individuals’ safety are counterfeit products that have made their way into the US drug supply chain and those advertised online and by unregulated sources,” the ADA said in the statement, published online on December 2, 2024, in Diabetes Care.

The statement, authored by Joshua J. Neumiller, PharmD, CDCES, of the Department of Pharmacotherapy, Washington State University, Spokane, and colleagues, states the following:

• Non–FDA-approved compounded incretin products are not recommended for use due to uncertainty about their content and resulting concerns about safety, quality, and effectiveness.
• If an incretin medication is unavailable (eg, in shortage), switching to a different FDA-approved medication is recommended as clinically appropriate to achieve and maintain individualized glucose-lowering, weight management, and/or cardiovascular and kidney risk reduction goals.
• Upon resolution of incretin product unavailability, reassess the appropriateness of resuming the original FDA-approved incretin medication.

The document points out that compounded products are not identical to the FDA-approved versions, may be distributed in nonstandard dosing devices, and may not provide sufficient user instructions.

However, “the ADA also recognizes that individuals and clinicians may still elect to use or recommend compounded products for financial or other reasons,” and therefore offers additional advice for the public, including the following:

• Discuss product use with their usual healthcare providers.
• Only use products that include dosing guidance.
• Verify that the compounding pharmacy is registered with FDA.

In addition, report any adverse events or medication errors to the FDA’s Medwatch.

A version of this article appeared on Medscape.com.

Even before the presidential election, the Federal Trade Commission’s (FTC) national ban on noncompete clauses faced a tough battle for survival in the courts. 

Now, legal specialists forecast a grim prognosis for the ban under Donald Trump’s return to the White House.

In April 2024, a divided FTC board approved a rule that would ban most noncompete agreements, which are the bane of many physicians in the states where they’re allowed. 

But a federal district’s court ruling put the ban on hold, and the Trump administration isn’t expected to support lifting the ban. 

“It is likely that the Trump administration will decline to defend the rule and may not even appeal the district court’s ruling, which means that the ban on noncompetes will not go into effect,” Steven Lubet, JD, a professor emeritus at Northwestern University Pritzker School of Law, Chicago, Illinois, said in an interview.

 

What’s in a Noncompete Clause?

Noncompete clauses in employee contracts typically restrict when and where workers can take future jobs. In medicine, supporters argue that the clauses are fair. Hospitals and practices provide a base of patients to physicians, they say, in return for their agreement not to go work for a competitor. 

But those opposed to these clauses argue that the restrictions harm careers and hurt patients by unfairly preventing physicians from moving to new jobs where they’re needed. 

At an April meeting, the FTC board voted 3 to 2 to ban noncompete clauses; some nonprofit organizations and senior executives were expected to be exempt. The FTC estimated that the move would save the healthcare system alone as much as $194 billion over 10 years. 

“A pandemic killed a million people in this country, and there are doctors who cannot work because of a noncompete,” declared FTC Commissioner Alvaro Bedoya. 

Hospitals protested the move. In a statement, the general counsel for the American Hospital Association called it “bad law, bad policy, and a clear sign of an agency run amok” and said the FTC ignored “mountains of contrary legal precedent and evidence about its adverse impacts on the health care markets.”

Although the American Medical Association does not support a total ban, its House of Delegates adopted policies in 2023 to support the prohibition of noncompete contracts for physicians employed by for-profit and nonprofit hospitals, hospital systems, or staffing companies. 

 

Texas Federal Judge Intervenes to Halt Ban

The ban was supposed to take effect on Sept. 4, 2024. But Texas federal judge Ada E. Brown struck down the ban in an Aug. 20 decision. She ruled that the FTC went beyond its authority.

“The district court based its ruling on a very dubious distinction between ‘unfair practices,’ which the FTC may prohibit, and ‘unfair competition,’ which, according to the court, it may not,” said Lubet. 

In fact, the ban should stand, he said. “This is a classic case of the government intervening on behalf of consumers/patients by prohibiting an unfair and harmful employment practice,” Lubet said. 

Amanda Hill, an attorney in Austin, Texas, who trains physicians about how to negotiate contracts, has a different take. “The Federal Trade Commission came down hard, and honestly, it really overstepped,” she said in an interview. “Congress needs to write laws, not regulatory bodies. I think all the lawyers went: ‘Good try, but you’re not going to get anywhere with that.’ ”

She noted that physicians themselves are divided over the value of noncompete clauses. “I would say 80% of my clients can’t stand noncompetes.” But another 20% own their own practices and hate the idea of losing their physicians to competitors, she said. 

 

Trump Isn’t Seen as Likely to Support Ban

While the Biden administration firmly supported a ban on noncompete clauses, there isn’t a strict Democratic-Republican divide over whether the agreements are a good idea. Some red states have embraced bans, and Hill said this can make sense from a Republican point of view: “We don’t want to run doctors out of town and out of the state because they think they’re going to be bound by big hospitals and corporate interests.”

In fact, former Florida congressman Matt Gaetz, a Republican briefly tapped as President-elect Trump’s nominee for attorney general, supports noncompete clauses. He filed a friend-of-the-court brief with the Texas judge that supported the FTC’s ruling, saying it is a “vindication of economic freedom and free enterprise.” 

But Republicans generally “believe that federal agencies are going too far and beyond the power granted to them by Congress,” Atlanta, Georgia, attorney Benjamin Fink, Esq., said in an interview.

And Trump is no fan of the FTC and its chair, Lina Khan, who may step down. Observers don’t expect that the Trump administration or a newly constituted FTC board will support an appeal of the Texas judge’s ruling.

“I don’t think anybody else — another agency or a private party — could step in place of the FTC if the FTC declines to defend the ban,” Atlanta attorney Neal F. Weinrich, Esq., said in an interview. In that case, “I think it ends.”

Attorneys Weinrich and Fink work at the same firm, which handles noncompete agreements for physicians. 

 

Noncompete Ban Advocates Turn to States 

Even if Kamala Harris had won the presidency, a national ban on noncompete clauses would have faced an uphill battle at the Supreme Court. 

“The Supreme Court majority has been unsympathetic to administrative agencies, interpreting their authority very narrowly,” said Lubet.

So what happens to noncompete clauses now? While bipartisan bills in Congress have tried to ban them, legislation is unlikely to pass now that Republicans will control both the House and Senate, Fink said. 

According to a recent article, 12 states prohibit noncompete clauses for physicians: Alabama, California, Colorado, Delaware, Massachusetts, Montana, New Hampshire, New Mexico, North Dakota, Oklahoma, Rhode Island, and South Dakota. 

The remaining states allow noncompetes in some form, often excluding them for employees earning below a certain threshold. For example, in Oregon, noncompete agreements may apply to employees earning more than $113,241. Most states have provisions to adjust the threshold annually. The District of Columbia permits 2-year noncompetes for “medical specialists” earning over $250,000 annually. 

Indiana employers can no longer enter into noncompete agreements with primary care providers. Other specialties may be subject to the clauses, except when the physician terminates the contract for cause or when an employer terminates the contract without cause. 

“I definitely think states are going to continue to restrict the use of noncompetes,” Fink said. 

Lubet has no disclosures. Hill, Fink, and Weinrich represent physicians in contract negotiations.

A version of this article appeared on Medscape.com.

Even before the presidential election, the Federal Trade Commission’s (FTC) national ban on noncompete clauses faced a tough battle for survival in the courts. 

Now, legal specialists forecast a grim prognosis for the ban under Donald Trump’s return to the White House.

In April 2024, a divided FTC board approved a rule that would ban most noncompete agreements, which are the bane of many physicians in the states where they’re allowed. 

But a federal district’s court ruling put the ban on hold, and the Trump administration isn’t expected to support lifting the ban. 

“It is likely that the Trump administration will decline to defend the rule and may not even appeal the district court’s ruling, which means that the ban on noncompetes will not go into effect,” Steven Lubet, JD, a professor emeritus at Northwestern University Pritzker School of Law, Chicago, Illinois, said in an interview.

 

What’s in a Noncompete Clause?

Noncompete clauses in employee contracts typically restrict when and where workers can take future jobs. In medicine, supporters argue that the clauses are fair. Hospitals and practices provide a base of patients to physicians, they say, in return for their agreement not to go work for a competitor. 

But those opposed to these clauses argue that the restrictions harm careers and hurt patients by unfairly preventing physicians from moving to new jobs where they’re needed. 

At an April meeting, the FTC board voted 3 to 2 to ban noncompete clauses; some nonprofit organizations and senior executives were expected to be exempt. The FTC estimated that the move would save the healthcare system alone as much as $194 billion over 10 years. 

“A pandemic killed a million people in this country, and there are doctors who cannot work because of a noncompete,” declared FTC Commissioner Alvaro Bedoya. 

Hospitals protested the move. In a statement, the general counsel for the American Hospital Association called it “bad law, bad policy, and a clear sign of an agency run amok” and said the FTC ignored “mountains of contrary legal precedent and evidence about its adverse impacts on the health care markets.”

Although the American Medical Association does not support a total ban, its House of Delegates adopted policies in 2023 to support the prohibition of noncompete contracts for physicians employed by for-profit and nonprofit hospitals, hospital systems, or staffing companies. 

 

Texas Federal Judge Intervenes to Halt Ban

The ban was supposed to take effect on Sept. 4, 2024. But Texas federal judge Ada E. Brown struck down the ban in an Aug. 20 decision. She ruled that the FTC went beyond its authority.

“The district court based its ruling on a very dubious distinction between ‘unfair practices,’ which the FTC may prohibit, and ‘unfair competition,’ which, according to the court, it may not,” said Lubet. 

In fact, the ban should stand, he said. “This is a classic case of the government intervening on behalf of consumers/patients by prohibiting an unfair and harmful employment practice,” Lubet said. 

Amanda Hill, an attorney in Austin, Texas, who trains physicians about how to negotiate contracts, has a different take. “The Federal Trade Commission came down hard, and honestly, it really overstepped,” she said in an interview. “Congress needs to write laws, not regulatory bodies. I think all the lawyers went: ‘Good try, but you’re not going to get anywhere with that.’ ”

She noted that physicians themselves are divided over the value of noncompete clauses. “I would say 80% of my clients can’t stand noncompetes.” But another 20% own their own practices and hate the idea of losing their physicians to competitors, she said. 

 

Trump Isn’t Seen as Likely to Support Ban

While the Biden administration firmly supported a ban on noncompete clauses, there isn’t a strict Democratic-Republican divide over whether the agreements are a good idea. Some red states have embraced bans, and Hill said this can make sense from a Republican point of view: “We don’t want to run doctors out of town and out of the state because they think they’re going to be bound by big hospitals and corporate interests.”

In fact, former Florida congressman Matt Gaetz, a Republican briefly tapped as President-elect Trump’s nominee for attorney general, supports noncompete clauses. He filed a friend-of-the-court brief with the Texas judge that supported the FTC’s ruling, saying it is a “vindication of economic freedom and free enterprise.” 

But Republicans generally “believe that federal agencies are going too far and beyond the power granted to them by Congress,” Atlanta, Georgia, attorney Benjamin Fink, Esq., said in an interview.

And Trump is no fan of the FTC and its chair, Lina Khan, who may step down. Observers don’t expect that the Trump administration or a newly constituted FTC board will support an appeal of the Texas judge’s ruling.

“I don’t think anybody else — another agency or a private party — could step in place of the FTC if the FTC declines to defend the ban,” Atlanta attorney Neal F. Weinrich, Esq., said in an interview. In that case, “I think it ends.”

Attorneys Weinrich and Fink work at the same firm, which handles noncompete agreements for physicians. 

 

Noncompete Ban Advocates Turn to States 

Even if Kamala Harris had won the presidency, a national ban on noncompete clauses would have faced an uphill battle at the Supreme Court. 

“The Supreme Court majority has been unsympathetic to administrative agencies, interpreting their authority very narrowly,” said Lubet.

So what happens to noncompete clauses now? While bipartisan bills in Congress have tried to ban them, legislation is unlikely to pass now that Republicans will control both the House and Senate, Fink said. 

According to a recent article, 12 states prohibit noncompete clauses for physicians: Alabama, California, Colorado, Delaware, Massachusetts, Montana, New Hampshire, New Mexico, North Dakota, Oklahoma, Rhode Island, and South Dakota. 

The remaining states allow noncompetes in some form, often excluding them for employees earning below a certain threshold. For example, in Oregon, noncompete agreements may apply to employees earning more than $113,241. Most states have provisions to adjust the threshold annually. The District of Columbia permits 2-year noncompetes for “medical specialists” earning over $250,000 annually. 

Indiana employers can no longer enter into noncompete agreements with primary care providers. Other specialties may be subject to the clauses, except when the physician terminates the contract for cause or when an employer terminates the contract without cause. 

“I definitely think states are going to continue to restrict the use of noncompetes,” Fink said. 

Lubet has no disclosures. Hill, Fink, and Weinrich represent physicians in contract negotiations.

A version of this article appeared on Medscape.com.

Even before the presidential election, the Federal Trade Commission’s (FTC) national ban on noncompete clauses faced a tough battle for survival in the courts. 

Now, legal specialists forecast a grim prognosis for the ban under Donald Trump’s return to the White House.

In April 2024, a divided FTC board approved a rule that would ban most noncompete agreements, which are the bane of many physicians in the states where they’re allowed. 

But a federal district’s court ruling put the ban on hold, and the Trump administration isn’t expected to support lifting the ban. 

“It is likely that the Trump administration will decline to defend the rule and may not even appeal the district court’s ruling, which means that the ban on noncompetes will not go into effect,” Steven Lubet, JD, a professor emeritus at Northwestern University Pritzker School of Law, Chicago, Illinois, said in an interview.

 

What’s in a Noncompete Clause?

Noncompete clauses in employee contracts typically restrict when and where workers can take future jobs. In medicine, supporters argue that the clauses are fair. Hospitals and practices provide a base of patients to physicians, they say, in return for their agreement not to go work for a competitor. 

But those opposed to these clauses argue that the restrictions harm careers and hurt patients by unfairly preventing physicians from moving to new jobs where they’re needed. 

At an April meeting, the FTC board voted 3 to 2 to ban noncompete clauses; some nonprofit organizations and senior executives were expected to be exempt. The FTC estimated that the move would save the healthcare system alone as much as $194 billion over 10 years. 

“A pandemic killed a million people in this country, and there are doctors who cannot work because of a noncompete,” declared FTC Commissioner Alvaro Bedoya. 

Hospitals protested the move. In a statement, the general counsel for the American Hospital Association called it “bad law, bad policy, and a clear sign of an agency run amok” and said the FTC ignored “mountains of contrary legal precedent and evidence about its adverse impacts on the health care markets.”

Although the American Medical Association does not support a total ban, its House of Delegates adopted policies in 2023 to support the prohibition of noncompete contracts for physicians employed by for-profit and nonprofit hospitals, hospital systems, or staffing companies. 

 

Texas Federal Judge Intervenes to Halt Ban

The ban was supposed to take effect on Sept. 4, 2024. But Texas federal judge Ada E. Brown struck down the ban in an Aug. 20 decision. She ruled that the FTC went beyond its authority.

“The district court based its ruling on a very dubious distinction between ‘unfair practices,’ which the FTC may prohibit, and ‘unfair competition,’ which, according to the court, it may not,” said Lubet. 

In fact, the ban should stand, he said. “This is a classic case of the government intervening on behalf of consumers/patients by prohibiting an unfair and harmful employment practice,” Lubet said. 

Amanda Hill, an attorney in Austin, Texas, who trains physicians about how to negotiate contracts, has a different take. “The Federal Trade Commission came down hard, and honestly, it really overstepped,” she said in an interview. “Congress needs to write laws, not regulatory bodies. I think all the lawyers went: ‘Good try, but you’re not going to get anywhere with that.’ ”

She noted that physicians themselves are divided over the value of noncompete clauses. “I would say 80% of my clients can’t stand noncompetes.” But another 20% own their own practices and hate the idea of losing their physicians to competitors, she said. 

 

Trump Isn’t Seen as Likely to Support Ban

While the Biden administration firmly supported a ban on noncompete clauses, there isn’t a strict Democratic-Republican divide over whether the agreements are a good idea. Some red states have embraced bans, and Hill said this can make sense from a Republican point of view: “We don’t want to run doctors out of town and out of the state because they think they’re going to be bound by big hospitals and corporate interests.”

In fact, former Florida congressman Matt Gaetz, a Republican briefly tapped as President-elect Trump’s nominee for attorney general, supports noncompete clauses. He filed a friend-of-the-court brief with the Texas judge that supported the FTC’s ruling, saying it is a “vindication of economic freedom and free enterprise.” 

But Republicans generally “believe that federal agencies are going too far and beyond the power granted to them by Congress,” Atlanta, Georgia, attorney Benjamin Fink, Esq., said in an interview.

And Trump is no fan of the FTC and its chair, Lina Khan, who may step down. Observers don’t expect that the Trump administration or a newly constituted FTC board will support an appeal of the Texas judge’s ruling.

“I don’t think anybody else — another agency or a private party — could step in place of the FTC if the FTC declines to defend the ban,” Atlanta attorney Neal F. Weinrich, Esq., said in an interview. In that case, “I think it ends.”

Attorneys Weinrich and Fink work at the same firm, which handles noncompete agreements for physicians. 

 

Noncompete Ban Advocates Turn to States 

Even if Kamala Harris had won the presidency, a national ban on noncompete clauses would have faced an uphill battle at the Supreme Court. 

“The Supreme Court majority has been unsympathetic to administrative agencies, interpreting their authority very narrowly,” said Lubet.

So what happens to noncompete clauses now? While bipartisan bills in Congress have tried to ban them, legislation is unlikely to pass now that Republicans will control both the House and Senate, Fink said. 

According to a recent article, 12 states prohibit noncompete clauses for physicians: Alabama, California, Colorado, Delaware, Massachusetts, Montana, New Hampshire, New Mexico, North Dakota, Oklahoma, Rhode Island, and South Dakota. 

The remaining states allow noncompetes in some form, often excluding them for employees earning below a certain threshold. For example, in Oregon, noncompete agreements may apply to employees earning more than $113,241. Most states have provisions to adjust the threshold annually. The District of Columbia permits 2-year noncompetes for “medical specialists” earning over $250,000 annually. 

Indiana employers can no longer enter into noncompete agreements with primary care providers. Other specialties may be subject to the clauses, except when the physician terminates the contract for cause or when an employer terminates the contract without cause. 

“I definitely think states are going to continue to restrict the use of noncompetes,” Fink said. 

Lubet has no disclosures. Hill, Fink, and Weinrich represent physicians in contract negotiations.

A version of this article appeared on Medscape.com.

WASHINGTON — Investigational treatments aimed specifically at reducing pain in knee osteoarthritis (OA) are moving forward in parallel with disease-modifying approaches.

“We still have very few treatments for the pain of osteoarthritis…It worries me that people think the only way forward is structure modification. I think while we’re waiting for some drugs to be structure modifying, we still need more pain relief. About 70% of people can’t tolerate or shouldn’t be on a [nonsteroidal anti-inflammatory drug], and that leaves a large number of people with pain,” Philip Conaghan, MBBS, PhD, Chair of Musculoskeletal Medicine at the University of Leeds in England, said in an interview.

At the annual meeting of the American College of Rheumatology, Conaghan, who is also honorary consultant rheumatologist for the Leeds Teaching Hospitals NHS Trust, presented new data for two novel approaches, both targeting peripheral nociceptive pain signaling.

In a late-breaking poster, he presented phase 2 trial data on RTX-GRT7039 (resiniferatoxin [RTX]), an agonist of the transient receptor potential vanilloid 1 that is a driver of OA pain. The trial investigated the efficacy and safety of a single intra-articular injection of RTX-GRT7039 in people with knee OA.

And separately, in a late-breaking oral abstract session, Conaghan presented phase 2 trial safety and efficacy data for another investigational agent called LEVI-04, a first-in-class neurotrophin receptor fusion protein (p75NTR-Fc) that supplements the endogenous protein and provides analgesia via inhibition of NT-3 activity.

“I think both have potential to provide good pain relief, through slightly different mechanisms,” Conaghan said in an interview.

Asked to comment, session moderator Gregory C. Gardner, MD, emeritus professor in the Division of Rheumatology at the University of Washington, Seattle, said in an interview: “I think the results are really exciting terms of the ability to control pain to a significant degree in patients with osteoarthritis.”

However, Gardner also said, “The molecules can be very expensive ... so who do we give them to? Will insurance companies pay for this simply for OA pain? They improve function ... so clearly, [they] will be a boon to treating osteoarthritis, but do we give them to people with only more advanced forms of osteoarthritis or earlier on?”

Moreover, Gardner said, “One of my concerns about treating osteoarthritis is I don’t want to do too good of a job treating pain in somebody who has a biomechanically abnormal joint. ... You’ve got a knee that’s worn out some of the cartilage, and now you feel like you can go out and play soccer again. That’s not a good thing. That joint will wear out very quickly, even though it doesn’t feel pain.”

Another OA expert, Matlock Jeffries, MD, director of the Arthritis Research Unit at the Oklahoma Medical Research Foundation, Oklahoma City, said in an interview, “I think we don’t focus nearly enough on pain, and that’s [partly] because the [Food and Drug Administration] has defined endpoints for knee OA trials that are radiographic. ... Patients do not care what their joint space narrowing is. They care what their pain is. And joint space changes and pain do not correlate in knee OA. ... About 20% or 30% of patients who have completely normal x-rays have a lot of pain…I hope that we’ll have some new OA pain therapeutics in the future because that’s what patients actually care about.”

But Jeffries noted that it will be very important to ensure that these agents don’t produce significant side effects, as had been seen previously in several large industry-sponsored trials of drugs targeting nerve growth factors.

“The big concern that we have in the field ... is that the nerve growth factor antibody trials were all stopped because there was a low but persistent risk of rapidly progressive OA in a small percent of patients. I think one of the questions in the field is whether targeting other things having to do with OA pain is going to result in similar bad outcomes. I think the answer is probably not, but that’s one thing that people do worry about, and they never really figured out why the [rapidly progressive OA] was happening.”

 

‘Potential to Provide Meaningful and Sustained Analgesia’

The phase 2 trial of RTX-GRT7039, funded by manufacturer Grünenthal, enrolled 40 patients with a baseline visual analog pain score (VAS) of > 40 mm on motion for average joint pain in the target knee over the past 2 days with or without analgesic medication and Kellgren-Lawrence grades 2-4.

They were randomized to receive a single intra-articular injection of 2 mg or 4 mg RTX-GRT7039 within 1 minute after receiving 5 mL ropivacaine (0.5%) or 4 mg or 8 mg RTX-GRT7039 administered 15 minutes after 5 mL ropivacaine pretreatment, or equivalent placebo treatments plus ropivacaine.

Plasma samples were collected for up to 2 hours, and VAS pain scores were collected for up to 3 hours post injection.

Reductions in VAS scores from baseline in the treated knee were seen in all RTX treatment groups as early as day 8 post injection and were maintained up to 6 months, while no reductions in VAS pain on motion scores were seen in the placebo group.

At 3 months, the absolute baseline-adjusted reductions in VAS scores were similar for RTX 2 mg (–39.75), RTX 4 mg (–40.20), and RTX 8 mg (–30.25), while the reduction in the placebo group was just –8.50. At 6 months, the mean absolute reduction in VAS score was numerically greater in the RTX 2-mg (–46.49), RTX 4-mg (–43.40), and RTX 8-mg (–38.60) groups vs the group that received RTX 4 mg within 1 minute after receiving ropivacaine (–22.00).

At both 3 and 6 months, a higher proportion of patients receiving any dose of RTX-GRT7039 achieved ≥ 50% and ≥ 70% reduction in pain on motion, compared with those who received placebo. All RTX-GRT7039 treatment groups reported a greater improvement in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) total score than the placebo group at both 3 and 6 months.

Rates of treatment-emergent adverse events were similar between the RTX groups (85.7%-90.9%) and placebo (85.7%) and slightly lower in the group that received RTX 4 mg within 1 minute of receiving ropivacaine (60.0%).

There was a trend toward greater procedural/injection site pain in the RTX treatment groups, compared with placebo, most commonly arthralgia (37.5%), headache (17.5%), and back pain (10%). This tended to peak around 0.5 hours post injection and resolve by 1.5-3.0 hours.

No treatment-related serious adverse events occurred, and no treatment-emergent adverse events led to discontinuation or death.

“This early-phase trial indicates that RTX-GRT7039 has the potential to provide meaningful and sustained analgesia for patients with knee OA pain,” Conaghan and colleagues wrote in their poster.

The drug is now being evaluated in three phase 3 trials (NCT05248386, NCT05449132, and NCT05377489).

 

LEVI-04: Modulation of NT-3 Appears to Work Safely

LEVI-04 was evaluated in a phase 2, 20-week, 13-center (Europe and Hong Kong) randomized, double-blind, placebo-controlled trial in 518 people with knee OA who had WOMAC pain subscale scores ≥ 20, mean average daily pain numeric rating scale score of 4-9, and radiographic Kellgren-Lawrence grade ≥ 2.

They were randomized to a total of five infusions of placebo or 0.3 mg/kg, 0.1 mg/kg, or 2 mg/kg LEVI-04 from baseline through week 16, with safety follow-up to week 30.

The primary endpoint, change in WOMAC pain from baseline to weeks 5 and 17, was met for all three doses. At 17 weeks, those were –2.79, –2.89, and –3.08 for 0.3 mg, 1.0 mg, and 2 mg, respectively, vs –2.28 for placebo (all P < .05).

Secondary endpoints, including WOMAC physical function, WOMAC stiffness, and Patient Global Assessment, and > 50% pain responders, were also all met at weeks 5 and 17. More than 50% of the LEVI-04–treated patients reported ≥ 50% reduction in pain, and > 25% reported ≥ 75% reduction at weeks 5 and 17.

“So, this modulation of NT-3 is working,” Conaghan commented.

There were no increased incidences of severe adverse events, treatment-emergent adverse events, or joint pathologies, including rapidly progressive OA, compared with placebo.

There were more paresthesias reported with the active drug, 2-4 vs 1 with placebo. “That says to me that the drug is working and that it’s having an effect on peripheral nerves, but luckily these were all mild or moderate and didn’t lead to any study withdrawal or discontinuation,” Conaghan said.

Phase 3 trials are in the planning stages, he noted.

 

Other Approaches to Treating OA Pain

Other approaches to treating OA pain have included methotrexate, for which Conaghan was also a coauthor on one paper that came out earlier in 2024. “This presumably works by treating inflammation, but it’s not clear if that is within-joint inflammation or systemic inflammation,” he said in an interview.

Another approach, using the weight loss drug semaglutide, was presented in April 2024 at the 2024 World Congress on Osteoarthritis annual meeting and published in October 2024 in The New England Journal of Medicine

The trial involving RTX-GRT7039 was funded by Grünenthal, and some study coauthors are employees of the company. The trial involving LEVI-04 was funded by Levicept, and some study coauthors are employees of the company. Conaghan is a consultant and/or speaker for Eli Lilly, Eupraxia Pharmaceuticals, Formation Bio, Galapagos, Genascence, GlaxoSmithKline, Grünenthal, Janssen Pharmaceuticals, Kolon TissueGene, Levicept, Medipost, Moebius, Novartis, Pacira, Sandoz, Stryker Corporation, and Takeda. Gardner and Jeffries had no disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Investigational treatments aimed specifically at reducing pain in knee osteoarthritis (OA) are moving forward in parallel with disease-modifying approaches.

“We still have very few treatments for the pain of osteoarthritis…It worries me that people think the only way forward is structure modification. I think while we’re waiting for some drugs to be structure modifying, we still need more pain relief. About 70% of people can’t tolerate or shouldn’t be on a [nonsteroidal anti-inflammatory drug], and that leaves a large number of people with pain,” Philip Conaghan, MBBS, PhD, Chair of Musculoskeletal Medicine at the University of Leeds in England, said in an interview.

At the annual meeting of the American College of Rheumatology, Conaghan, who is also honorary consultant rheumatologist for the Leeds Teaching Hospitals NHS Trust, presented new data for two novel approaches, both targeting peripheral nociceptive pain signaling.

In a late-breaking poster, he presented phase 2 trial data on RTX-GRT7039 (resiniferatoxin [RTX]), an agonist of the transient receptor potential vanilloid 1 that is a driver of OA pain. The trial investigated the efficacy and safety of a single intra-articular injection of RTX-GRT7039 in people with knee OA.

And separately, in a late-breaking oral abstract session, Conaghan presented phase 2 trial safety and efficacy data for another investigational agent called LEVI-04, a first-in-class neurotrophin receptor fusion protein (p75NTR-Fc) that supplements the endogenous protein and provides analgesia via inhibition of NT-3 activity.

“I think both have potential to provide good pain relief, through slightly different mechanisms,” Conaghan said in an interview.

Asked to comment, session moderator Gregory C. Gardner, MD, emeritus professor in the Division of Rheumatology at the University of Washington, Seattle, said in an interview: “I think the results are really exciting terms of the ability to control pain to a significant degree in patients with osteoarthritis.”

However, Gardner also said, “The molecules can be very expensive ... so who do we give them to? Will insurance companies pay for this simply for OA pain? They improve function ... so clearly, [they] will be a boon to treating osteoarthritis, but do we give them to people with only more advanced forms of osteoarthritis or earlier on?”

Moreover, Gardner said, “One of my concerns about treating osteoarthritis is I don’t want to do too good of a job treating pain in somebody who has a biomechanically abnormal joint. ... You’ve got a knee that’s worn out some of the cartilage, and now you feel like you can go out and play soccer again. That’s not a good thing. That joint will wear out very quickly, even though it doesn’t feel pain.”

Another OA expert, Matlock Jeffries, MD, director of the Arthritis Research Unit at the Oklahoma Medical Research Foundation, Oklahoma City, said in an interview, “I think we don’t focus nearly enough on pain, and that’s [partly] because the [Food and Drug Administration] has defined endpoints for knee OA trials that are radiographic. ... Patients do not care what their joint space narrowing is. They care what their pain is. And joint space changes and pain do not correlate in knee OA. ... About 20% or 30% of patients who have completely normal x-rays have a lot of pain…I hope that we’ll have some new OA pain therapeutics in the future because that’s what patients actually care about.”

But Jeffries noted that it will be very important to ensure that these agents don’t produce significant side effects, as had been seen previously in several large industry-sponsored trials of drugs targeting nerve growth factors.

“The big concern that we have in the field ... is that the nerve growth factor antibody trials were all stopped because there was a low but persistent risk of rapidly progressive OA in a small percent of patients. I think one of the questions in the field is whether targeting other things having to do with OA pain is going to result in similar bad outcomes. I think the answer is probably not, but that’s one thing that people do worry about, and they never really figured out why the [rapidly progressive OA] was happening.”

 

‘Potential to Provide Meaningful and Sustained Analgesia’

The phase 2 trial of RTX-GRT7039, funded by manufacturer Grünenthal, enrolled 40 patients with a baseline visual analog pain score (VAS) of > 40 mm on motion for average joint pain in the target knee over the past 2 days with or without analgesic medication and Kellgren-Lawrence grades 2-4.

They were randomized to receive a single intra-articular injection of 2 mg or 4 mg RTX-GRT7039 within 1 minute after receiving 5 mL ropivacaine (0.5%) or 4 mg or 8 mg RTX-GRT7039 administered 15 minutes after 5 mL ropivacaine pretreatment, or equivalent placebo treatments plus ropivacaine.

Plasma samples were collected for up to 2 hours, and VAS pain scores were collected for up to 3 hours post injection.

Reductions in VAS scores from baseline in the treated knee were seen in all RTX treatment groups as early as day 8 post injection and were maintained up to 6 months, while no reductions in VAS pain on motion scores were seen in the placebo group.

At 3 months, the absolute baseline-adjusted reductions in VAS scores were similar for RTX 2 mg (–39.75), RTX 4 mg (–40.20), and RTX 8 mg (–30.25), while the reduction in the placebo group was just –8.50. At 6 months, the mean absolute reduction in VAS score was numerically greater in the RTX 2-mg (–46.49), RTX 4-mg (–43.40), and RTX 8-mg (–38.60) groups vs the group that received RTX 4 mg within 1 minute after receiving ropivacaine (–22.00).

At both 3 and 6 months, a higher proportion of patients receiving any dose of RTX-GRT7039 achieved ≥ 50% and ≥ 70% reduction in pain on motion, compared with those who received placebo. All RTX-GRT7039 treatment groups reported a greater improvement in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) total score than the placebo group at both 3 and 6 months.

Rates of treatment-emergent adverse events were similar between the RTX groups (85.7%-90.9%) and placebo (85.7%) and slightly lower in the group that received RTX 4 mg within 1 minute of receiving ropivacaine (60.0%).

There was a trend toward greater procedural/injection site pain in the RTX treatment groups, compared with placebo, most commonly arthralgia (37.5%), headache (17.5%), and back pain (10%). This tended to peak around 0.5 hours post injection and resolve by 1.5-3.0 hours.

No treatment-related serious adverse events occurred, and no treatment-emergent adverse events led to discontinuation or death.

“This early-phase trial indicates that RTX-GRT7039 has the potential to provide meaningful and sustained analgesia for patients with knee OA pain,” Conaghan and colleagues wrote in their poster.

The drug is now being evaluated in three phase 3 trials (NCT05248386, NCT05449132, and NCT05377489).

 

LEVI-04: Modulation of NT-3 Appears to Work Safely

LEVI-04 was evaluated in a phase 2, 20-week, 13-center (Europe and Hong Kong) randomized, double-blind, placebo-controlled trial in 518 people with knee OA who had WOMAC pain subscale scores ≥ 20, mean average daily pain numeric rating scale score of 4-9, and radiographic Kellgren-Lawrence grade ≥ 2.

They were randomized to a total of five infusions of placebo or 0.3 mg/kg, 0.1 mg/kg, or 2 mg/kg LEVI-04 from baseline through week 16, with safety follow-up to week 30.

The primary endpoint, change in WOMAC pain from baseline to weeks 5 and 17, was met for all three doses. At 17 weeks, those were –2.79, –2.89, and –3.08 for 0.3 mg, 1.0 mg, and 2 mg, respectively, vs –2.28 for placebo (all P < .05).

Secondary endpoints, including WOMAC physical function, WOMAC stiffness, and Patient Global Assessment, and > 50% pain responders, were also all met at weeks 5 and 17. More than 50% of the LEVI-04–treated patients reported ≥ 50% reduction in pain, and > 25% reported ≥ 75% reduction at weeks 5 and 17.

“So, this modulation of NT-3 is working,” Conaghan commented.

There were no increased incidences of severe adverse events, treatment-emergent adverse events, or joint pathologies, including rapidly progressive OA, compared with placebo.

There were more paresthesias reported with the active drug, 2-4 vs 1 with placebo. “That says to me that the drug is working and that it’s having an effect on peripheral nerves, but luckily these were all mild or moderate and didn’t lead to any study withdrawal or discontinuation,” Conaghan said.

Phase 3 trials are in the planning stages, he noted.

 

Other Approaches to Treating OA Pain

Other approaches to treating OA pain have included methotrexate, for which Conaghan was also a coauthor on one paper that came out earlier in 2024. “This presumably works by treating inflammation, but it’s not clear if that is within-joint inflammation or systemic inflammation,” he said in an interview.

Another approach, using the weight loss drug semaglutide, was presented in April 2024 at the 2024 World Congress on Osteoarthritis annual meeting and published in October 2024 in The New England Journal of Medicine

The trial involving RTX-GRT7039 was funded by Grünenthal, and some study coauthors are employees of the company. The trial involving LEVI-04 was funded by Levicept, and some study coauthors are employees of the company. Conaghan is a consultant and/or speaker for Eli Lilly, Eupraxia Pharmaceuticals, Formation Bio, Galapagos, Genascence, GlaxoSmithKline, Grünenthal, Janssen Pharmaceuticals, Kolon TissueGene, Levicept, Medipost, Moebius, Novartis, Pacira, Sandoz, Stryker Corporation, and Takeda. Gardner and Jeffries had no disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Investigational treatments aimed specifically at reducing pain in knee osteoarthritis (OA) are moving forward in parallel with disease-modifying approaches.

“We still have very few treatments for the pain of osteoarthritis…It worries me that people think the only way forward is structure modification. I think while we’re waiting for some drugs to be structure modifying, we still need more pain relief. About 70% of people can’t tolerate or shouldn’t be on a [nonsteroidal anti-inflammatory drug], and that leaves a large number of people with pain,” Philip Conaghan, MBBS, PhD, Chair of Musculoskeletal Medicine at the University of Leeds in England, said in an interview.

At the annual meeting of the American College of Rheumatology, Conaghan, who is also honorary consultant rheumatologist for the Leeds Teaching Hospitals NHS Trust, presented new data for two novel approaches, both targeting peripheral nociceptive pain signaling.

In a late-breaking poster, he presented phase 2 trial data on RTX-GRT7039 (resiniferatoxin [RTX]), an agonist of the transient receptor potential vanilloid 1 that is a driver of OA pain. The trial investigated the efficacy and safety of a single intra-articular injection of RTX-GRT7039 in people with knee OA.

And separately, in a late-breaking oral abstract session, Conaghan presented phase 2 trial safety and efficacy data for another investigational agent called LEVI-04, a first-in-class neurotrophin receptor fusion protein (p75NTR-Fc) that supplements the endogenous protein and provides analgesia via inhibition of NT-3 activity.

“I think both have potential to provide good pain relief, through slightly different mechanisms,” Conaghan said in an interview.

Asked to comment, session moderator Gregory C. Gardner, MD, emeritus professor in the Division of Rheumatology at the University of Washington, Seattle, said in an interview: “I think the results are really exciting terms of the ability to control pain to a significant degree in patients with osteoarthritis.”

However, Gardner also said, “The molecules can be very expensive ... so who do we give them to? Will insurance companies pay for this simply for OA pain? They improve function ... so clearly, [they] will be a boon to treating osteoarthritis, but do we give them to people with only more advanced forms of osteoarthritis or earlier on?”

Moreover, Gardner said, “One of my concerns about treating osteoarthritis is I don’t want to do too good of a job treating pain in somebody who has a biomechanically abnormal joint. ... You’ve got a knee that’s worn out some of the cartilage, and now you feel like you can go out and play soccer again. That’s not a good thing. That joint will wear out very quickly, even though it doesn’t feel pain.”

Another OA expert, Matlock Jeffries, MD, director of the Arthritis Research Unit at the Oklahoma Medical Research Foundation, Oklahoma City, said in an interview, “I think we don’t focus nearly enough on pain, and that’s [partly] because the [Food and Drug Administration] has defined endpoints for knee OA trials that are radiographic. ... Patients do not care what their joint space narrowing is. They care what their pain is. And joint space changes and pain do not correlate in knee OA. ... About 20% or 30% of patients who have completely normal x-rays have a lot of pain…I hope that we’ll have some new OA pain therapeutics in the future because that’s what patients actually care about.”

But Jeffries noted that it will be very important to ensure that these agents don’t produce significant side effects, as had been seen previously in several large industry-sponsored trials of drugs targeting nerve growth factors.

“The big concern that we have in the field ... is that the nerve growth factor antibody trials were all stopped because there was a low but persistent risk of rapidly progressive OA in a small percent of patients. I think one of the questions in the field is whether targeting other things having to do with OA pain is going to result in similar bad outcomes. I think the answer is probably not, but that’s one thing that people do worry about, and they never really figured out why the [rapidly progressive OA] was happening.”

 

‘Potential to Provide Meaningful and Sustained Analgesia’

The phase 2 trial of RTX-GRT7039, funded by manufacturer Grünenthal, enrolled 40 patients with a baseline visual analog pain score (VAS) of > 40 mm on motion for average joint pain in the target knee over the past 2 days with or without analgesic medication and Kellgren-Lawrence grades 2-4.

They were randomized to receive a single intra-articular injection of 2 mg or 4 mg RTX-GRT7039 within 1 minute after receiving 5 mL ropivacaine (0.5%) or 4 mg or 8 mg RTX-GRT7039 administered 15 minutes after 5 mL ropivacaine pretreatment, or equivalent placebo treatments plus ropivacaine.

Plasma samples were collected for up to 2 hours, and VAS pain scores were collected for up to 3 hours post injection.

Reductions in VAS scores from baseline in the treated knee were seen in all RTX treatment groups as early as day 8 post injection and were maintained up to 6 months, while no reductions in VAS pain on motion scores were seen in the placebo group.

At 3 months, the absolute baseline-adjusted reductions in VAS scores were similar for RTX 2 mg (–39.75), RTX 4 mg (–40.20), and RTX 8 mg (–30.25), while the reduction in the placebo group was just –8.50. At 6 months, the mean absolute reduction in VAS score was numerically greater in the RTX 2-mg (–46.49), RTX 4-mg (–43.40), and RTX 8-mg (–38.60) groups vs the group that received RTX 4 mg within 1 minute after receiving ropivacaine (–22.00).

At both 3 and 6 months, a higher proportion of patients receiving any dose of RTX-GRT7039 achieved ≥ 50% and ≥ 70% reduction in pain on motion, compared with those who received placebo. All RTX-GRT7039 treatment groups reported a greater improvement in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) total score than the placebo group at both 3 and 6 months.

Rates of treatment-emergent adverse events were similar between the RTX groups (85.7%-90.9%) and placebo (85.7%) and slightly lower in the group that received RTX 4 mg within 1 minute of receiving ropivacaine (60.0%).

There was a trend toward greater procedural/injection site pain in the RTX treatment groups, compared with placebo, most commonly arthralgia (37.5%), headache (17.5%), and back pain (10%). This tended to peak around 0.5 hours post injection and resolve by 1.5-3.0 hours.

No treatment-related serious adverse events occurred, and no treatment-emergent adverse events led to discontinuation or death.

“This early-phase trial indicates that RTX-GRT7039 has the potential to provide meaningful and sustained analgesia for patients with knee OA pain,” Conaghan and colleagues wrote in their poster.

The drug is now being evaluated in three phase 3 trials (NCT05248386, NCT05449132, and NCT05377489).

 

LEVI-04: Modulation of NT-3 Appears to Work Safely

LEVI-04 was evaluated in a phase 2, 20-week, 13-center (Europe and Hong Kong) randomized, double-blind, placebo-controlled trial in 518 people with knee OA who had WOMAC pain subscale scores ≥ 20, mean average daily pain numeric rating scale score of 4-9, and radiographic Kellgren-Lawrence grade ≥ 2.

They were randomized to a total of five infusions of placebo or 0.3 mg/kg, 0.1 mg/kg, or 2 mg/kg LEVI-04 from baseline through week 16, with safety follow-up to week 30.

The primary endpoint, change in WOMAC pain from baseline to weeks 5 and 17, was met for all three doses. At 17 weeks, those were –2.79, –2.89, and –3.08 for 0.3 mg, 1.0 mg, and 2 mg, respectively, vs –2.28 for placebo (all P < .05).

Secondary endpoints, including WOMAC physical function, WOMAC stiffness, and Patient Global Assessment, and > 50% pain responders, were also all met at weeks 5 and 17. More than 50% of the LEVI-04–treated patients reported ≥ 50% reduction in pain, and > 25% reported ≥ 75% reduction at weeks 5 and 17.

“So, this modulation of NT-3 is working,” Conaghan commented.

There were no increased incidences of severe adverse events, treatment-emergent adverse events, or joint pathologies, including rapidly progressive OA, compared with placebo.

There were more paresthesias reported with the active drug, 2-4 vs 1 with placebo. “That says to me that the drug is working and that it’s having an effect on peripheral nerves, but luckily these were all mild or moderate and didn’t lead to any study withdrawal or discontinuation,” Conaghan said.

Phase 3 trials are in the planning stages, he noted.

 

Other Approaches to Treating OA Pain

Other approaches to treating OA pain have included methotrexate, for which Conaghan was also a coauthor on one paper that came out earlier in 2024. “This presumably works by treating inflammation, but it’s not clear if that is within-joint inflammation or systemic inflammation,” he said in an interview.

Another approach, using the weight loss drug semaglutide, was presented in April 2024 at the 2024 World Congress on Osteoarthritis annual meeting and published in October 2024 in The New England Journal of Medicine

The trial involving RTX-GRT7039 was funded by Grünenthal, and some study coauthors are employees of the company. The trial involving LEVI-04 was funded by Levicept, and some study coauthors are employees of the company. Conaghan is a consultant and/or speaker for Eli Lilly, Eupraxia Pharmaceuticals, Formation Bio, Galapagos, Genascence, GlaxoSmithKline, Grünenthal, Janssen Pharmaceuticals, Kolon TissueGene, Levicept, Medipost, Moebius, Novartis, Pacira, Sandoz, Stryker Corporation, and Takeda. Gardner and Jeffries had no disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with serum ferritin levels higher than 1000 μg/L show a 91% increased risk for any fracture, with a doubled risk for vertebral and humerus fractures compared with those without iron overload.

 

METHODOLOGY:

• Iron overload’s association with decreased bone mineral density is established, but its relationship to osteoporotic fracture risk has remained understudied and inconsistent across fracture sites.
• Researchers conducted a population-based cohort study using a UK general practice database to evaluate the fracture risk in 20,264 patients with iron overload and 192,956 matched controls without elevated ferritin (mean age, 57 years; about 40% women).
• Patients with iron overload were identified as those with laboratory-confirmed iron overload (serum ferritin levels > 1000 μg/L; n = 13,510) or a diagnosis of an iron overloading disorder, such as thalassemia major, sickle cell disease, or hemochromatosis (n = 6754).
• The primary outcome of interest was the first occurrence of an osteoporotic fracture after the diagnosis of iron overload or first record of high ferritin.
• A sensitivity analysis was conducted to check the impact of laboratory-confirmed iron overload on the risk for osteoporotic fracture compared with a diagnosis code without elevated ferritin.

TAKEAWAY:

• In the overall cohort, patients with iron overload had a 55% higher risk for any osteoporotic fracture than control individuals (adjusted hazard ratio [aHR], 1.55; 95% CI, 1.42-1.68), with the highest risk observed for vertebral fractures (aHR, 1.97; 95% CI, 1.63-2.37) and humerus fractures (aHR, 1.91; 95% CI, 1.61-2.26).
• Patients with laboratory-confirmed iron overload showed a 91% increased risk for any fracture (aHR, 1.91; 95% CI, 1.73-2.10), with a 2.5-fold higher risk observed for vertebral fractures (aHR, 2.51; 95% CI, 2.01-3.12), followed by humerus fractures (aHR, 2.41; 95% CI, 1.96-2.95).
• There was no increased risk for fracture at any site in patients with a diagnosis of an iron overloading disorder but no laboratory-confirmed iron overload.
• No sex-specific differences were identified in the association between iron overload and fracture risk.

IN PRACTICE:

“The main clinical message from our findings is that clinicians should consider iron overloading as a risk factor for fracture. Importantly, among high-risk patients presenting with serum ferritin values exceeding 1000 μg/L, osteoporosis screening and treatment strategies should be initiated in accordance with the guidelines for patients with hepatic disease,” the authors wrote.

 

SOURCE:

The study was led by Andrea Michelle Burden, PhD, Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zürich in Switzerland, and was published online in The Journal of Clinical Endocrinology & Metabolism.

 

LIMITATIONS:

The study could not assess the duration of iron overload on fracture risk, and thus, patients could enter the cohort with a single elevated serum ferritin value that may not have reflected systemic iron overload. The authors also acknowledged potential exposure misclassification among matched control individuals because only 2.9% had a serum ferritin value available at baseline. Also, researchers were unable to adjust for inflammation status due to the limited availability of C-reactive protein measurements and the lack of leukocyte count data in primary care settings.

 

DISCLOSURES:

This study received support through grants from the German Research Foundation. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients with serum ferritin levels higher than 1000 μg/L show a 91% increased risk for any fracture, with a doubled risk for vertebral and humerus fractures compared with those without iron overload.

 

METHODOLOGY:

• Iron overload’s association with decreased bone mineral density is established, but its relationship to osteoporotic fracture risk has remained understudied and inconsistent across fracture sites.
• Researchers conducted a population-based cohort study using a UK general practice database to evaluate the fracture risk in 20,264 patients with iron overload and 192,956 matched controls without elevated ferritin (mean age, 57 years; about 40% women).
• Patients with iron overload were identified as those with laboratory-confirmed iron overload (serum ferritin levels > 1000 μg/L; n = 13,510) or a diagnosis of an iron overloading disorder, such as thalassemia major, sickle cell disease, or hemochromatosis (n = 6754).
• The primary outcome of interest was the first occurrence of an osteoporotic fracture after the diagnosis of iron overload or first record of high ferritin.
• A sensitivity analysis was conducted to check the impact of laboratory-confirmed iron overload on the risk for osteoporotic fracture compared with a diagnosis code without elevated ferritin.

TAKEAWAY:

• In the overall cohort, patients with iron overload had a 55% higher risk for any osteoporotic fracture than control individuals (adjusted hazard ratio [aHR], 1.55; 95% CI, 1.42-1.68), with the highest risk observed for vertebral fractures (aHR, 1.97; 95% CI, 1.63-2.37) and humerus fractures (aHR, 1.91; 95% CI, 1.61-2.26).
• Patients with laboratory-confirmed iron overload showed a 91% increased risk for any fracture (aHR, 1.91; 95% CI, 1.73-2.10), with a 2.5-fold higher risk observed for vertebral fractures (aHR, 2.51; 95% CI, 2.01-3.12), followed by humerus fractures (aHR, 2.41; 95% CI, 1.96-2.95).
• There was no increased risk for fracture at any site in patients with a diagnosis of an iron overloading disorder but no laboratory-confirmed iron overload.
• No sex-specific differences were identified in the association between iron overload and fracture risk.

IN PRACTICE:

“The main clinical message from our findings is that clinicians should consider iron overloading as a risk factor for fracture. Importantly, among high-risk patients presenting with serum ferritin values exceeding 1000 μg/L, osteoporosis screening and treatment strategies should be initiated in accordance with the guidelines for patients with hepatic disease,” the authors wrote.

 

SOURCE:

The study was led by Andrea Michelle Burden, PhD, Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zürich in Switzerland, and was published online in The Journal of Clinical Endocrinology & Metabolism.

 

LIMITATIONS:

The study could not assess the duration of iron overload on fracture risk, and thus, patients could enter the cohort with a single elevated serum ferritin value that may not have reflected systemic iron overload. The authors also acknowledged potential exposure misclassification among matched control individuals because only 2.9% had a serum ferritin value available at baseline. Also, researchers were unable to adjust for inflammation status due to the limited availability of C-reactive protein measurements and the lack of leukocyte count data in primary care settings.

 

DISCLOSURES:

This study received support through grants from the German Research Foundation. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients with serum ferritin levels higher than 1000 μg/L show a 91% increased risk for any fracture, with a doubled risk for vertebral and humerus fractures compared with those without iron overload.

 

METHODOLOGY:

• Iron overload’s association with decreased bone mineral density is established, but its relationship to osteoporotic fracture risk has remained understudied and inconsistent across fracture sites.
• Researchers conducted a population-based cohort study using a UK general practice database to evaluate the fracture risk in 20,264 patients with iron overload and 192,956 matched controls without elevated ferritin (mean age, 57 years; about 40% women).
• Patients with iron overload were identified as those with laboratory-confirmed iron overload (serum ferritin levels > 1000 μg/L; n = 13,510) or a diagnosis of an iron overloading disorder, such as thalassemia major, sickle cell disease, or hemochromatosis (n = 6754).
• The primary outcome of interest was the first occurrence of an osteoporotic fracture after the diagnosis of iron overload or first record of high ferritin.
• A sensitivity analysis was conducted to check the impact of laboratory-confirmed iron overload on the risk for osteoporotic fracture compared with a diagnosis code without elevated ferritin.

TAKEAWAY:

• In the overall cohort, patients with iron overload had a 55% higher risk for any osteoporotic fracture than control individuals (adjusted hazard ratio [aHR], 1.55; 95% CI, 1.42-1.68), with the highest risk observed for vertebral fractures (aHR, 1.97; 95% CI, 1.63-2.37) and humerus fractures (aHR, 1.91; 95% CI, 1.61-2.26).
• Patients with laboratory-confirmed iron overload showed a 91% increased risk for any fracture (aHR, 1.91; 95% CI, 1.73-2.10), with a 2.5-fold higher risk observed for vertebral fractures (aHR, 2.51; 95% CI, 2.01-3.12), followed by humerus fractures (aHR, 2.41; 95% CI, 1.96-2.95).
• There was no increased risk for fracture at any site in patients with a diagnosis of an iron overloading disorder but no laboratory-confirmed iron overload.
• No sex-specific differences were identified in the association between iron overload and fracture risk.

IN PRACTICE:

“The main clinical message from our findings is that clinicians should consider iron overloading as a risk factor for fracture. Importantly, among high-risk patients presenting with serum ferritin values exceeding 1000 μg/L, osteoporosis screening and treatment strategies should be initiated in accordance with the guidelines for patients with hepatic disease,” the authors wrote.

 

SOURCE:

The study was led by Andrea Michelle Burden, PhD, Institute of Pharmaceutical Sciences, Department of Chemistry and Applied Biosciences, ETH Zürich in Switzerland, and was published online in The Journal of Clinical Endocrinology & Metabolism.

 

LIMITATIONS:

The study could not assess the duration of iron overload on fracture risk, and thus, patients could enter the cohort with a single elevated serum ferritin value that may not have reflected systemic iron overload. The authors also acknowledged potential exposure misclassification among matched control individuals because only 2.9% had a serum ferritin value available at baseline. Also, researchers were unable to adjust for inflammation status due to the limited availability of C-reactive protein measurements and the lack of leukocyte count data in primary care settings.

 

DISCLOSURES:

This study received support through grants from the German Research Foundation. The authors declared no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

The word “malnutrition” probably brings to mind images of very thin patients with catabolic illness. But it really just means “poor nutrition,” which can — and often does — apply to patients with overweight or obesity.

That’s because malnutrition doesn’t occur simply because of a lack of calories, but rather because there is a gap in the nutrition the body requires and the nutrition it receives.

Each day, clinicians see patients with chronic conditions related to malnutrition. That list includes diabetes and hypertension, which can be promoted by excess intake of certain nutrients (carbohydrates and sodium) or inadequate intake of others (fiber, protein, potassium, magnesium, and calcium).

 

Diet Education Is Vital in Chronic Disease Management

Diet education is without a doubt a core pillar of chronic disease management. Nutrition therapy is recommended in treatment guidelines for the management of some of the most commonly seen chronic conditions such as hypertension, diabetes, and kidney disease. But in one study, only 58% of physicians, nurses and other health professionals surveyed had received formal nutrition education and only 40% were confident in their ability to provide nutrition education to patients.

As a registered dietitian, I welcome referrals for both prevention and management of chronic diseases with open arms. But medical nutrition therapy with a registered dietitian may not be realistic for all patients owing to financial, geographic, or other constraints. So, their best option may be the few minutes that a physician or physician extender has to spare at the end of their appointment.

But time constraints may result in clinicians turning to short, easy-to-remember messages such as “Don’t eat anything white” or “Only shop the edges of the grocery store.” Although catchy, this type of advice can inadvertently encourage patients to skip over foods that are actually very nutrient dense. For example, white foods such as onions, turnips, mushrooms, cauliflower, and even popcorn are low in calories and high in nutritional value. The center aisles of the grocery store may harbor high-carbohydrate breakfast cereals and potato chips, but they are also home to legumes, nuts, and canned and frozen fruits and vegetables.

What may be more effective is educating the patient on the importance of focusing on the nutrient density of foods, rather than simply limiting certain food groups or colors.

 

How to Work Nutrient Density into the Conversation

Nutrient density is a concept that refers to the proportion of nutrients to calories in a food item: essentially, a food’s qualitative nutritional value. It provides more depth than simply referring to foods as being high or low in calories, healthy or unhealthy, or good or bad.

Educating patients about nutrition density and encouraging a focus on foods that are low in calories and high in vitamins and minerals can help address micronutrient deficiencies, which may be more common than previously thought and linked to the chronic diseases that we see daily. It is worth noting that some foods that are not low in calories are still nutrient dense. Avocados, liver, and nuts come to mind as foods that are high in calories, but they have additional nutrients such as fiber, potassium, antioxidants, vitamin A, iron, and selenium that can still make them an excellent choice if they are part of a well-balanced diet.

I fear that we often underestimate our patients. We worry that not providing them with a list of acceptable foods will set them up for failure. But, in my experience, that list of “good” and “bad” foods may be useful for a week or so but will eventually become lost on the fridge under children’s artwork and save-the-dates.

Patients know that potato chips offer little more than fat, carbs, and salt and that they’re a poor choice for long-term health. What they might not know is that cocktail peanuts can also satisfy the craving for a salty snack, with more than four times the protein, twice the fiber, and just over half of the sodium found in the same serving size of regular salted potato chips. Peanuts have the added bonus of being high in heart-healthy monounsaturated fatty acids.

The best thing that clinicians can do with just a few minutes of time for diet education is to talk to patients about the nutrient density of whole foods and caution patients against highly processed foods, because processing can decrease nutritional content. Our most effective option is to explain why a varied diet with focus on fruits, vegetables, lean protein, nuts, legumes, and healthy fats is beneficial for cardiovascular and metabolic health. After that, all that is left is to trust the patient to make the right choices for their health.

Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The word “malnutrition” probably brings to mind images of very thin patients with catabolic illness. But it really just means “poor nutrition,” which can — and often does — apply to patients with overweight or obesity.

That’s because malnutrition doesn’t occur simply because of a lack of calories, but rather because there is a gap in the nutrition the body requires and the nutrition it receives.

Each day, clinicians see patients with chronic conditions related to malnutrition. That list includes diabetes and hypertension, which can be promoted by excess intake of certain nutrients (carbohydrates and sodium) or inadequate intake of others (fiber, protein, potassium, magnesium, and calcium).

 

Diet Education Is Vital in Chronic Disease Management

Diet education is without a doubt a core pillar of chronic disease management. Nutrition therapy is recommended in treatment guidelines for the management of some of the most commonly seen chronic conditions such as hypertension, diabetes, and kidney disease. But in one study, only 58% of physicians, nurses and other health professionals surveyed had received formal nutrition education and only 40% were confident in their ability to provide nutrition education to patients.

As a registered dietitian, I welcome referrals for both prevention and management of chronic diseases with open arms. But medical nutrition therapy with a registered dietitian may not be realistic for all patients owing to financial, geographic, or other constraints. So, their best option may be the few minutes that a physician or physician extender has to spare at the end of their appointment.

But time constraints may result in clinicians turning to short, easy-to-remember messages such as “Don’t eat anything white” or “Only shop the edges of the grocery store.” Although catchy, this type of advice can inadvertently encourage patients to skip over foods that are actually very nutrient dense. For example, white foods such as onions, turnips, mushrooms, cauliflower, and even popcorn are low in calories and high in nutritional value. The center aisles of the grocery store may harbor high-carbohydrate breakfast cereals and potato chips, but they are also home to legumes, nuts, and canned and frozen fruits and vegetables.

What may be more effective is educating the patient on the importance of focusing on the nutrient density of foods, rather than simply limiting certain food groups or colors.

 

How to Work Nutrient Density into the Conversation

Nutrient density is a concept that refers to the proportion of nutrients to calories in a food item: essentially, a food’s qualitative nutritional value. It provides more depth than simply referring to foods as being high or low in calories, healthy or unhealthy, or good or bad.

Educating patients about nutrition density and encouraging a focus on foods that are low in calories and high in vitamins and minerals can help address micronutrient deficiencies, which may be more common than previously thought and linked to the chronic diseases that we see daily. It is worth noting that some foods that are not low in calories are still nutrient dense. Avocados, liver, and nuts come to mind as foods that are high in calories, but they have additional nutrients such as fiber, potassium, antioxidants, vitamin A, iron, and selenium that can still make them an excellent choice if they are part of a well-balanced diet.

I fear that we often underestimate our patients. We worry that not providing them with a list of acceptable foods will set them up for failure. But, in my experience, that list of “good” and “bad” foods may be useful for a week or so but will eventually become lost on the fridge under children’s artwork and save-the-dates.

Patients know that potato chips offer little more than fat, carbs, and salt and that they’re a poor choice for long-term health. What they might not know is that cocktail peanuts can also satisfy the craving for a salty snack, with more than four times the protein, twice the fiber, and just over half of the sodium found in the same serving size of regular salted potato chips. Peanuts have the added bonus of being high in heart-healthy monounsaturated fatty acids.

The best thing that clinicians can do with just a few minutes of time for diet education is to talk to patients about the nutrient density of whole foods and caution patients against highly processed foods, because processing can decrease nutritional content. Our most effective option is to explain why a varied diet with focus on fruits, vegetables, lean protein, nuts, legumes, and healthy fats is beneficial for cardiovascular and metabolic health. After that, all that is left is to trust the patient to make the right choices for their health.

Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The word “malnutrition” probably brings to mind images of very thin patients with catabolic illness. But it really just means “poor nutrition,” which can — and often does — apply to patients with overweight or obesity.

That’s because malnutrition doesn’t occur simply because of a lack of calories, but rather because there is a gap in the nutrition the body requires and the nutrition it receives.

Each day, clinicians see patients with chronic conditions related to malnutrition. That list includes diabetes and hypertension, which can be promoted by excess intake of certain nutrients (carbohydrates and sodium) or inadequate intake of others (fiber, protein, potassium, magnesium, and calcium).

 

Diet Education Is Vital in Chronic Disease Management

Diet education is without a doubt a core pillar of chronic disease management. Nutrition therapy is recommended in treatment guidelines for the management of some of the most commonly seen chronic conditions such as hypertension, diabetes, and kidney disease. But in one study, only 58% of physicians, nurses and other health professionals surveyed had received formal nutrition education and only 40% were confident in their ability to provide nutrition education to patients.

As a registered dietitian, I welcome referrals for both prevention and management of chronic diseases with open arms. But medical nutrition therapy with a registered dietitian may not be realistic for all patients owing to financial, geographic, or other constraints. So, their best option may be the few minutes that a physician or physician extender has to spare at the end of their appointment.

But time constraints may result in clinicians turning to short, easy-to-remember messages such as “Don’t eat anything white” or “Only shop the edges of the grocery store.” Although catchy, this type of advice can inadvertently encourage patients to skip over foods that are actually very nutrient dense. For example, white foods such as onions, turnips, mushrooms, cauliflower, and even popcorn are low in calories and high in nutritional value. The center aisles of the grocery store may harbor high-carbohydrate breakfast cereals and potato chips, but they are also home to legumes, nuts, and canned and frozen fruits and vegetables.

What may be more effective is educating the patient on the importance of focusing on the nutrient density of foods, rather than simply limiting certain food groups or colors.

 

How to Work Nutrient Density into the Conversation

Nutrient density is a concept that refers to the proportion of nutrients to calories in a food item: essentially, a food’s qualitative nutritional value. It provides more depth than simply referring to foods as being high or low in calories, healthy or unhealthy, or good or bad.

Educating patients about nutrition density and encouraging a focus on foods that are low in calories and high in vitamins and minerals can help address micronutrient deficiencies, which may be more common than previously thought and linked to the chronic diseases that we see daily. It is worth noting that some foods that are not low in calories are still nutrient dense. Avocados, liver, and nuts come to mind as foods that are high in calories, but they have additional nutrients such as fiber, potassium, antioxidants, vitamin A, iron, and selenium that can still make them an excellent choice if they are part of a well-balanced diet.

I fear that we often underestimate our patients. We worry that not providing them with a list of acceptable foods will set them up for failure. But, in my experience, that list of “good” and “bad” foods may be useful for a week or so but will eventually become lost on the fridge under children’s artwork and save-the-dates.

Patients know that potato chips offer little more than fat, carbs, and salt and that they’re a poor choice for long-term health. What they might not know is that cocktail peanuts can also satisfy the craving for a salty snack, with more than four times the protein, twice the fiber, and just over half of the sodium found in the same serving size of regular salted potato chips. Peanuts have the added bonus of being high in heart-healthy monounsaturated fatty acids.

The best thing that clinicians can do with just a few minutes of time for diet education is to talk to patients about the nutrient density of whole foods and caution patients against highly processed foods, because processing can decrease nutritional content. Our most effective option is to explain why a varied diet with focus on fruits, vegetables, lean protein, nuts, legumes, and healthy fats is beneficial for cardiovascular and metabolic health. After that, all that is left is to trust the patient to make the right choices for their health.

Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Nearly every patient I start on incretin therapy for weight loss asks me the same question, which is, will I have to stay on this forever? The answer is probably yes, but I think it’s much more nuanced than that because A) forever is a long time and B) I think there are various ways to approach this.

I want people to start just saying, let’s see how this works, because not everyone’s going to lose the same amount of weight or respond in the same way. I say let’s try it, but don’t stop it suddenly. If we decide at some point you don’t need quite the same dose, we can reduce the dose and maybe even reduce the frequency of giving it, but you don’t want to stop cold turkey because you may well regain the weight, and that’s obviously not our desired outcome.

There have been multiple clinical trials in which people started on an incretin hormone, either a glucagon-like peptide 1 (GLP-1) receptor agonist or a dual hormone, and they’ve actually shown that stopping it and then continuing patients on a placebo vs active drug results in continued weight gain over time vs either weight maintenance or weight loss when they remain on the incretin hormone. Clearly, on average, people will regain the weight, but that isn’t always true. 

One of the things I think is really important is that, from the get-go on starting on these hormones, people start working with a lifestyle plan, whether it’s working with a coach or an online program. However they approach this, it’s important to start changing habits and increasing exercise.

I can’t say how important this is enough, because people need to increase their physical activity to enhance the benefits of these agents and also to help retain lean body mass. I don’t want people losing a large amount of lean body mass as they go through the process of weight loss. 

I set the stage for the fact that I expect people to adhere to a lifestyle program, and maybe losing weight with the medications is going to help them do even better because they’re going to see positive outcomes.

When they get to the point of weight maintenance, I think we need to reinforce lifestyle. I either go down on the dose given weekly or I start having patients take the dose every other week, for instance, as opposed to every week, and then sometimes every month. Depending on the patient, I get them potentially to a lower dose, and then they’re able to maintain the weight as long as they improved their lifestyle along with the changes in the medication.

I tell people we’ll work with the drug, we’ll work with their metabolic needs, that there are many benefits to being on incretin hormone therapy, but I think it’s important that we can do this on an individualized basis. The thing I don’t want to happen, though, is for people to start on it and then stop it, and then start on it and stop it because they may lose weight, regain weight, get side effects, get used to the side effects, stop it, and start it.

As we know, that’s not the best way to do this, and I think it’s not healthy for people to do that either. I know it’s been somewhat problematic with supply chain issues, but hopefully we’ll be able to start these agents, reach the desired outcome in terms of weight loss, and then help patients maintain that weight with a combination of both medication and lifestyle.

Dr. Peters, professor, Department of Clinical Medicine, Keck School of Medicine; Director, University of Southern California Westside Center for Diabetes, Los Angeles, disclosed ties with Abbott Diabetes Care, Becton Dickinson; Boehringer Ingelheim Pharmaceuticals, Eli Lilly, Lexicon Pharmaceuticals, Livongo; Medscape; Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

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

This transcript has been edited for clarity. 

Nearly every patient I start on incretin therapy for weight loss asks me the same question, which is, will I have to stay on this forever? The answer is probably yes, but I think it’s much more nuanced than that because A) forever is a long time and B) I think there are various ways to approach this.

I want people to start just saying, let’s see how this works, because not everyone’s going to lose the same amount of weight or respond in the same way. I say let’s try it, but don’t stop it suddenly. If we decide at some point you don’t need quite the same dose, we can reduce the dose and maybe even reduce the frequency of giving it, but you don’t want to stop cold turkey because you may well regain the weight, and that’s obviously not our desired outcome.

There have been multiple clinical trials in which people started on an incretin hormone, either a glucagon-like peptide 1 (GLP-1) receptor agonist or a dual hormone, and they’ve actually shown that stopping it and then continuing patients on a placebo vs active drug results in continued weight gain over time vs either weight maintenance or weight loss when they remain on the incretin hormone. Clearly, on average, people will regain the weight, but that isn’t always true. 

One of the things I think is really important is that, from the get-go on starting on these hormones, people start working with a lifestyle plan, whether it’s working with a coach or an online program. However they approach this, it’s important to start changing habits and increasing exercise.

I can’t say how important this is enough, because people need to increase their physical activity to enhance the benefits of these agents and also to help retain lean body mass. I don’t want people losing a large amount of lean body mass as they go through the process of weight loss. 

I set the stage for the fact that I expect people to adhere to a lifestyle program, and maybe losing weight with the medications is going to help them do even better because they’re going to see positive outcomes.

When they get to the point of weight maintenance, I think we need to reinforce lifestyle. I either go down on the dose given weekly or I start having patients take the dose every other week, for instance, as opposed to every week, and then sometimes every month. Depending on the patient, I get them potentially to a lower dose, and then they’re able to maintain the weight as long as they improved their lifestyle along with the changes in the medication.

I tell people we’ll work with the drug, we’ll work with their metabolic needs, that there are many benefits to being on incretin hormone therapy, but I think it’s important that we can do this on an individualized basis. The thing I don’t want to happen, though, is for people to start on it and then stop it, and then start on it and stop it because they may lose weight, regain weight, get side effects, get used to the side effects, stop it, and start it.

As we know, that’s not the best way to do this, and I think it’s not healthy for people to do that either. I know it’s been somewhat problematic with supply chain issues, but hopefully we’ll be able to start these agents, reach the desired outcome in terms of weight loss, and then help patients maintain that weight with a combination of both medication and lifestyle.

Dr. Peters, professor, Department of Clinical Medicine, Keck School of Medicine; Director, University of Southern California Westside Center for Diabetes, Los Angeles, disclosed ties with Abbott Diabetes Care, Becton Dickinson; Boehringer Ingelheim Pharmaceuticals, Eli Lilly, Lexicon Pharmaceuticals, Livongo; Medscape; Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

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

This transcript has been edited for clarity. 

Nearly every patient I start on incretin therapy for weight loss asks me the same question, which is, will I have to stay on this forever? The answer is probably yes, but I think it’s much more nuanced than that because A) forever is a long time and B) I think there are various ways to approach this.

I want people to start just saying, let’s see how this works, because not everyone’s going to lose the same amount of weight or respond in the same way. I say let’s try it, but don’t stop it suddenly. If we decide at some point you don’t need quite the same dose, we can reduce the dose and maybe even reduce the frequency of giving it, but you don’t want to stop cold turkey because you may well regain the weight, and that’s obviously not our desired outcome.

There have been multiple clinical trials in which people started on an incretin hormone, either a glucagon-like peptide 1 (GLP-1) receptor agonist or a dual hormone, and they’ve actually shown that stopping it and then continuing patients on a placebo vs active drug results in continued weight gain over time vs either weight maintenance or weight loss when they remain on the incretin hormone. Clearly, on average, people will regain the weight, but that isn’t always true. 

One of the things I think is really important is that, from the get-go on starting on these hormones, people start working with a lifestyle plan, whether it’s working with a coach or an online program. However they approach this, it’s important to start changing habits and increasing exercise.

I can’t say how important this is enough, because people need to increase their physical activity to enhance the benefits of these agents and also to help retain lean body mass. I don’t want people losing a large amount of lean body mass as they go through the process of weight loss. 

I set the stage for the fact that I expect people to adhere to a lifestyle program, and maybe losing weight with the medications is going to help them do even better because they’re going to see positive outcomes.

When they get to the point of weight maintenance, I think we need to reinforce lifestyle. I either go down on the dose given weekly or I start having patients take the dose every other week, for instance, as opposed to every week, and then sometimes every month. Depending on the patient, I get them potentially to a lower dose, and then they’re able to maintain the weight as long as they improved their lifestyle along with the changes in the medication.

I tell people we’ll work with the drug, we’ll work with their metabolic needs, that there are many benefits to being on incretin hormone therapy, but I think it’s important that we can do this on an individualized basis. The thing I don’t want to happen, though, is for people to start on it and then stop it, and then start on it and stop it because they may lose weight, regain weight, get side effects, get used to the side effects, stop it, and start it.

As we know, that’s not the best way to do this, and I think it’s not healthy for people to do that either. I know it’s been somewhat problematic with supply chain issues, but hopefully we’ll be able to start these agents, reach the desired outcome in terms of weight loss, and then help patients maintain that weight with a combination of both medication and lifestyle.

Dr. Peters, professor, Department of Clinical Medicine, Keck School of Medicine; Director, University of Southern California Westside Center for Diabetes, Los Angeles, disclosed ties with Abbott Diabetes Care, Becton Dickinson; Boehringer Ingelheim Pharmaceuticals, Eli Lilly, Lexicon Pharmaceuticals, Livongo; Medscape; Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

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