Clinical Endocrinology News

Although obesity affects more than 1 billion people worldwide, according to a global analysis published in The Lancet, it still lacks a clear “identity” in research, social perception, and the healthcare sector. This lack of clarity hinders accurate diagnoses and treatments, while also perpetuating stigma and prejudice. Specialists argue that obesity is a chronic disease rather than just a condition that leads to other diseases.

At the latest International Congress on Obesity held in São Paulo, Brazil from June 26 to 29, The Lancet Commission on the Definition and Diagnosis of Clinical Obesity announced that it is conducting a global study to create a clear definition for obesity. This condition is often wrongly associated solely with individual choices. Ricardo Cohen, MD, PhD, coordinator of the Obesity and Diabetes Specialized Center at the Oswaldo Cruz German Hospital, São Paulo, and a key researcher in the study, made the announcement. “The current definition of obesity is too broad and ineffective for our needs,” said Dr. Cohen.

Dr. Cohen highlighted several challenges stemming from the lack of a precise definition, including confusion between prevention and treatment strategies, inadequate access to evidence-based treatments, and misconceptions about obesity and its reversibility. He also pointed out the limited understanding of the metabolic and biological complexity of the disease. “Society is comfortable with the current scenario because people are commonly blamed for their obesity. This is evident in the acceptance of so-called ‘magic solutions,’ such as fad diets, and the idea that obesity is merely a result of overeating and underexercising,” he said, noting the mental health damage that this perception can cause.

The difficulty in defining obesity stems from its common classification as a risk factor rather than a disease, said Dr. Cohen. Obesity meets the criteria to be considered a disease, such as well-defined pathophysiologic and etiologic mechanisms. In this way, obesity resembles diabetes and depressive disorders, which are classified as diseases based on the same criteria. This inconsistency, maintained by societal perceptions and the healthcare sector, creates confusion. Many professionals still lack a clear understanding of obesity as a disease.

This confusion perpetuates stigma and ignores the unique metabolic function in individuals. As a result, treatments often focus on preventing secondary diseases like diabetes and hypertension rather than on addressing obesity itself. Dr. Cohen recounted the case of a patient with fatigue, knee pain, and osteolysis who couldn’t perform daily activities but did not receive the necessary care. “If he had diabetes, he could have access to treatment because diabetes is recognized as a disease and needs to be treated. But since obesity is not recognized as such, he was sent home.”

To address these challenges, The Lancet Commission’s study, which is expected to be published this year, aims to establish clear diagnostic criteria for adults and children. Drawing inspiration from medical disciplines with well-established diagnostic criteria, such as rheumatology and psychiatry, the research has defined 18 criteria for adults and 14 for children.

The study also redefines treatment outcomes, sets standards for clinical remission of obesity, and proposes clear recommendations for clinical practice and public health policies. The ultimate goal, according to Dr. Cohen, is to transform the global treatment spectrum of obesity and improve access to necessary care.

“Our plan is to recognize obesity as a disease so that health policies, societal attitudes, and treatments will address it more effectively. This approach will also help reduce the harm caused by stigma and prejudice,” concluded Dr. Cohen.

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

Although obesity affects more than 1 billion people worldwide, according to a global analysis published in The Lancet, it still lacks a clear “identity” in research, social perception, and the healthcare sector. This lack of clarity hinders accurate diagnoses and treatments, while also perpetuating stigma and prejudice. Specialists argue that obesity is a chronic disease rather than just a condition that leads to other diseases.

At the latest International Congress on Obesity held in São Paulo, Brazil from June 26 to 29, The Lancet Commission on the Definition and Diagnosis of Clinical Obesity announced that it is conducting a global study to create a clear definition for obesity. This condition is often wrongly associated solely with individual choices. Ricardo Cohen, MD, PhD, coordinator of the Obesity and Diabetes Specialized Center at the Oswaldo Cruz German Hospital, São Paulo, and a key researcher in the study, made the announcement. “The current definition of obesity is too broad and ineffective for our needs,” said Dr. Cohen.

Dr. Cohen highlighted several challenges stemming from the lack of a precise definition, including confusion between prevention and treatment strategies, inadequate access to evidence-based treatments, and misconceptions about obesity and its reversibility. He also pointed out the limited understanding of the metabolic and biological complexity of the disease. “Society is comfortable with the current scenario because people are commonly blamed for their obesity. This is evident in the acceptance of so-called ‘magic solutions,’ such as fad diets, and the idea that obesity is merely a result of overeating and underexercising,” he said, noting the mental health damage that this perception can cause.

The difficulty in defining obesity stems from its common classification as a risk factor rather than a disease, said Dr. Cohen. Obesity meets the criteria to be considered a disease, such as well-defined pathophysiologic and etiologic mechanisms. In this way, obesity resembles diabetes and depressive disorders, which are classified as diseases based on the same criteria. This inconsistency, maintained by societal perceptions and the healthcare sector, creates confusion. Many professionals still lack a clear understanding of obesity as a disease.

This confusion perpetuates stigma and ignores the unique metabolic function in individuals. As a result, treatments often focus on preventing secondary diseases like diabetes and hypertension rather than on addressing obesity itself. Dr. Cohen recounted the case of a patient with fatigue, knee pain, and osteolysis who couldn’t perform daily activities but did not receive the necessary care. “If he had diabetes, he could have access to treatment because diabetes is recognized as a disease and needs to be treated. But since obesity is not recognized as such, he was sent home.”

To address these challenges, The Lancet Commission’s study, which is expected to be published this year, aims to establish clear diagnostic criteria for adults and children. Drawing inspiration from medical disciplines with well-established diagnostic criteria, such as rheumatology and psychiatry, the research has defined 18 criteria for adults and 14 for children.

The study also redefines treatment outcomes, sets standards for clinical remission of obesity, and proposes clear recommendations for clinical practice and public health policies. The ultimate goal, according to Dr. Cohen, is to transform the global treatment spectrum of obesity and improve access to necessary care.

“Our plan is to recognize obesity as a disease so that health policies, societal attitudes, and treatments will address it more effectively. This approach will also help reduce the harm caused by stigma and prejudice,” concluded Dr. Cohen.

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

Although obesity affects more than 1 billion people worldwide, according to a global analysis published in The Lancet, it still lacks a clear “identity” in research, social perception, and the healthcare sector. This lack of clarity hinders accurate diagnoses and treatments, while also perpetuating stigma and prejudice. Specialists argue that obesity is a chronic disease rather than just a condition that leads to other diseases.

At the latest International Congress on Obesity held in São Paulo, Brazil from June 26 to 29, The Lancet Commission on the Definition and Diagnosis of Clinical Obesity announced that it is conducting a global study to create a clear definition for obesity. This condition is often wrongly associated solely with individual choices. Ricardo Cohen, MD, PhD, coordinator of the Obesity and Diabetes Specialized Center at the Oswaldo Cruz German Hospital, São Paulo, and a key researcher in the study, made the announcement. “The current definition of obesity is too broad and ineffective for our needs,” said Dr. Cohen.

Dr. Cohen highlighted several challenges stemming from the lack of a precise definition, including confusion between prevention and treatment strategies, inadequate access to evidence-based treatments, and misconceptions about obesity and its reversibility. He also pointed out the limited understanding of the metabolic and biological complexity of the disease. “Society is comfortable with the current scenario because people are commonly blamed for their obesity. This is evident in the acceptance of so-called ‘magic solutions,’ such as fad diets, and the idea that obesity is merely a result of overeating and underexercising,” he said, noting the mental health damage that this perception can cause.

The difficulty in defining obesity stems from its common classification as a risk factor rather than a disease, said Dr. Cohen. Obesity meets the criteria to be considered a disease, such as well-defined pathophysiologic and etiologic mechanisms. In this way, obesity resembles diabetes and depressive disorders, which are classified as diseases based on the same criteria. This inconsistency, maintained by societal perceptions and the healthcare sector, creates confusion. Many professionals still lack a clear understanding of obesity as a disease.

This confusion perpetuates stigma and ignores the unique metabolic function in individuals. As a result, treatments often focus on preventing secondary diseases like diabetes and hypertension rather than on addressing obesity itself. Dr. Cohen recounted the case of a patient with fatigue, knee pain, and osteolysis who couldn’t perform daily activities but did not receive the necessary care. “If he had diabetes, he could have access to treatment because diabetes is recognized as a disease and needs to be treated. But since obesity is not recognized as such, he was sent home.”

To address these challenges, The Lancet Commission’s study, which is expected to be published this year, aims to establish clear diagnostic criteria for adults and children. Drawing inspiration from medical disciplines with well-established diagnostic criteria, such as rheumatology and psychiatry, the research has defined 18 criteria for adults and 14 for children.

The study also redefines treatment outcomes, sets standards for clinical remission of obesity, and proposes clear recommendations for clinical practice and public health policies. The ultimate goal, according to Dr. Cohen, is to transform the global treatment spectrum of obesity and improve access to necessary care.

“Our plan is to recognize obesity as a disease so that health policies, societal attitudes, and treatments will address it more effectively. This approach will also help reduce the harm caused by stigma and prejudice,” concluded Dr. Cohen.

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

An ancient virus that infected our ancestors tens of millions of years ago may be helping to fuel cancer today, according to a fascinating new study in Science Advances. Targeting these viral remnants still lingering in our DNA could lead to more effective cancer treatment with fewer side effects, the researchers said.

The study “gives a better understanding of how gene regulation can be impacted by these ancient retroviral sequences,” said Dixie Mager, PhD, scientist emeritus at the Terry Fox Laboratory at the British Columbia Cancer Research Institute, Vancouver, British Columbia, Canada. (Mager was not involved in the study.)

Long thought to be “junk” DNA with no biologic function, “endogenous retroviruses,” which have mutated over time and lost their ability to create the virus, are now known to regulate genes — allowing some genes to turn on and off. Research in recent years suggests they may play a role in diseases like cancer.

But scientists weren’t exactly sure what that role was, said senior study author Edward Chuong, PhD, a genome biologist at the University of Colorado Boulder.

Most studies have looked at whether endogenous retroviruses code for proteins that influence cancer. But these ancient viral strands usually don’t code for proteins at all.

Dr. Chuong took a different approach. Inspired by scientists who’ve studied how viral remnants regulate positive processes (immunity, brain development, or placenta development), he and his team explored whether some might regulate genes that, once activated, help cancer thrive.

Borrowing from epigenomic analysis data (data on molecules that alter gene expression) for 21 cancers mapped by the Cancer Genome Atlas, the researchers identified 19 virus-derived DNA sequences that bind to regulatory proteins more in cancer cells than in healthy cells. All of these could potentially act as gene regulators that promote cancer.

The researchers homed in on one sequence, called LTR10, because it showed especially high activity in several cancers, including lung and colorectal cancer. This DNA segment comes from a virus that entered our ancestors’ genome 30 million years ago, and it’s activated in a third of colorectal cancers.

Using the gene editing technology clustered regularly interspaced short palindromic repeats (CRISPR), Dr. Chuong’s team silenced LTR10 in colorectal cancer cells, altering the gene sequence so it couldn’t bind to regulatory proteins. Doing so dampened the activity of nearby cancer-promoting genes.

“They still behaved like cancer cells,” Dr. Chuong said. But “it made the cancer cells more susceptible to radiation. That would imply that the presence of that viral ‘switch’ actually helped those cancer cells survive radiation therapy.”

Previously, two studies had found that viral regulators play a role in promoting two types of cancer: Leukemia and prostate cancer. The new study shows these two cases weren’t flukes. All 21 cancers they looked at had at least one of those 19 viral elements, presumably working as cancer enhancers.

The study also identified what activates LTR10 to make it promote cancer. The culprit is a regulator protein called mitogen-activated protein (MAP) kinase, which is overactivated in about 40% of all human cancers.

Some cancer drugs — MAP kinase inhibitors — already target MAP kinase, and they’re often the first ones prescribed when a patient is diagnosed with cancer, Dr. Chuong said. As with many cancer treatments, doctors don’t know why they work, just that they do.

“By understanding the mechanisms in the cell, we might be able to make them work better or further optimize their treatment,” he said.

“MAP kinase inhibitors are really like a sledgehammer to the cell,” Dr. Chuong said — meaning they affect many cellular processes, not just those related to cancer.

“If we’re able to say that these viral switches are what’s important, then that could potentially help us develop a more targeted therapy that uses something like CRISPR to silence these viral elements,” he said. Or it could help providers choose a MAP kinase inhibitor from among the dozens available best suited to treat an individual patient and avoid side effects.  

Still, whether the findings translate to real cancer patients remains to be seen. “It’s very, very hard to go the final step of showing in a patient that these actually make a difference in the cancer,” Dr. Mager said.

More lab research, human trials, and at least a few years will be needed before this discovery could help treat cancer. “Directly targeting these elements as a therapy would be at least 5 years out,” Dr. Chuong said, “partly because that application would rely on CRISPR epigenome editing technology that is still being developed for clinical use.”
 

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

An ancient virus that infected our ancestors tens of millions of years ago may be helping to fuel cancer today, according to a fascinating new study in Science Advances. Targeting these viral remnants still lingering in our DNA could lead to more effective cancer treatment with fewer side effects, the researchers said.

The study “gives a better understanding of how gene regulation can be impacted by these ancient retroviral sequences,” said Dixie Mager, PhD, scientist emeritus at the Terry Fox Laboratory at the British Columbia Cancer Research Institute, Vancouver, British Columbia, Canada. (Mager was not involved in the study.)

Long thought to be “junk” DNA with no biologic function, “endogenous retroviruses,” which have mutated over time and lost their ability to create the virus, are now known to regulate genes — allowing some genes to turn on and off. Research in recent years suggests they may play a role in diseases like cancer.

But scientists weren’t exactly sure what that role was, said senior study author Edward Chuong, PhD, a genome biologist at the University of Colorado Boulder.

Most studies have looked at whether endogenous retroviruses code for proteins that influence cancer. But these ancient viral strands usually don’t code for proteins at all.

Dr. Chuong took a different approach. Inspired by scientists who’ve studied how viral remnants regulate positive processes (immunity, brain development, or placenta development), he and his team explored whether some might regulate genes that, once activated, help cancer thrive.

Borrowing from epigenomic analysis data (data on molecules that alter gene expression) for 21 cancers mapped by the Cancer Genome Atlas, the researchers identified 19 virus-derived DNA sequences that bind to regulatory proteins more in cancer cells than in healthy cells. All of these could potentially act as gene regulators that promote cancer.

The researchers homed in on one sequence, called LTR10, because it showed especially high activity in several cancers, including lung and colorectal cancer. This DNA segment comes from a virus that entered our ancestors’ genome 30 million years ago, and it’s activated in a third of colorectal cancers.

Using the gene editing technology clustered regularly interspaced short palindromic repeats (CRISPR), Dr. Chuong’s team silenced LTR10 in colorectal cancer cells, altering the gene sequence so it couldn’t bind to regulatory proteins. Doing so dampened the activity of nearby cancer-promoting genes.

“They still behaved like cancer cells,” Dr. Chuong said. But “it made the cancer cells more susceptible to radiation. That would imply that the presence of that viral ‘switch’ actually helped those cancer cells survive radiation therapy.”

Previously, two studies had found that viral regulators play a role in promoting two types of cancer: Leukemia and prostate cancer. The new study shows these two cases weren’t flukes. All 21 cancers they looked at had at least one of those 19 viral elements, presumably working as cancer enhancers.

The study also identified what activates LTR10 to make it promote cancer. The culprit is a regulator protein called mitogen-activated protein (MAP) kinase, which is overactivated in about 40% of all human cancers.

Some cancer drugs — MAP kinase inhibitors — already target MAP kinase, and they’re often the first ones prescribed when a patient is diagnosed with cancer, Dr. Chuong said. As with many cancer treatments, doctors don’t know why they work, just that they do.

“By understanding the mechanisms in the cell, we might be able to make them work better or further optimize their treatment,” he said.

“MAP kinase inhibitors are really like a sledgehammer to the cell,” Dr. Chuong said — meaning they affect many cellular processes, not just those related to cancer.

“If we’re able to say that these viral switches are what’s important, then that could potentially help us develop a more targeted therapy that uses something like CRISPR to silence these viral elements,” he said. Or it could help providers choose a MAP kinase inhibitor from among the dozens available best suited to treat an individual patient and avoid side effects.  

Still, whether the findings translate to real cancer patients remains to be seen. “It’s very, very hard to go the final step of showing in a patient that these actually make a difference in the cancer,” Dr. Mager said.

More lab research, human trials, and at least a few years will be needed before this discovery could help treat cancer. “Directly targeting these elements as a therapy would be at least 5 years out,” Dr. Chuong said, “partly because that application would rely on CRISPR epigenome editing technology that is still being developed for clinical use.”
 

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

An ancient virus that infected our ancestors tens of millions of years ago may be helping to fuel cancer today, according to a fascinating new study in Science Advances. Targeting these viral remnants still lingering in our DNA could lead to more effective cancer treatment with fewer side effects, the researchers said.

The study “gives a better understanding of how gene regulation can be impacted by these ancient retroviral sequences,” said Dixie Mager, PhD, scientist emeritus at the Terry Fox Laboratory at the British Columbia Cancer Research Institute, Vancouver, British Columbia, Canada. (Mager was not involved in the study.)

Long thought to be “junk” DNA with no biologic function, “endogenous retroviruses,” which have mutated over time and lost their ability to create the virus, are now known to regulate genes — allowing some genes to turn on and off. Research in recent years suggests they may play a role in diseases like cancer.

But scientists weren’t exactly sure what that role was, said senior study author Edward Chuong, PhD, a genome biologist at the University of Colorado Boulder.

Most studies have looked at whether endogenous retroviruses code for proteins that influence cancer. But these ancient viral strands usually don’t code for proteins at all.

Dr. Chuong took a different approach. Inspired by scientists who’ve studied how viral remnants regulate positive processes (immunity, brain development, or placenta development), he and his team explored whether some might regulate genes that, once activated, help cancer thrive.

Borrowing from epigenomic analysis data (data on molecules that alter gene expression) for 21 cancers mapped by the Cancer Genome Atlas, the researchers identified 19 virus-derived DNA sequences that bind to regulatory proteins more in cancer cells than in healthy cells. All of these could potentially act as gene regulators that promote cancer.

The researchers homed in on one sequence, called LTR10, because it showed especially high activity in several cancers, including lung and colorectal cancer. This DNA segment comes from a virus that entered our ancestors’ genome 30 million years ago, and it’s activated in a third of colorectal cancers.

Using the gene editing technology clustered regularly interspaced short palindromic repeats (CRISPR), Dr. Chuong’s team silenced LTR10 in colorectal cancer cells, altering the gene sequence so it couldn’t bind to regulatory proteins. Doing so dampened the activity of nearby cancer-promoting genes.

“They still behaved like cancer cells,” Dr. Chuong said. But “it made the cancer cells more susceptible to radiation. That would imply that the presence of that viral ‘switch’ actually helped those cancer cells survive radiation therapy.”

Previously, two studies had found that viral regulators play a role in promoting two types of cancer: Leukemia and prostate cancer. The new study shows these two cases weren’t flukes. All 21 cancers they looked at had at least one of those 19 viral elements, presumably working as cancer enhancers.

The study also identified what activates LTR10 to make it promote cancer. The culprit is a regulator protein called mitogen-activated protein (MAP) kinase, which is overactivated in about 40% of all human cancers.

Some cancer drugs — MAP kinase inhibitors — already target MAP kinase, and they’re often the first ones prescribed when a patient is diagnosed with cancer, Dr. Chuong said. As with many cancer treatments, doctors don’t know why they work, just that they do.

“By understanding the mechanisms in the cell, we might be able to make them work better or further optimize their treatment,” he said.

“MAP kinase inhibitors are really like a sledgehammer to the cell,” Dr. Chuong said — meaning they affect many cellular processes, not just those related to cancer.

“If we’re able to say that these viral switches are what’s important, then that could potentially help us develop a more targeted therapy that uses something like CRISPR to silence these viral elements,” he said. Or it could help providers choose a MAP kinase inhibitor from among the dozens available best suited to treat an individual patient and avoid side effects.  

Still, whether the findings translate to real cancer patients remains to be seen. “It’s very, very hard to go the final step of showing in a patient that these actually make a difference in the cancer,” Dr. Mager said.

More lab research, human trials, and at least a few years will be needed before this discovery could help treat cancer. “Directly targeting these elements as a therapy would be at least 5 years out,” Dr. Chuong said, “partly because that application would rely on CRISPR epigenome editing technology that is still being developed for clinical use.”
 

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

This transcript has been edited for clarity. 

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at New York University Grossman School of Medicine in New York City. 

There are many things screwy with our healthcare system. Many of you [reading] this are dealing with bureaucracy, paperwork, all sorts of constraints, restraints, and requirements that sometimes make the practice of medicine, or even nursing, difficult.

I don’t think I’ve seen anything screwier, from a moral point of view, than the system we have that allows for preauthorization by third-party payers, or insurers, in order to give care to patients. It’s pretty clear that a third-party payer has a conflict of interest. It’s simple: They don’t want to spend money.

Their goal as profit-making companies is to reduce what it is that they’re going to authorize. That clearly is driving how the preauthorization process works. We’re not getting a neutral review by third parties of the appropriateness of treatment recommendations or somebody saying, this is the standard of care and this is what ought to happen.

We’re letting the people who have the pocketbooks and the wallets have prior approval of what the doctor thinks is correct. That is really not the way to practice medicine. 

We now have more evidence about what really is going on. A doctor was recently interviewed by ProPublica and said that she had worked for Cigna as a reviewer. Basically, the message she got from that insurer was to speed it up, go fast, and basically “deny, deny, deny” when she got requests. Those are her words, not mine.

We get a peek under the tent of how this works, and Dr. Day is basically saying she had to leave because she just didn’t feel that it was evidence-driven. It was driven by concerns about who’s going to lose money or make money.

If you want to check to see whether something is appropriate, the question becomes, who ought to do prior review? 

Who does it now? Sometimes doctors. Sometimes nurses who aren’t in the specialty where the request is coming in for preapproval. I’ve even seen situations where some companies use nurses in other countries, such as the Philippines, to do preapproval. They send them information, like a clip, to use to deny things that basically is boilerplate language, whatever the request is.

Looming up now, some insurers are starting to think, well, maybe artificial intelligence could do it. Just review the written request, trigger certain responses on the part of the artificial intelligence — it can deny the claims just as well as a human — and maybe it’s even cheaper to set up that system for the insurer.

This is ethically nuts. We need to have a system where doctors’ judgments drive what patients get. You listen to doctors, as I do, about preapproval access and they say patients sometimes give up trying to get what they think is needed. Continuity of care is interrupted if they have to keep making requests all the time.

There are adverse events when the thing that the doctor thought was most appropriate isn’t approved and something else is used that is less safe or less efficacious. It isn’t in patient interest to have the person with the wallet saying, this is what we think you need, and then having unqualified people or even automated intelligence with no accountability and no transparency get involved in preauthorization.

This system costs us money because middlemen are doing all this work. It basically becomes one of the huge scandals, in my view, of our health system, that doctors don’t ultimately decide what the patient needs. A preauthorizing third party or robot, without transparency, without accountability, and behind closed doors second-guesses what’s going on.

I’m Art Caplan at the Division of Medical Ethics at the New York University Grossman School of Medicine.

Arthur L. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York, New York, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). Serves as a contributing author and advisor for Medscape.

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

This transcript has been edited for clarity. 

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at New York University Grossman School of Medicine in New York City. 

There are many things screwy with our healthcare system. Many of you [reading] this are dealing with bureaucracy, paperwork, all sorts of constraints, restraints, and requirements that sometimes make the practice of medicine, or even nursing, difficult.

I don’t think I’ve seen anything screwier, from a moral point of view, than the system we have that allows for preauthorization by third-party payers, or insurers, in order to give care to patients. It’s pretty clear that a third-party payer has a conflict of interest. It’s simple: They don’t want to spend money.

Their goal as profit-making companies is to reduce what it is that they’re going to authorize. That clearly is driving how the preauthorization process works. We’re not getting a neutral review by third parties of the appropriateness of treatment recommendations or somebody saying, this is the standard of care and this is what ought to happen.

We’re letting the people who have the pocketbooks and the wallets have prior approval of what the doctor thinks is correct. That is really not the way to practice medicine. 

We now have more evidence about what really is going on. A doctor was recently interviewed by ProPublica and said that she had worked for Cigna as a reviewer. Basically, the message she got from that insurer was to speed it up, go fast, and basically “deny, deny, deny” when she got requests. Those are her words, not mine.

We get a peek under the tent of how this works, and Dr. Day is basically saying she had to leave because she just didn’t feel that it was evidence-driven. It was driven by concerns about who’s going to lose money or make money.

If you want to check to see whether something is appropriate, the question becomes, who ought to do prior review? 

Who does it now? Sometimes doctors. Sometimes nurses who aren’t in the specialty where the request is coming in for preapproval. I’ve even seen situations where some companies use nurses in other countries, such as the Philippines, to do preapproval. They send them information, like a clip, to use to deny things that basically is boilerplate language, whatever the request is.

Looming up now, some insurers are starting to think, well, maybe artificial intelligence could do it. Just review the written request, trigger certain responses on the part of the artificial intelligence — it can deny the claims just as well as a human — and maybe it’s even cheaper to set up that system for the insurer.

This is ethically nuts. We need to have a system where doctors’ judgments drive what patients get. You listen to doctors, as I do, about preapproval access and they say patients sometimes give up trying to get what they think is needed. Continuity of care is interrupted if they have to keep making requests all the time.

There are adverse events when the thing that the doctor thought was most appropriate isn’t approved and something else is used that is less safe or less efficacious. It isn’t in patient interest to have the person with the wallet saying, this is what we think you need, and then having unqualified people or even automated intelligence with no accountability and no transparency get involved in preauthorization.

This system costs us money because middlemen are doing all this work. It basically becomes one of the huge scandals, in my view, of our health system, that doctors don’t ultimately decide what the patient needs. A preauthorizing third party or robot, without transparency, without accountability, and behind closed doors second-guesses what’s going on.

I’m Art Caplan at the Division of Medical Ethics at the New York University Grossman School of Medicine.

Arthur L. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York, New York, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). Serves as a contributing author and advisor for Medscape.

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

This transcript has been edited for clarity. 

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at New York University Grossman School of Medicine in New York City. 

There are many things screwy with our healthcare system. Many of you [reading] this are dealing with bureaucracy, paperwork, all sorts of constraints, restraints, and requirements that sometimes make the practice of medicine, or even nursing, difficult.

I don’t think I’ve seen anything screwier, from a moral point of view, than the system we have that allows for preauthorization by third-party payers, or insurers, in order to give care to patients. It’s pretty clear that a third-party payer has a conflict of interest. It’s simple: They don’t want to spend money.

Their goal as profit-making companies is to reduce what it is that they’re going to authorize. That clearly is driving how the preauthorization process works. We’re not getting a neutral review by third parties of the appropriateness of treatment recommendations or somebody saying, this is the standard of care and this is what ought to happen.

We’re letting the people who have the pocketbooks and the wallets have prior approval of what the doctor thinks is correct. That is really not the way to practice medicine. 

We now have more evidence about what really is going on. A doctor was recently interviewed by ProPublica and said that she had worked for Cigna as a reviewer. Basically, the message she got from that insurer was to speed it up, go fast, and basically “deny, deny, deny” when she got requests. Those are her words, not mine.

We get a peek under the tent of how this works, and Dr. Day is basically saying she had to leave because she just didn’t feel that it was evidence-driven. It was driven by concerns about who’s going to lose money or make money.

If you want to check to see whether something is appropriate, the question becomes, who ought to do prior review? 

Who does it now? Sometimes doctors. Sometimes nurses who aren’t in the specialty where the request is coming in for preapproval. I’ve even seen situations where some companies use nurses in other countries, such as the Philippines, to do preapproval. They send them information, like a clip, to use to deny things that basically is boilerplate language, whatever the request is.

Looming up now, some insurers are starting to think, well, maybe artificial intelligence could do it. Just review the written request, trigger certain responses on the part of the artificial intelligence — it can deny the claims just as well as a human — and maybe it’s even cheaper to set up that system for the insurer.

This is ethically nuts. We need to have a system where doctors’ judgments drive what patients get. You listen to doctors, as I do, about preapproval access and they say patients sometimes give up trying to get what they think is needed. Continuity of care is interrupted if they have to keep making requests all the time.

There are adverse events when the thing that the doctor thought was most appropriate isn’t approved and something else is used that is less safe or less efficacious. It isn’t in patient interest to have the person with the wallet saying, this is what we think you need, and then having unqualified people or even automated intelligence with no accountability and no transparency get involved in preauthorization.

This system costs us money because middlemen are doing all this work. It basically becomes one of the huge scandals, in my view, of our health system, that doctors don’t ultimately decide what the patient needs. A preauthorizing third party or robot, without transparency, without accountability, and behind closed doors second-guesses what’s going on.

I’m Art Caplan at the Division of Medical Ethics at the New York University Grossman School of Medicine.

Arthur L. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York, New York, has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position). Serves as a contributing author and advisor for Medscape.

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

Lipedema affects about 11% of cisgender women, according to the Brazilian Society of Angiology and Vascular Surgery. Yet the condition remains wrapped in uncertainties. Despite significant advancements in understanding its physiology, diagnosis, and treatment, more clarity is needed as awareness and diagnoses increase.

At the latest International Congress on Obesity (ICO) in São Paulo, Brazil, Philipp Scherer, PhD, director of the Touchstone Diabetes Center, discussed the complexities of lipedema. “It is an extremely frustrating condition for someone like me, who has spent a lifetime studying functional and dysfunctional adipose tissue. We are trying to understand the physiology of this pathology, but it is challenging, and so far, we have not been able to find a concrete answer,” he noted.

Lipedema is characterized by the abnormal accumulation of subcutaneous adipose tissue, especially in the lower limbs, and almost exclusively affects cisgender women. The reason for this gender disparity is unclear. It could be an intrinsic characteristic of the disease or a result from clinicians’ lack of familiarity with lipedema, which often leads to misdiagnosis as obesity. This misdiagnosis results in fewer men seeking treatment.

Research has predominantly focused on women, and evidence suggests that hormones play a crucial role in the disease’s pathophysiology. Lipedema typically manifests during periods of hormonal changes, such as puberty, pregnancy, menopause, and hormone replacement therapies, reinforcing the idea that hormones significantly influence the condition’s development and progression.
 

Main Symptoms

Jonathan Kartt, CEO of the Lipedema Foundation, emphasized that intense pain in the areas of adipose tissue accumulation is a hallmark symptom of lipedema, setting it apart from obesity. Pain levels can vary widely among patients, ranging from moderate to severe, with unbearable peaks on certain days. Mr. Kartt stressed the importance of recognizing and addressing this often underestimated symptom.

Lipedema is characterized by a bilateral, symmetrical increase in mass compared with the rest of the body. This is commonly distinguished by the “cuff sign,” a separation between normal tissue in the feet and abnormal tissue from the ankle upward. Other frequent symptoms include a feeling of heaviness, discomfort, fatigue, frequent bruising, and tiredness. A notable sign is the presence of subcutaneous nodules with a texture similar to that of rice grains, which are crucial for differentiating lipedema from other conditions. Palpation during anamnesis is essential to identify these nodules and confirm the diagnosis.

“It is crucial to investigate the family history for genetic predisposition. Additionally, it is fundamental to ask whether, even with weight loss, the affected areas retain accumulated fat. Hormonal changes, pain symptoms, and impact on quality of life should also be carefully evaluated,” advised Mr. Kartt.
 

Diagnostic Tools

André Murad, MD, a clinical consultant at the Instituto Lipedema Brazil, has been exploring new diagnostic approaches for lipedema beyond traditional anamnesis. During his presentation at the ICO, he shared studies on the efficacy of imaging exams such as ultrasound, tomography, and MRI in diagnosing the characteristic lipedema-associated increase in subcutaneous tissue.

He also discussed lymphangiography and lymphoscintigraphy, highlighting the use of magnetic resonance lymphangiography to evaluate dilated lymphatic vessels often observed in patients with lipedema. “By injecting contrast into the feet, this technique allows the evaluation of vessels, which are usually dilated, indicating characteristic lymphatic system overload in lipedema. Lymphoscintigraphy is crucial for detecting associated lymphedema, revealing delayed lymphatic flow and asymmetry between limbs in cases of lipedema without lymphedema,” he explained.

Despite the various diagnostic options, Dr. Murad highlighted two highly effective studies. A Brazilian study used ultrasound to establish a cutoff point of 11.7 mm in the pretibial subcutaneous tissue thickness, achieving 96% specificity for diagnosis. Another study emphasized the value of dual-energy x-ray absorptiometry (DXA), which demonstrated 95% sensitivity. This method assesses fat distribution by correlating the amount present in the legs with the total body, providing a cost-effective and accessible option for specialists.

“DXA allows for a precise mathematical evaluation of fat distribution relative to the total body. A ratio of 0.38 in the leg-to-body relationship is a significant indicator of high suspicion of lipedema,” highlighted Dr. Murad. “In clinical practice, many patients self-diagnose with lipedema, but the clinical exam often reveals no disproportion, with the leg-to-body ratio below 0.38 being common in these cases,” he added.
 

Treatment Approaches

Treatments for lipedema are still evolving, with considerable debate about the best approach. While some specialists advocate exclusively for conservative treatment, others recommend combining these methods with surgical interventions, depending on the stage of the disease. The relative novelty of lipedema and the scarcity of robust, long-term studies contribute to the uncertainty around treatment efficacy.

Conservative treatment typically includes compression, lymphatic drainage techniques, and pressure therapy. An active lifestyle and a healthy diet are also recommended. Although these measures do not prevent the accumulation of adipose tissue, they help reduce inflammation and improve quality of life. “Even though the causes of lipedema are not fully known, lifestyle management is essential for controlling symptoms, starting with an anti-inflammatory diet,” emphasized Dr. Murad.

Because insulin promotes lipogenesis, a diet that avoids spikes in glycemic and insulin levels is advisable. Insulin resistance can exacerbate edema formation, so a Mediterranean diet may be beneficial. This diet limits fast-absorbing carbohydrates, such as added sugar, refined grains, and ultraprocessed foods, while promoting complex carbohydrates from whole grains and legumes.

Dr. Murad also presented a study evaluating the potential benefits of a low-carbohydrate, high-fat diet for patients with lipedema. The study demonstrated weight loss, reduced body fat, controlled leg volume, and, notably, pain relief.

For more advanced stages of lipedema, plastic surgery is often considered when conservative approaches do not yield satisfactory results. Some specialists advocate for surgery as an effective way to remove diseased adipose cells and reduce excess fat accumulation, which can improve physical appearance and associated pain. There is a growing consensus that surgical intervention should be performed early, ideally in stage I of IV, to maximize efficacy and prevent disease progression.

Fábio Masato Kamamoto, MD, a plastic surgeon and director of the Instituto Lipedema Brazil, shared insights into surgical treatments for lipedema. He discussed techniques from liposuction to advanced skin retraction and dermolipectomy, crucial for addressing more advanced stages of the condition. “It’s a complex process that demands precision to protect the lymphatic system, especially considering the characteristic nodules of lipedema,” he noted.

Dr. Kamamoto discussed a former patient with stage III lipedema. In the initial stage, he performed liposuction, removing 8 L of fat and 3.4 kg of skin. After 6 months, a follow-up procedure resulted in a total removal of 15 kg. Complementary procedures, such as microneedling, were performed to stimulate collagen production and reduce skin sagging. In addition to cosmetic improvements, the procedure also removed the distinctive lipedema nodules, which Mr. Kartt described as feeling like “rice grains.” Removing these nodules significantly alleviates pain, according to Dr. Kamamoto.

The benefits of surgical treatment for lipedema can be long lasting. Dr. Kamamoto noted that fat tends not to reaccumulate in treated areas, with patients often experiencing lower weight, reduced edema, and decreased pain over time. “While we hope that patients do not regain weight, the benefits of surgery persist even if weight is regained. Therefore, combining conservative and surgical treatments remains a valid and effective approach,” he concluded.

Dr. Scherer highlighted that despite various approaches, there is still no definitive “magic signature” that fully explains lipedema. This lack of clarity directly affects the effectiveness of diagnoses and treatments. He expressed hope that future integration of data from different studies and approaches will lead to the identification of a clinically useful molecular signature. “The true cause of lipedema remains unknown, requiring more speculation, hypothesis formulation, and testing for significant discoveries. This situation is frustrating, as the disease affects many women who lack a clear diagnosis that differentiates them from patients with obesity, as well as evidence-based recommendations,” he concluded.
 

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

Lipedema affects about 11% of cisgender women, according to the Brazilian Society of Angiology and Vascular Surgery. Yet the condition remains wrapped in uncertainties. Despite significant advancements in understanding its physiology, diagnosis, and treatment, more clarity is needed as awareness and diagnoses increase.

At the latest International Congress on Obesity (ICO) in São Paulo, Brazil, Philipp Scherer, PhD, director of the Touchstone Diabetes Center, discussed the complexities of lipedema. “It is an extremely frustrating condition for someone like me, who has spent a lifetime studying functional and dysfunctional adipose tissue. We are trying to understand the physiology of this pathology, but it is challenging, and so far, we have not been able to find a concrete answer,” he noted.

Lipedema is characterized by the abnormal accumulation of subcutaneous adipose tissue, especially in the lower limbs, and almost exclusively affects cisgender women. The reason for this gender disparity is unclear. It could be an intrinsic characteristic of the disease or a result from clinicians’ lack of familiarity with lipedema, which often leads to misdiagnosis as obesity. This misdiagnosis results in fewer men seeking treatment.

Research has predominantly focused on women, and evidence suggests that hormones play a crucial role in the disease’s pathophysiology. Lipedema typically manifests during periods of hormonal changes, such as puberty, pregnancy, menopause, and hormone replacement therapies, reinforcing the idea that hormones significantly influence the condition’s development and progression.
 

Main Symptoms

Jonathan Kartt, CEO of the Lipedema Foundation, emphasized that intense pain in the areas of adipose tissue accumulation is a hallmark symptom of lipedema, setting it apart from obesity. Pain levels can vary widely among patients, ranging from moderate to severe, with unbearable peaks on certain days. Mr. Kartt stressed the importance of recognizing and addressing this often underestimated symptom.

Lipedema is characterized by a bilateral, symmetrical increase in mass compared with the rest of the body. This is commonly distinguished by the “cuff sign,” a separation between normal tissue in the feet and abnormal tissue from the ankle upward. Other frequent symptoms include a feeling of heaviness, discomfort, fatigue, frequent bruising, and tiredness. A notable sign is the presence of subcutaneous nodules with a texture similar to that of rice grains, which are crucial for differentiating lipedema from other conditions. Palpation during anamnesis is essential to identify these nodules and confirm the diagnosis.

“It is crucial to investigate the family history for genetic predisposition. Additionally, it is fundamental to ask whether, even with weight loss, the affected areas retain accumulated fat. Hormonal changes, pain symptoms, and impact on quality of life should also be carefully evaluated,” advised Mr. Kartt.
 

Diagnostic Tools

André Murad, MD, a clinical consultant at the Instituto Lipedema Brazil, has been exploring new diagnostic approaches for lipedema beyond traditional anamnesis. During his presentation at the ICO, he shared studies on the efficacy of imaging exams such as ultrasound, tomography, and MRI in diagnosing the characteristic lipedema-associated increase in subcutaneous tissue.

He also discussed lymphangiography and lymphoscintigraphy, highlighting the use of magnetic resonance lymphangiography to evaluate dilated lymphatic vessels often observed in patients with lipedema. “By injecting contrast into the feet, this technique allows the evaluation of vessels, which are usually dilated, indicating characteristic lymphatic system overload in lipedema. Lymphoscintigraphy is crucial for detecting associated lymphedema, revealing delayed lymphatic flow and asymmetry between limbs in cases of lipedema without lymphedema,” he explained.

Despite the various diagnostic options, Dr. Murad highlighted two highly effective studies. A Brazilian study used ultrasound to establish a cutoff point of 11.7 mm in the pretibial subcutaneous tissue thickness, achieving 96% specificity for diagnosis. Another study emphasized the value of dual-energy x-ray absorptiometry (DXA), which demonstrated 95% sensitivity. This method assesses fat distribution by correlating the amount present in the legs with the total body, providing a cost-effective and accessible option for specialists.

“DXA allows for a precise mathematical evaluation of fat distribution relative to the total body. A ratio of 0.38 in the leg-to-body relationship is a significant indicator of high suspicion of lipedema,” highlighted Dr. Murad. “In clinical practice, many patients self-diagnose with lipedema, but the clinical exam often reveals no disproportion, with the leg-to-body ratio below 0.38 being common in these cases,” he added.
 

Treatment Approaches

Treatments for lipedema are still evolving, with considerable debate about the best approach. While some specialists advocate exclusively for conservative treatment, others recommend combining these methods with surgical interventions, depending on the stage of the disease. The relative novelty of lipedema and the scarcity of robust, long-term studies contribute to the uncertainty around treatment efficacy.

Conservative treatment typically includes compression, lymphatic drainage techniques, and pressure therapy. An active lifestyle and a healthy diet are also recommended. Although these measures do not prevent the accumulation of adipose tissue, they help reduce inflammation and improve quality of life. “Even though the causes of lipedema are not fully known, lifestyle management is essential for controlling symptoms, starting with an anti-inflammatory diet,” emphasized Dr. Murad.

Because insulin promotes lipogenesis, a diet that avoids spikes in glycemic and insulin levels is advisable. Insulin resistance can exacerbate edema formation, so a Mediterranean diet may be beneficial. This diet limits fast-absorbing carbohydrates, such as added sugar, refined grains, and ultraprocessed foods, while promoting complex carbohydrates from whole grains and legumes.

Dr. Murad also presented a study evaluating the potential benefits of a low-carbohydrate, high-fat diet for patients with lipedema. The study demonstrated weight loss, reduced body fat, controlled leg volume, and, notably, pain relief.

For more advanced stages of lipedema, plastic surgery is often considered when conservative approaches do not yield satisfactory results. Some specialists advocate for surgery as an effective way to remove diseased adipose cells and reduce excess fat accumulation, which can improve physical appearance and associated pain. There is a growing consensus that surgical intervention should be performed early, ideally in stage I of IV, to maximize efficacy and prevent disease progression.

Fábio Masato Kamamoto, MD, a plastic surgeon and director of the Instituto Lipedema Brazil, shared insights into surgical treatments for lipedema. He discussed techniques from liposuction to advanced skin retraction and dermolipectomy, crucial for addressing more advanced stages of the condition. “It’s a complex process that demands precision to protect the lymphatic system, especially considering the characteristic nodules of lipedema,” he noted.

Dr. Kamamoto discussed a former patient with stage III lipedema. In the initial stage, he performed liposuction, removing 8 L of fat and 3.4 kg of skin. After 6 months, a follow-up procedure resulted in a total removal of 15 kg. Complementary procedures, such as microneedling, were performed to stimulate collagen production and reduce skin sagging. In addition to cosmetic improvements, the procedure also removed the distinctive lipedema nodules, which Mr. Kartt described as feeling like “rice grains.” Removing these nodules significantly alleviates pain, according to Dr. Kamamoto.

The benefits of surgical treatment for lipedema can be long lasting. Dr. Kamamoto noted that fat tends not to reaccumulate in treated areas, with patients often experiencing lower weight, reduced edema, and decreased pain over time. “While we hope that patients do not regain weight, the benefits of surgery persist even if weight is regained. Therefore, combining conservative and surgical treatments remains a valid and effective approach,” he concluded.

Dr. Scherer highlighted that despite various approaches, there is still no definitive “magic signature” that fully explains lipedema. This lack of clarity directly affects the effectiveness of diagnoses and treatments. He expressed hope that future integration of data from different studies and approaches will lead to the identification of a clinically useful molecular signature. “The true cause of lipedema remains unknown, requiring more speculation, hypothesis formulation, and testing for significant discoveries. This situation is frustrating, as the disease affects many women who lack a clear diagnosis that differentiates them from patients with obesity, as well as evidence-based recommendations,” he concluded.
 

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

Lipedema affects about 11% of cisgender women, according to the Brazilian Society of Angiology and Vascular Surgery. Yet the condition remains wrapped in uncertainties. Despite significant advancements in understanding its physiology, diagnosis, and treatment, more clarity is needed as awareness and diagnoses increase.

At the latest International Congress on Obesity (ICO) in São Paulo, Brazil, Philipp Scherer, PhD, director of the Touchstone Diabetes Center, discussed the complexities of lipedema. “It is an extremely frustrating condition for someone like me, who has spent a lifetime studying functional and dysfunctional adipose tissue. We are trying to understand the physiology of this pathology, but it is challenging, and so far, we have not been able to find a concrete answer,” he noted.

Lipedema is characterized by the abnormal accumulation of subcutaneous adipose tissue, especially in the lower limbs, and almost exclusively affects cisgender women. The reason for this gender disparity is unclear. It could be an intrinsic characteristic of the disease or a result from clinicians’ lack of familiarity with lipedema, which often leads to misdiagnosis as obesity. This misdiagnosis results in fewer men seeking treatment.

Research has predominantly focused on women, and evidence suggests that hormones play a crucial role in the disease’s pathophysiology. Lipedema typically manifests during periods of hormonal changes, such as puberty, pregnancy, menopause, and hormone replacement therapies, reinforcing the idea that hormones significantly influence the condition’s development and progression.
 

Main Symptoms

Jonathan Kartt, CEO of the Lipedema Foundation, emphasized that intense pain in the areas of adipose tissue accumulation is a hallmark symptom of lipedema, setting it apart from obesity. Pain levels can vary widely among patients, ranging from moderate to severe, with unbearable peaks on certain days. Mr. Kartt stressed the importance of recognizing and addressing this often underestimated symptom.

Lipedema is characterized by a bilateral, symmetrical increase in mass compared with the rest of the body. This is commonly distinguished by the “cuff sign,” a separation between normal tissue in the feet and abnormal tissue from the ankle upward. Other frequent symptoms include a feeling of heaviness, discomfort, fatigue, frequent bruising, and tiredness. A notable sign is the presence of subcutaneous nodules with a texture similar to that of rice grains, which are crucial for differentiating lipedema from other conditions. Palpation during anamnesis is essential to identify these nodules and confirm the diagnosis.

“It is crucial to investigate the family history for genetic predisposition. Additionally, it is fundamental to ask whether, even with weight loss, the affected areas retain accumulated fat. Hormonal changes, pain symptoms, and impact on quality of life should also be carefully evaluated,” advised Mr. Kartt.
 

Diagnostic Tools

André Murad, MD, a clinical consultant at the Instituto Lipedema Brazil, has been exploring new diagnostic approaches for lipedema beyond traditional anamnesis. During his presentation at the ICO, he shared studies on the efficacy of imaging exams such as ultrasound, tomography, and MRI in diagnosing the characteristic lipedema-associated increase in subcutaneous tissue.

He also discussed lymphangiography and lymphoscintigraphy, highlighting the use of magnetic resonance lymphangiography to evaluate dilated lymphatic vessels often observed in patients with lipedema. “By injecting contrast into the feet, this technique allows the evaluation of vessels, which are usually dilated, indicating characteristic lymphatic system overload in lipedema. Lymphoscintigraphy is crucial for detecting associated lymphedema, revealing delayed lymphatic flow and asymmetry between limbs in cases of lipedema without lymphedema,” he explained.

Despite the various diagnostic options, Dr. Murad highlighted two highly effective studies. A Brazilian study used ultrasound to establish a cutoff point of 11.7 mm in the pretibial subcutaneous tissue thickness, achieving 96% specificity for diagnosis. Another study emphasized the value of dual-energy x-ray absorptiometry (DXA), which demonstrated 95% sensitivity. This method assesses fat distribution by correlating the amount present in the legs with the total body, providing a cost-effective and accessible option for specialists.

“DXA allows for a precise mathematical evaluation of fat distribution relative to the total body. A ratio of 0.38 in the leg-to-body relationship is a significant indicator of high suspicion of lipedema,” highlighted Dr. Murad. “In clinical practice, many patients self-diagnose with lipedema, but the clinical exam often reveals no disproportion, with the leg-to-body ratio below 0.38 being common in these cases,” he added.
 

Treatment Approaches

Treatments for lipedema are still evolving, with considerable debate about the best approach. While some specialists advocate exclusively for conservative treatment, others recommend combining these methods with surgical interventions, depending on the stage of the disease. The relative novelty of lipedema and the scarcity of robust, long-term studies contribute to the uncertainty around treatment efficacy.

Conservative treatment typically includes compression, lymphatic drainage techniques, and pressure therapy. An active lifestyle and a healthy diet are also recommended. Although these measures do not prevent the accumulation of adipose tissue, they help reduce inflammation and improve quality of life. “Even though the causes of lipedema are not fully known, lifestyle management is essential for controlling symptoms, starting with an anti-inflammatory diet,” emphasized Dr. Murad.

Because insulin promotes lipogenesis, a diet that avoids spikes in glycemic and insulin levels is advisable. Insulin resistance can exacerbate edema formation, so a Mediterranean diet may be beneficial. This diet limits fast-absorbing carbohydrates, such as added sugar, refined grains, and ultraprocessed foods, while promoting complex carbohydrates from whole grains and legumes.

Dr. Murad also presented a study evaluating the potential benefits of a low-carbohydrate, high-fat diet for patients with lipedema. The study demonstrated weight loss, reduced body fat, controlled leg volume, and, notably, pain relief.

For more advanced stages of lipedema, plastic surgery is often considered when conservative approaches do not yield satisfactory results. Some specialists advocate for surgery as an effective way to remove diseased adipose cells and reduce excess fat accumulation, which can improve physical appearance and associated pain. There is a growing consensus that surgical intervention should be performed early, ideally in stage I of IV, to maximize efficacy and prevent disease progression.

Fábio Masato Kamamoto, MD, a plastic surgeon and director of the Instituto Lipedema Brazil, shared insights into surgical treatments for lipedema. He discussed techniques from liposuction to advanced skin retraction and dermolipectomy, crucial for addressing more advanced stages of the condition. “It’s a complex process that demands precision to protect the lymphatic system, especially considering the characteristic nodules of lipedema,” he noted.

Dr. Kamamoto discussed a former patient with stage III lipedema. In the initial stage, he performed liposuction, removing 8 L of fat and 3.4 kg of skin. After 6 months, a follow-up procedure resulted in a total removal of 15 kg. Complementary procedures, such as microneedling, were performed to stimulate collagen production and reduce skin sagging. In addition to cosmetic improvements, the procedure also removed the distinctive lipedema nodules, which Mr. Kartt described as feeling like “rice grains.” Removing these nodules significantly alleviates pain, according to Dr. Kamamoto.

The benefits of surgical treatment for lipedema can be long lasting. Dr. Kamamoto noted that fat tends not to reaccumulate in treated areas, with patients often experiencing lower weight, reduced edema, and decreased pain over time. “While we hope that patients do not regain weight, the benefits of surgery persist even if weight is regained. Therefore, combining conservative and surgical treatments remains a valid and effective approach,” he concluded.

Dr. Scherer highlighted that despite various approaches, there is still no definitive “magic signature” that fully explains lipedema. This lack of clarity directly affects the effectiveness of diagnoses and treatments. He expressed hope that future integration of data from different studies and approaches will lead to the identification of a clinically useful molecular signature. “The true cause of lipedema remains unknown, requiring more speculation, hypothesis formulation, and testing for significant discoveries. This situation is frustrating, as the disease affects many women who lack a clear diagnosis that differentiates them from patients with obesity, as well as evidence-based recommendations,” he concluded.
 

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

TOPLINE:

A less favorable balance between physical activity (PA) and sitting time (ST) is associated with a higher risk for all-cause mortality.

METHODOLOGY:

• Researchers evaluated the association between PA and ST with the risk for mortality in 5836 middle-aged and older Australian adults (mean age, 56.4 years; 45% men) from the Australian Diabetes, Obesity and Lifestyle Study.
• The Physical Activity and Sitting Time Balance Index (PASTBI) was calculated by dividing the total duration of daily PA by the duration of daily ST.
• Participants were categorized into quartiles on the basis of their PASTBI score, ranging from low PA/high ST to high PA/low ST.
• The primary outcome was all-cause mortality.

TAKEAWAY:

• During a median follow-up time of 14.3 years, 885 (15%) all-cause deaths were reported.
• The risk for all-cause mortality was 47% higher in participants with lower engagement in PA and higher ST (low PASTBI) than those with higher engagement in PA and lower ST (high PASTBI; adjusted hazard ratio, 1.47; 95% confidence interval, 1.21-1.79).

IN PRACTICE:

“The utility of the PASTBI in identifying relationships with mortality risk further highlights the importance of achieving a healthier balance in the dual health behaviors of PA [physical activity] and ST [sitting time],” the authors wrote.

SOURCE:

The study was led by Roslin Botlero, MBBS, MPH, PhD, of the School of Public Health and Preventive Medicine at Monash University in Melbourne, Australia. It was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on self-reported data for PA and ST, which may have introduced recall or reporting bias. The generalizability of the findings is restricted to a specific set of self-reported questionnaires. Even after adjustment for several potential confounders, other unmeasured or unknown confounders may have influenced the association between PASTBI and all-cause mortality.
 

DISCLOSURES:

The Australian Diabetes, Obesity and Lifestyle Study was sponsored by the National Health and Medical Research Council, the Australian Government Department of Health and Aged Care, and others. 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:

A less favorable balance between physical activity (PA) and sitting time (ST) is associated with a higher risk for all-cause mortality.

METHODOLOGY:

• Researchers evaluated the association between PA and ST with the risk for mortality in 5836 middle-aged and older Australian adults (mean age, 56.4 years; 45% men) from the Australian Diabetes, Obesity and Lifestyle Study.
• The Physical Activity and Sitting Time Balance Index (PASTBI) was calculated by dividing the total duration of daily PA by the duration of daily ST.
• Participants were categorized into quartiles on the basis of their PASTBI score, ranging from low PA/high ST to high PA/low ST.
• The primary outcome was all-cause mortality.

TAKEAWAY:

• During a median follow-up time of 14.3 years, 885 (15%) all-cause deaths were reported.
• The risk for all-cause mortality was 47% higher in participants with lower engagement in PA and higher ST (low PASTBI) than those with higher engagement in PA and lower ST (high PASTBI; adjusted hazard ratio, 1.47; 95% confidence interval, 1.21-1.79).

IN PRACTICE:

“The utility of the PASTBI in identifying relationships with mortality risk further highlights the importance of achieving a healthier balance in the dual health behaviors of PA [physical activity] and ST [sitting time],” the authors wrote.

SOURCE:

The study was led by Roslin Botlero, MBBS, MPH, PhD, of the School of Public Health and Preventive Medicine at Monash University in Melbourne, Australia. It was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on self-reported data for PA and ST, which may have introduced recall or reporting bias. The generalizability of the findings is restricted to a specific set of self-reported questionnaires. Even after adjustment for several potential confounders, other unmeasured or unknown confounders may have influenced the association between PASTBI and all-cause mortality.
 

DISCLOSURES:

The Australian Diabetes, Obesity and Lifestyle Study was sponsored by the National Health and Medical Research Council, the Australian Government Department of Health and Aged Care, and others. 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:

A less favorable balance between physical activity (PA) and sitting time (ST) is associated with a higher risk for all-cause mortality.

METHODOLOGY:

• Researchers evaluated the association between PA and ST with the risk for mortality in 5836 middle-aged and older Australian adults (mean age, 56.4 years; 45% men) from the Australian Diabetes, Obesity and Lifestyle Study.
• The Physical Activity and Sitting Time Balance Index (PASTBI) was calculated by dividing the total duration of daily PA by the duration of daily ST.
• Participants were categorized into quartiles on the basis of their PASTBI score, ranging from low PA/high ST to high PA/low ST.
• The primary outcome was all-cause mortality.

TAKEAWAY:

• During a median follow-up time of 14.3 years, 885 (15%) all-cause deaths were reported.
• The risk for all-cause mortality was 47% higher in participants with lower engagement in PA and higher ST (low PASTBI) than those with higher engagement in PA and lower ST (high PASTBI; adjusted hazard ratio, 1.47; 95% confidence interval, 1.21-1.79).

IN PRACTICE:

“The utility of the PASTBI in identifying relationships with mortality risk further highlights the importance of achieving a healthier balance in the dual health behaviors of PA [physical activity] and ST [sitting time],” the authors wrote.

SOURCE:

The study was led by Roslin Botlero, MBBS, MPH, PhD, of the School of Public Health and Preventive Medicine at Monash University in Melbourne, Australia. It was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on self-reported data for PA and ST, which may have introduced recall or reporting bias. The generalizability of the findings is restricted to a specific set of self-reported questionnaires. Even after adjustment for several potential confounders, other unmeasured or unknown confounders may have influenced the association between PASTBI and all-cause mortality.
 

DISCLOSURES:

The Australian Diabetes, Obesity and Lifestyle Study was sponsored by the National Health and Medical Research Council, the Australian Government Department of Health and Aged Care, and others. 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:

Very high and very low levels of high-density lipoprotein cholesterol (HDL-C) are linked to a higher risk for kidney disease in women with type 2 diabetes (T2D), but not in men.

METHODOLOGY:

• Studies have reported a strong association between low HDL-C levels and the risk for diabetic kidney disease, but whether higher HDL-C levels can influence the risk for diabetic kidney disease remains unclear.
• Researchers conducted a cross-sectional observational study of 936 patients with T2D (mean age, about 60 years; 41% women; 33% with diabetic kidney disease) from the Endocrinology Department at the Jinhua Hospital between September 2020 and July 2021.
• To examine the relationship between HDL-C levels and the risk for diabetic kidney disease, researchers used logistic regression to assess the continuous and categorical associations and a restricted cubic spline curve to assess the nonlinear association.
• HDL-C levels were categorized into four groups, with 0.40-0.96 mmol/L corresponding to the lowest quartile and 1.32-6.27 mmol/L corresponding to the highest quartile.
• The researchers observed a U-shaped association between HDL-C levels and the risk for diabetic kidney disease (P_nonlinear = .010) and selected two threshold values of 0.95 and 1.54 mmol/L.

TAKEAWAY:

• The risk for diabetic kidney disease was higher when the HDL-C levels were < 0.95 mmol/L or > 1.54 mmol/L.
• Compared with patients with HDL-C levels in the range of 0.95-1.54 mmol/L, those with very high and very low HDL-C levels had a 128% and 77% increased risk for diabetic kidney disease, respectively.
• The association was significant in women (P = .006) and not in men (P = .054), after adjusting for confounding factors.
• HDL-C level as a continuous variable was not associated with the risk for kidney disease (P = .902).

IN PRACTICE:

“Although HDL-C is generally considered a cardiovascular protective factor, at very high levels, this protective effect does not seem to hold true and may be associated with an increased DKD [diabetic kidney disease] risk,” the authors wrote.

SOURCE:

This study was led by Huabin Wang, from the Department of Clinical Laboratory, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China, and was published online in Scientific Reports.

LIMITATIONS:

The cross-sectional nature of the study limited the ability to establish a causal relationship between high HDL-C levels and the risk for diabetic kidney disease. The sample size of the study was relatively small at the higher end of the HDL-C concentration spectrum. Moreover, the study did not consider other potential confounding factors such as diet, sedentary lifestyle, obesity, genetic diseases, drug effects on HDL-C levels, and fluctuating estrogen levels, which could affect the overall findings.

DISCLOSURES:

The study was funded by the Department of Science and Technology of Zhejiang Province, China, and The Science and Technology Bureau of Jinhua City. The authors declared no competing interests.

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

TOPLINE:

Very high and very low levels of high-density lipoprotein cholesterol (HDL-C) are linked to a higher risk for kidney disease in women with type 2 diabetes (T2D), but not in men.

METHODOLOGY:

• Studies have reported a strong association between low HDL-C levels and the risk for diabetic kidney disease, but whether higher HDL-C levels can influence the risk for diabetic kidney disease remains unclear.
• Researchers conducted a cross-sectional observational study of 936 patients with T2D (mean age, about 60 years; 41% women; 33% with diabetic kidney disease) from the Endocrinology Department at the Jinhua Hospital between September 2020 and July 2021.
• To examine the relationship between HDL-C levels and the risk for diabetic kidney disease, researchers used logistic regression to assess the continuous and categorical associations and a restricted cubic spline curve to assess the nonlinear association.
• HDL-C levels were categorized into four groups, with 0.40-0.96 mmol/L corresponding to the lowest quartile and 1.32-6.27 mmol/L corresponding to the highest quartile.
• The researchers observed a U-shaped association between HDL-C levels and the risk for diabetic kidney disease (P_nonlinear = .010) and selected two threshold values of 0.95 and 1.54 mmol/L.

TAKEAWAY:

• The risk for diabetic kidney disease was higher when the HDL-C levels were < 0.95 mmol/L or > 1.54 mmol/L.
• Compared with patients with HDL-C levels in the range of 0.95-1.54 mmol/L, those with very high and very low HDL-C levels had a 128% and 77% increased risk for diabetic kidney disease, respectively.
• The association was significant in women (P = .006) and not in men (P = .054), after adjusting for confounding factors.
• HDL-C level as a continuous variable was not associated with the risk for kidney disease (P = .902).

IN PRACTICE:

“Although HDL-C is generally considered a cardiovascular protective factor, at very high levels, this protective effect does not seem to hold true and may be associated with an increased DKD [diabetic kidney disease] risk,” the authors wrote.

SOURCE:

This study was led by Huabin Wang, from the Department of Clinical Laboratory, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China, and was published online in Scientific Reports.

LIMITATIONS:

The cross-sectional nature of the study limited the ability to establish a causal relationship between high HDL-C levels and the risk for diabetic kidney disease. The sample size of the study was relatively small at the higher end of the HDL-C concentration spectrum. Moreover, the study did not consider other potential confounding factors such as diet, sedentary lifestyle, obesity, genetic diseases, drug effects on HDL-C levels, and fluctuating estrogen levels, which could affect the overall findings.

DISCLOSURES:

The study was funded by the Department of Science and Technology of Zhejiang Province, China, and The Science and Technology Bureau of Jinhua City. The authors declared no competing interests.

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

TOPLINE:

Very high and very low levels of high-density lipoprotein cholesterol (HDL-C) are linked to a higher risk for kidney disease in women with type 2 diabetes (T2D), but not in men.

METHODOLOGY:

• Studies have reported a strong association between low HDL-C levels and the risk for diabetic kidney disease, but whether higher HDL-C levels can influence the risk for diabetic kidney disease remains unclear.
• Researchers conducted a cross-sectional observational study of 936 patients with T2D (mean age, about 60 years; 41% women; 33% with diabetic kidney disease) from the Endocrinology Department at the Jinhua Hospital between September 2020 and July 2021.
• To examine the relationship between HDL-C levels and the risk for diabetic kidney disease, researchers used logistic regression to assess the continuous and categorical associations and a restricted cubic spline curve to assess the nonlinear association.
• HDL-C levels were categorized into four groups, with 0.40-0.96 mmol/L corresponding to the lowest quartile and 1.32-6.27 mmol/L corresponding to the highest quartile.
• The researchers observed a U-shaped association between HDL-C levels and the risk for diabetic kidney disease (P_nonlinear = .010) and selected two threshold values of 0.95 and 1.54 mmol/L.

TAKEAWAY:

• The risk for diabetic kidney disease was higher when the HDL-C levels were < 0.95 mmol/L or > 1.54 mmol/L.
• Compared with patients with HDL-C levels in the range of 0.95-1.54 mmol/L, those with very high and very low HDL-C levels had a 128% and 77% increased risk for diabetic kidney disease, respectively.
• The association was significant in women (P = .006) and not in men (P = .054), after adjusting for confounding factors.
• HDL-C level as a continuous variable was not associated with the risk for kidney disease (P = .902).

IN PRACTICE:

“Although HDL-C is generally considered a cardiovascular protective factor, at very high levels, this protective effect does not seem to hold true and may be associated with an increased DKD [diabetic kidney disease] risk,” the authors wrote.

SOURCE:

This study was led by Huabin Wang, from the Department of Clinical Laboratory, Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China, and was published online in Scientific Reports.

LIMITATIONS:

The cross-sectional nature of the study limited the ability to establish a causal relationship between high HDL-C levels and the risk for diabetic kidney disease. The sample size of the study was relatively small at the higher end of the HDL-C concentration spectrum. Moreover, the study did not consider other potential confounding factors such as diet, sedentary lifestyle, obesity, genetic diseases, drug effects on HDL-C levels, and fluctuating estrogen levels, which could affect the overall findings.

DISCLOSURES:

The study was funded by the Department of Science and Technology of Zhejiang Province, China, and The Science and Technology Bureau of Jinhua City. The authors declared no competing interests.

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

Increasingly recognized as a multifactorial disease, obesity demands an approach that involves multiple healthcare professionals. For psychologist Andréa Levy, coordinator and founder of the nongovernmental organization Obesity Brazil, addressing the patient’s “psychological weight” is crucial.

In an interview with this news organization, Ms. Levy, who was one of the speakers at the International Congress on Obesity in 2024, emphasized the importance of integrating emotional and behavioral aspects into treatment, because these factors often influence eating habits and weight gain.

She also highlighted the essential collaboration between endocrinologists, nutritionists, psychiatrists, and psychologists, who must work together to provide comprehensive and effective care to patients.
 

How do psychological factors affect the treatment of obesity?

Psychological factors are important triggers for weight gain. As the degree of obesity increases, so does the predisposition to mental health problems such as anxiety, mood disorders, personality disorders, and eating disorders. Understanding these factors is important because accurate psychodiagnosis is essential for effective disease treatment.

Without a proper diagnosis, the treatment may be incomplete and omit relevant factors. For example, a person with undiagnosed depression who is starting treatment for weight loss may feel discouraged and low on energy. He or she may wrongly attribute these symptoms to the diet or surgery. Similarly, someone undergoing bariatric surgery may confuse malnutrition symptoms with depression, resulting in inadequate treatment with antidepressants and possible iatrogenic complications.

Furthermore, psychotherapy and psychological follow-up are essential to help the individual organize better and understand the treatment and the disease itself. This is especially important in stigmatized diseases and those subject to prejudice such as obesity, where understanding and acceptance are often challenging, which affects treatment adherence.

Is the collaboration between psychologist and psychiatrist always necessary?

Often, it is necessary to have the support of both a psychologist and a psychiatrist. The process generally begins with a good psychodiagnosis. Initially, there may not be a case that requires treatment, but it is important to perform this evaluation to rule out any issues.

The follow-up, unlike weekly psychotherapy, can be monthly or at an interval agreed on with the patient. It is crucial to help him or her navigate the various stages of obesity treatment. For example, the patient may be going through a period of mourning or separation, or a happier moment, such as the beginning of a relationship or the birth of a child in the family. These moments affect eating habits and need to be well managed.

Depending on the degree of the pathology, such as depression, severe binge-eating disorder, or personality disorders, the psychologist works in conjunction with the psychiatrist. When we talk about obesity, we are possibly also talking about a psychiatric population because it is a disease that, besides being highly recurrent, involves many other factors, such as the gaze of others, difficulty with dressing, body pains, mobility, and relationships. Therefore, having this disease alone is already a trigger for disorders such as depression.
 

What is the main evidence regarding the psychological follow-up of patients with obesity?

Several studies have investigated the relationship between obesity and mental health. Research indicates that the greater the obesity, the higher the likelihood of a positive diagnosis for a psychiatric disorder. Additionally, there is evidence of the benefits of psychological treatment for patients with obesity.

A study published in the Journal of Clinical Endocrinology and Metabolism addressed the impact of cognitive-behavioral therapy (CBT), which helps patients manage goals and treat maladaptive behaviors such as binge-eating disorders. CBT has a modest effect on weight loss, but its integration as part of a lifestyle modification amplifies the results of this loss.

Recent research also shows that weight loss through bariatric surgery offers significant psychological benefits. In the past, it was believed that this procedure could cause depression and other severe psychiatric disorders, but it is now more than proven that weight loss, when done properly and without misconduct or malnutrition, improves psychological and psychiatric issues.
 

How does psychological follow-up affect the use of medication during obesity treatment?

Many people who take medications, such as corticosteroids for chronic pain or psychiatric medications, may experience weight gain. It is essential to discuss these issues with the psychiatrist because if the patient already has a predisposition to weight gain, medication X should be chosen instead of medication Y, or the dosage should be adjusted. The psychiatrist needs to understand obesity to medicate correctly. Other types of medication, such as chemotherapeutics, may also cause weight gain, often resulting in more abdominal obesity.

There is also lipedema, a hormone-dependent disease that is different from obesity. In this disease, the person gains weight mainly in the legs and arms. In this case, bariatric surgery may result in weight loss only in specific areas, causing disproportionality and difficulty in understanding for the patient. Therefore, when treating obesity, it is important to analyze the patient from all angles: psychological, physiologic, and physical, considering the diversity of the body, its functioning, and hormonal reactions.

Although psychologists do not prescribe medications, they often explain their functioning to the patient. For example, if a patient is taking a glucagon-like peptide 1 analog and experiences initial nausea, he or she may stop using the treatment because the wrong dose had been started. In this case, the psychologist can explain how the medication works and encourage the patient to discuss adjustments with the doctor, avoiding premature discontinuation.
 

How has the mental health follow-up of patients with obesity evolved over the years?

I started working with people with obesity 25 years ago, when I myself underwent bariatric surgery. At that time, surgeons were used to “solving” the problem and sending the person home. Often, the patient did not even return for surgical follow-up because, in theory, the problem was solved.

Over time, I believe that surgeons learned to talk to the patient, understanding that there is a whole process that even involves creating a bond with the individual who underwent the surgical procedure. Within this process, the importance of the mental health of patients was recognized, and how common it is to confuse a degree of malnutrition with a mental disorder.

Even though I am not a nutritionist, I need to know the difference between a case of malnutrition and depression. So, it is a whole set of factors that needs to be worked on like an orchestra. It is not necessary for this work to be done in the same physical space, but dialogue is important.

Of course, there are things that the patient will only share with the psychologist or with the surgeon, but there are also pieces of information that need to be shared for positive management. I have had patients who were afraid to go back to the nutritionist because they did not lose weight. If they are afraid, it is because the professional is guiding them incorrectly.
 

What tips would you give to clinicians regarding the psychological approach to people with obesity?

Accessibility is crucial. When someone tells me they are dealing with obesity and depression, I usually ask, “Did you know you have two chronic diseases?” It is essential to explain these concepts because the patient may often think they are free after a successful diet and weight loss, which is not true because of the high relapse associated with obesity. Depression and anxiety follow similar patterns. If the same person wears prescription glasses, I interact by saying, “Did you know you have three chronic diseases?” This question often causes surprise. “I hadn’t thought of that.”

It is essential to use accessible language for the patient to understand the functioning of the disease. More important than choosing a treatment approach is understanding the pathophysiology of obesity and its psychological impact. This avoids a one-size-fits-all approach for all patients.

For example, the impact on someone who developed obesity in childhood after suffering physical, moral, or sexual abuse will probably be deeper than on someone in a healthy family who gained weight after becoming sedentary. Each life story requires a personalized approach.

Sometimes, a patient with mild obesity (grade 1) may not seem to need specific interventions at first glance, but it is crucial to listen to his or her story. Similarly, patients with severe obesity (grades 3 or 4) who resist surgery are entitled to other treatment options, and this is perfectly valid. Therefore, it is always important to ask, “Who is this person? What does obesity represent in their story?” Then propose the most appropriate treatment.

Ms. Levy reported having no relevant financial relationships.
 

This story was translated from the Medscape Portuguese edition 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.

Increasingly recognized as a multifactorial disease, obesity demands an approach that involves multiple healthcare professionals. For psychologist Andréa Levy, coordinator and founder of the nongovernmental organization Obesity Brazil, addressing the patient’s “psychological weight” is crucial.

In an interview with this news organization, Ms. Levy, who was one of the speakers at the International Congress on Obesity in 2024, emphasized the importance of integrating emotional and behavioral aspects into treatment, because these factors often influence eating habits and weight gain.

She also highlighted the essential collaboration between endocrinologists, nutritionists, psychiatrists, and psychologists, who must work together to provide comprehensive and effective care to patients.
 

How do psychological factors affect the treatment of obesity?

Psychological factors are important triggers for weight gain. As the degree of obesity increases, so does the predisposition to mental health problems such as anxiety, mood disorders, personality disorders, and eating disorders. Understanding these factors is important because accurate psychodiagnosis is essential for effective disease treatment.

Without a proper diagnosis, the treatment may be incomplete and omit relevant factors. For example, a person with undiagnosed depression who is starting treatment for weight loss may feel discouraged and low on energy. He or she may wrongly attribute these symptoms to the diet or surgery. Similarly, someone undergoing bariatric surgery may confuse malnutrition symptoms with depression, resulting in inadequate treatment with antidepressants and possible iatrogenic complications.

Furthermore, psychotherapy and psychological follow-up are essential to help the individual organize better and understand the treatment and the disease itself. This is especially important in stigmatized diseases and those subject to prejudice such as obesity, where understanding and acceptance are often challenging, which affects treatment adherence.

Is the collaboration between psychologist and psychiatrist always necessary?

Often, it is necessary to have the support of both a psychologist and a psychiatrist. The process generally begins with a good psychodiagnosis. Initially, there may not be a case that requires treatment, but it is important to perform this evaluation to rule out any issues.

The follow-up, unlike weekly psychotherapy, can be monthly or at an interval agreed on with the patient. It is crucial to help him or her navigate the various stages of obesity treatment. For example, the patient may be going through a period of mourning or separation, or a happier moment, such as the beginning of a relationship or the birth of a child in the family. These moments affect eating habits and need to be well managed.

Depending on the degree of the pathology, such as depression, severe binge-eating disorder, or personality disorders, the psychologist works in conjunction with the psychiatrist. When we talk about obesity, we are possibly also talking about a psychiatric population because it is a disease that, besides being highly recurrent, involves many other factors, such as the gaze of others, difficulty with dressing, body pains, mobility, and relationships. Therefore, having this disease alone is already a trigger for disorders such as depression.
 

What is the main evidence regarding the psychological follow-up of patients with obesity?

Several studies have investigated the relationship between obesity and mental health. Research indicates that the greater the obesity, the higher the likelihood of a positive diagnosis for a psychiatric disorder. Additionally, there is evidence of the benefits of psychological treatment for patients with obesity.

A study published in the Journal of Clinical Endocrinology and Metabolism addressed the impact of cognitive-behavioral therapy (CBT), which helps patients manage goals and treat maladaptive behaviors such as binge-eating disorders. CBT has a modest effect on weight loss, but its integration as part of a lifestyle modification amplifies the results of this loss.

Recent research also shows that weight loss through bariatric surgery offers significant psychological benefits. In the past, it was believed that this procedure could cause depression and other severe psychiatric disorders, but it is now more than proven that weight loss, when done properly and without misconduct or malnutrition, improves psychological and psychiatric issues.
 

How does psychological follow-up affect the use of medication during obesity treatment?

Many people who take medications, such as corticosteroids for chronic pain or psychiatric medications, may experience weight gain. It is essential to discuss these issues with the psychiatrist because if the patient already has a predisposition to weight gain, medication X should be chosen instead of medication Y, or the dosage should be adjusted. The psychiatrist needs to understand obesity to medicate correctly. Other types of medication, such as chemotherapeutics, may also cause weight gain, often resulting in more abdominal obesity.

There is also lipedema, a hormone-dependent disease that is different from obesity. In this disease, the person gains weight mainly in the legs and arms. In this case, bariatric surgery may result in weight loss only in specific areas, causing disproportionality and difficulty in understanding for the patient. Therefore, when treating obesity, it is important to analyze the patient from all angles: psychological, physiologic, and physical, considering the diversity of the body, its functioning, and hormonal reactions.

Although psychologists do not prescribe medications, they often explain their functioning to the patient. For example, if a patient is taking a glucagon-like peptide 1 analog and experiences initial nausea, he or she may stop using the treatment because the wrong dose had been started. In this case, the psychologist can explain how the medication works and encourage the patient to discuss adjustments with the doctor, avoiding premature discontinuation.
 

How has the mental health follow-up of patients with obesity evolved over the years?

I started working with people with obesity 25 years ago, when I myself underwent bariatric surgery. At that time, surgeons were used to “solving” the problem and sending the person home. Often, the patient did not even return for surgical follow-up because, in theory, the problem was solved.

Over time, I believe that surgeons learned to talk to the patient, understanding that there is a whole process that even involves creating a bond with the individual who underwent the surgical procedure. Within this process, the importance of the mental health of patients was recognized, and how common it is to confuse a degree of malnutrition with a mental disorder.

Even though I am not a nutritionist, I need to know the difference between a case of malnutrition and depression. So, it is a whole set of factors that needs to be worked on like an orchestra. It is not necessary for this work to be done in the same physical space, but dialogue is important.

Of course, there are things that the patient will only share with the psychologist or with the surgeon, but there are also pieces of information that need to be shared for positive management. I have had patients who were afraid to go back to the nutritionist because they did not lose weight. If they are afraid, it is because the professional is guiding them incorrectly.
 

What tips would you give to clinicians regarding the psychological approach to people with obesity?

Accessibility is crucial. When someone tells me they are dealing with obesity and depression, I usually ask, “Did you know you have two chronic diseases?” It is essential to explain these concepts because the patient may often think they are free after a successful diet and weight loss, which is not true because of the high relapse associated with obesity. Depression and anxiety follow similar patterns. If the same person wears prescription glasses, I interact by saying, “Did you know you have three chronic diseases?” This question often causes surprise. “I hadn’t thought of that.”

It is essential to use accessible language for the patient to understand the functioning of the disease. More important than choosing a treatment approach is understanding the pathophysiology of obesity and its psychological impact. This avoids a one-size-fits-all approach for all patients.

For example, the impact on someone who developed obesity in childhood after suffering physical, moral, or sexual abuse will probably be deeper than on someone in a healthy family who gained weight after becoming sedentary. Each life story requires a personalized approach.

Sometimes, a patient with mild obesity (grade 1) may not seem to need specific interventions at first glance, but it is crucial to listen to his or her story. Similarly, patients with severe obesity (grades 3 or 4) who resist surgery are entitled to other treatment options, and this is perfectly valid. Therefore, it is always important to ask, “Who is this person? What does obesity represent in their story?” Then propose the most appropriate treatment.

Ms. Levy reported having no relevant financial relationships.
 

This story was translated from the Medscape Portuguese edition 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.

Increasingly recognized as a multifactorial disease, obesity demands an approach that involves multiple healthcare professionals. For psychologist Andréa Levy, coordinator and founder of the nongovernmental organization Obesity Brazil, addressing the patient’s “psychological weight” is crucial.

In an interview with this news organization, Ms. Levy, who was one of the speakers at the International Congress on Obesity in 2024, emphasized the importance of integrating emotional and behavioral aspects into treatment, because these factors often influence eating habits and weight gain.

She also highlighted the essential collaboration between endocrinologists, nutritionists, psychiatrists, and psychologists, who must work together to provide comprehensive and effective care to patients.
 

How do psychological factors affect the treatment of obesity?

Psychological factors are important triggers for weight gain. As the degree of obesity increases, so does the predisposition to mental health problems such as anxiety, mood disorders, personality disorders, and eating disorders. Understanding these factors is important because accurate psychodiagnosis is essential for effective disease treatment.

Without a proper diagnosis, the treatment may be incomplete and omit relevant factors. For example, a person with undiagnosed depression who is starting treatment for weight loss may feel discouraged and low on energy. He or she may wrongly attribute these symptoms to the diet or surgery. Similarly, someone undergoing bariatric surgery may confuse malnutrition symptoms with depression, resulting in inadequate treatment with antidepressants and possible iatrogenic complications.

Furthermore, psychotherapy and psychological follow-up are essential to help the individual organize better and understand the treatment and the disease itself. This is especially important in stigmatized diseases and those subject to prejudice such as obesity, where understanding and acceptance are often challenging, which affects treatment adherence.

Is the collaboration between psychologist and psychiatrist always necessary?

Often, it is necessary to have the support of both a psychologist and a psychiatrist. The process generally begins with a good psychodiagnosis. Initially, there may not be a case that requires treatment, but it is important to perform this evaluation to rule out any issues.

The follow-up, unlike weekly psychotherapy, can be monthly or at an interval agreed on with the patient. It is crucial to help him or her navigate the various stages of obesity treatment. For example, the patient may be going through a period of mourning or separation, or a happier moment, such as the beginning of a relationship or the birth of a child in the family. These moments affect eating habits and need to be well managed.

Depending on the degree of the pathology, such as depression, severe binge-eating disorder, or personality disorders, the psychologist works in conjunction with the psychiatrist. When we talk about obesity, we are possibly also talking about a psychiatric population because it is a disease that, besides being highly recurrent, involves many other factors, such as the gaze of others, difficulty with dressing, body pains, mobility, and relationships. Therefore, having this disease alone is already a trigger for disorders such as depression.
 

What is the main evidence regarding the psychological follow-up of patients with obesity?

Several studies have investigated the relationship between obesity and mental health. Research indicates that the greater the obesity, the higher the likelihood of a positive diagnosis for a psychiatric disorder. Additionally, there is evidence of the benefits of psychological treatment for patients with obesity.

A study published in the Journal of Clinical Endocrinology and Metabolism addressed the impact of cognitive-behavioral therapy (CBT), which helps patients manage goals and treat maladaptive behaviors such as binge-eating disorders. CBT has a modest effect on weight loss, but its integration as part of a lifestyle modification amplifies the results of this loss.

Recent research also shows that weight loss through bariatric surgery offers significant psychological benefits. In the past, it was believed that this procedure could cause depression and other severe psychiatric disorders, but it is now more than proven that weight loss, when done properly and without misconduct or malnutrition, improves psychological and psychiatric issues.
 

How does psychological follow-up affect the use of medication during obesity treatment?

Many people who take medications, such as corticosteroids for chronic pain or psychiatric medications, may experience weight gain. It is essential to discuss these issues with the psychiatrist because if the patient already has a predisposition to weight gain, medication X should be chosen instead of medication Y, or the dosage should be adjusted. The psychiatrist needs to understand obesity to medicate correctly. Other types of medication, such as chemotherapeutics, may also cause weight gain, often resulting in more abdominal obesity.

There is also lipedema, a hormone-dependent disease that is different from obesity. In this disease, the person gains weight mainly in the legs and arms. In this case, bariatric surgery may result in weight loss only in specific areas, causing disproportionality and difficulty in understanding for the patient. Therefore, when treating obesity, it is important to analyze the patient from all angles: psychological, physiologic, and physical, considering the diversity of the body, its functioning, and hormonal reactions.

Although psychologists do not prescribe medications, they often explain their functioning to the patient. For example, if a patient is taking a glucagon-like peptide 1 analog and experiences initial nausea, he or she may stop using the treatment because the wrong dose had been started. In this case, the psychologist can explain how the medication works and encourage the patient to discuss adjustments with the doctor, avoiding premature discontinuation.
 

How has the mental health follow-up of patients with obesity evolved over the years?

I started working with people with obesity 25 years ago, when I myself underwent bariatric surgery. At that time, surgeons were used to “solving” the problem and sending the person home. Often, the patient did not even return for surgical follow-up because, in theory, the problem was solved.

Over time, I believe that surgeons learned to talk to the patient, understanding that there is a whole process that even involves creating a bond with the individual who underwent the surgical procedure. Within this process, the importance of the mental health of patients was recognized, and how common it is to confuse a degree of malnutrition with a mental disorder.

Even though I am not a nutritionist, I need to know the difference between a case of malnutrition and depression. So, it is a whole set of factors that needs to be worked on like an orchestra. It is not necessary for this work to be done in the same physical space, but dialogue is important.

Of course, there are things that the patient will only share with the psychologist or with the surgeon, but there are also pieces of information that need to be shared for positive management. I have had patients who were afraid to go back to the nutritionist because they did not lose weight. If they are afraid, it is because the professional is guiding them incorrectly.
 

What tips would you give to clinicians regarding the psychological approach to people with obesity?

Accessibility is crucial. When someone tells me they are dealing with obesity and depression, I usually ask, “Did you know you have two chronic diseases?” It is essential to explain these concepts because the patient may often think they are free after a successful diet and weight loss, which is not true because of the high relapse associated with obesity. Depression and anxiety follow similar patterns. If the same person wears prescription glasses, I interact by saying, “Did you know you have three chronic diseases?” This question often causes surprise. “I hadn’t thought of that.”

It is essential to use accessible language for the patient to understand the functioning of the disease. More important than choosing a treatment approach is understanding the pathophysiology of obesity and its psychological impact. This avoids a one-size-fits-all approach for all patients.

For example, the impact on someone who developed obesity in childhood after suffering physical, moral, or sexual abuse will probably be deeper than on someone in a healthy family who gained weight after becoming sedentary. Each life story requires a personalized approach.

Sometimes, a patient with mild obesity (grade 1) may not seem to need specific interventions at first glance, but it is crucial to listen to his or her story. Similarly, patients with severe obesity (grades 3 or 4) who resist surgery are entitled to other treatment options, and this is perfectly valid. Therefore, it is always important to ask, “Who is this person? What does obesity represent in their story?” Then propose the most appropriate treatment.

Ms. Levy reported having no relevant financial relationships.
 

This story was translated from the Medscape Portuguese edition 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.

Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.

Statins Are Not Bad For the Liver

When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.

But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).¹ A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.² Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.

In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.³ The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.⁴

Statins Do Not Cause Muscle Pain in Most Patients

Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.⁵ Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.

Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.⁶ Muscle-related side effects were reported by 60% of former statin users and 25% of current users.

Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.⁷ Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.

Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.⁸ Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
 

Statins Are Likely Helpful In the Very Elderly

Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.

2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.

3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.

4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.

5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.

6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.

7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.

8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.

9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.

Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.

Statins Are Not Bad For the Liver

When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.

But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).¹ A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.² Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.

In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.³ The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.⁴

Statins Do Not Cause Muscle Pain in Most Patients

Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.⁵ Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.

Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.⁶ Muscle-related side effects were reported by 60% of former statin users and 25% of current users.

Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.⁷ Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.

Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.⁸ Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
 

Statins Are Likely Helpful In the Very Elderly

Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.

2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.

3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.

4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.

5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.

6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.

7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.

8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.

9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.

Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.

Statins Are Not Bad For the Liver

When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.

But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).¹ A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.² Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.

In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.³ The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.⁴

Statins Do Not Cause Muscle Pain in Most Patients

Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.⁵ Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.

Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.⁶ Muscle-related side effects were reported by 60% of former statin users and 25% of current users.

Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.⁷ Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.

Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.⁸ Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
 

Statins Are Likely Helpful In the Very Elderly

Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.

2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.

3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.

4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.

5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.

6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.

7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.

8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.

9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.

TOPLINE:

Higher levels of some serum medium-chain fatty acids found in coconut oil, palm kernel oil, and milk products are associated with a reduced risk for type 2 diabetes (T2D). This inverse relationship is more pronounced in individuals with a high genetic risk or physical inactivity.

METHODOLOGY:

• Studies reporting a link between dietary medium-chain fatty acids and a reduced risk for T2D have been based on food intake questionnaires, but serum samples are likely to be a more precise and objective basis for understanding metabolic relationships.
• To assess the association between medium-chain fatty acids and T2D risk, the researchers conducted a nested case-control study within the prospective China Cardiometabolic Disease and Cancer Cohort Study.
• They included 1707 individuals who developed diabetes during a median follow-up of 3.03 years and added a propensity-matched normoglycemic control group for a total of 3414 individuals (mean age, 57.56 years; 59.4% women), all with normal glucose regulation at baseline.
• Researchers investigated associations of baseline levels of five serum medium-chain fatty acids — octanoic acid, nonanoic acid, decanoic acid, undecanoic acid, and lauric acid — between individuals with T2D and control participants and stratified by risk factors, including diabetes genetic susceptibility.
• The genetic risk scores were calculated as a weighted sum of 86 T2D-associated single nucleotide polymorphisms.

TAKEAWAY:

• In an inverse association, each standard deviation increase in the baseline serum levels of octanoic acid and nonanoic acid decreased the odds of T2D by 10% and 16%, respectively (odds ratio [OR], 0.90; 95% CI, 0.82-0.98 and OR, 0.84; 95% CI, 0.74-0.95, respectively; all P < .05).
• , with significant interactions observed for octanoic, nonanoic, and decanoic acids (P for interaction = .042, .034, and .037, respectively).
• Moreover, the negative relationship between octanoic acid and the risk for diabetes was stronger in those with a high genetic risk, with a significant interaction (P for interaction = .003).
• No significant associations were observed between the levels of decanoic, undecanoic, and lauric acids and the overall risk for incident diabetes.

IN PRACTICE:

“Our findings generally support the protective effect of MCFAs [medium-chain fatty acids] but also emphasize the personalized approaches in improving serum MCFA profiles for T2D prevention, which could be tailored according to individuals’ genetic and lifestyle profiles,” the authors wrote.

SOURCE:

The study was led by Xiaojing Jia, MD, and Hong Lin, PhD, of the Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study’s follow-up duration of 3 years was short, which may have compromised the statistical power of the analysis. The long-term effects of medium-chain fatty acids on the risk for diabetes may not be captured as they were assessed only at baseline. The study population was limited to Chinese adults older than 40 years, which may affect the generalizability of the findings to other ethnicities and age groups.

DISCLOSURES:

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:

Higher levels of some serum medium-chain fatty acids found in coconut oil, palm kernel oil, and milk products are associated with a reduced risk for type 2 diabetes (T2D). This inverse relationship is more pronounced in individuals with a high genetic risk or physical inactivity.

METHODOLOGY:

• Studies reporting a link between dietary medium-chain fatty acids and a reduced risk for T2D have been based on food intake questionnaires, but serum samples are likely to be a more precise and objective basis for understanding metabolic relationships.
• To assess the association between medium-chain fatty acids and T2D risk, the researchers conducted a nested case-control study within the prospective China Cardiometabolic Disease and Cancer Cohort Study.
• They included 1707 individuals who developed diabetes during a median follow-up of 3.03 years and added a propensity-matched normoglycemic control group for a total of 3414 individuals (mean age, 57.56 years; 59.4% women), all with normal glucose regulation at baseline.
• Researchers investigated associations of baseline levels of five serum medium-chain fatty acids — octanoic acid, nonanoic acid, decanoic acid, undecanoic acid, and lauric acid — between individuals with T2D and control participants and stratified by risk factors, including diabetes genetic susceptibility.
• The genetic risk scores were calculated as a weighted sum of 86 T2D-associated single nucleotide polymorphisms.

TAKEAWAY:

• In an inverse association, each standard deviation increase in the baseline serum levels of octanoic acid and nonanoic acid decreased the odds of T2D by 10% and 16%, respectively (odds ratio [OR], 0.90; 95% CI, 0.82-0.98 and OR, 0.84; 95% CI, 0.74-0.95, respectively; all P < .05).
• , with significant interactions observed for octanoic, nonanoic, and decanoic acids (P for interaction = .042, .034, and .037, respectively).
• Moreover, the negative relationship between octanoic acid and the risk for diabetes was stronger in those with a high genetic risk, with a significant interaction (P for interaction = .003).
• No significant associations were observed between the levels of decanoic, undecanoic, and lauric acids and the overall risk for incident diabetes.

IN PRACTICE:

“Our findings generally support the protective effect of MCFAs [medium-chain fatty acids] but also emphasize the personalized approaches in improving serum MCFA profiles for T2D prevention, which could be tailored according to individuals’ genetic and lifestyle profiles,” the authors wrote.

SOURCE:

The study was led by Xiaojing Jia, MD, and Hong Lin, PhD, of the Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study’s follow-up duration of 3 years was short, which may have compromised the statistical power of the analysis. The long-term effects of medium-chain fatty acids on the risk for diabetes may not be captured as they were assessed only at baseline. The study population was limited to Chinese adults older than 40 years, which may affect the generalizability of the findings to other ethnicities and age groups.

DISCLOSURES:

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:

Higher levels of some serum medium-chain fatty acids found in coconut oil, palm kernel oil, and milk products are associated with a reduced risk for type 2 diabetes (T2D). This inverse relationship is more pronounced in individuals with a high genetic risk or physical inactivity.

METHODOLOGY:

• Studies reporting a link between dietary medium-chain fatty acids and a reduced risk for T2D have been based on food intake questionnaires, but serum samples are likely to be a more precise and objective basis for understanding metabolic relationships.
• To assess the association between medium-chain fatty acids and T2D risk, the researchers conducted a nested case-control study within the prospective China Cardiometabolic Disease and Cancer Cohort Study.
• They included 1707 individuals who developed diabetes during a median follow-up of 3.03 years and added a propensity-matched normoglycemic control group for a total of 3414 individuals (mean age, 57.56 years; 59.4% women), all with normal glucose regulation at baseline.
• Researchers investigated associations of baseline levels of five serum medium-chain fatty acids — octanoic acid, nonanoic acid, decanoic acid, undecanoic acid, and lauric acid — between individuals with T2D and control participants and stratified by risk factors, including diabetes genetic susceptibility.
• The genetic risk scores were calculated as a weighted sum of 86 T2D-associated single nucleotide polymorphisms.

TAKEAWAY:

• In an inverse association, each standard deviation increase in the baseline serum levels of octanoic acid and nonanoic acid decreased the odds of T2D by 10% and 16%, respectively (odds ratio [OR], 0.90; 95% CI, 0.82-0.98 and OR, 0.84; 95% CI, 0.74-0.95, respectively; all P < .05).
• , with significant interactions observed for octanoic, nonanoic, and decanoic acids (P for interaction = .042, .034, and .037, respectively).
• Moreover, the negative relationship between octanoic acid and the risk for diabetes was stronger in those with a high genetic risk, with a significant interaction (P for interaction = .003).
• No significant associations were observed between the levels of decanoic, undecanoic, and lauric acids and the overall risk for incident diabetes.

IN PRACTICE:

“Our findings generally support the protective effect of MCFAs [medium-chain fatty acids] but also emphasize the personalized approaches in improving serum MCFA profiles for T2D prevention, which could be tailored according to individuals’ genetic and lifestyle profiles,” the authors wrote.

SOURCE:

The study was led by Xiaojing Jia, MD, and Hong Lin, PhD, of the Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study’s follow-up duration of 3 years was short, which may have compromised the statistical power of the analysis. The long-term effects of medium-chain fatty acids on the risk for diabetes may not be captured as they were assessed only at baseline. The study population was limited to Chinese adults older than 40 years, which may affect the generalizability of the findings to other ethnicities and age groups.

DISCLOSURES:

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.

Patients are overdosing on compounded semaglutide due to errors in measuring and self-administering the drug and due to clinicians miscalculating doses that may differ from US Food and Drug Administration (FDA)–approved products.

The FDA published an alert on July 26 after receiving reports of dosing errors involving compounded semaglutide injectable products dispensed in multidose vials. Adverse events included gastrointestinal effects, fainting, dehydration, headache, gallstones, and acute pancreatitis. Some patients required hospitalization.
 

Why the Risks?

FDA-approved semaglutide injectable products are dosed in milligrams, have standard concentrations, and are currently only available in prefilled pens.

Compounded semaglutide products may differ from approved products in ways that contribute to potential errors — for example, in multidose vials and prefilled syringes. In addition, product concentrations may vary depending on the compounder, and even a single compounder may offer multiple concentrations of semaglutide.

Instructions for a compounded drug, if provided, may tell users to administer semaglutide injections in “units,” the volume of which may vary depending on the concentration — rather than in milligrams. In some instances, patients received syringes significantly larger than the prescribed volume.
 

Common Errors

The FDA has received reports related to patients mistakenly taking more than the prescribed dose from a multidose vial — sometimes 5-20 times more than the intended dose.

Several reports described clinicians incorrectly calculating the intended dose when converting from milligrams to units or milliliters. In one case, a patient couldn’t get clarity on dosing instructions from the telemedicine provider who prescribed the compounded semaglutide, leading the patient to search online for medical advice. This resulted in the patient taking five times the intended dose.

In another example, one clinician prescribed 20 units instead of two units, affecting three patients who, after receiving 10 times the intended dose, experienced nausea and vomiting.

Another clinician, who also takes semaglutide himself, tried to recalculate his own dose in units and ended up self-administering a dose 10 times higher than intended.

The FDA previously warned about potential risks from the use of compounded drugs during a shortage as is the case with semaglutide. While compounded drugs can “sometimes” be helpful, according to the agency, “compounded drugs pose a higher risk to patients than FDA-approved drugs because compounded drugs do not undergo FDA premarket review for safety, effectiveness, or quality.”

Patients are overdosing on compounded semaglutide due to errors in measuring and self-administering the drug and due to clinicians miscalculating doses that may differ from US Food and Drug Administration (FDA)–approved products.

The FDA published an alert on July 26 after receiving reports of dosing errors involving compounded semaglutide injectable products dispensed in multidose vials. Adverse events included gastrointestinal effects, fainting, dehydration, headache, gallstones, and acute pancreatitis. Some patients required hospitalization.
 

Why the Risks?

FDA-approved semaglutide injectable products are dosed in milligrams, have standard concentrations, and are currently only available in prefilled pens.

Compounded semaglutide products may differ from approved products in ways that contribute to potential errors — for example, in multidose vials and prefilled syringes. In addition, product concentrations may vary depending on the compounder, and even a single compounder may offer multiple concentrations of semaglutide.

Instructions for a compounded drug, if provided, may tell users to administer semaglutide injections in “units,” the volume of which may vary depending on the concentration — rather than in milligrams. In some instances, patients received syringes significantly larger than the prescribed volume.
 

Common Errors

The FDA has received reports related to patients mistakenly taking more than the prescribed dose from a multidose vial — sometimes 5-20 times more than the intended dose.

Several reports described clinicians incorrectly calculating the intended dose when converting from milligrams to units or milliliters. In one case, a patient couldn’t get clarity on dosing instructions from the telemedicine provider who prescribed the compounded semaglutide, leading the patient to search online for medical advice. This resulted in the patient taking five times the intended dose.

In another example, one clinician prescribed 20 units instead of two units, affecting three patients who, after receiving 10 times the intended dose, experienced nausea and vomiting.

Another clinician, who also takes semaglutide himself, tried to recalculate his own dose in units and ended up self-administering a dose 10 times higher than intended.

The FDA previously warned about potential risks from the use of compounded drugs during a shortage as is the case with semaglutide. While compounded drugs can “sometimes” be helpful, according to the agency, “compounded drugs pose a higher risk to patients than FDA-approved drugs because compounded drugs do not undergo FDA premarket review for safety, effectiveness, or quality.”

Patients are overdosing on compounded semaglutide due to errors in measuring and self-administering the drug and due to clinicians miscalculating doses that may differ from US Food and Drug Administration (FDA)–approved products.

The FDA published an alert on July 26 after receiving reports of dosing errors involving compounded semaglutide injectable products dispensed in multidose vials. Adverse events included gastrointestinal effects, fainting, dehydration, headache, gallstones, and acute pancreatitis. Some patients required hospitalization.
 

Why the Risks?

FDA-approved semaglutide injectable products are dosed in milligrams, have standard concentrations, and are currently only available in prefilled pens.

Compounded semaglutide products may differ from approved products in ways that contribute to potential errors — for example, in multidose vials and prefilled syringes. In addition, product concentrations may vary depending on the compounder, and even a single compounder may offer multiple concentrations of semaglutide.

Instructions for a compounded drug, if provided, may tell users to administer semaglutide injections in “units,” the volume of which may vary depending on the concentration — rather than in milligrams. In some instances, patients received syringes significantly larger than the prescribed volume.
 

Common Errors

The FDA has received reports related to patients mistakenly taking more than the prescribed dose from a multidose vial — sometimes 5-20 times more than the intended dose.

Several reports described clinicians incorrectly calculating the intended dose when converting from milligrams to units or milliliters. In one case, a patient couldn’t get clarity on dosing instructions from the telemedicine provider who prescribed the compounded semaglutide, leading the patient to search online for medical advice. This resulted in the patient taking five times the intended dose.

In another example, one clinician prescribed 20 units instead of two units, affecting three patients who, after receiving 10 times the intended dose, experienced nausea and vomiting.

Another clinician, who also takes semaglutide himself, tried to recalculate his own dose in units and ended up self-administering a dose 10 times higher than intended.

The FDA previously warned about potential risks from the use of compounded drugs during a shortage as is the case with semaglutide. While compounded drugs can “sometimes” be helpful, according to the agency, “compounded drugs pose a higher risk to patients than FDA-approved drugs because compounded drugs do not undergo FDA premarket review for safety, effectiveness, or quality.”