Family Practice News

TOPLINE:

Compared with the general population, patients with urticaria had a 49% higher risk of developing cancer in the first year following diagnosis, which decreased to 6% in subsequent years, in a cohort study using Danish healthcare databases.

METHODOLOGY:

• Researchers conducted a retrospective cohort study using data from Danish healthcare registries and compared the incident cancer risk between patients with urticaria and the risk in the general population.
• They identified 87,507 patients (58% women) with a primary or secondary first-time hospital outpatient clinic, emergency room, or inpatient diagnosis of urticaria between 1980 and 2022, who were followed for a median of 10.1 years.
• Incident cancers, including nonmelanoma skin cancer, were identified using the Danish Cancer Registry and classified by the extent of spread at the time of diagnosis.
• This study computed the absolute cancer risk within the first year of an urticaria diagnosis and standardized incidence ratios (SIRs), with 95% CIs standardized to Danish national cancer rates.

TAKEAWAY:

• For the first year of follow-up, the absolute risk for all cancer types was 0.7%, and it was 29.5% for subsequent years. The overall SIR for all types of cancer was 1.09 (95% CI, 1.06-1.11), which was based on 7788 observed cancer cases compared with 7161 cases expected over the entire follow-up period.
• Within the first year of follow-up, 588 patients with urticaria were diagnosed with cancer, for an SIR of 1.49 (95% CI, 1.38-1.62) for all cancer types.
• After the first year, the SIR for all cancer sites decreased and stabilized at 1.06 (95% CI, 1.04-1.09), with 7200 observed cancer cases.
• The risk was highest for hematological cancers in the first year, particularly Hodgkin lymphoma (SIR, 5.35; 95% CI, 2.56-9.85).

IN PRACTICE:

“Our study suggests that urticaria may be a marker of occult cancer and that it is associated with a slightly increased long-term cancer risk,” the authors wrote.

SOURCE:

The study was led by Sissel B.T. Sørensen, departments of dermatology and rheumatology, Aarhus University Hospital, Aarhus, Denmark. It was published online on June 27, 2024, in the British Journal of Dermatology.

LIMITATIONS:

The study is limited by its observational design and reliance on registry data, which may be subject to misclassification or incomplete information. In addition, the study could not assess individual patient factors such as lifestyle or genetic predispositions that may influence cancer risk, and the results may not be generalizable to other populations. Finally, the exact biologic mechanisms linking urticaria and cancer remain unclear, warranting further investigation.

DISCLOSURES:

The study did not receive any funding. The authors reported that they had no relevant 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 first appeared on Medscape.com.

TOPLINE:

Compared with the general population, patients with urticaria had a 49% higher risk of developing cancer in the first year following diagnosis, which decreased to 6% in subsequent years, in a cohort study using Danish healthcare databases.

METHODOLOGY:

• Researchers conducted a retrospective cohort study using data from Danish healthcare registries and compared the incident cancer risk between patients with urticaria and the risk in the general population.
• They identified 87,507 patients (58% women) with a primary or secondary first-time hospital outpatient clinic, emergency room, or inpatient diagnosis of urticaria between 1980 and 2022, who were followed for a median of 10.1 years.
• Incident cancers, including nonmelanoma skin cancer, were identified using the Danish Cancer Registry and classified by the extent of spread at the time of diagnosis.
• This study computed the absolute cancer risk within the first year of an urticaria diagnosis and standardized incidence ratios (SIRs), with 95% CIs standardized to Danish national cancer rates.

TAKEAWAY:

• For the first year of follow-up, the absolute risk for all cancer types was 0.7%, and it was 29.5% for subsequent years. The overall SIR for all types of cancer was 1.09 (95% CI, 1.06-1.11), which was based on 7788 observed cancer cases compared with 7161 cases expected over the entire follow-up period.
• Within the first year of follow-up, 588 patients with urticaria were diagnosed with cancer, for an SIR of 1.49 (95% CI, 1.38-1.62) for all cancer types.
• After the first year, the SIR for all cancer sites decreased and stabilized at 1.06 (95% CI, 1.04-1.09), with 7200 observed cancer cases.
• The risk was highest for hematological cancers in the first year, particularly Hodgkin lymphoma (SIR, 5.35; 95% CI, 2.56-9.85).

IN PRACTICE:

“Our study suggests that urticaria may be a marker of occult cancer and that it is associated with a slightly increased long-term cancer risk,” the authors wrote.

SOURCE:

The study was led by Sissel B.T. Sørensen, departments of dermatology and rheumatology, Aarhus University Hospital, Aarhus, Denmark. It was published online on June 27, 2024, in the British Journal of Dermatology.

LIMITATIONS:

The study is limited by its observational design and reliance on registry data, which may be subject to misclassification or incomplete information. In addition, the study could not assess individual patient factors such as lifestyle or genetic predispositions that may influence cancer risk, and the results may not be generalizable to other populations. Finally, the exact biologic mechanisms linking urticaria and cancer remain unclear, warranting further investigation.

DISCLOSURES:

The study did not receive any funding. The authors reported that they had no relevant 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 first appeared on Medscape.com.

TOPLINE:

Compared with the general population, patients with urticaria had a 49% higher risk of developing cancer in the first year following diagnosis, which decreased to 6% in subsequent years, in a cohort study using Danish healthcare databases.

METHODOLOGY:

• Researchers conducted a retrospective cohort study using data from Danish healthcare registries and compared the incident cancer risk between patients with urticaria and the risk in the general population.
• They identified 87,507 patients (58% women) with a primary or secondary first-time hospital outpatient clinic, emergency room, or inpatient diagnosis of urticaria between 1980 and 2022, who were followed for a median of 10.1 years.
• Incident cancers, including nonmelanoma skin cancer, were identified using the Danish Cancer Registry and classified by the extent of spread at the time of diagnosis.
• This study computed the absolute cancer risk within the first year of an urticaria diagnosis and standardized incidence ratios (SIRs), with 95% CIs standardized to Danish national cancer rates.

TAKEAWAY:

• For the first year of follow-up, the absolute risk for all cancer types was 0.7%, and it was 29.5% for subsequent years. The overall SIR for all types of cancer was 1.09 (95% CI, 1.06-1.11), which was based on 7788 observed cancer cases compared with 7161 cases expected over the entire follow-up period.
• Within the first year of follow-up, 588 patients with urticaria were diagnosed with cancer, for an SIR of 1.49 (95% CI, 1.38-1.62) for all cancer types.
• After the first year, the SIR for all cancer sites decreased and stabilized at 1.06 (95% CI, 1.04-1.09), with 7200 observed cancer cases.
• The risk was highest for hematological cancers in the first year, particularly Hodgkin lymphoma (SIR, 5.35; 95% CI, 2.56-9.85).

IN PRACTICE:

“Our study suggests that urticaria may be a marker of occult cancer and that it is associated with a slightly increased long-term cancer risk,” the authors wrote.

SOURCE:

The study was led by Sissel B.T. Sørensen, departments of dermatology and rheumatology, Aarhus University Hospital, Aarhus, Denmark. It was published online on June 27, 2024, in the British Journal of Dermatology.

LIMITATIONS:

The study is limited by its observational design and reliance on registry data, which may be subject to misclassification or incomplete information. In addition, the study could not assess individual patient factors such as lifestyle or genetic predispositions that may influence cancer risk, and the results may not be generalizable to other populations. Finally, the exact biologic mechanisms linking urticaria and cancer remain unclear, warranting further investigation.

DISCLOSURES:

The study did not receive any funding. The authors reported that they had no relevant 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 first appeared on Medscape.com.

Yes, there’s still much to find offensive, but South Park: The End of Obesity, in just 51 minutes, does more to explain some of obesity’s realities, its pharmacotherapy, and weight bias than the mainstream media has done perhaps ever. 

The mini-movie follows the plight of Eric Cartman, the fictional South Parkian child with severe obesity. 

South Park got everything right. The movie starts in a medical center where discussions with Cartman, his mother, and his doctor make it clear that obesity isn’t something that Cartman chose and is perhaps the most distressing aspect of his life. This certainly echoes study findings which report that quality-of-life scores in children with severe obesity are lower than those of children with newly diagnosed on-treatment cancers. As to how obesity erodes a child’s quality of life, no doubt part of its impact stems from obesity being a top source of schoolyard bullying, which is reflected by Cartman as he imagines his life without it. 

Cartman’s mother explains that of course they’ve tried diet and exercise, but that intentional behavior change alone hasn’t been sufficient to sustainably move the scale’s needle — a truth for the vast majority of people with obesity. But here, unlike in many actual doctors’ offices, Cartman’s doctor doesn’t spend time doubting or cajoling; instead, he does his job — which is to inform his patient, without judgment, about a pharmaceutical option that has proved to be beneficial. He accurately describes these medications as ushering in “a whole new era of medicine, a miracle really” that can “help people lose vast amounts of weight.”

The kicker, though, comes next. The doctor explains that insurance companies cover the medications only for patients with diabetes, “so if you can’t afford them, you’re just kind of out of luck.” This is changing somewhat now, at least here in Canada, where two of our main private insurers have changed their base coverages to make antiobesity medications something employers need to opt out of rather than opt into, but certainly they’re not covered by US Medicare for weight management, nor by our version of the same here in Canada.

But even for those who have coverage, there are hoops to jump through, which is highlighted by the incredible efforts made by Cartman and his friends to get his insurance plan to cover the medications. Thwarted at every turn, despite the undeniable benefits of these medications to health and quality of life, they are forced to turn to compounding — a phenomenon certainly pervasive here in North America whereby compounding pharmacies claim to be able to provide glucagon-like peptide-1 (GLP-1) analogs with comparable efficacy at a fraction of the price, but without the same rigor of proof of purity or efficacy. 

Also covered by South Park is that the GLP-1 analog supply is impacted by use by people who don’t meet approved medical criteria and are using the medications for aesthetic purposes. This speaks to the incredible societal pressure to be thin and to the comfort of some physicians to inappropriately prescribe these medications. This is covered by the subplot of South Park’s weed farmer, Randy, who in turn delivers an important insight into how it feels to use a GLP-1 analog: “I think there’s something wrong with these drugs ... I feel satisfied. With any drugs I want to do more and more, but with these drugs I feel like I want things less. With these drugs you don’t really crave anything.” The sentiment is echoed by Cartman, who exclaims, “I think I’m full. I’ve never known that feeling before in my life, but I’m full.”

It’s remarkable that South Park, a show built on serving up politically incorrect offense, covers obesity and its treatment with more accuracy, nuance, and compassion than does society as a whole. The show notes that obesity is a biological condition (it is), that when it comes to health (in America) “you have to have some f-ing willpower.” But where they explicitly mean having willpower in terms of filing and pursing insurance claims (you do), explains that drug companies are making antiobesity medications more expensive in America than anywhere else in the world (they are), and finally delivers this quote, which, while missing the biological basis of behavior and hunger with respect to obesity, certainly sums up why blame has no place in the discourse:

“We have sugar companies, pharmaceutical companies, and insurance companies all just trying to figure out how to make money off our health. It isn’t fair to put the blame on anyone for their weight.”

No, it’s not.

This movie should be required viewing in medical schools.
 

Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.

A version of this article appeared on Medscape.com.

Yes, there’s still much to find offensive, but South Park: The End of Obesity, in just 51 minutes, does more to explain some of obesity’s realities, its pharmacotherapy, and weight bias than the mainstream media has done perhaps ever. 

The mini-movie follows the plight of Eric Cartman, the fictional South Parkian child with severe obesity. 

South Park got everything right. The movie starts in a medical center where discussions with Cartman, his mother, and his doctor make it clear that obesity isn’t something that Cartman chose and is perhaps the most distressing aspect of his life. This certainly echoes study findings which report that quality-of-life scores in children with severe obesity are lower than those of children with newly diagnosed on-treatment cancers. As to how obesity erodes a child’s quality of life, no doubt part of its impact stems from obesity being a top source of schoolyard bullying, which is reflected by Cartman as he imagines his life without it. 

Cartman’s mother explains that of course they’ve tried diet and exercise, but that intentional behavior change alone hasn’t been sufficient to sustainably move the scale’s needle — a truth for the vast majority of people with obesity. But here, unlike in many actual doctors’ offices, Cartman’s doctor doesn’t spend time doubting or cajoling; instead, he does his job — which is to inform his patient, without judgment, about a pharmaceutical option that has proved to be beneficial. He accurately describes these medications as ushering in “a whole new era of medicine, a miracle really” that can “help people lose vast amounts of weight.”

The kicker, though, comes next. The doctor explains that insurance companies cover the medications only for patients with diabetes, “so if you can’t afford them, you’re just kind of out of luck.” This is changing somewhat now, at least here in Canada, where two of our main private insurers have changed their base coverages to make antiobesity medications something employers need to opt out of rather than opt into, but certainly they’re not covered by US Medicare for weight management, nor by our version of the same here in Canada.

But even for those who have coverage, there are hoops to jump through, which is highlighted by the incredible efforts made by Cartman and his friends to get his insurance plan to cover the medications. Thwarted at every turn, despite the undeniable benefits of these medications to health and quality of life, they are forced to turn to compounding — a phenomenon certainly pervasive here in North America whereby compounding pharmacies claim to be able to provide glucagon-like peptide-1 (GLP-1) analogs with comparable efficacy at a fraction of the price, but without the same rigor of proof of purity or efficacy. 

Also covered by South Park is that the GLP-1 analog supply is impacted by use by people who don’t meet approved medical criteria and are using the medications for aesthetic purposes. This speaks to the incredible societal pressure to be thin and to the comfort of some physicians to inappropriately prescribe these medications. This is covered by the subplot of South Park’s weed farmer, Randy, who in turn delivers an important insight into how it feels to use a GLP-1 analog: “I think there’s something wrong with these drugs ... I feel satisfied. With any drugs I want to do more and more, but with these drugs I feel like I want things less. With these drugs you don’t really crave anything.” The sentiment is echoed by Cartman, who exclaims, “I think I’m full. I’ve never known that feeling before in my life, but I’m full.”

It’s remarkable that South Park, a show built on serving up politically incorrect offense, covers obesity and its treatment with more accuracy, nuance, and compassion than does society as a whole. The show notes that obesity is a biological condition (it is), that when it comes to health (in America) “you have to have some f-ing willpower.” But where they explicitly mean having willpower in terms of filing and pursing insurance claims (you do), explains that drug companies are making antiobesity medications more expensive in America than anywhere else in the world (they are), and finally delivers this quote, which, while missing the biological basis of behavior and hunger with respect to obesity, certainly sums up why blame has no place in the discourse:

“We have sugar companies, pharmaceutical companies, and insurance companies all just trying to figure out how to make money off our health. It isn’t fair to put the blame on anyone for their weight.”

No, it’s not.

This movie should be required viewing in medical schools.
 

Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.

A version of this article appeared on Medscape.com.

Yes, there’s still much to find offensive, but South Park: The End of Obesity, in just 51 minutes, does more to explain some of obesity’s realities, its pharmacotherapy, and weight bias than the mainstream media has done perhaps ever. 

The mini-movie follows the plight of Eric Cartman, the fictional South Parkian child with severe obesity. 

South Park got everything right. The movie starts in a medical center where discussions with Cartman, his mother, and his doctor make it clear that obesity isn’t something that Cartman chose and is perhaps the most distressing aspect of his life. This certainly echoes study findings which report that quality-of-life scores in children with severe obesity are lower than those of children with newly diagnosed on-treatment cancers. As to how obesity erodes a child’s quality of life, no doubt part of its impact stems from obesity being a top source of schoolyard bullying, which is reflected by Cartman as he imagines his life without it. 

Cartman’s mother explains that of course they’ve tried diet and exercise, but that intentional behavior change alone hasn’t been sufficient to sustainably move the scale’s needle — a truth for the vast majority of people with obesity. But here, unlike in many actual doctors’ offices, Cartman’s doctor doesn’t spend time doubting or cajoling; instead, he does his job — which is to inform his patient, without judgment, about a pharmaceutical option that has proved to be beneficial. He accurately describes these medications as ushering in “a whole new era of medicine, a miracle really” that can “help people lose vast amounts of weight.”

The kicker, though, comes next. The doctor explains that insurance companies cover the medications only for patients with diabetes, “so if you can’t afford them, you’re just kind of out of luck.” This is changing somewhat now, at least here in Canada, where two of our main private insurers have changed their base coverages to make antiobesity medications something employers need to opt out of rather than opt into, but certainly they’re not covered by US Medicare for weight management, nor by our version of the same here in Canada.

But even for those who have coverage, there are hoops to jump through, which is highlighted by the incredible efforts made by Cartman and his friends to get his insurance plan to cover the medications. Thwarted at every turn, despite the undeniable benefits of these medications to health and quality of life, they are forced to turn to compounding — a phenomenon certainly pervasive here in North America whereby compounding pharmacies claim to be able to provide glucagon-like peptide-1 (GLP-1) analogs with comparable efficacy at a fraction of the price, but without the same rigor of proof of purity or efficacy. 

Also covered by South Park is that the GLP-1 analog supply is impacted by use by people who don’t meet approved medical criteria and are using the medications for aesthetic purposes. This speaks to the incredible societal pressure to be thin and to the comfort of some physicians to inappropriately prescribe these medications. This is covered by the subplot of South Park’s weed farmer, Randy, who in turn delivers an important insight into how it feels to use a GLP-1 analog: “I think there’s something wrong with these drugs ... I feel satisfied. With any drugs I want to do more and more, but with these drugs I feel like I want things less. With these drugs you don’t really crave anything.” The sentiment is echoed by Cartman, who exclaims, “I think I’m full. I’ve never known that feeling before in my life, but I’m full.”

It’s remarkable that South Park, a show built on serving up politically incorrect offense, covers obesity and its treatment with more accuracy, nuance, and compassion than does society as a whole. The show notes that obesity is a biological condition (it is), that when it comes to health (in America) “you have to have some f-ing willpower.” But where they explicitly mean having willpower in terms of filing and pursing insurance claims (you do), explains that drug companies are making antiobesity medications more expensive in America than anywhere else in the world (they are), and finally delivers this quote, which, while missing the biological basis of behavior and hunger with respect to obesity, certainly sums up why blame has no place in the discourse:

“We have sugar companies, pharmaceutical companies, and insurance companies all just trying to figure out how to make money off our health. It isn’t fair to put the blame on anyone for their weight.”

No, it’s not.

This movie should be required viewing in medical schools.
 

Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.

A version of this article appeared on Medscape.com.

Bothersome urinary symptoms and incontinence at 12 months post partum are common and treatable, so screening for those symptoms as well as associated depression and anxiety is essential, write authors of a new study.

Sonia Bhandari Randhawa, MD, with the Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center in Dallas, led the study published in Urogynecology, which identified factors associated with persistent stress urinary incontinence (SUI), marked by leakage from sudden movements such as coughing or jumping; urgency UI (UUI), leakage after a sudden and intense need to urinate, even if the bladder isn’t full; and other overall bothersome urinary symptoms 1 year after delivery.
 

Associations by Subtype

Dr. Randhawa analyzed data provided by 419 patients (77% Hispanic White and 22% non-Hispanic Black). After multivariable analysis, SUI (n = 136, 32.5%) was significantly associated with greater body mass index (BMI) at the time of delivery and greater depression screening scores. Factors not associated included fetal birth weight, mode of delivery, degree of laceration, and breastfeeding status.

UUI (n = 69, 16.5%) was significantly associated with more births and higher anxiety screening scores. Women with overall urinary symptom bother also had significantly more births and higher anxiety screening scores.

“These findings support the [American College of Obstetricians and Gynecologists] recommendations for routine mental health and urinary incontinence screening in the postpartum period,” said Gena Dunivan, MD, director of the Division of Urogynecology and Pelvic Reconstructive Surgery at University of Alabama–Birmingham, who was not part of the study. “Routine screening for these issues will hopefully reduce the stigma, allowing more patients to receive the help they deserve.”
 

1 in 3 Postpartum Patients Affected by Urinary Incontinence

About one third of postpartum patients are affected by urinary incontinence, which is linked with poorer quality of life and mental health outcomes, the authors note.

Estimates of incontinence frequency post partum vary depending on the population studied, differences in subgroups, and definition of urinary incontinence. A strength of the study was its sizable population, made up almost entirely of Hispanic White and non-Hispanic Black women receiving care at a large safety-net hospital.

“This study has important clinical implications for postpartum patients,” the authors write. “Given an array of proven treatment options for both UUI and SUI, maternal health surveillance needs to include routine inquiry about UI to overcome patients’ reluctance for seeking care. Next, as elevated BMI was identified as a risk factor for persistent postpartum SUI, maintaining a healthy weight should be routinely encouraged during antenatal and postpartum clinic visits.”

Lauren Giugale, MD, director of UPMC’s Magee-Womens Hospital Postpartum Pelvic Floor Healing Clinic in Pittsburgh, Pennsylvania, says an important aspect of the study is that it measured urinary symptoms 1 year after delivery and shows that these symptoms persist. “A lot of studies look more short term,” she noted.

She also pointed to the study’s population of Black and Hispanic women, populations which “have been pretty hard to capture in urogynecology research. It’s important for us to understand these urinary symptoms are affecting those women as well as White women.”
 

Association With Anxiety

The association between postpartum depression scores and SUI is important, she says, but Dr. Randhawa’s team also “uniquely looked at anxiety scores in postpartum women. They showed an association between anxiety scores and UUI, so there’s certainly a potential impact of postpartum urinary symptoms on maternal mental health and maternal well-being.” The relationship between anxiety and depression and postpartum urinary symptoms is not well understood and warrants further research, she says.

In her role, Dr. Giugale says, she always asks about urinary symptoms, particularly in postpartum women. But she notes that some ob.gyn.s without urogynecology training may not prioritize those questions amid all the other information they need to cover.

She says she tells her residents to ask patients pointedly, “Are you having any urine leakage? Patients may not think it’s a problem that can be addressed. We do patients a disservice when we don’t ask the important questions that might potentially impact patients’ lives.”

The authors and Dr. Giugale and Dr. Dunivan report no relevant financial relationships.

Bothersome urinary symptoms and incontinence at 12 months post partum are common and treatable, so screening for those symptoms as well as associated depression and anxiety is essential, write authors of a new study.

Sonia Bhandari Randhawa, MD, with the Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center in Dallas, led the study published in Urogynecology, which identified factors associated with persistent stress urinary incontinence (SUI), marked by leakage from sudden movements such as coughing or jumping; urgency UI (UUI), leakage after a sudden and intense need to urinate, even if the bladder isn’t full; and other overall bothersome urinary symptoms 1 year after delivery.
 

Associations by Subtype

Dr. Randhawa analyzed data provided by 419 patients (77% Hispanic White and 22% non-Hispanic Black). After multivariable analysis, SUI (n = 136, 32.5%) was significantly associated with greater body mass index (BMI) at the time of delivery and greater depression screening scores. Factors not associated included fetal birth weight, mode of delivery, degree of laceration, and breastfeeding status.

UUI (n = 69, 16.5%) was significantly associated with more births and higher anxiety screening scores. Women with overall urinary symptom bother also had significantly more births and higher anxiety screening scores.

“These findings support the [American College of Obstetricians and Gynecologists] recommendations for routine mental health and urinary incontinence screening in the postpartum period,” said Gena Dunivan, MD, director of the Division of Urogynecology and Pelvic Reconstructive Surgery at University of Alabama–Birmingham, who was not part of the study. “Routine screening for these issues will hopefully reduce the stigma, allowing more patients to receive the help they deserve.”
 

1 in 3 Postpartum Patients Affected by Urinary Incontinence

About one third of postpartum patients are affected by urinary incontinence, which is linked with poorer quality of life and mental health outcomes, the authors note.

Estimates of incontinence frequency post partum vary depending on the population studied, differences in subgroups, and definition of urinary incontinence. A strength of the study was its sizable population, made up almost entirely of Hispanic White and non-Hispanic Black women receiving care at a large safety-net hospital.

“This study has important clinical implications for postpartum patients,” the authors write. “Given an array of proven treatment options for both UUI and SUI, maternal health surveillance needs to include routine inquiry about UI to overcome patients’ reluctance for seeking care. Next, as elevated BMI was identified as a risk factor for persistent postpartum SUI, maintaining a healthy weight should be routinely encouraged during antenatal and postpartum clinic visits.”

Lauren Giugale, MD, director of UPMC’s Magee-Womens Hospital Postpartum Pelvic Floor Healing Clinic in Pittsburgh, Pennsylvania, says an important aspect of the study is that it measured urinary symptoms 1 year after delivery and shows that these symptoms persist. “A lot of studies look more short term,” she noted.

She also pointed to the study’s population of Black and Hispanic women, populations which “have been pretty hard to capture in urogynecology research. It’s important for us to understand these urinary symptoms are affecting those women as well as White women.”
 

Association With Anxiety

The association between postpartum depression scores and SUI is important, she says, but Dr. Randhawa’s team also “uniquely looked at anxiety scores in postpartum women. They showed an association between anxiety scores and UUI, so there’s certainly a potential impact of postpartum urinary symptoms on maternal mental health and maternal well-being.” The relationship between anxiety and depression and postpartum urinary symptoms is not well understood and warrants further research, she says.

In her role, Dr. Giugale says, she always asks about urinary symptoms, particularly in postpartum women. But she notes that some ob.gyn.s without urogynecology training may not prioritize those questions amid all the other information they need to cover.

She says she tells her residents to ask patients pointedly, “Are you having any urine leakage? Patients may not think it’s a problem that can be addressed. We do patients a disservice when we don’t ask the important questions that might potentially impact patients’ lives.”

The authors and Dr. Giugale and Dr. Dunivan report no relevant financial relationships.

Bothersome urinary symptoms and incontinence at 12 months post partum are common and treatable, so screening for those symptoms as well as associated depression and anxiety is essential, write authors of a new study.

Sonia Bhandari Randhawa, MD, with the Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center in Dallas, led the study published in Urogynecology, which identified factors associated with persistent stress urinary incontinence (SUI), marked by leakage from sudden movements such as coughing or jumping; urgency UI (UUI), leakage after a sudden and intense need to urinate, even if the bladder isn’t full; and other overall bothersome urinary symptoms 1 year after delivery.
 

Associations by Subtype

Dr. Randhawa analyzed data provided by 419 patients (77% Hispanic White and 22% non-Hispanic Black). After multivariable analysis, SUI (n = 136, 32.5%) was significantly associated with greater body mass index (BMI) at the time of delivery and greater depression screening scores. Factors not associated included fetal birth weight, mode of delivery, degree of laceration, and breastfeeding status.

UUI (n = 69, 16.5%) was significantly associated with more births and higher anxiety screening scores. Women with overall urinary symptom bother also had significantly more births and higher anxiety screening scores.

“These findings support the [American College of Obstetricians and Gynecologists] recommendations for routine mental health and urinary incontinence screening in the postpartum period,” said Gena Dunivan, MD, director of the Division of Urogynecology and Pelvic Reconstructive Surgery at University of Alabama–Birmingham, who was not part of the study. “Routine screening for these issues will hopefully reduce the stigma, allowing more patients to receive the help they deserve.”
 

1 in 3 Postpartum Patients Affected by Urinary Incontinence

About one third of postpartum patients are affected by urinary incontinence, which is linked with poorer quality of life and mental health outcomes, the authors note.

Estimates of incontinence frequency post partum vary depending on the population studied, differences in subgroups, and definition of urinary incontinence. A strength of the study was its sizable population, made up almost entirely of Hispanic White and non-Hispanic Black women receiving care at a large safety-net hospital.

“This study has important clinical implications for postpartum patients,” the authors write. “Given an array of proven treatment options for both UUI and SUI, maternal health surveillance needs to include routine inquiry about UI to overcome patients’ reluctance for seeking care. Next, as elevated BMI was identified as a risk factor for persistent postpartum SUI, maintaining a healthy weight should be routinely encouraged during antenatal and postpartum clinic visits.”

Lauren Giugale, MD, director of UPMC’s Magee-Womens Hospital Postpartum Pelvic Floor Healing Clinic in Pittsburgh, Pennsylvania, says an important aspect of the study is that it measured urinary symptoms 1 year after delivery and shows that these symptoms persist. “A lot of studies look more short term,” she noted.

She also pointed to the study’s population of Black and Hispanic women, populations which “have been pretty hard to capture in urogynecology research. It’s important for us to understand these urinary symptoms are affecting those women as well as White women.”
 

Association With Anxiety

The association between postpartum depression scores and SUI is important, she says, but Dr. Randhawa’s team also “uniquely looked at anxiety scores in postpartum women. They showed an association between anxiety scores and UUI, so there’s certainly a potential impact of postpartum urinary symptoms on maternal mental health and maternal well-being.” The relationship between anxiety and depression and postpartum urinary symptoms is not well understood and warrants further research, she says.

In her role, Dr. Giugale says, she always asks about urinary symptoms, particularly in postpartum women. But she notes that some ob.gyn.s without urogynecology training may not prioritize those questions amid all the other information they need to cover.

She says she tells her residents to ask patients pointedly, “Are you having any urine leakage? Patients may not think it’s a problem that can be addressed. We do patients a disservice when we don’t ask the important questions that might potentially impact patients’ lives.”

The authors and Dr. Giugale and Dr. Dunivan report no relevant financial relationships.

Should a patient with high lipoprotein (a), or Lp(a), be started on low-dose aspirin?

This is the conundrum facing many physicians and patients, but even getting to that point will require more availability and coverage of tests and a greater appreciation of the risk associated with Lp(a), said cardiologists.
 

Lp(a): The Silent Risk

On Lp(a) Awareness Day, C. Michael Gibson, MD, MA, CEO of the Baim Institute for Clinical Research, Boston, Massachusetts, and PERFUSE took the opportunity to talk about his experiences with testing on X.

The professor of medicine at Harvard Medical School, also in Boston, said he was surprised to find that he had a very high calcium score, despite a low-density lipoprotein (LDL) cholesterol level of just 70 mg/dL. Eventually, he found out that he had a “very, very high Lp(a),” which was particularly concerning because his grandfather died of a heart attack at 45 years of age.

But how much risk does that represent?

A 2022 consensus statement from the European Atherosclerosis Society (EAS) highlighted that epidemiologic and genetic studies “strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes,” even at very low LDL cholesterol levels.

This is because Lp(a) has proinflammatory and proatherosclerotic properties, and high levels are associated with both micro- and macrocalcification of the aortic valve. Findings from a US registry study also suggest the threshold related to increased cardiovascular risk may differ for primary and secondary prevention populations (J Am Coll Cardiol. 2024 Mar 5;83[9]:873-886).

Lp(a) is, however, genetically determined, and there are no drugs available that directly lower levels, although some are on the horizon. In the meantime, the experts behind the consensus statement recommend that all adults be tested at least once in their lifetime.
 

Testing Cost and Availability

This recommendation has been translated into guidelines in “many, many” countries, said lead author Florian Kronenberg, MD, MAE, Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria, but “we are far away from reaching that goal.”

“We’ve got a real problem,” added Stephen Nicholls, MD, PhD, director of the Victorian Heart Institute and a professor of cardiology at Monash University, Melbourne, Australia, as there is “not a country in the world where there’s good access to Lp(a) testing.”

Dr. Kronenberg said that the consensus statement “created a kind of momentum” toward universal testing.

Ulrich Laufs, MD, PhD, professor and chair, Department of Cardiology, University Hospital Leipzig, Leipzig, Germany, agreed, saying that, overall, Lp(a) testing has “increased dramatically,” albeit from “extremely low levels.”

Dr. Kronenberg believes that “we have to be really patient.” He cited a lack of knowledge among physicians as one of the biggest barriers to greater uptake of testing.

“There is still no appreciation of the role of Lp(a),” agreed Alberico L. Catapano, MD, PhD, director of Cardiovascular Research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, Italy, and past president of the EAS.

“That’s why it’s not mentioned” to patients, he said. “What is really needed is to inform physician colleagues that Lp(a) is not only a risk factor but is the cause” of atherosclerotic cardiovascular disease (ASCVD).

Dr. Kronenberg said that the pressure for testing can often come from the patient themselves.

Physicians then question why the patient wants to be tested when there are no medications to treat it, he added. “We really tried very hard when we did the consensus paper to say that we should perform the test and give people advice on what to do.”

Dr. Catapano believes that another major obstacle is the cost of the test, which remains high “because very few people do it,” and there is some debate over which test to use.

Taken together, these issues have meant that “payers are really struggling with the idea of funding Lp(a),” said Dr. Nicholls, adding that “there seems to be this fixation on: ‘Well, if you can’t lower Lp(a), why measure it?’ ”

Rather than blame the payers, he says there is a need to educate about the science behind testing and underline that Lp(a) is an “important risk enhancer” for cardiovascular disease.

“Because if we’re going to make people pay out of pocket, then you’re creating a massive equity issue in that only those who can afford the test have it.”
 

High Lp(a) Now What?

But once the test has been performed, there then comes the question as to what to do about the result.

“Before we get anywhere near an agent that effectively lowers Lp(a) and get it into the clinic, there are lots of things that we can do today,” said Dr. Nicholls.

If someone has an intermediate or high background cardiovascular risk and they have got a high Lp(a) level, they “should be treated more intensively, as we know that high Lp(a) patients do better if their LDL cholesterol and their blood pressure is lower.”

For Dr. Catapano, this means having the “same mindset as you do with [a patient with] high blood pressure, high LDL cholesterol, and so on, because it’s exactly the same thing: It’s interacting with your other risk factors to increase your overall risk.”

Dr. Gibson agreed. Through a range of measures, including weight loss and statin therapy, he was able to reduce his overall cardiovascular risk, and his LDL cholesterol level dropped to just 20 mg/dL.
 

A Role for Aspirin?

However, one debate that has been rolling on in recent months is whether to start patients with elevated Lp(a) on low-dose aspirin.

It gained added momentum when Pablo Corral, MD, a lipidologist and a professor in the School of Medicine, Pharmacology Department, FASTA University, Mar del Plata, Buenos Aires, Argentina, highlighted the issue on X.

He pointed to a recent study, which showed that regular aspirin use was associated with a significantly lower rate of ASCVD mortality in adults without clinical ASCVD but who had elevated Lp(a).

Dr. Nicholls said that, when you “peel away the layers” of the current evidence, there is some suggestion that Lp(a)may be prothrombotic. “So in theory, perhaps aspirin might be maybe more intuitively useful there.”

He noted that the ASPREE primary prevention study found that low-dose aspirin in older adults resulted in a significantly higher risk for major hemorrhage over placebo and did not significantly reduce the risk for cardiovascular disease.

But an analysis he and his colleagues did suggest that aspirin may indeed benefit older individuals if they have elevated Lp(a) genotypes.
 

An Individual Decision

For Dr. Kronenberg and Dr. Laufs, there is currently a lack of appropriate data to make a recommendation either way, particularly for primary prevention.

They warned that the risk for thrombosis in patients with mildly elevated Lp(a) cannot be discounted, and in most cases either “the existing risk of bleeding exceeds the beneficial effects [of aspirin], or it’s not indicated,” said Dr. Laufs.

“When we make a recommendation, we should have evidence-based data,” Dr. Kronenberg said, but, at the moment, people “somehow put their finger in the air and see” which way the wind is blowing.

Dr. Catapano urged patients to talk to their physician, as even low-dose aspirin is “very potent” at inhibiting platelets.

Dr. Gibson agreed, saying that he is in two minds, as the potential benefit has to be weighed against the bleeding risk.

He personally takes low-dose aspirin because “I know I have a low bleeding risk,” but it is a decision “that has to be taken individually between a patient and their physician.”

Dr. Gibson, Dr. Kronenberg, Dr. Nicholls, and Dr. Catapano all reported conflicts of interest with numerous pharmaceutical companies and organizations.

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

Should a patient with high lipoprotein (a), or Lp(a), be started on low-dose aspirin?

This is the conundrum facing many physicians and patients, but even getting to that point will require more availability and coverage of tests and a greater appreciation of the risk associated with Lp(a), said cardiologists.
 

Lp(a): The Silent Risk

On Lp(a) Awareness Day, C. Michael Gibson, MD, MA, CEO of the Baim Institute for Clinical Research, Boston, Massachusetts, and PERFUSE took the opportunity to talk about his experiences with testing on X.

The professor of medicine at Harvard Medical School, also in Boston, said he was surprised to find that he had a very high calcium score, despite a low-density lipoprotein (LDL) cholesterol level of just 70 mg/dL. Eventually, he found out that he had a “very, very high Lp(a),” which was particularly concerning because his grandfather died of a heart attack at 45 years of age.

But how much risk does that represent?

A 2022 consensus statement from the European Atherosclerosis Society (EAS) highlighted that epidemiologic and genetic studies “strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes,” even at very low LDL cholesterol levels.

This is because Lp(a) has proinflammatory and proatherosclerotic properties, and high levels are associated with both micro- and macrocalcification of the aortic valve. Findings from a US registry study also suggest the threshold related to increased cardiovascular risk may differ for primary and secondary prevention populations (J Am Coll Cardiol. 2024 Mar 5;83[9]:873-886).

Lp(a) is, however, genetically determined, and there are no drugs available that directly lower levels, although some are on the horizon. In the meantime, the experts behind the consensus statement recommend that all adults be tested at least once in their lifetime.
 

Testing Cost and Availability

This recommendation has been translated into guidelines in “many, many” countries, said lead author Florian Kronenberg, MD, MAE, Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria, but “we are far away from reaching that goal.”

“We’ve got a real problem,” added Stephen Nicholls, MD, PhD, director of the Victorian Heart Institute and a professor of cardiology at Monash University, Melbourne, Australia, as there is “not a country in the world where there’s good access to Lp(a) testing.”

Dr. Kronenberg said that the consensus statement “created a kind of momentum” toward universal testing.

Ulrich Laufs, MD, PhD, professor and chair, Department of Cardiology, University Hospital Leipzig, Leipzig, Germany, agreed, saying that, overall, Lp(a) testing has “increased dramatically,” albeit from “extremely low levels.”

Dr. Kronenberg believes that “we have to be really patient.” He cited a lack of knowledge among physicians as one of the biggest barriers to greater uptake of testing.

“There is still no appreciation of the role of Lp(a),” agreed Alberico L. Catapano, MD, PhD, director of Cardiovascular Research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, Italy, and past president of the EAS.

“That’s why it’s not mentioned” to patients, he said. “What is really needed is to inform physician colleagues that Lp(a) is not only a risk factor but is the cause” of atherosclerotic cardiovascular disease (ASCVD).

Dr. Kronenberg said that the pressure for testing can often come from the patient themselves.

Physicians then question why the patient wants to be tested when there are no medications to treat it, he added. “We really tried very hard when we did the consensus paper to say that we should perform the test and give people advice on what to do.”

Dr. Catapano believes that another major obstacle is the cost of the test, which remains high “because very few people do it,” and there is some debate over which test to use.

Taken together, these issues have meant that “payers are really struggling with the idea of funding Lp(a),” said Dr. Nicholls, adding that “there seems to be this fixation on: ‘Well, if you can’t lower Lp(a), why measure it?’ ”

Rather than blame the payers, he says there is a need to educate about the science behind testing and underline that Lp(a) is an “important risk enhancer” for cardiovascular disease.

“Because if we’re going to make people pay out of pocket, then you’re creating a massive equity issue in that only those who can afford the test have it.”
 

High Lp(a) Now What?

But once the test has been performed, there then comes the question as to what to do about the result.

“Before we get anywhere near an agent that effectively lowers Lp(a) and get it into the clinic, there are lots of things that we can do today,” said Dr. Nicholls.

If someone has an intermediate or high background cardiovascular risk and they have got a high Lp(a) level, they “should be treated more intensively, as we know that high Lp(a) patients do better if their LDL cholesterol and their blood pressure is lower.”

For Dr. Catapano, this means having the “same mindset as you do with [a patient with] high blood pressure, high LDL cholesterol, and so on, because it’s exactly the same thing: It’s interacting with your other risk factors to increase your overall risk.”

Dr. Gibson agreed. Through a range of measures, including weight loss and statin therapy, he was able to reduce his overall cardiovascular risk, and his LDL cholesterol level dropped to just 20 mg/dL.
 

A Role for Aspirin?

However, one debate that has been rolling on in recent months is whether to start patients with elevated Lp(a) on low-dose aspirin.

It gained added momentum when Pablo Corral, MD, a lipidologist and a professor in the School of Medicine, Pharmacology Department, FASTA University, Mar del Plata, Buenos Aires, Argentina, highlighted the issue on X.

He pointed to a recent study, which showed that regular aspirin use was associated with a significantly lower rate of ASCVD mortality in adults without clinical ASCVD but who had elevated Lp(a).

Dr. Nicholls said that, when you “peel away the layers” of the current evidence, there is some suggestion that Lp(a)may be prothrombotic. “So in theory, perhaps aspirin might be maybe more intuitively useful there.”

He noted that the ASPREE primary prevention study found that low-dose aspirin in older adults resulted in a significantly higher risk for major hemorrhage over placebo and did not significantly reduce the risk for cardiovascular disease.

But an analysis he and his colleagues did suggest that aspirin may indeed benefit older individuals if they have elevated Lp(a) genotypes.
 

An Individual Decision

For Dr. Kronenberg and Dr. Laufs, there is currently a lack of appropriate data to make a recommendation either way, particularly for primary prevention.

They warned that the risk for thrombosis in patients with mildly elevated Lp(a) cannot be discounted, and in most cases either “the existing risk of bleeding exceeds the beneficial effects [of aspirin], or it’s not indicated,” said Dr. Laufs.

“When we make a recommendation, we should have evidence-based data,” Dr. Kronenberg said, but, at the moment, people “somehow put their finger in the air and see” which way the wind is blowing.

Dr. Catapano urged patients to talk to their physician, as even low-dose aspirin is “very potent” at inhibiting platelets.

Dr. Gibson agreed, saying that he is in two minds, as the potential benefit has to be weighed against the bleeding risk.

He personally takes low-dose aspirin because “I know I have a low bleeding risk,” but it is a decision “that has to be taken individually between a patient and their physician.”

Dr. Gibson, Dr. Kronenberg, Dr. Nicholls, and Dr. Catapano all reported conflicts of interest with numerous pharmaceutical companies and organizations.

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

Should a patient with high lipoprotein (a), or Lp(a), be started on low-dose aspirin?

This is the conundrum facing many physicians and patients, but even getting to that point will require more availability and coverage of tests and a greater appreciation of the risk associated with Lp(a), said cardiologists.
 

Lp(a): The Silent Risk

On Lp(a) Awareness Day, C. Michael Gibson, MD, MA, CEO of the Baim Institute for Clinical Research, Boston, Massachusetts, and PERFUSE took the opportunity to talk about his experiences with testing on X.

The professor of medicine at Harvard Medical School, also in Boston, said he was surprised to find that he had a very high calcium score, despite a low-density lipoprotein (LDL) cholesterol level of just 70 mg/dL. Eventually, he found out that he had a “very, very high Lp(a),” which was particularly concerning because his grandfather died of a heart attack at 45 years of age.

But how much risk does that represent?

A 2022 consensus statement from the European Atherosclerosis Society (EAS) highlighted that epidemiologic and genetic studies “strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes,” even at very low LDL cholesterol levels.

This is because Lp(a) has proinflammatory and proatherosclerotic properties, and high levels are associated with both micro- and macrocalcification of the aortic valve. Findings from a US registry study also suggest the threshold related to increased cardiovascular risk may differ for primary and secondary prevention populations (J Am Coll Cardiol. 2024 Mar 5;83[9]:873-886).

Lp(a) is, however, genetically determined, and there are no drugs available that directly lower levels, although some are on the horizon. In the meantime, the experts behind the consensus statement recommend that all adults be tested at least once in their lifetime.
 

Testing Cost and Availability

This recommendation has been translated into guidelines in “many, many” countries, said lead author Florian Kronenberg, MD, MAE, Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria, but “we are far away from reaching that goal.”

“We’ve got a real problem,” added Stephen Nicholls, MD, PhD, director of the Victorian Heart Institute and a professor of cardiology at Monash University, Melbourne, Australia, as there is “not a country in the world where there’s good access to Lp(a) testing.”

Dr. Kronenberg said that the consensus statement “created a kind of momentum” toward universal testing.

Ulrich Laufs, MD, PhD, professor and chair, Department of Cardiology, University Hospital Leipzig, Leipzig, Germany, agreed, saying that, overall, Lp(a) testing has “increased dramatically,” albeit from “extremely low levels.”

Dr. Kronenberg believes that “we have to be really patient.” He cited a lack of knowledge among physicians as one of the biggest barriers to greater uptake of testing.

“There is still no appreciation of the role of Lp(a),” agreed Alberico L. Catapano, MD, PhD, director of Cardiovascular Research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, Italy, and past president of the EAS.

“That’s why it’s not mentioned” to patients, he said. “What is really needed is to inform physician colleagues that Lp(a) is not only a risk factor but is the cause” of atherosclerotic cardiovascular disease (ASCVD).

Dr. Kronenberg said that the pressure for testing can often come from the patient themselves.

Physicians then question why the patient wants to be tested when there are no medications to treat it, he added. “We really tried very hard when we did the consensus paper to say that we should perform the test and give people advice on what to do.”

Dr. Catapano believes that another major obstacle is the cost of the test, which remains high “because very few people do it,” and there is some debate over which test to use.

Taken together, these issues have meant that “payers are really struggling with the idea of funding Lp(a),” said Dr. Nicholls, adding that “there seems to be this fixation on: ‘Well, if you can’t lower Lp(a), why measure it?’ ”

Rather than blame the payers, he says there is a need to educate about the science behind testing and underline that Lp(a) is an “important risk enhancer” for cardiovascular disease.

“Because if we’re going to make people pay out of pocket, then you’re creating a massive equity issue in that only those who can afford the test have it.”
 

High Lp(a) Now What?

But once the test has been performed, there then comes the question as to what to do about the result.

“Before we get anywhere near an agent that effectively lowers Lp(a) and get it into the clinic, there are lots of things that we can do today,” said Dr. Nicholls.

If someone has an intermediate or high background cardiovascular risk and they have got a high Lp(a) level, they “should be treated more intensively, as we know that high Lp(a) patients do better if their LDL cholesterol and their blood pressure is lower.”

For Dr. Catapano, this means having the “same mindset as you do with [a patient with] high blood pressure, high LDL cholesterol, and so on, because it’s exactly the same thing: It’s interacting with your other risk factors to increase your overall risk.”

Dr. Gibson agreed. Through a range of measures, including weight loss and statin therapy, he was able to reduce his overall cardiovascular risk, and his LDL cholesterol level dropped to just 20 mg/dL.
 

A Role for Aspirin?

However, one debate that has been rolling on in recent months is whether to start patients with elevated Lp(a) on low-dose aspirin.

It gained added momentum when Pablo Corral, MD, a lipidologist and a professor in the School of Medicine, Pharmacology Department, FASTA University, Mar del Plata, Buenos Aires, Argentina, highlighted the issue on X.

He pointed to a recent study, which showed that regular aspirin use was associated with a significantly lower rate of ASCVD mortality in adults without clinical ASCVD but who had elevated Lp(a).

Dr. Nicholls said that, when you “peel away the layers” of the current evidence, there is some suggestion that Lp(a)may be prothrombotic. “So in theory, perhaps aspirin might be maybe more intuitively useful there.”

He noted that the ASPREE primary prevention study found that low-dose aspirin in older adults resulted in a significantly higher risk for major hemorrhage over placebo and did not significantly reduce the risk for cardiovascular disease.

But an analysis he and his colleagues did suggest that aspirin may indeed benefit older individuals if they have elevated Lp(a) genotypes.
 

An Individual Decision

For Dr. Kronenberg and Dr. Laufs, there is currently a lack of appropriate data to make a recommendation either way, particularly for primary prevention.

They warned that the risk for thrombosis in patients with mildly elevated Lp(a) cannot be discounted, and in most cases either “the existing risk of bleeding exceeds the beneficial effects [of aspirin], or it’s not indicated,” said Dr. Laufs.

“When we make a recommendation, we should have evidence-based data,” Dr. Kronenberg said, but, at the moment, people “somehow put their finger in the air and see” which way the wind is blowing.

Dr. Catapano urged patients to talk to their physician, as even low-dose aspirin is “very potent” at inhibiting platelets.

Dr. Gibson agreed, saying that he is in two minds, as the potential benefit has to be weighed against the bleeding risk.

He personally takes low-dose aspirin because “I know I have a low bleeding risk,” but it is a decision “that has to be taken individually between a patient and their physician.”

Dr. Gibson, Dr. Kronenberg, Dr. Nicholls, and Dr. Catapano all reported conflicts of interest with numerous pharmaceutical companies and organizations.

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

ORLANDO, Florida — Clinicians should keep in mind concerns about overdiagnosis of thyroid cancer when prescribing glucagon-like peptide 1 (GLP-1) drugs, as the US boxed warning about this risk for this class of medicines for certain tumors in mice could trigger excess screening, an expert endocrinologist said.

Speaking at the annual American Diabetes Association (ADA) 84th Scientific Sessions, Elizabeth N. Pearce, MD, MSc, a professor of medicine at Boston University, Boston, reviewed the different approaches US and European regulators have taken for the GLP-1 drugs. She also explained the current concerns about the wide use of thyroid screening in general and how these intersect with the rapid uptake of the GLP-1 drugs.

“We should not be screening for thyroid nodules before or during GLP-1 receptor agonist treatment just because the patients are on these medications,” said Dr. Pearce, who is also a former board president of the American Thyroid Association (ATA). “We do not want to contribute to this epidemic of overdiagnosis of thyroid cancer.”

The ATA and the US Preventive Services Task Force (USPSTF) are among the health organizations that have in recent years sought to boost public awareness of the potential risks for excess screening of thyroid nodules. In 2017, the USPSTF, which influences insurance coverage, recommended against routine screening for thyroid cancer in asymptomatic adults. At that time, the incidence of thyroid cancer detection had increased by 4.5% per year over a decade, faster than for any other cancer, but without a corresponding change in the mortality rate, USPSTF said.

“Unequivocally, the thyroid cancer mortality has not kept pace with thyroid cancer detection,” Dr. Pearce said at the ADA meeting. “We’ve been diagnosing a lot of small thyroid cancers that people would otherwise have been destined to die with and not die of.”

Dr. Pearce said clinicians should be careful not to overly restrict access to GLP-1 drugs due to concerns about thyroid cancer — and they should use care in screening nodules.

It’s possible that the weight loss experienced by people taking GLP-1 drugs may make preexisting thyroid nodules more prominent, Dr. Pearce said. It’s also likely that the US boxed warning on thyroid risk on GLP-1 drugs makes clinicians and patients more likely to look for these kinds of growths.

Dr. Pearce urged adherence to guidelines such as the ones the ATA published in 2015 for assessing nodules.

In an interview with this news organization, Dr. Pearce noted the frequency of CT scans in US medical practice in turning up many incidental thyroid nodules, a finding that can cause some panic for patients and their clinicians.

But it helps to put these findings in context, as by the age of 50, about 40% of women will have at least one thyroid nodule, making this a very common finding, she said.

“The vast majority are not malignant,” Dr. Pearce said. “When you explain this to patients, it alleviates anxiety.”
 

The US, European Union Differences

In the United States, the label for GLP-1 drugs starts with a boxed warning about thyroid C-cell tumors seen in rodents given these medicines in testing.

It’s unknown if the medicines could cause medullary thyroid carcinoma (MTC) in humans, the label adds. The drug is contraindicated in patients with a personal or family history of MTC or multiple endocrine neoplasia syndrome 2, the boxed warning says. This is based largely on data seen in laboratory rats.

“It’s a big black box warning that gets people’s attention,” Dr. Pearce said. “Important to note that if you practice in Europe, you will not be familiar with this labeling because it doesn’t exist there. They’ve never had this warning on the European package.”

The European Medicines Agency (EMA) does include information about the results of rodent studies as part of the discussion of known and potential risks for GLP-1 drugs but has not emphasized it in the same way as the US drug labels do.

For example, the public assessment report posted on the EMA website for semaglutide (Ozempic, Novo Nordisk) notes that nonlethal thyroid C-cell tumors “observed in rodents are a class effect for GLP-1 receptor agonists.” It’s possible that these may be due to a particular sensitivity in rodents, the report said.

“The relevance for humans is considered to be low but cannot be completely excluded,” the EMA report said in the product information section of the report.

There has been ongoing interest in the issue.

The EMA’s Pharmacovigilance Risk Assessment Committee (PRAC) in October concluded that the available evidence does not support a causal association between GLP-1 receptor agonists and thyroid cancer.

The EMA’s PRAC safety committee said it began assessing the evidence about a possible connection following the publication of a study in 2022 in the journal Diabetes Care. That paper reported on an analysis that suggested increased risk for all thyroid cancer and medullary thyroid cancer with the use of GLP-1 drugs, particularly after 1-3 years of treatment.

The EMA’s PRAC said that in making its decision, it also considered other published papers on this topic as well as clinical and postmarketing data on GLP-1 drugs.

In an email interview, Jean-Luc Faillie, MD, PhD, corresponding author of the Diabetes Care paper, called for continued “vigilance and prudence in clinical practice” with GLP-1 drugs.

His paper reported on a case-control analysis on the basis of reports from the French national healthcare insurance system database, looking at people who had taken GLP-1 drugs and similar people who had not.

Due to a lack of a specific diagnostic code for medullary thyroid cancers, the researchers used a composite definition combining thyroid cancer diagnosis with several calcitonin tests, a carcinoembryonic antigen test, or a specific treatment (vandetanib) to identify potential cases of this cancer.

It’s possible that this method could have led to overestimation of MTC among the cases of thyroid cancer, wrote Dr. Faillie, who is a professor at France’s Université de Montpellier, Montpellier, France, and part of its pharmacological vigilance service.

“Nevertheless, it’s crucial to emphasize that any potential overestimation of MTC cases would likely apply equally to both GLP-1 receptor agonist–exposed and unexposed groups,” Dr. Faillie wrote. “Therefore, it should not significantly impact our main findings regarding the suggested increased risk associated with GLP-1 receptor agonist use.”

Dr. Pearce disclosed honoraria for speaking at the Merck China Forum. Dr. Faille and his coauthors reported no conflicts of interest in the publication of their study. Their research was supported by the French Medicines Agency (Agence Nationale de Sécurité du Médicament et des Produits de Santé, grant 2019S015) in the context of a partnership with the Health Product Epidemiology Scientific Interest Group (EPI-PHARE). The study was part of France’s Drugs Systematized Assessment in Real-Life Environment (DRUGS-SAFEr) research program.

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

ORLANDO, Florida — Clinicians should keep in mind concerns about overdiagnosis of thyroid cancer when prescribing glucagon-like peptide 1 (GLP-1) drugs, as the US boxed warning about this risk for this class of medicines for certain tumors in mice could trigger excess screening, an expert endocrinologist said.

Speaking at the annual American Diabetes Association (ADA) 84th Scientific Sessions, Elizabeth N. Pearce, MD, MSc, a professor of medicine at Boston University, Boston, reviewed the different approaches US and European regulators have taken for the GLP-1 drugs. She also explained the current concerns about the wide use of thyroid screening in general and how these intersect with the rapid uptake of the GLP-1 drugs.

“We should not be screening for thyroid nodules before or during GLP-1 receptor agonist treatment just because the patients are on these medications,” said Dr. Pearce, who is also a former board president of the American Thyroid Association (ATA). “We do not want to contribute to this epidemic of overdiagnosis of thyroid cancer.”

The ATA and the US Preventive Services Task Force (USPSTF) are among the health organizations that have in recent years sought to boost public awareness of the potential risks for excess screening of thyroid nodules. In 2017, the USPSTF, which influences insurance coverage, recommended against routine screening for thyroid cancer in asymptomatic adults. At that time, the incidence of thyroid cancer detection had increased by 4.5% per year over a decade, faster than for any other cancer, but without a corresponding change in the mortality rate, USPSTF said.

“Unequivocally, the thyroid cancer mortality has not kept pace with thyroid cancer detection,” Dr. Pearce said at the ADA meeting. “We’ve been diagnosing a lot of small thyroid cancers that people would otherwise have been destined to die with and not die of.”

Dr. Pearce said clinicians should be careful not to overly restrict access to GLP-1 drugs due to concerns about thyroid cancer — and they should use care in screening nodules.

It’s possible that the weight loss experienced by people taking GLP-1 drugs may make preexisting thyroid nodules more prominent, Dr. Pearce said. It’s also likely that the US boxed warning on thyroid risk on GLP-1 drugs makes clinicians and patients more likely to look for these kinds of growths.

Dr. Pearce urged adherence to guidelines such as the ones the ATA published in 2015 for assessing nodules.

In an interview with this news organization, Dr. Pearce noted the frequency of CT scans in US medical practice in turning up many incidental thyroid nodules, a finding that can cause some panic for patients and their clinicians.

But it helps to put these findings in context, as by the age of 50, about 40% of women will have at least one thyroid nodule, making this a very common finding, she said.

“The vast majority are not malignant,” Dr. Pearce said. “When you explain this to patients, it alleviates anxiety.”
 

The US, European Union Differences

In the United States, the label for GLP-1 drugs starts with a boxed warning about thyroid C-cell tumors seen in rodents given these medicines in testing.

It’s unknown if the medicines could cause medullary thyroid carcinoma (MTC) in humans, the label adds. The drug is contraindicated in patients with a personal or family history of MTC or multiple endocrine neoplasia syndrome 2, the boxed warning says. This is based largely on data seen in laboratory rats.

“It’s a big black box warning that gets people’s attention,” Dr. Pearce said. “Important to note that if you practice in Europe, you will not be familiar with this labeling because it doesn’t exist there. They’ve never had this warning on the European package.”

The European Medicines Agency (EMA) does include information about the results of rodent studies as part of the discussion of known and potential risks for GLP-1 drugs but has not emphasized it in the same way as the US drug labels do.

For example, the public assessment report posted on the EMA website for semaglutide (Ozempic, Novo Nordisk) notes that nonlethal thyroid C-cell tumors “observed in rodents are a class effect for GLP-1 receptor agonists.” It’s possible that these may be due to a particular sensitivity in rodents, the report said.

“The relevance for humans is considered to be low but cannot be completely excluded,” the EMA report said in the product information section of the report.

There has been ongoing interest in the issue.

The EMA’s Pharmacovigilance Risk Assessment Committee (PRAC) in October concluded that the available evidence does not support a causal association between GLP-1 receptor agonists and thyroid cancer.

The EMA’s PRAC safety committee said it began assessing the evidence about a possible connection following the publication of a study in 2022 in the journal Diabetes Care. That paper reported on an analysis that suggested increased risk for all thyroid cancer and medullary thyroid cancer with the use of GLP-1 drugs, particularly after 1-3 years of treatment.

The EMA’s PRAC said that in making its decision, it also considered other published papers on this topic as well as clinical and postmarketing data on GLP-1 drugs.

In an email interview, Jean-Luc Faillie, MD, PhD, corresponding author of the Diabetes Care paper, called for continued “vigilance and prudence in clinical practice” with GLP-1 drugs.

His paper reported on a case-control analysis on the basis of reports from the French national healthcare insurance system database, looking at people who had taken GLP-1 drugs and similar people who had not.

Due to a lack of a specific diagnostic code for medullary thyroid cancers, the researchers used a composite definition combining thyroid cancer diagnosis with several calcitonin tests, a carcinoembryonic antigen test, or a specific treatment (vandetanib) to identify potential cases of this cancer.

It’s possible that this method could have led to overestimation of MTC among the cases of thyroid cancer, wrote Dr. Faillie, who is a professor at France’s Université de Montpellier, Montpellier, France, and part of its pharmacological vigilance service.

“Nevertheless, it’s crucial to emphasize that any potential overestimation of MTC cases would likely apply equally to both GLP-1 receptor agonist–exposed and unexposed groups,” Dr. Faillie wrote. “Therefore, it should not significantly impact our main findings regarding the suggested increased risk associated with GLP-1 receptor agonist use.”

Dr. Pearce disclosed honoraria for speaking at the Merck China Forum. Dr. Faille and his coauthors reported no conflicts of interest in the publication of their study. Their research was supported by the French Medicines Agency (Agence Nationale de Sécurité du Médicament et des Produits de Santé, grant 2019S015) in the context of a partnership with the Health Product Epidemiology Scientific Interest Group (EPI-PHARE). The study was part of France’s Drugs Systematized Assessment in Real-Life Environment (DRUGS-SAFEr) research program.

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

ORLANDO, Florida — Clinicians should keep in mind concerns about overdiagnosis of thyroid cancer when prescribing glucagon-like peptide 1 (GLP-1) drugs, as the US boxed warning about this risk for this class of medicines for certain tumors in mice could trigger excess screening, an expert endocrinologist said.

Speaking at the annual American Diabetes Association (ADA) 84th Scientific Sessions, Elizabeth N. Pearce, MD, MSc, a professor of medicine at Boston University, Boston, reviewed the different approaches US and European regulators have taken for the GLP-1 drugs. She also explained the current concerns about the wide use of thyroid screening in general and how these intersect with the rapid uptake of the GLP-1 drugs.

“We should not be screening for thyroid nodules before or during GLP-1 receptor agonist treatment just because the patients are on these medications,” said Dr. Pearce, who is also a former board president of the American Thyroid Association (ATA). “We do not want to contribute to this epidemic of overdiagnosis of thyroid cancer.”

The ATA and the US Preventive Services Task Force (USPSTF) are among the health organizations that have in recent years sought to boost public awareness of the potential risks for excess screening of thyroid nodules. In 2017, the USPSTF, which influences insurance coverage, recommended against routine screening for thyroid cancer in asymptomatic adults. At that time, the incidence of thyroid cancer detection had increased by 4.5% per year over a decade, faster than for any other cancer, but without a corresponding change in the mortality rate, USPSTF said.

“Unequivocally, the thyroid cancer mortality has not kept pace with thyroid cancer detection,” Dr. Pearce said at the ADA meeting. “We’ve been diagnosing a lot of small thyroid cancers that people would otherwise have been destined to die with and not die of.”

Dr. Pearce said clinicians should be careful not to overly restrict access to GLP-1 drugs due to concerns about thyroid cancer — and they should use care in screening nodules.

It’s possible that the weight loss experienced by people taking GLP-1 drugs may make preexisting thyroid nodules more prominent, Dr. Pearce said. It’s also likely that the US boxed warning on thyroid risk on GLP-1 drugs makes clinicians and patients more likely to look for these kinds of growths.

Dr. Pearce urged adherence to guidelines such as the ones the ATA published in 2015 for assessing nodules.

In an interview with this news organization, Dr. Pearce noted the frequency of CT scans in US medical practice in turning up many incidental thyroid nodules, a finding that can cause some panic for patients and their clinicians.

But it helps to put these findings in context, as by the age of 50, about 40% of women will have at least one thyroid nodule, making this a very common finding, she said.

“The vast majority are not malignant,” Dr. Pearce said. “When you explain this to patients, it alleviates anxiety.”
 

The US, European Union Differences

In the United States, the label for GLP-1 drugs starts with a boxed warning about thyroid C-cell tumors seen in rodents given these medicines in testing.

It’s unknown if the medicines could cause medullary thyroid carcinoma (MTC) in humans, the label adds. The drug is contraindicated in patients with a personal or family history of MTC or multiple endocrine neoplasia syndrome 2, the boxed warning says. This is based largely on data seen in laboratory rats.

“It’s a big black box warning that gets people’s attention,” Dr. Pearce said. “Important to note that if you practice in Europe, you will not be familiar with this labeling because it doesn’t exist there. They’ve never had this warning on the European package.”

The European Medicines Agency (EMA) does include information about the results of rodent studies as part of the discussion of known and potential risks for GLP-1 drugs but has not emphasized it in the same way as the US drug labels do.

For example, the public assessment report posted on the EMA website for semaglutide (Ozempic, Novo Nordisk) notes that nonlethal thyroid C-cell tumors “observed in rodents are a class effect for GLP-1 receptor agonists.” It’s possible that these may be due to a particular sensitivity in rodents, the report said.

“The relevance for humans is considered to be low but cannot be completely excluded,” the EMA report said in the product information section of the report.

There has been ongoing interest in the issue.

The EMA’s Pharmacovigilance Risk Assessment Committee (PRAC) in October concluded that the available evidence does not support a causal association between GLP-1 receptor agonists and thyroid cancer.

The EMA’s PRAC safety committee said it began assessing the evidence about a possible connection following the publication of a study in 2022 in the journal Diabetes Care. That paper reported on an analysis that suggested increased risk for all thyroid cancer and medullary thyroid cancer with the use of GLP-1 drugs, particularly after 1-3 years of treatment.

The EMA’s PRAC said that in making its decision, it also considered other published papers on this topic as well as clinical and postmarketing data on GLP-1 drugs.

In an email interview, Jean-Luc Faillie, MD, PhD, corresponding author of the Diabetes Care paper, called for continued “vigilance and prudence in clinical practice” with GLP-1 drugs.

His paper reported on a case-control analysis on the basis of reports from the French national healthcare insurance system database, looking at people who had taken GLP-1 drugs and similar people who had not.

Due to a lack of a specific diagnostic code for medullary thyroid cancers, the researchers used a composite definition combining thyroid cancer diagnosis with several calcitonin tests, a carcinoembryonic antigen test, or a specific treatment (vandetanib) to identify potential cases of this cancer.

It’s possible that this method could have led to overestimation of MTC among the cases of thyroid cancer, wrote Dr. Faillie, who is a professor at France’s Université de Montpellier, Montpellier, France, and part of its pharmacological vigilance service.

“Nevertheless, it’s crucial to emphasize that any potential overestimation of MTC cases would likely apply equally to both GLP-1 receptor agonist–exposed and unexposed groups,” Dr. Faillie wrote. “Therefore, it should not significantly impact our main findings regarding the suggested increased risk associated with GLP-1 receptor agonist use.”

Dr. Pearce disclosed honoraria for speaking at the Merck China Forum. Dr. Faille and his coauthors reported no conflicts of interest in the publication of their study. Their research was supported by the French Medicines Agency (Agence Nationale de Sécurité du Médicament et des Produits de Santé, grant 2019S015) in the context of a partnership with the Health Product Epidemiology Scientific Interest Group (EPI-PHARE). The study was part of France’s Drugs Systematized Assessment in Real-Life Environment (DRUGS-SAFEr) research program.

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

This transcript has been edited for clarity. 

My oldest daughter is at sleepaway camp for a couple of weeks, and the camp has a photographer who goes around all day taking pictures of the kids, which get uploaded to a private Facebook group. In the past, I would go online every day (or, okay, several times a day) and scroll through all those pictures looking for one that features my kid. 

I don’t have to do that anymore. This year, I simply uploaded a picture of my daughter to an app and artificial intelligence (AI) takes care of the rest, recognizing her face amidst the sea of smiling children, and flagging just those photos for me to peruse. It’s amazing, really. And a bit scary.

The fact that facial recognition has penetrated the summer camp market should tell you that the tech is truly ubiquitous. But today we’re going to think a bit more about what AI can do with a picture of your face, because the power of facial recognition is not just skin deep.

What’s got me hot and bothered about facial images is this paper, appearing in Cell Metabolism, which adds a new layer to the standard facial-analysis playbook: facial temperature.

To understand this paper, you need to understand a whole field of research that is developing various different “clocks” for age. 

It turns out that age really is just a number. Our cells, our proteins, our biochemistry can be analyzed to give different numbers. These “clocks,” as distinct from the calendar we usually use to measure our age, might have more predictive power than the number itself. 

There are numerous molecular clocks, such as telomere length, that not only correlate with calendar age but are superior to calendar age in predicting age-related complications. Testing telomere length typically requires a blood sample — and remains costly. But we can use other sources to estimate age; how about a photo?

I mean, we do this all the time when we meet someone new or, as a physician, when we meet a new patient. I have often written that a patient “appears younger than their stated age,” and we’ve all had the experience of hearing how old someone is and being shocked. I mean, have you seen Sharon Stone recently? She’s 66 years old. Okay — to be fair, there might be some outside help there. But you get the point.

Back to the Cell Metabolism paper. Researchers report on multiple algorithms to obtain an “age” from a picture of an individual’s face. 

The first algorithm is pretty straightforward. Researchers collected 2811 images, all of Han Chinese individuals ranging in age from 20 to 90 years, and reconstructed a 3D facial map from those. 

memubrocheposwowrutaphewrowrimijebrauulathaleswot

prosterechiwremedrijatreclewrivudruwabruluphestespepustostuwruslunusliprukibejifrireshichethupiphemohothastesiwepriseputreualachigovusheruchodrenespestestepebeniphesivuchabrewrajichuphadrililicludrop

phatritribeuacrispicishabrejajuchephebrihedricevoshavivevospitheshuvotretegutrobujawoclodrirekuboswestekiclamacrawrijaveuithejabruvasistebrasicrugonetrowowuuishecropholiclumabristanawreswushislebaphaprihewreshagubreshiclicredrugostubrilegatrid

vatuthoviclobrauucushosudruswudevudrocetujoshoclouibastouetomacafrepreduprehachiwrewiprespirucacleslestisusposholemislunauutrocetetristiclejagewrehisloslecrithewru

thiprapesliposhuphidracloricucluwrispichikilatrehuuubiphadrumuslihouudrupakaprochadidrebijoj

be

swiprabuwroceslidrowruthoshodrulapropithuuucapilechuchoribubrathujireswovifrophuswemaslowruswijajadihogaspabestetrigupreclekushefrowaphowruspupuvatrataspeprolidecuwrowrafratejithucawodisowetinetodreche

br

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

My oldest daughter is at sleepaway camp for a couple of weeks, and the camp has a photographer who goes around all day taking pictures of the kids, which get uploaded to a private Facebook group. In the past, I would go online every day (or, okay, several times a day) and scroll through all those pictures looking for one that features my kid. 

I don’t have to do that anymore. This year, I simply uploaded a picture of my daughter to an app and artificial intelligence (AI) takes care of the rest, recognizing her face amidst the sea of smiling children, and flagging just those photos for me to peruse. It’s amazing, really. And a bit scary.

The fact that facial recognition has penetrated the summer camp market should tell you that the tech is truly ubiquitous. But today we’re going to think a bit more about what AI can do with a picture of your face, because the power of facial recognition is not just skin deep.

What’s got me hot and bothered about facial images is this paper, appearing in Cell Metabolism, which adds a new layer to the standard facial-analysis playbook: facial temperature.

To understand this paper, you need to understand a whole field of research that is developing various different “clocks” for age. 

It turns out that age really is just a number. Our cells, our proteins, our biochemistry can be analyzed to give different numbers. These “clocks,” as distinct from the calendar we usually use to measure our age, might have more predictive power than the number itself. 

There are numerous molecular clocks, such as telomere length, that not only correlate with calendar age but are superior to calendar age in predicting age-related complications. Testing telomere length typically requires a blood sample — and remains costly. But we can use other sources to estimate age; how about a photo?

I mean, we do this all the time when we meet someone new or, as a physician, when we meet a new patient. I have often written that a patient “appears younger than their stated age,” and we’ve all had the experience of hearing how old someone is and being shocked. I mean, have you seen Sharon Stone recently? She’s 66 years old. Okay — to be fair, there might be some outside help there. But you get the point.

Back to the Cell Metabolism paper. Researchers report on multiple algorithms to obtain an “age” from a picture of an individual’s face. 

The first algorithm is pretty straightforward. Researchers collected 2811 images, all of Han Chinese individuals ranging in age from 20 to 90 years, and reconstructed a 3D facial map from those. 

memubrocheposwowrutaphewrowrimijebrauulathaleswot

prosterechiwremedrijatreclewrivudruwabruluphestespepustostuwruslunusliprukibejifrireshichethupiphemohothastesiwepriseputreualachigovusheruchodrenespestestepebeniphesivuchabrewrajichuphadrililicludrop

phatritribeuacrispicishabrejajuchephebrihedricevoshavivevospitheshuvotretegutrobujawoclodrirekuboswestekiclamacrawrijaveuithejabruvasistebrasicrugonetrowowuuishecropholiclumabristanawreswushislebaphaprihewreshagubreshiclicredrugostubrilegatrid

vatuthoviclobrauucushosudruswudevudrocetujoshoclouibastouetomacafrepreduprehachiwrewiprespirucacleslestisusposholemislunauutrocetetristiclejagewrehisloslecrithewru

thiprapesliposhuphidracloricucluwrispichikilatrehuuubiphadrumuslihouudrupakaprochadidrebijoj

be

swiprabuwroceslidrowruthoshodrulapropithuuucapilechuchoribubrathujireswovifrophuswemaslowruswijajadihogaspabestetrigupreclekushefrowaphowruspupuvatrataspeprolidecuwrowrafratejithucawodisowetinetodreche

br

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

My oldest daughter is at sleepaway camp for a couple of weeks, and the camp has a photographer who goes around all day taking pictures of the kids, which get uploaded to a private Facebook group. In the past, I would go online every day (or, okay, several times a day) and scroll through all those pictures looking for one that features my kid. 

I don’t have to do that anymore. This year, I simply uploaded a picture of my daughter to an app and artificial intelligence (AI) takes care of the rest, recognizing her face amidst the sea of smiling children, and flagging just those photos for me to peruse. It’s amazing, really. And a bit scary.

The fact that facial recognition has penetrated the summer camp market should tell you that the tech is truly ubiquitous. But today we’re going to think a bit more about what AI can do with a picture of your face, because the power of facial recognition is not just skin deep.

What’s got me hot and bothered about facial images is this paper, appearing in Cell Metabolism, which adds a new layer to the standard facial-analysis playbook: facial temperature.

To understand this paper, you need to understand a whole field of research that is developing various different “clocks” for age. 

It turns out that age really is just a number. Our cells, our proteins, our biochemistry can be analyzed to give different numbers. These “clocks,” as distinct from the calendar we usually use to measure our age, might have more predictive power than the number itself. 

There are numerous molecular clocks, such as telomere length, that not only correlate with calendar age but are superior to calendar age in predicting age-related complications. Testing telomere length typically requires a blood sample — and remains costly. But we can use other sources to estimate age; how about a photo?

I mean, we do this all the time when we meet someone new or, as a physician, when we meet a new patient. I have often written that a patient “appears younger than their stated age,” and we’ve all had the experience of hearing how old someone is and being shocked. I mean, have you seen Sharon Stone recently? She’s 66 years old. Okay — to be fair, there might be some outside help there. But you get the point.

Back to the Cell Metabolism paper. Researchers report on multiple algorithms to obtain an “age” from a picture of an individual’s face. 

The first algorithm is pretty straightforward. Researchers collected 2811 images, all of Han Chinese individuals ranging in age from 20 to 90 years, and reconstructed a 3D facial map from those. 

memubrocheposwowrutaphewrowrimijebrauulathaleswot

prosterechiwremedrijatreclewrivudruwabruluphestespepustostuwruslunusliprukibejifrireshichethupiphemohothastesiwepriseputreualachigovusheruchodrenespestestepebeniphesivuchabrewrajichuphadrililicludrop

phatritribeuacrispicishabrejajuchephebrihedricevoshavivevospitheshuvotretegutrobujawoclodrirekuboswestekiclamacrawrijaveuithejabruvasistebrasicrugonetrowowuuishecropholiclumabristanawreswushislebaphaprihewreshagubreshiclicredrugostubrilegatrid

vatuthoviclobrauucushosudruswudevudrocetujoshoclouibastouetomacafrepreduprehachiwrewiprespirucacleslestisusposholemislunauutrocetetristiclejagewrehisloslecrithewru

thiprapesliposhuphidracloricucluwrispichikilatrehuuubiphadrumuslihouudrupakaprochadidrebijoj

be

swiprabuwroceslidrowruthoshodrulapropithuuucapilechuchoribubrathujireswovifrophuswemaslowruswijajadihogaspabestetrigupreclekushefrowaphowruspupuvatrataspeprolidecuwrowrafratejithucawodisowetinetodreche

br

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

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

ORLANDO, FLORIDA — What to prioritize first in managing early diabetes? That was the question debated on an expert panel at the American Diabetes Association (ADA) 84th Scientific Sessions, with impassioned responses ranging from a plea to “treat obesity first,” to a James Carville–inspired counterpoint of “it’s the glucose, stupid.” 

With a focus on preventing complications and inducing remission rounding out the four positions argued, Session Moderator Ravi Retnakaran, MD, of the University of Toronto, noted that the options reflect the tricky choices clinicians treating patients with diabetes are pressed to make on a daily basis.

“In clinical decision-making [for early diabetes], we are faced with weighing each of these variables for the individual patient, and while all are good options, strong arguments can be made for prioritizing each — with the potential of each choice to influence or improve all of the others,” Dr. Retnakaran told this news organization.
 

Which to Prioritize First?

Making the obesity first argument, Ania M. Jastreboff, MD, PhD, associate professor and director of the Yale Obesity Research Center at Yale School of Medicine, New Haven, Connecticut, noted the striking statistic that nearly 90% of people with type 2 diabetes have overweight or obesity and discussed the ever-expanding data showing the benefits of drugs including glucagon-like peptide 1 (GLP-1) receptor agonists not just in weight loss but also in kidney, cardiovascular, and, as presented at the meeting, sleep apnea improvement.

She contrasted the experiences of two patients with obesity: One treated for the obesity upon type 2 diagnosis — who had a quick normalization of lipids and hypertension soon after the obesity treatment — and the other presenting after 10 years with type 2 diabetes — who was on therapy for hypertension and hyperlipidemia but not for obesity and whose diseases were not as easily treated by that point.

“Why are we treating all the downstream effects and we’re not treating the disease that is potentially the root cause of all these other diseases?” Dr. Jastreboff said.
 

Complications?

Arguing in favor of focusing on complications, Roopa Mehta, MD, PhD, with the department of endocrinology and metabolism at Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán (INCMNSZ), Mexico City, made the case that stakes don’t get any higher in diabetes than when it comes the looming threat of potentially fatal complications.

Acute myocardial infarction, stroke, amputation, and end-stage renal disease are all on the list of unwanted outcomes and need to be considered even in the earliest stages, as data show early onset type 2 diabetes is linked to life expectancy.

“The main goal of management has always been to prevent complications,” she noted. Citing ADA guidelines, Dr. Mehta underscored the benefits of first- and second-line therapy of metformin, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and GLP-1 receptor agonists for most patients.
 

Remission?

Discussing the priority of putting patients into disease remission, Roy Taylor, MD, professor of medicine and metabolism at Newcastle University and Newcastle Hospitals NHS in Newcastle upon Tyne, England, and author of the book Life Without Diabetes, focused on an evidence-based alternative to achieving remission — a nonpharmacologic approach that avoids costly and sometimes inaccessible drugs.

In the intervention, described in the DiRECT randomized trial and subsequently in the UK National Health Service Type 2 Diabetes Path to Remission Program, patients with overweight or obesity were placed on a highly restrictive diet of just 800-900 calories a day for 12-20 weeks, followed by maintenance for 12 months, and they not only achieved weight loss but also achieved diabetes remission, in some cases long term.

Acknowledging that “this is not for everyone,” Dr. Taylor asserted that “we have to realize there is a substantial minority of people who want to be healthy but who don’t want to be medicalized,” he said.

“They want their health, and they can do extremely well.”
 

Glucose?

In taking his self-titled “it’s the glucose, stupid” stand, David M. Nathan, MD, of the Diabetes Center, Massachusetts General Hospital, Harvard Medical School, in Boston, cited extensive evidence showing that early intensive blood glucose control with treatment including sulfonylureas, insulin, or metformin significantly reduced the risk for complications in type 2 diabetes 15 or more years later, including renal failure, blindness, amputation, and myocardial infarctions, in addition to a reduction in diabetes-related death.

“In many of these studies, you saw the benefit even in the setting of weight-gain,” Dr. Nathan underscored.

He further noted the “sobering” findings of the Look AHEAD study, which had to be stopped due to futility when an intensive lifestyle/weight loss intervention showed no significant benefits in terms of cardiovascular disease in people with type 2 diabetes at a median follow-up of 9.6 years.

Ultimately, “diabetes, type 1 and type 2, remains a gluco-centric disease,” Dr. Nathan asserted. “Hyperglycemia is the only universal link between all forms of diabetes and mortality, and the long-term complications of diabetes are intimately associated with hyperglycemia.”
 

Tackling the Caveats

The ensuing panel discussion did not fail to deliver in delving into key areas of contention, particularly in terms of GLP-1 treatment.

Regarding a lack of data on the potential long-term effects of GLP-1s: “Yes, there are a huge number of studies [on GLP-1 receptor agonists], but they are, in general, over short periods of time and driven by pharma, who get in and get out as quickly as they can and have little in the way of interest to do comparative effectiveness studies,” Dr. Nathan argued.

“Meanwhile, this is like the crack cocaine of medications — patients have to stay on it for a lifetime or they will regain the weight — are you concerned at all about a lifetime of exposure to GLP-1 [drugs]?” he asked the panel.

Dr. Jastreboff responded that the first GLP-1 receptor agonist medications were approved in 2005, nearly 20 years ago, by the US Food and Drug Administration.

“Do I think we need long-term lifetime data? Absolutely,” she said. “We need to do our due diligence, we need to be careful, we need to monitor patients, and when and if there are signals, we need to follow them.”

What about the notorious gastrointestinal side effects of the drugs? “A majority of them are mitigated by slow up-titration,” Dr. Jastreboff noted.

“If patients have nausea, I do not go up [in dose]. I invite patients to tell me if they’re having vomiting because I don’t want anybody to have it, and I can count on one hand how many of my patients do.”

Dr. Mehta added the concern that as the drugs’ popularity soars, “a lot of doctors don’t know when they need to put the brakes on [weight coming off too quickly].”

She underscored that “we are not treating obesity for weight loss or for cosmetic reasons — this is about optimizing health.”

Dr. Jastreboff noted that in her practice, “I down-titrate if they’re losing weight too quickly.”

“If the patient is losing more than 1% per week of their body weight, then I slow down to make sure they’re getting the nutrients that they need, that they have enough energy to exercise, and that they’re prioritizing protein and fruits and vegetables in their diet.

“We just need to go slow, and yes, we need to follow them long term,” she said.

Chiming in from the audience, Julio Rosenstock, MD, a recognized thought leader in type 2 diabetes, offered his own take on the issues, describing Dr. Taylor’s very low–calorie diet suggestion as “not realistic” and Dr. Nathan’s glucose-first argument to be “stuck in the past.”

Based on modern-day evidence, “there is no reason on earth to start [diabetes treatment] with only metformin,” asserted Dr. Rosenstock, director of the Velocity Clinical Research center at Medical City and clinical professor of medicine at the University of Texas Southwestern Medical Center, Dallas.

“We need to start at the very least with metformin and a sodium-glucose cotransporter 2 (SGLT2) inhibitor from day 1, and then, if it’s affordable and there is access, with a GLP-1 receptor agonist,” he said.

“There is nothing better these days than those agents that consistently have shown a reduction of cardiovascular events and slowing of kidney disease progression.”

Overall, however, “I think you are all right,” he added, a sentiment shared by most.

Noting that the discussion as a whole represents a virtual sea change from the evidence-based options that would have been discussed only a decade ago, Dr. Retnakaran summed up his take-home message: “Stay tuned.

“You could easily see things changing in the next decade to come as we get more data and evidence to support what we ultimately should prioritize an early type 2 diabetes, so this is an exciting time.”

Dr. Retnakaran disclosed ties with Novo Nordisk, Boehringer Ingelheim, Novartis, Sanofi, and Eli Lilly. Dr. Jastreboff disclosed ties with Amgen, AstraZeneca, Boehringer Ingelheim, Biohaven, Eli Lilly, Intellihealth, Novo Nordisk, Pfizer, Regeneron, Scholar Rock, Structure Therapeutics, Terms Pharmaceutical, Weight Watchers, and Zealand Pharmaceuticals. Dr. Roopa had relationships with Novo Nordisk, Boehringer Ingelheim, Amgen, AstraZeneca, Eli Lilly, Silanes, and Sanofi. Dr. Taylor received lecture fees from Novartis, Lilly, Abbott, and Nestle Health and research funding from Diabetes UK and is an advisor to Fast800. Dr. Rosenstock reported relationships with Applied Therapeutics, AstraZeneca, Biomea Fusion, Boehringer Ingelheim, Eli Lilly and Company, Hanmi, Merck, Oramed, Structure Therapeutics, Novartis, Novo Nordisk, Pfizer, Ragor, and Sanofi. Dr. Nathan had no disclosures to report.
 

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

ORLANDO, FLORIDA — What to prioritize first in managing early diabetes? That was the question debated on an expert panel at the American Diabetes Association (ADA) 84th Scientific Sessions, with impassioned responses ranging from a plea to “treat obesity first,” to a James Carville–inspired counterpoint of “it’s the glucose, stupid.” 

With a focus on preventing complications and inducing remission rounding out the four positions argued, Session Moderator Ravi Retnakaran, MD, of the University of Toronto, noted that the options reflect the tricky choices clinicians treating patients with diabetes are pressed to make on a daily basis.

“In clinical decision-making [for early diabetes], we are faced with weighing each of these variables for the individual patient, and while all are good options, strong arguments can be made for prioritizing each — with the potential of each choice to influence or improve all of the others,” Dr. Retnakaran told this news organization.
 

Which to Prioritize First?

Making the obesity first argument, Ania M. Jastreboff, MD, PhD, associate professor and director of the Yale Obesity Research Center at Yale School of Medicine, New Haven, Connecticut, noted the striking statistic that nearly 90% of people with type 2 diabetes have overweight or obesity and discussed the ever-expanding data showing the benefits of drugs including glucagon-like peptide 1 (GLP-1) receptor agonists not just in weight loss but also in kidney, cardiovascular, and, as presented at the meeting, sleep apnea improvement.

She contrasted the experiences of two patients with obesity: One treated for the obesity upon type 2 diagnosis — who had a quick normalization of lipids and hypertension soon after the obesity treatment — and the other presenting after 10 years with type 2 diabetes — who was on therapy for hypertension and hyperlipidemia but not for obesity and whose diseases were not as easily treated by that point.

“Why are we treating all the downstream effects and we’re not treating the disease that is potentially the root cause of all these other diseases?” Dr. Jastreboff said.
 

Complications?

Arguing in favor of focusing on complications, Roopa Mehta, MD, PhD, with the department of endocrinology and metabolism at Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán (INCMNSZ), Mexico City, made the case that stakes don’t get any higher in diabetes than when it comes the looming threat of potentially fatal complications.

Acute myocardial infarction, stroke, amputation, and end-stage renal disease are all on the list of unwanted outcomes and need to be considered even in the earliest stages, as data show early onset type 2 diabetes is linked to life expectancy.

“The main goal of management has always been to prevent complications,” she noted. Citing ADA guidelines, Dr. Mehta underscored the benefits of first- and second-line therapy of metformin, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and GLP-1 receptor agonists for most patients.
 

Remission?

Discussing the priority of putting patients into disease remission, Roy Taylor, MD, professor of medicine and metabolism at Newcastle University and Newcastle Hospitals NHS in Newcastle upon Tyne, England, and author of the book Life Without Diabetes, focused on an evidence-based alternative to achieving remission — a nonpharmacologic approach that avoids costly and sometimes inaccessible drugs.

In the intervention, described in the DiRECT randomized trial and subsequently in the UK National Health Service Type 2 Diabetes Path to Remission Program, patients with overweight or obesity were placed on a highly restrictive diet of just 800-900 calories a day for 12-20 weeks, followed by maintenance for 12 months, and they not only achieved weight loss but also achieved diabetes remission, in some cases long term.

Acknowledging that “this is not for everyone,” Dr. Taylor asserted that “we have to realize there is a substantial minority of people who want to be healthy but who don’t want to be medicalized,” he said.

“They want their health, and they can do extremely well.”
 

Glucose?

In taking his self-titled “it’s the glucose, stupid” stand, David M. Nathan, MD, of the Diabetes Center, Massachusetts General Hospital, Harvard Medical School, in Boston, cited extensive evidence showing that early intensive blood glucose control with treatment including sulfonylureas, insulin, or metformin significantly reduced the risk for complications in type 2 diabetes 15 or more years later, including renal failure, blindness, amputation, and myocardial infarctions, in addition to a reduction in diabetes-related death.

“In many of these studies, you saw the benefit even in the setting of weight-gain,” Dr. Nathan underscored.

He further noted the “sobering” findings of the Look AHEAD study, which had to be stopped due to futility when an intensive lifestyle/weight loss intervention showed no significant benefits in terms of cardiovascular disease in people with type 2 diabetes at a median follow-up of 9.6 years.

Ultimately, “diabetes, type 1 and type 2, remains a gluco-centric disease,” Dr. Nathan asserted. “Hyperglycemia is the only universal link between all forms of diabetes and mortality, and the long-term complications of diabetes are intimately associated with hyperglycemia.”
 

Tackling the Caveats

The ensuing panel discussion did not fail to deliver in delving into key areas of contention, particularly in terms of GLP-1 treatment.

Regarding a lack of data on the potential long-term effects of GLP-1s: “Yes, there are a huge number of studies [on GLP-1 receptor agonists], but they are, in general, over short periods of time and driven by pharma, who get in and get out as quickly as they can and have little in the way of interest to do comparative effectiveness studies,” Dr. Nathan argued.

“Meanwhile, this is like the crack cocaine of medications — patients have to stay on it for a lifetime or they will regain the weight — are you concerned at all about a lifetime of exposure to GLP-1 [drugs]?” he asked the panel.

Dr. Jastreboff responded that the first GLP-1 receptor agonist medications were approved in 2005, nearly 20 years ago, by the US Food and Drug Administration.

“Do I think we need long-term lifetime data? Absolutely,” she said. “We need to do our due diligence, we need to be careful, we need to monitor patients, and when and if there are signals, we need to follow them.”

What about the notorious gastrointestinal side effects of the drugs? “A majority of them are mitigated by slow up-titration,” Dr. Jastreboff noted.

“If patients have nausea, I do not go up [in dose]. I invite patients to tell me if they’re having vomiting because I don’t want anybody to have it, and I can count on one hand how many of my patients do.”

Dr. Mehta added the concern that as the drugs’ popularity soars, “a lot of doctors don’t know when they need to put the brakes on [weight coming off too quickly].”

She underscored that “we are not treating obesity for weight loss or for cosmetic reasons — this is about optimizing health.”

Dr. Jastreboff noted that in her practice, “I down-titrate if they’re losing weight too quickly.”

“If the patient is losing more than 1% per week of their body weight, then I slow down to make sure they’re getting the nutrients that they need, that they have enough energy to exercise, and that they’re prioritizing protein and fruits and vegetables in their diet.

“We just need to go slow, and yes, we need to follow them long term,” she said.

Chiming in from the audience, Julio Rosenstock, MD, a recognized thought leader in type 2 diabetes, offered his own take on the issues, describing Dr. Taylor’s very low–calorie diet suggestion as “not realistic” and Dr. Nathan’s glucose-first argument to be “stuck in the past.”

Based on modern-day evidence, “there is no reason on earth to start [diabetes treatment] with only metformin,” asserted Dr. Rosenstock, director of the Velocity Clinical Research center at Medical City and clinical professor of medicine at the University of Texas Southwestern Medical Center, Dallas.

“We need to start at the very least with metformin and a sodium-glucose cotransporter 2 (SGLT2) inhibitor from day 1, and then, if it’s affordable and there is access, with a GLP-1 receptor agonist,” he said.

“There is nothing better these days than those agents that consistently have shown a reduction of cardiovascular events and slowing of kidney disease progression.”

Overall, however, “I think you are all right,” he added, a sentiment shared by most.

Noting that the discussion as a whole represents a virtual sea change from the evidence-based options that would have been discussed only a decade ago, Dr. Retnakaran summed up his take-home message: “Stay tuned.

“You could easily see things changing in the next decade to come as we get more data and evidence to support what we ultimately should prioritize an early type 2 diabetes, so this is an exciting time.”

Dr. Retnakaran disclosed ties with Novo Nordisk, Boehringer Ingelheim, Novartis, Sanofi, and Eli Lilly. Dr. Jastreboff disclosed ties with Amgen, AstraZeneca, Boehringer Ingelheim, Biohaven, Eli Lilly, Intellihealth, Novo Nordisk, Pfizer, Regeneron, Scholar Rock, Structure Therapeutics, Terms Pharmaceutical, Weight Watchers, and Zealand Pharmaceuticals. Dr. Roopa had relationships with Novo Nordisk, Boehringer Ingelheim, Amgen, AstraZeneca, Eli Lilly, Silanes, and Sanofi. Dr. Taylor received lecture fees from Novartis, Lilly, Abbott, and Nestle Health and research funding from Diabetes UK and is an advisor to Fast800. Dr. Rosenstock reported relationships with Applied Therapeutics, AstraZeneca, Biomea Fusion, Boehringer Ingelheim, Eli Lilly and Company, Hanmi, Merck, Oramed, Structure Therapeutics, Novartis, Novo Nordisk, Pfizer, Ragor, and Sanofi. Dr. Nathan had no disclosures to report.
 

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

ORLANDO, FLORIDA — What to prioritize first in managing early diabetes? That was the question debated on an expert panel at the American Diabetes Association (ADA) 84th Scientific Sessions, with impassioned responses ranging from a plea to “treat obesity first,” to a James Carville–inspired counterpoint of “it’s the glucose, stupid.” 

With a focus on preventing complications and inducing remission rounding out the four positions argued, Session Moderator Ravi Retnakaran, MD, of the University of Toronto, noted that the options reflect the tricky choices clinicians treating patients with diabetes are pressed to make on a daily basis.

“In clinical decision-making [for early diabetes], we are faced with weighing each of these variables for the individual patient, and while all are good options, strong arguments can be made for prioritizing each — with the potential of each choice to influence or improve all of the others,” Dr. Retnakaran told this news organization.
 

Which to Prioritize First?

Making the obesity first argument, Ania M. Jastreboff, MD, PhD, associate professor and director of the Yale Obesity Research Center at Yale School of Medicine, New Haven, Connecticut, noted the striking statistic that nearly 90% of people with type 2 diabetes have overweight or obesity and discussed the ever-expanding data showing the benefits of drugs including glucagon-like peptide 1 (GLP-1) receptor agonists not just in weight loss but also in kidney, cardiovascular, and, as presented at the meeting, sleep apnea improvement.

She contrasted the experiences of two patients with obesity: One treated for the obesity upon type 2 diagnosis — who had a quick normalization of lipids and hypertension soon after the obesity treatment — and the other presenting after 10 years with type 2 diabetes — who was on therapy for hypertension and hyperlipidemia but not for obesity and whose diseases were not as easily treated by that point.

“Why are we treating all the downstream effects and we’re not treating the disease that is potentially the root cause of all these other diseases?” Dr. Jastreboff said.
 

Complications?

Arguing in favor of focusing on complications, Roopa Mehta, MD, PhD, with the department of endocrinology and metabolism at Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán (INCMNSZ), Mexico City, made the case that stakes don’t get any higher in diabetes than when it comes the looming threat of potentially fatal complications.

Acute myocardial infarction, stroke, amputation, and end-stage renal disease are all on the list of unwanted outcomes and need to be considered even in the earliest stages, as data show early onset type 2 diabetes is linked to life expectancy.

“The main goal of management has always been to prevent complications,” she noted. Citing ADA guidelines, Dr. Mehta underscored the benefits of first- and second-line therapy of metformin, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and GLP-1 receptor agonists for most patients.
 

Remission?

Discussing the priority of putting patients into disease remission, Roy Taylor, MD, professor of medicine and metabolism at Newcastle University and Newcastle Hospitals NHS in Newcastle upon Tyne, England, and author of the book Life Without Diabetes, focused on an evidence-based alternative to achieving remission — a nonpharmacologic approach that avoids costly and sometimes inaccessible drugs.

In the intervention, described in the DiRECT randomized trial and subsequently in the UK National Health Service Type 2 Diabetes Path to Remission Program, patients with overweight or obesity were placed on a highly restrictive diet of just 800-900 calories a day for 12-20 weeks, followed by maintenance for 12 months, and they not only achieved weight loss but also achieved diabetes remission, in some cases long term.

Acknowledging that “this is not for everyone,” Dr. Taylor asserted that “we have to realize there is a substantial minority of people who want to be healthy but who don’t want to be medicalized,” he said.

“They want their health, and they can do extremely well.”
 

Glucose?

In taking his self-titled “it’s the glucose, stupid” stand, David M. Nathan, MD, of the Diabetes Center, Massachusetts General Hospital, Harvard Medical School, in Boston, cited extensive evidence showing that early intensive blood glucose control with treatment including sulfonylureas, insulin, or metformin significantly reduced the risk for complications in type 2 diabetes 15 or more years later, including renal failure, blindness, amputation, and myocardial infarctions, in addition to a reduction in diabetes-related death.

“In many of these studies, you saw the benefit even in the setting of weight-gain,” Dr. Nathan underscored.

He further noted the “sobering” findings of the Look AHEAD study, which had to be stopped due to futility when an intensive lifestyle/weight loss intervention showed no significant benefits in terms of cardiovascular disease in people with type 2 diabetes at a median follow-up of 9.6 years.

Ultimately, “diabetes, type 1 and type 2, remains a gluco-centric disease,” Dr. Nathan asserted. “Hyperglycemia is the only universal link between all forms of diabetes and mortality, and the long-term complications of diabetes are intimately associated with hyperglycemia.”
 

Tackling the Caveats

The ensuing panel discussion did not fail to deliver in delving into key areas of contention, particularly in terms of GLP-1 treatment.

Regarding a lack of data on the potential long-term effects of GLP-1s: “Yes, there are a huge number of studies [on GLP-1 receptor agonists], but they are, in general, over short periods of time and driven by pharma, who get in and get out as quickly as they can and have little in the way of interest to do comparative effectiveness studies,” Dr. Nathan argued.

“Meanwhile, this is like the crack cocaine of medications — patients have to stay on it for a lifetime or they will regain the weight — are you concerned at all about a lifetime of exposure to GLP-1 [drugs]?” he asked the panel.

Dr. Jastreboff responded that the first GLP-1 receptor agonist medications were approved in 2005, nearly 20 years ago, by the US Food and Drug Administration.

“Do I think we need long-term lifetime data? Absolutely,” she said. “We need to do our due diligence, we need to be careful, we need to monitor patients, and when and if there are signals, we need to follow them.”

What about the notorious gastrointestinal side effects of the drugs? “A majority of them are mitigated by slow up-titration,” Dr. Jastreboff noted.

“If patients have nausea, I do not go up [in dose]. I invite patients to tell me if they’re having vomiting because I don’t want anybody to have it, and I can count on one hand how many of my patients do.”

Dr. Mehta added the concern that as the drugs’ popularity soars, “a lot of doctors don’t know when they need to put the brakes on [weight coming off too quickly].”

She underscored that “we are not treating obesity for weight loss or for cosmetic reasons — this is about optimizing health.”

Dr. Jastreboff noted that in her practice, “I down-titrate if they’re losing weight too quickly.”

“If the patient is losing more than 1% per week of their body weight, then I slow down to make sure they’re getting the nutrients that they need, that they have enough energy to exercise, and that they’re prioritizing protein and fruits and vegetables in their diet.

“We just need to go slow, and yes, we need to follow them long term,” she said.

Chiming in from the audience, Julio Rosenstock, MD, a recognized thought leader in type 2 diabetes, offered his own take on the issues, describing Dr. Taylor’s very low–calorie diet suggestion as “not realistic” and Dr. Nathan’s glucose-first argument to be “stuck in the past.”

Based on modern-day evidence, “there is no reason on earth to start [diabetes treatment] with only metformin,” asserted Dr. Rosenstock, director of the Velocity Clinical Research center at Medical City and clinical professor of medicine at the University of Texas Southwestern Medical Center, Dallas.

“We need to start at the very least with metformin and a sodium-glucose cotransporter 2 (SGLT2) inhibitor from day 1, and then, if it’s affordable and there is access, with a GLP-1 receptor agonist,” he said.

“There is nothing better these days than those agents that consistently have shown a reduction of cardiovascular events and slowing of kidney disease progression.”

Overall, however, “I think you are all right,” he added, a sentiment shared by most.

Noting that the discussion as a whole represents a virtual sea change from the evidence-based options that would have been discussed only a decade ago, Dr. Retnakaran summed up his take-home message: “Stay tuned.

“You could easily see things changing in the next decade to come as we get more data and evidence to support what we ultimately should prioritize an early type 2 diabetes, so this is an exciting time.”

Dr. Retnakaran disclosed ties with Novo Nordisk, Boehringer Ingelheim, Novartis, Sanofi, and Eli Lilly. Dr. Jastreboff disclosed ties with Amgen, AstraZeneca, Boehringer Ingelheim, Biohaven, Eli Lilly, Intellihealth, Novo Nordisk, Pfizer, Regeneron, Scholar Rock, Structure Therapeutics, Terms Pharmaceutical, Weight Watchers, and Zealand Pharmaceuticals. Dr. Roopa had relationships with Novo Nordisk, Boehringer Ingelheim, Amgen, AstraZeneca, Eli Lilly, Silanes, and Sanofi. Dr. Taylor received lecture fees from Novartis, Lilly, Abbott, and Nestle Health and research funding from Diabetes UK and is an advisor to Fast800. Dr. Rosenstock reported relationships with Applied Therapeutics, AstraZeneca, Biomea Fusion, Boehringer Ingelheim, Eli Lilly and Company, Hanmi, Merck, Oramed, Structure Therapeutics, Novartis, Novo Nordisk, Pfizer, Ragor, and Sanofi. Dr. Nathan had no disclosures to report.
 

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

TOPLINE:

A triple combination therapy (TCT) of metformin, dapagliflozin, and saxagliptin is an effective and safe treatment option for drug-naive patients with type 2 diabetes (T2D) compared with stepwise add-on therapy.

METHODOLOGY:

• Current guidelines recommend early combination therapy to extend the time to treatment failure, reduce the risk for diabetic complications, and prevent clinical inertia in patients with T2D.
• This randomized controlled open-label trial conducted at nine sites in South Korea included 105 drug-naive patients with T2D (mean age, 49.5 years; 32.4% women) who either received triple therapy (metformin, dapagliflozin, and saxagliptin) or stepwise add-on therapy (initiated with metformin, followed by glimepiride and sitagliptin for those with baseline hemoglobin A1c levels < 9.0% or with initial dual metformin and glimepiride in those with A1c levels ≥ 9.0% followed by sitagliptin).
• The primary outcome was the proportion of patients who achieved A1c levels < 6.5% without hypoglycemia, weight gain ≥ 5%, or discontinuation of drugs because of adverse events at week 104.
• The secondary outcomes were the proportion of patients whose A1c levels dropped to < 7.0% at weeks 56 and 104 and dropped to < 6.5% at week 56, all without hypoglycemia, weight gain, nor discontinuation due to adverse events.

TAKEAWAY:

• At week 104, a higher proportion of patients in the triple therapy group achieved the primary outcome than those in the stepwise add-on therapy group (39.0% vs 17.1%; P = .027).
• In both groups, a similar proportion of patients (46.3%) achieved A1c levels < 6.5% at week 104, but the proportion of patients without hypoglycemia, weight gain, or discontinuation because of adverse events was higher in the triple therapy group than those in the stepwise add-on therapy group (83.3% vs 38.0%; P < .001).

IN PRACTICE:

The authors wrote: “Although the glycemic efficacy of each drug in the TCT was modest, the combination of these drugs resulted in a 2-year durable glycemic efficacy, with greater than a 2.5% reduction in A1c levels from baseline. The overall results of this study suggest a novel strategy for initial combination therapy in newly diagnosed T2D patients.”

SOURCE:

The study was led by Nam Hoon Kim, MD, of the Department of Internal Medicine, Korea University College of Medicine, Seoul. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study had a relatively small sample size as compared with previous clinical trials. More people in the standard therapy group had A1c levels ≥ 9.0%, which resulted in more than double the number of people receiving dual combination therapy over monotherapy in that group. The trial duration was insufficient to evaluate the cardiovascular outcomes.

DISCLOSURES:

The study was funded by AstraZeneca. Some authors reported financial ties with AstraZeneca and other pharmaceutical and medical device companies as members of advisory boards or recipients of grants, consulting fees, honoraria, or lecture fees.

A version of this article appeared on Medscape.com.

TOPLINE:

A triple combination therapy (TCT) of metformin, dapagliflozin, and saxagliptin is an effective and safe treatment option for drug-naive patients with type 2 diabetes (T2D) compared with stepwise add-on therapy.

METHODOLOGY:

• Current guidelines recommend early combination therapy to extend the time to treatment failure, reduce the risk for diabetic complications, and prevent clinical inertia in patients with T2D.
• This randomized controlled open-label trial conducted at nine sites in South Korea included 105 drug-naive patients with T2D (mean age, 49.5 years; 32.4% women) who either received triple therapy (metformin, dapagliflozin, and saxagliptin) or stepwise add-on therapy (initiated with metformin, followed by glimepiride and sitagliptin for those with baseline hemoglobin A1c levels < 9.0% or with initial dual metformin and glimepiride in those with A1c levels ≥ 9.0% followed by sitagliptin).
• The primary outcome was the proportion of patients who achieved A1c levels < 6.5% without hypoglycemia, weight gain ≥ 5%, or discontinuation of drugs because of adverse events at week 104.
• The secondary outcomes were the proportion of patients whose A1c levels dropped to < 7.0% at weeks 56 and 104 and dropped to < 6.5% at week 56, all without hypoglycemia, weight gain, nor discontinuation due to adverse events.

TAKEAWAY:

• At week 104, a higher proportion of patients in the triple therapy group achieved the primary outcome than those in the stepwise add-on therapy group (39.0% vs 17.1%; P = .027).
• In both groups, a similar proportion of patients (46.3%) achieved A1c levels < 6.5% at week 104, but the proportion of patients without hypoglycemia, weight gain, or discontinuation because of adverse events was higher in the triple therapy group than those in the stepwise add-on therapy group (83.3% vs 38.0%; P < .001).

IN PRACTICE:

The authors wrote: “Although the glycemic efficacy of each drug in the TCT was modest, the combination of these drugs resulted in a 2-year durable glycemic efficacy, with greater than a 2.5% reduction in A1c levels from baseline. The overall results of this study suggest a novel strategy for initial combination therapy in newly diagnosed T2D patients.”

SOURCE:

The study was led by Nam Hoon Kim, MD, of the Department of Internal Medicine, Korea University College of Medicine, Seoul. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study had a relatively small sample size as compared with previous clinical trials. More people in the standard therapy group had A1c levels ≥ 9.0%, which resulted in more than double the number of people receiving dual combination therapy over monotherapy in that group. The trial duration was insufficient to evaluate the cardiovascular outcomes.

DISCLOSURES:

The study was funded by AstraZeneca. Some authors reported financial ties with AstraZeneca and other pharmaceutical and medical device companies as members of advisory boards or recipients of grants, consulting fees, honoraria, or lecture fees.

A version of this article appeared on Medscape.com.

TOPLINE:

A triple combination therapy (TCT) of metformin, dapagliflozin, and saxagliptin is an effective and safe treatment option for drug-naive patients with type 2 diabetes (T2D) compared with stepwise add-on therapy.

METHODOLOGY:

• Current guidelines recommend early combination therapy to extend the time to treatment failure, reduce the risk for diabetic complications, and prevent clinical inertia in patients with T2D.
• This randomized controlled open-label trial conducted at nine sites in South Korea included 105 drug-naive patients with T2D (mean age, 49.5 years; 32.4% women) who either received triple therapy (metformin, dapagliflozin, and saxagliptin) or stepwise add-on therapy (initiated with metformin, followed by glimepiride and sitagliptin for those with baseline hemoglobin A1c levels < 9.0% or with initial dual metformin and glimepiride in those with A1c levels ≥ 9.0% followed by sitagliptin).
• The primary outcome was the proportion of patients who achieved A1c levels < 6.5% without hypoglycemia, weight gain ≥ 5%, or discontinuation of drugs because of adverse events at week 104.
• The secondary outcomes were the proportion of patients whose A1c levels dropped to < 7.0% at weeks 56 and 104 and dropped to < 6.5% at week 56, all without hypoglycemia, weight gain, nor discontinuation due to adverse events.

TAKEAWAY:

• At week 104, a higher proportion of patients in the triple therapy group achieved the primary outcome than those in the stepwise add-on therapy group (39.0% vs 17.1%; P = .027).
• In both groups, a similar proportion of patients (46.3%) achieved A1c levels < 6.5% at week 104, but the proportion of patients without hypoglycemia, weight gain, or discontinuation because of adverse events was higher in the triple therapy group than those in the stepwise add-on therapy group (83.3% vs 38.0%; P < .001).

IN PRACTICE:

The authors wrote: “Although the glycemic efficacy of each drug in the TCT was modest, the combination of these drugs resulted in a 2-year durable glycemic efficacy, with greater than a 2.5% reduction in A1c levels from baseline. The overall results of this study suggest a novel strategy for initial combination therapy in newly diagnosed T2D patients.”

SOURCE:

The study was led by Nam Hoon Kim, MD, of the Department of Internal Medicine, Korea University College of Medicine, Seoul. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study had a relatively small sample size as compared with previous clinical trials. More people in the standard therapy group had A1c levels ≥ 9.0%, which resulted in more than double the number of people receiving dual combination therapy over monotherapy in that group. The trial duration was insufficient to evaluate the cardiovascular outcomes.

DISCLOSURES:

The study was funded by AstraZeneca. Some authors reported financial ties with AstraZeneca and other pharmaceutical and medical device companies as members of advisory boards or recipients of grants, consulting fees, honoraria, or lecture fees.

A version of this article appeared on Medscape.com.