Clinical Endocrinology News

Over a period of 5 years, the likelihood of major adverse cardiovascular events (MACE) in patients with psoriasis and dyslipidemia who were on statin therapy was 40% greater than that in non-psoriasis patients with dyslipidemia on statin therapy, even after adjusting for covariates, results from a large retrospective study showed.

“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.

Dr. Ormaza Vera

Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.

To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.

Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).

“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.

She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.

Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”

The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.

A version of this article appeared on Medscape.com .

Over a period of 5 years, the likelihood of major adverse cardiovascular events (MACE) in patients with psoriasis and dyslipidemia who were on statin therapy was 40% greater than that in non-psoriasis patients with dyslipidemia on statin therapy, even after adjusting for covariates, results from a large retrospective study showed.

“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.

Dr. Ormaza Vera

Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.

To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.

Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).

“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.

She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.

Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”

The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.

A version of this article appeared on Medscape.com .

Over a period of 5 years, the likelihood of major adverse cardiovascular events (MACE) in patients with psoriasis and dyslipidemia who were on statin therapy was 40% greater than that in non-psoriasis patients with dyslipidemia on statin therapy, even after adjusting for covariates, results from a large retrospective study showed.

“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.

Dr. Ormaza Vera

Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.

To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.

Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).

“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.

She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.

Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”

The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.

A version of this article appeared on Medscape.com .

BOSTON — New Endocrine Society guidelines call for limiting vitamin D supplementation beyond the daily recommended intake to specific risk groups and advises against routine 25-hydroxyvitamin D [25(OH)D] testing in healthy individuals. 

The evidence-based document was presented on June 3, 2024, at the Endocrine Society annual meeting, and simultaneously published in The Journal of Clinical Endocrinology and Metabolism. It advises that people who may benefit from vitamin D supplementation include: 

• Children aged 1-18 years to prevent rickets and to potentially lower the risk for respiratory tract infections
• Pregnant people to lower the risk for maternal and fetal or neonatal complications
• Adults older than 75 years to lower the risk for mortality
• Adults with prediabetes to lower the risk for type 2 diabetes

In those groups, the recommendation is for daily (rather than intermittent) empiric vitamin D supplementation of more than what was recommended in 2011 by the National Academy of Medicine (NAM), which was then called the Institute of Medicine (IOM): 600 IU/d for those aged 1-70 years and 800 IU/d for those older than 70 years. The document acknowledges that the optimal dose for these populations isn’t known, but it provides the dose ranges that were used in the trials cited as evidence for the recommendations. 

In contrast, the document advises against more vitamin D than the recommended daily intake for most healthier adults younger than 75 years and recommends against testing for blood vitamin D levels in the general population, including those with obesity or darker complexions. 

Guideline author Anastassios G. Pittas, MD, professor of medicine at Tufts University School of Medicine, Boston, told this news organization, “this guideline refers to people who are otherwise healthy, and there’s no clear indication for vitamin D, such as people with already established osteoporosis. This guideline is not relevant to them.”

Dr. Pittas also noted, “there’s no single question and single answer about the role of vitamin D in health and disease, which is what people often want to know. There are many questions, and we cannot answer all of them.”

Panel Chair Marie B. Demay, MD, professor of medicine at Harvard Medical School, Boston, told this news organization that indeed the panel was limited by lack of randomized clinical trial evidence to answer many important questions. “There is a paucity of data regarding definition of optimal levels and optimal intake of vitamin D for preventing specific diseases ... What we really need are large scale clinical trials and biomarkers so we can predict disease outcome before it happens.”

Overall, Dr. Demay said, “The recommendations are that populations adhere to the [NAM/IOM] dietary recommended intakes, and there are certain populations that will likely benefit from levels of intake above [those].” 

Asked to comment, session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine, noted that screening for vitamin D is quite common in clinical practice, but the recommendation against doing so makes sense. 

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it. That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life ... Screening is probably not worthwhile in any age group.”

Dr. Rosen, who was an author on the 2011 NAM/IOM dietary reference intakes, said that since then, new data have come out regarding the role of vitamin D in mortality in people older than 75 years, benefit in children with regard to respiratory illness, and the potential benefit of vitamin D in pregnancy. “Otherwise, I think we’re going over a lot of the same stuff that we’ve talked about since I was on the IOM panel 15 years ago ... But I think the level of evidence and rigor with which they did it is really impressive.”

However, Simeon I. Taylor, MD, professor of medicine at the University of Maryland, Baltimore, expressed disappointment that the document was limited to healthy people. “Although acknowledging challenges in managing vitamin D status in patients with several diseases, [such as] chronic kidney disease or inflammatory bowel disease, the new guidelines do not provide sufficient guidance for practicing physicians about how to manage these complex patients.”

In addition, Dr. Taylor said that the guidelines “do not explicitly consider the literature suggesting that alternative testing strategies may provide more relevant insights into vitamin D status. Just as variation in levels of thyroid-binding globulin have convinced endocrinologists not to rely on measurement of total thyroxine; interindividual variation in levels of vitamin D binding protein must be accounted for to interpret measurements of total levels of 25(OH)D. It would have been useful to explicitly consider the possible value of measuring vitamin D binding protein-independent indices of vitamin D status.”

Dr. Taylor also raised the same point as an audience member did during the Q&A period regarding patients with osteoporosis or osteopenia. “The value and utility of the new guidelines would be greatly strengthened by providing guidance for how to approach this important and very large group of individuals.”

Dr. Taylor did say that the document has “several strengths, including the fact that they acknowledge the major limitations of the quality of relevant evidence derived from clinical trials.” 

In an accompanying commentary, the guideline authors delve into the issues of skin pigmentation and race as they pertain to vitamin D metabolism, writing: 

The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants’ skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations.

Dr. Pittas and Dr. Demay have no disclosures relevant to this clinical practice guideline. Dr. Rosen has no disclosures. Dr. Taylor serves as a consultant for Ionis Pharmaceuticals.
 

A version of this article appeared on Medscape.com.

BOSTON — New Endocrine Society guidelines call for limiting vitamin D supplementation beyond the daily recommended intake to specific risk groups and advises against routine 25-hydroxyvitamin D [25(OH)D] testing in healthy individuals. 

The evidence-based document was presented on June 3, 2024, at the Endocrine Society annual meeting, and simultaneously published in The Journal of Clinical Endocrinology and Metabolism. It advises that people who may benefit from vitamin D supplementation include: 

• Children aged 1-18 years to prevent rickets and to potentially lower the risk for respiratory tract infections
• Pregnant people to lower the risk for maternal and fetal or neonatal complications
• Adults older than 75 years to lower the risk for mortality
• Adults with prediabetes to lower the risk for type 2 diabetes

In those groups, the recommendation is for daily (rather than intermittent) empiric vitamin D supplementation of more than what was recommended in 2011 by the National Academy of Medicine (NAM), which was then called the Institute of Medicine (IOM): 600 IU/d for those aged 1-70 years and 800 IU/d for those older than 70 years. The document acknowledges that the optimal dose for these populations isn’t known, but it provides the dose ranges that were used in the trials cited as evidence for the recommendations. 

In contrast, the document advises against more vitamin D than the recommended daily intake for most healthier adults younger than 75 years and recommends against testing for blood vitamin D levels in the general population, including those with obesity or darker complexions. 

Guideline author Anastassios G. Pittas, MD, professor of medicine at Tufts University School of Medicine, Boston, told this news organization, “this guideline refers to people who are otherwise healthy, and there’s no clear indication for vitamin D, such as people with already established osteoporosis. This guideline is not relevant to them.”

Dr. Pittas also noted, “there’s no single question and single answer about the role of vitamin D in health and disease, which is what people often want to know. There are many questions, and we cannot answer all of them.”

Panel Chair Marie B. Demay, MD, professor of medicine at Harvard Medical School, Boston, told this news organization that indeed the panel was limited by lack of randomized clinical trial evidence to answer many important questions. “There is a paucity of data regarding definition of optimal levels and optimal intake of vitamin D for preventing specific diseases ... What we really need are large scale clinical trials and biomarkers so we can predict disease outcome before it happens.”

Overall, Dr. Demay said, “The recommendations are that populations adhere to the [NAM/IOM] dietary recommended intakes, and there are certain populations that will likely benefit from levels of intake above [those].” 

Asked to comment, session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine, noted that screening for vitamin D is quite common in clinical practice, but the recommendation against doing so makes sense. 

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it. That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life ... Screening is probably not worthwhile in any age group.”

Dr. Rosen, who was an author on the 2011 NAM/IOM dietary reference intakes, said that since then, new data have come out regarding the role of vitamin D in mortality in people older than 75 years, benefit in children with regard to respiratory illness, and the potential benefit of vitamin D in pregnancy. “Otherwise, I think we’re going over a lot of the same stuff that we’ve talked about since I was on the IOM panel 15 years ago ... But I think the level of evidence and rigor with which they did it is really impressive.”

However, Simeon I. Taylor, MD, professor of medicine at the University of Maryland, Baltimore, expressed disappointment that the document was limited to healthy people. “Although acknowledging challenges in managing vitamin D status in patients with several diseases, [such as] chronic kidney disease or inflammatory bowel disease, the new guidelines do not provide sufficient guidance for practicing physicians about how to manage these complex patients.”

In addition, Dr. Taylor said that the guidelines “do not explicitly consider the literature suggesting that alternative testing strategies may provide more relevant insights into vitamin D status. Just as variation in levels of thyroid-binding globulin have convinced endocrinologists not to rely on measurement of total thyroxine; interindividual variation in levels of vitamin D binding protein must be accounted for to interpret measurements of total levels of 25(OH)D. It would have been useful to explicitly consider the possible value of measuring vitamin D binding protein-independent indices of vitamin D status.”

Dr. Taylor also raised the same point as an audience member did during the Q&A period regarding patients with osteoporosis or osteopenia. “The value and utility of the new guidelines would be greatly strengthened by providing guidance for how to approach this important and very large group of individuals.”

Dr. Taylor did say that the document has “several strengths, including the fact that they acknowledge the major limitations of the quality of relevant evidence derived from clinical trials.” 

In an accompanying commentary, the guideline authors delve into the issues of skin pigmentation and race as they pertain to vitamin D metabolism, writing: 

The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants’ skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations.

Dr. Pittas and Dr. Demay have no disclosures relevant to this clinical practice guideline. Dr. Rosen has no disclosures. Dr. Taylor serves as a consultant for Ionis Pharmaceuticals.
 

A version of this article appeared on Medscape.com.

BOSTON — New Endocrine Society guidelines call for limiting vitamin D supplementation beyond the daily recommended intake to specific risk groups and advises against routine 25-hydroxyvitamin D [25(OH)D] testing in healthy individuals. 

The evidence-based document was presented on June 3, 2024, at the Endocrine Society annual meeting, and simultaneously published in The Journal of Clinical Endocrinology and Metabolism. It advises that people who may benefit from vitamin D supplementation include: 

• Children aged 1-18 years to prevent rickets and to potentially lower the risk for respiratory tract infections
• Pregnant people to lower the risk for maternal and fetal or neonatal complications
• Adults older than 75 years to lower the risk for mortality
• Adults with prediabetes to lower the risk for type 2 diabetes

In those groups, the recommendation is for daily (rather than intermittent) empiric vitamin D supplementation of more than what was recommended in 2011 by the National Academy of Medicine (NAM), which was then called the Institute of Medicine (IOM): 600 IU/d for those aged 1-70 years and 800 IU/d for those older than 70 years. The document acknowledges that the optimal dose for these populations isn’t known, but it provides the dose ranges that were used in the trials cited as evidence for the recommendations. 

In contrast, the document advises against more vitamin D than the recommended daily intake for most healthier adults younger than 75 years and recommends against testing for blood vitamin D levels in the general population, including those with obesity or darker complexions. 

Guideline author Anastassios G. Pittas, MD, professor of medicine at Tufts University School of Medicine, Boston, told this news organization, “this guideline refers to people who are otherwise healthy, and there’s no clear indication for vitamin D, such as people with already established osteoporosis. This guideline is not relevant to them.”

Dr. Pittas also noted, “there’s no single question and single answer about the role of vitamin D in health and disease, which is what people often want to know. There are many questions, and we cannot answer all of them.”

Panel Chair Marie B. Demay, MD, professor of medicine at Harvard Medical School, Boston, told this news organization that indeed the panel was limited by lack of randomized clinical trial evidence to answer many important questions. “There is a paucity of data regarding definition of optimal levels and optimal intake of vitamin D for preventing specific diseases ... What we really need are large scale clinical trials and biomarkers so we can predict disease outcome before it happens.”

Overall, Dr. Demay said, “The recommendations are that populations adhere to the [NAM/IOM] dietary recommended intakes, and there are certain populations that will likely benefit from levels of intake above [those].” 

Asked to comment, session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine, noted that screening for vitamin D is quite common in clinical practice, but the recommendation against doing so makes sense. 

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it. That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life ... Screening is probably not worthwhile in any age group.”

Dr. Rosen, who was an author on the 2011 NAM/IOM dietary reference intakes, said that since then, new data have come out regarding the role of vitamin D in mortality in people older than 75 years, benefit in children with regard to respiratory illness, and the potential benefit of vitamin D in pregnancy. “Otherwise, I think we’re going over a lot of the same stuff that we’ve talked about since I was on the IOM panel 15 years ago ... But I think the level of evidence and rigor with which they did it is really impressive.”

However, Simeon I. Taylor, MD, professor of medicine at the University of Maryland, Baltimore, expressed disappointment that the document was limited to healthy people. “Although acknowledging challenges in managing vitamin D status in patients with several diseases, [such as] chronic kidney disease or inflammatory bowel disease, the new guidelines do not provide sufficient guidance for practicing physicians about how to manage these complex patients.”

In addition, Dr. Taylor said that the guidelines “do not explicitly consider the literature suggesting that alternative testing strategies may provide more relevant insights into vitamin D status. Just as variation in levels of thyroid-binding globulin have convinced endocrinologists not to rely on measurement of total thyroxine; interindividual variation in levels of vitamin D binding protein must be accounted for to interpret measurements of total levels of 25(OH)D. It would have been useful to explicitly consider the possible value of measuring vitamin D binding protein-independent indices of vitamin D status.”

Dr. Taylor also raised the same point as an audience member did during the Q&A period regarding patients with osteoporosis or osteopenia. “The value and utility of the new guidelines would be greatly strengthened by providing guidance for how to approach this important and very large group of individuals.”

Dr. Taylor did say that the document has “several strengths, including the fact that they acknowledge the major limitations of the quality of relevant evidence derived from clinical trials.” 

In an accompanying commentary, the guideline authors delve into the issues of skin pigmentation and race as they pertain to vitamin D metabolism, writing: 

The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants’ skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations.

Dr. Pittas and Dr. Demay have no disclosures relevant to this clinical practice guideline. Dr. Rosen has no disclosures. Dr. Taylor serves as a consultant for Ionis Pharmaceuticals.
 

A version of this article appeared on Medscape.com.

The glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide (Ozempic, Wegovy) enhances taste sensitivity, changes brain responses to sweet tastes and may even alter expression of genes in the tongue associated with taste bud development, according to new research presented at the annual meeting of the Endocrine Society, held in Boston. 

“Some studies have reported that individuals living with obesity often perceive tastes as less intense,” noted Mojca Jensterle Sever, PhD, of the University Medical Centre in Ljubljana, Slovenia, who presented the work. Research also suggests that “populations prone to obesity have an inherently elevated desire for sweet and energy-dense foods,” she continued. 

Studies in animal models have also previously shown that GLP-1 plays an important role in taste sensitivity, but it was not known if this hormone also influenced human taste perception. 

In this proof-of-concept study, researchers randomly assigned 30 women with polycystic ovary syndrome (PCOS) to either 1 mg of semaglutide, administered once a week, or placebo for 16 weeks. Participants were on average 34 years old with a body mass index (BMI) of 36.4. Participants with PCOS were selected with the “aim to reduce variability in taste perception across different phases of the menstrual cycle,” Dr. Sever said. 

Prior to the intervention, researchers tested participants’ taste sensitivity using 16 taste strips infused with four different concentrations of sweet, sour, salty, and bitter substances. Participants were asked to identify the taste of each strip. Every correct answer counted as one point, with a possible total of 16 points overall. Tongue biopsies were conducted for gene expression analysis. 

Researchers also used functional MRI (fMRI) to evaluate brain responses to a series of calorie-dense, low-calorie, and non-food visual cues as well as to sweet taste stimulus. A sweet solution was administered on the tongue 30 minutes before and after participants consumed a standardized meal: a high-protein enriched nutritional drink. 

These tests were repeated after 16 weeks. 

At the end of the study, the women taking semaglutide increased their taste sensitivity from 11.9 to 14.4 points; the estimated treatment difference from the control group was 2.5 points (95% CI, 1.7 - 3.3). 

The semaglutide group also exhibited decreased activation of the putamen (a structure in the brain involved with the brain’s reward system) on fMRI in response to calorie-dense cues. In response to sweet taste stimulus, those taking semaglutide showed increased activation of angular gyrus on MRI compared with the placebo group. The angular gyrus is part of the brain’s parietal lobe and is involved with language, memory, reasoning, and attention.

Lastly, researchers identified differential mRNA expression in the genes EYA, PRMT8, CRLF1, and CYP1B1, which are associated with taste bud development, renewal, and differentiation.

The findings are “fascinating, because we think about all of the factors that this new class of agents are able to improve, but taste is often not something that we look at, though there have been very strong associations,” said Gitanjali Srivastava, MD, of Vanderbilt University, Nashville, Tennessee, who moderated the session.

“Is it possible that another mechanism of action for this class of agents is perhaps indirectly altering our taste perception,” she posited, and, because of that, “we have an altered sense of satiety and hunger?”

Dr. Sever noted Dr. Several limitations to the study, including that only specific tastes were evaluated in a controlled study environment, “which may not reflect everyday experience,” she said. Taste perception can also vary widely from person to person, and changes in mRNA expression do not necessarily reflect changes in protein levels or activity.

“Our study should be seen and interpreted as a proof-of-concept study,” Dr. Sever added, with additional research needed to explore the relationship between semaglutide and taste perception.

Dr. Srivastava consults for Novo Nordisk, Eli Lilly, and Rhythm Pharmaceuticals. She has received research grant support from Eli Lilly. Dr. Sever reports no relevant financial relationships. 

A version of this article appeared on Medscape.com .

The glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide (Ozempic, Wegovy) enhances taste sensitivity, changes brain responses to sweet tastes and may even alter expression of genes in the tongue associated with taste bud development, according to new research presented at the annual meeting of the Endocrine Society, held in Boston. 

“Some studies have reported that individuals living with obesity often perceive tastes as less intense,” noted Mojca Jensterle Sever, PhD, of the University Medical Centre in Ljubljana, Slovenia, who presented the work. Research also suggests that “populations prone to obesity have an inherently elevated desire for sweet and energy-dense foods,” she continued. 

Studies in animal models have also previously shown that GLP-1 plays an important role in taste sensitivity, but it was not known if this hormone also influenced human taste perception. 

In this proof-of-concept study, researchers randomly assigned 30 women with polycystic ovary syndrome (PCOS) to either 1 mg of semaglutide, administered once a week, or placebo for 16 weeks. Participants were on average 34 years old with a body mass index (BMI) of 36.4. Participants with PCOS were selected with the “aim to reduce variability in taste perception across different phases of the menstrual cycle,” Dr. Sever said. 

Prior to the intervention, researchers tested participants’ taste sensitivity using 16 taste strips infused with four different concentrations of sweet, sour, salty, and bitter substances. Participants were asked to identify the taste of each strip. Every correct answer counted as one point, with a possible total of 16 points overall. Tongue biopsies were conducted for gene expression analysis. 

Researchers also used functional MRI (fMRI) to evaluate brain responses to a series of calorie-dense, low-calorie, and non-food visual cues as well as to sweet taste stimulus. A sweet solution was administered on the tongue 30 minutes before and after participants consumed a standardized meal: a high-protein enriched nutritional drink. 

These tests were repeated after 16 weeks. 

At the end of the study, the women taking semaglutide increased their taste sensitivity from 11.9 to 14.4 points; the estimated treatment difference from the control group was 2.5 points (95% CI, 1.7 - 3.3). 

The semaglutide group also exhibited decreased activation of the putamen (a structure in the brain involved with the brain’s reward system) on fMRI in response to calorie-dense cues. In response to sweet taste stimulus, those taking semaglutide showed increased activation of angular gyrus on MRI compared with the placebo group. The angular gyrus is part of the brain’s parietal lobe and is involved with language, memory, reasoning, and attention.

Lastly, researchers identified differential mRNA expression in the genes EYA, PRMT8, CRLF1, and CYP1B1, which are associated with taste bud development, renewal, and differentiation.

The findings are “fascinating, because we think about all of the factors that this new class of agents are able to improve, but taste is often not something that we look at, though there have been very strong associations,” said Gitanjali Srivastava, MD, of Vanderbilt University, Nashville, Tennessee, who moderated the session.

“Is it possible that another mechanism of action for this class of agents is perhaps indirectly altering our taste perception,” she posited, and, because of that, “we have an altered sense of satiety and hunger?”

Dr. Sever noted Dr. Several limitations to the study, including that only specific tastes were evaluated in a controlled study environment, “which may not reflect everyday experience,” she said. Taste perception can also vary widely from person to person, and changes in mRNA expression do not necessarily reflect changes in protein levels or activity.

“Our study should be seen and interpreted as a proof-of-concept study,” Dr. Sever added, with additional research needed to explore the relationship between semaglutide and taste perception.

Dr. Srivastava consults for Novo Nordisk, Eli Lilly, and Rhythm Pharmaceuticals. She has received research grant support from Eli Lilly. Dr. Sever reports no relevant financial relationships. 

A version of this article appeared on Medscape.com .

The glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide (Ozempic, Wegovy) enhances taste sensitivity, changes brain responses to sweet tastes and may even alter expression of genes in the tongue associated with taste bud development, according to new research presented at the annual meeting of the Endocrine Society, held in Boston. 

“Some studies have reported that individuals living with obesity often perceive tastes as less intense,” noted Mojca Jensterle Sever, PhD, of the University Medical Centre in Ljubljana, Slovenia, who presented the work. Research also suggests that “populations prone to obesity have an inherently elevated desire for sweet and energy-dense foods,” she continued. 

Studies in animal models have also previously shown that GLP-1 plays an important role in taste sensitivity, but it was not known if this hormone also influenced human taste perception. 

In this proof-of-concept study, researchers randomly assigned 30 women with polycystic ovary syndrome (PCOS) to either 1 mg of semaglutide, administered once a week, or placebo for 16 weeks. Participants were on average 34 years old with a body mass index (BMI) of 36.4. Participants with PCOS were selected with the “aim to reduce variability in taste perception across different phases of the menstrual cycle,” Dr. Sever said. 

Prior to the intervention, researchers tested participants’ taste sensitivity using 16 taste strips infused with four different concentrations of sweet, sour, salty, and bitter substances. Participants were asked to identify the taste of each strip. Every correct answer counted as one point, with a possible total of 16 points overall. Tongue biopsies were conducted for gene expression analysis. 

Researchers also used functional MRI (fMRI) to evaluate brain responses to a series of calorie-dense, low-calorie, and non-food visual cues as well as to sweet taste stimulus. A sweet solution was administered on the tongue 30 minutes before and after participants consumed a standardized meal: a high-protein enriched nutritional drink. 

These tests were repeated after 16 weeks. 

At the end of the study, the women taking semaglutide increased their taste sensitivity from 11.9 to 14.4 points; the estimated treatment difference from the control group was 2.5 points (95% CI, 1.7 - 3.3). 

The semaglutide group also exhibited decreased activation of the putamen (a structure in the brain involved with the brain’s reward system) on fMRI in response to calorie-dense cues. In response to sweet taste stimulus, those taking semaglutide showed increased activation of angular gyrus on MRI compared with the placebo group. The angular gyrus is part of the brain’s parietal lobe and is involved with language, memory, reasoning, and attention.

Lastly, researchers identified differential mRNA expression in the genes EYA, PRMT8, CRLF1, and CYP1B1, which are associated with taste bud development, renewal, and differentiation.

The findings are “fascinating, because we think about all of the factors that this new class of agents are able to improve, but taste is often not something that we look at, though there have been very strong associations,” said Gitanjali Srivastava, MD, of Vanderbilt University, Nashville, Tennessee, who moderated the session.

“Is it possible that another mechanism of action for this class of agents is perhaps indirectly altering our taste perception,” she posited, and, because of that, “we have an altered sense of satiety and hunger?”

Dr. Sever noted Dr. Several limitations to the study, including that only specific tastes were evaluated in a controlled study environment, “which may not reflect everyday experience,” she said. Taste perception can also vary widely from person to person, and changes in mRNA expression do not necessarily reflect changes in protein levels or activity.

“Our study should be seen and interpreted as a proof-of-concept study,” Dr. Sever added, with additional research needed to explore the relationship between semaglutide and taste perception.

Dr. Srivastava consults for Novo Nordisk, Eli Lilly, and Rhythm Pharmaceuticals. She has received research grant support from Eli Lilly. Dr. Sever reports no relevant financial relationships. 

A version of this article appeared on Medscape.com .

My crystal ball says that Big Food’s ongoing development and marketing of products designed for the reduced appetites of people taking anti-obesity medications will simultaneously be welcomed by their target market and scorned by self-righteous, healthy-living, just-try-harder, isn’t-this-just-feeding-the-problem hypocrites. 

For the privileged, self-righteous, healthy-living crowd, the right to enjoy dietary indulgences and conveniences is inversely proportional to your weight. Often, judgment isn’t cast on the less-than-perfect choices of those with so-called “normal” weight; that’s often not the case for those with obesity. 

Think you’re free from this paradigm? If you are, good for you. But I’d wager that there are plenty of readers who state that they’re free from bias, but when standing in supermarket checkout lines, they scrutinize and silently pass judgment on the contents of the grocery carts of people with obesity or, similarly, on the orders of people with obesity in fast-food restaurants.

Yet, there are bags of chips and cookies in most of our weekly carts, and who among us doesn’t, at times, grab some greasy comfort or convenience?

Unfortunately, the fuel for these sorts of judgments — implicit weight bias — is not only pervasive but also durable. A recent study of temporal changes to implicit biases demonstrated that unlike biases about race, skin tone, sexuality, age, and disability — between 2007 and 2016, tested levels of these implicit bias were seen to be in decline —biases about weight remain stable.

As to the products themselves, according to the recent article, they’ll be smaller, lower in calories, and high in protein and fat. To put it another way, compared with their nonshrunken counterparts, the food products will lead to the consumption of fewer calories while providing a potentially more-sating macronutrient distribution: a win-win. And no doubt, their sales won’t be restricted to those taking anti-obesity medications and, consequently, will provide everyone the ability to purchase and enjoy smaller dietary indulgences. 

With that said, I’d be remiss if I didn’t assert that the discussion of the merits or lack thereof of these sorts of offerings is misguided and pointless in that the food industry’s job is not one of social service provision or preventive healthcare. As I’ve written in the past, the food industry is neither friend, foe, nor partner. The food industry’s one job is to sell food, and if they see a market opportunity, they’ll take it. In this case, that turns out to be refreshing in a sense in that unlike moral-panic scolds, the food industry doesn’t judge its customers’ right to buy its products on the basis of how much their customers weigh. 

Whereas the food industry’s response to anti-obesity medications’ impact on appetite may be to embrace it, many others’, including in medicine, seem to involve some degree of judgment or scorn. Yes, our behavior has an impact on our weight, but intentional behavior change in the name of weight requires multiple layers of deep and perpetual privilege. And yes, our environment is indeed a tremendous contributor to the challenge of obesity, but the world is full of medical conditions influenced or caused by our environment. Yet, discussions around how medications fail to address obesity’s root cause are the only such root-cause discussions I ever see. 

Put more plainly, “how dare we develop medications for conditions influenced by our environment” is an odd stance to take in a world full of conditions influenced by our environments and where our environments’ primary change-driver is sales. Products that support the use of medications that improve life’s quality while markedly reducing the risk for an ever-growing number of conditions should be celebrated. 

Dr. Freedhoff has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; received research grant from Novo Nordisk; publicly shared opinions via Weighty Matters and social media.

A version of this article appeared on Medscape.com.

My crystal ball says that Big Food’s ongoing development and marketing of products designed for the reduced appetites of people taking anti-obesity medications will simultaneously be welcomed by their target market and scorned by self-righteous, healthy-living, just-try-harder, isn’t-this-just-feeding-the-problem hypocrites. 

For the privileged, self-righteous, healthy-living crowd, the right to enjoy dietary indulgences and conveniences is inversely proportional to your weight. Often, judgment isn’t cast on the less-than-perfect choices of those with so-called “normal” weight; that’s often not the case for those with obesity. 

Think you’re free from this paradigm? If you are, good for you. But I’d wager that there are plenty of readers who state that they’re free from bias, but when standing in supermarket checkout lines, they scrutinize and silently pass judgment on the contents of the grocery carts of people with obesity or, similarly, on the orders of people with obesity in fast-food restaurants.

Yet, there are bags of chips and cookies in most of our weekly carts, and who among us doesn’t, at times, grab some greasy comfort or convenience?

Unfortunately, the fuel for these sorts of judgments — implicit weight bias — is not only pervasive but also durable. A recent study of temporal changes to implicit biases demonstrated that unlike biases about race, skin tone, sexuality, age, and disability — between 2007 and 2016, tested levels of these implicit bias were seen to be in decline —biases about weight remain stable.

As to the products themselves, according to the recent article, they’ll be smaller, lower in calories, and high in protein and fat. To put it another way, compared with their nonshrunken counterparts, the food products will lead to the consumption of fewer calories while providing a potentially more-sating macronutrient distribution: a win-win. And no doubt, their sales won’t be restricted to those taking anti-obesity medications and, consequently, will provide everyone the ability to purchase and enjoy smaller dietary indulgences. 

With that said, I’d be remiss if I didn’t assert that the discussion of the merits or lack thereof of these sorts of offerings is misguided and pointless in that the food industry’s job is not one of social service provision or preventive healthcare. As I’ve written in the past, the food industry is neither friend, foe, nor partner. The food industry’s one job is to sell food, and if they see a market opportunity, they’ll take it. In this case, that turns out to be refreshing in a sense in that unlike moral-panic scolds, the food industry doesn’t judge its customers’ right to buy its products on the basis of how much their customers weigh. 

Whereas the food industry’s response to anti-obesity medications’ impact on appetite may be to embrace it, many others’, including in medicine, seem to involve some degree of judgment or scorn. Yes, our behavior has an impact on our weight, but intentional behavior change in the name of weight requires multiple layers of deep and perpetual privilege. And yes, our environment is indeed a tremendous contributor to the challenge of obesity, but the world is full of medical conditions influenced or caused by our environment. Yet, discussions around how medications fail to address obesity’s root cause are the only such root-cause discussions I ever see. 

Put more plainly, “how dare we develop medications for conditions influenced by our environment” is an odd stance to take in a world full of conditions influenced by our environments and where our environments’ primary change-driver is sales. Products that support the use of medications that improve life’s quality while markedly reducing the risk for an ever-growing number of conditions should be celebrated. 

Dr. Freedhoff has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; received research grant from Novo Nordisk; publicly shared opinions via Weighty Matters and social media.

A version of this article appeared on Medscape.com.

My crystal ball says that Big Food’s ongoing development and marketing of products designed for the reduced appetites of people taking anti-obesity medications will simultaneously be welcomed by their target market and scorned by self-righteous, healthy-living, just-try-harder, isn’t-this-just-feeding-the-problem hypocrites. 

For the privileged, self-righteous, healthy-living crowd, the right to enjoy dietary indulgences and conveniences is inversely proportional to your weight. Often, judgment isn’t cast on the less-than-perfect choices of those with so-called “normal” weight; that’s often not the case for those with obesity. 

Think you’re free from this paradigm? If you are, good for you. But I’d wager that there are plenty of readers who state that they’re free from bias, but when standing in supermarket checkout lines, they scrutinize and silently pass judgment on the contents of the grocery carts of people with obesity or, similarly, on the orders of people with obesity in fast-food restaurants.

Yet, there are bags of chips and cookies in most of our weekly carts, and who among us doesn’t, at times, grab some greasy comfort or convenience?

Unfortunately, the fuel for these sorts of judgments — implicit weight bias — is not only pervasive but also durable. A recent study of temporal changes to implicit biases demonstrated that unlike biases about race, skin tone, sexuality, age, and disability — between 2007 and 2016, tested levels of these implicit bias were seen to be in decline —biases about weight remain stable.

As to the products themselves, according to the recent article, they’ll be smaller, lower in calories, and high in protein and fat. To put it another way, compared with their nonshrunken counterparts, the food products will lead to the consumption of fewer calories while providing a potentially more-sating macronutrient distribution: a win-win. And no doubt, their sales won’t be restricted to those taking anti-obesity medications and, consequently, will provide everyone the ability to purchase and enjoy smaller dietary indulgences. 

With that said, I’d be remiss if I didn’t assert that the discussion of the merits or lack thereof of these sorts of offerings is misguided and pointless in that the food industry’s job is not one of social service provision or preventive healthcare. As I’ve written in the past, the food industry is neither friend, foe, nor partner. The food industry’s one job is to sell food, and if they see a market opportunity, they’ll take it. In this case, that turns out to be refreshing in a sense in that unlike moral-panic scolds, the food industry doesn’t judge its customers’ right to buy its products on the basis of how much their customers weigh. 

Whereas the food industry’s response to anti-obesity medications’ impact on appetite may be to embrace it, many others’, including in medicine, seem to involve some degree of judgment or scorn. Yes, our behavior has an impact on our weight, but intentional behavior change in the name of weight requires multiple layers of deep and perpetual privilege. And yes, our environment is indeed a tremendous contributor to the challenge of obesity, but the world is full of medical conditions influenced or caused by our environment. Yet, discussions around how medications fail to address obesity’s root cause are the only such root-cause discussions I ever see. 

Put more plainly, “how dare we develop medications for conditions influenced by our environment” is an odd stance to take in a world full of conditions influenced by our environments and where our environments’ primary change-driver is sales. Products that support the use of medications that improve life’s quality while markedly reducing the risk for an ever-growing number of conditions should be celebrated. 

Dr. Freedhoff has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; received research grant from Novo Nordisk; publicly shared opinions via Weighty Matters and social media.

A version of this article appeared on Medscape.com.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

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

A version of this article appeared on Medscape.com.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

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

A version of this article appeared on Medscape.com.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

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

A version of this article appeared on Medscape.com.

TOPLINE:

Women with low bone density are more likely to report their first fragility hip fracture in their 60s rather than at older ages.

METHODOLOGY:

• Researchers used hip fracture data from the National Health and Nutrition Examination Survey for 2009-2010, 2013-2014, and 2017-2018.
• They included women older than 60 years with a bone mineral density T score ≤ −1 at the femur neck, measured by dual-energy x-ray absorptiometry.
• Fragility fractures are defined as a self-reported hip fracture resulting from a fall from standing height or less.

TAKEAWAY:

• The number of women in their 60s who reported their first hip fracture grew by 50% from 2009 to 2018.
• The opposite was true for women in their 70s and 80s who reported fewer first hip fractures over the study period.
• Reported fragility hip fractures in women overall decreased by half from 2009 to 2018.
• The prevalence of women with osteoporosis (T score ≤ −2.5) grew from 18.1% to 21.3% over 10 years.

IN PRACTICE:

The decrease in fractures overall and in women older than 70 years “may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education, and environmental modifications targeted toward the elderly population,” the authors wrote. The findings also underscore the importance of earlier bone health awareness in primary care to curb the rising trend in younger women, they added.

SOURCE:

The study was led by Avica Atri, MD, of Albert Einstein Medical Center in Philadelphia. She presented the findings at ENDO 2024: The Endocrine Society Annual Meeting.

LIMITATIONS:

The study was retrospective in nature and included self-reported health data.

DISCLOSURES:

The study received no commercial funding. The authors have reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Women with low bone density are more likely to report their first fragility hip fracture in their 60s rather than at older ages.

METHODOLOGY:

• Researchers used hip fracture data from the National Health and Nutrition Examination Survey for 2009-2010, 2013-2014, and 2017-2018.
• They included women older than 60 years with a bone mineral density T score ≤ −1 at the femur neck, measured by dual-energy x-ray absorptiometry.
• Fragility fractures are defined as a self-reported hip fracture resulting from a fall from standing height or less.

TAKEAWAY:

• The number of women in their 60s who reported their first hip fracture grew by 50% from 2009 to 2018.
• The opposite was true for women in their 70s and 80s who reported fewer first hip fractures over the study period.
• Reported fragility hip fractures in women overall decreased by half from 2009 to 2018.
• The prevalence of women with osteoporosis (T score ≤ −2.5) grew from 18.1% to 21.3% over 10 years.

IN PRACTICE:

The decrease in fractures overall and in women older than 70 years “may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education, and environmental modifications targeted toward the elderly population,” the authors wrote. The findings also underscore the importance of earlier bone health awareness in primary care to curb the rising trend in younger women, they added.

SOURCE:

The study was led by Avica Atri, MD, of Albert Einstein Medical Center in Philadelphia. She presented the findings at ENDO 2024: The Endocrine Society Annual Meeting.

LIMITATIONS:

The study was retrospective in nature and included self-reported health data.

DISCLOSURES:

The study received no commercial funding. The authors have reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Women with low bone density are more likely to report their first fragility hip fracture in their 60s rather than at older ages.

METHODOLOGY:

• Researchers used hip fracture data from the National Health and Nutrition Examination Survey for 2009-2010, 2013-2014, and 2017-2018.
• They included women older than 60 years with a bone mineral density T score ≤ −1 at the femur neck, measured by dual-energy x-ray absorptiometry.
• Fragility fractures are defined as a self-reported hip fracture resulting from a fall from standing height or less.

TAKEAWAY:

• The number of women in their 60s who reported their first hip fracture grew by 50% from 2009 to 2018.
• The opposite was true for women in their 70s and 80s who reported fewer first hip fractures over the study period.
• Reported fragility hip fractures in women overall decreased by half from 2009 to 2018.
• The prevalence of women with osteoporosis (T score ≤ −2.5) grew from 18.1% to 21.3% over 10 years.

IN PRACTICE:

The decrease in fractures overall and in women older than 70 years “may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education, and environmental modifications targeted toward the elderly population,” the authors wrote. The findings also underscore the importance of earlier bone health awareness in primary care to curb the rising trend in younger women, they added.

SOURCE:

The study was led by Avica Atri, MD, of Albert Einstein Medical Center in Philadelphia. She presented the findings at ENDO 2024: The Endocrine Society Annual Meeting.

LIMITATIONS:

The study was retrospective in nature and included self-reported health data.

DISCLOSURES:

The study received no commercial funding. The authors have reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Tricia Ward: Hi. I’m Tricia Ward, from theheart.org/Medscape Cardiology. I’m joined today by Dr Matthew Budoff. He is professor of medicine at UCLA and the endowed chair of preventive cardiology at the Lundquist Institute. Welcome, Dr Budoff. 

Matthew J. Budoff, MD: Thank you. 

Dietary Calcium vs Coronary Calcium

Ms. Ward: The reason I wanted to talk to you today is because there have been some recent studies linking calcium supplements to an increased risk for cardiovascular disease. I’m old enough to remember when we used to tell people that dietary calcium and coronary calcium weren’t connected and weren’t the same. Were we wrong?

Dr. Budoff: I think there’s a large amount of mixed data out there still. The US Preventive Services Task Force looked into this a number of years ago and said there’s no association between calcium supplementation and increased risk for cardiovascular disease. 

As you mentioned, there are a couple of newer studies that point us toward a relationship. I think that we still have a little bit of a mixed bag, but we need to dive a little deeper into that to figure out what’s going on. 

Ms. Ward: Does it appear to be connected to calcium in the form of supplements vs calcium from foods? 

Dr. Budoff: We looked very carefully at dietary calcium in the MESA study, the multiethnic study of atherosclerosis. There is no relationship between dietary calcium intake and coronary calcium or cardiovascular events. We’re talking mostly about supplements now when we talk about this increased risk that we’re seeing.
 

Does Vitamin D Exacerbate Risk? 

Ms. Ward: Because it’s seen with supplements, is that likely because that’s a much higher concentration of calcium coming in or do you think it’s something inherent in its being in the form of a supplement?

Dr. Budoff: I think there are two things. One, it’s definitely a higher concentration all at once. You get many more milligrams at a time when you take a supplement than if you had a high-calcium food or drink.

Also, most supplements have vitamin D as well. I think vitamin D and calcium work synergistically. When you give them both together simultaneously, I think that may have more of a potentiating effect that might exacerbate any potential risk. 

Ms. Ward: Is there any reason to think there might be a difference in type of calcium supplement? I always think of the chalky tablet form vs calcium chews. 

Dr. Budoff: I’m not aware of a difference in the supplement type. I think the vitamin D issue is a big problem because we all have patients who take thousands of units of vitamin D — just crazy numbers. People advocate really high numbers and that stays in the system. 

Personally, I think part of the explanation is that with very high levels of vitamin D on top of calcium supplementation, you now absorb it better. You now get it into the bone, but maybe also into the coronary arteries. If you’re very high in vitamin D and then are taking a large calcium supplement, it might be the calcium/vitamin D combination that’s giving us some trouble. I think people on vitamin D supplements really need to watch their levels and not get supratherapeutic. 

Ms. Ward: With the vitamin D? 

Dr. Budoff: With the vitamin D.
 

Diabetes and Renal Function

Ms. Ward: In some of the studies, there seems to be a higher risk in patients with diabetes. Is there any reason why that would be?

Dr. Budoff: I can’t think of a reason exactly why with diabetes per se, except for renal disease. Patients with diabetes have more intrinsic renal disease, proteinuria, and even a reduced eGFR. We’ve seen that the kidney is very strongly tied to this. We have a very strong relationship, in work I’ve done a decade ago now, showing that calcium supplementation (in the form of phosphate binders) in patients on dialysis or with advanced renal disease is linked to much higher coronary calcium progression. 

We did prospective, randomized trials showing that calcium intake as binders to reduce phosphorus led to more coronary calcium. We always thought that was just relegated to the renal population, and there might be an overlap here with the diabetes and more renal disease. I have a feeling that it has to do with more of that. It might be regulation of parathyroid hormone as well, which might be more abnormal in patients with diabetes. 
 

Avoid Supratherapeutic Vitamin D Levels

Ms. Ward:: What are you telling your patients? 

Dr. Budoff: I tell patients with normal kidney function that the bone will modulate 99.9% of the calcium uptake. If they have osteopenia or osteoporosis, regardless of their calcium score, I’m very comfortable putting them on supplements. 

I’m a little more cautious with the vitamin D levels, and I keep an eye on that and regulate how much vitamin D they get based on their levels. I get them into the normal range, but I don’t want them supratherapeutic. You can even follow their calcium score. Again, we’ve shown that if you’re taking too much calcium, your calcium score will go up. I can just check it again in a couple of years to make sure that it’s safe. 

Ms. Ward:: In terms of vitamin D levels, when you’re saying “supratherapeutic,” what levels do you consider a safe amount to take?

Dr. Budoff: I’d like them under 100 ng/mL as far as their upper level. Normal is around 70 ng/mL at most labs. I try to keep them in the normal range. I don’t even want them to be high-normal if I’m going to be concomitantly giving them calcium supplements. Of course, if they have renal insufficiency, then I’m much more cautious. We’ve even seen calcium supplements raise the serum calcium, which you never see with dietary calcium. That’s another potential proof that it might be too much too fast. 

For renal patients, even in mild renal insufficiency, maybe even in diabetes where we’ve seen a signal, maybe aim lower in the amount of calcium supplementation if diet is insufficient, and aim a little lower in vitamin D targets, and I think you’ll be in a safer place. 

Ms. Ward: Is there anything else you want to add? 

Dr. Budoff: The evidence is still evolving. I’d say that it’s interesting and maybe a little frustrating that we don’t have a final answer on all of this. I would stay tuned for more data because we’re looking at many of the epidemiologic studies to try to see what happens in the real world, with both dietary intake of calcium and calcium supplementation. 

Ms. Ward: Thank you very much for joining me today. 

Dr. Budoff: It’s a pleasure. Thanks for having me. 

Dr. Budoff disclosed being a speaker for Amarin Pharma.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Tricia Ward: Hi. I’m Tricia Ward, from theheart.org/Medscape Cardiology. I’m joined today by Dr Matthew Budoff. He is professor of medicine at UCLA and the endowed chair of preventive cardiology at the Lundquist Institute. Welcome, Dr Budoff. 

Matthew J. Budoff, MD: Thank you. 

Dietary Calcium vs Coronary Calcium

Ms. Ward: The reason I wanted to talk to you today is because there have been some recent studies linking calcium supplements to an increased risk for cardiovascular disease. I’m old enough to remember when we used to tell people that dietary calcium and coronary calcium weren’t connected and weren’t the same. Were we wrong?

Dr. Budoff: I think there’s a large amount of mixed data out there still. The US Preventive Services Task Force looked into this a number of years ago and said there’s no association between calcium supplementation and increased risk for cardiovascular disease. 

As you mentioned, there are a couple of newer studies that point us toward a relationship. I think that we still have a little bit of a mixed bag, but we need to dive a little deeper into that to figure out what’s going on. 

Ms. Ward: Does it appear to be connected to calcium in the form of supplements vs calcium from foods? 

Dr. Budoff: We looked very carefully at dietary calcium in the MESA study, the multiethnic study of atherosclerosis. There is no relationship between dietary calcium intake and coronary calcium or cardiovascular events. We’re talking mostly about supplements now when we talk about this increased risk that we’re seeing.
 

Does Vitamin D Exacerbate Risk? 

Ms. Ward: Because it’s seen with supplements, is that likely because that’s a much higher concentration of calcium coming in or do you think it’s something inherent in its being in the form of a supplement?

Dr. Budoff: I think there are two things. One, it’s definitely a higher concentration all at once. You get many more milligrams at a time when you take a supplement than if you had a high-calcium food or drink.

Also, most supplements have vitamin D as well. I think vitamin D and calcium work synergistically. When you give them both together simultaneously, I think that may have more of a potentiating effect that might exacerbate any potential risk. 

Ms. Ward: Is there any reason to think there might be a difference in type of calcium supplement? I always think of the chalky tablet form vs calcium chews. 

Dr. Budoff: I’m not aware of a difference in the supplement type. I think the vitamin D issue is a big problem because we all have patients who take thousands of units of vitamin D — just crazy numbers. People advocate really high numbers and that stays in the system. 

Personally, I think part of the explanation is that with very high levels of vitamin D on top of calcium supplementation, you now absorb it better. You now get it into the bone, but maybe also into the coronary arteries. If you’re very high in vitamin D and then are taking a large calcium supplement, it might be the calcium/vitamin D combination that’s giving us some trouble. I think people on vitamin D supplements really need to watch their levels and not get supratherapeutic. 

Ms. Ward: With the vitamin D? 

Dr. Budoff: With the vitamin D.
 

Diabetes and Renal Function

Ms. Ward: In some of the studies, there seems to be a higher risk in patients with diabetes. Is there any reason why that would be?

Dr. Budoff: I can’t think of a reason exactly why with diabetes per se, except for renal disease. Patients with diabetes have more intrinsic renal disease, proteinuria, and even a reduced eGFR. We’ve seen that the kidney is very strongly tied to this. We have a very strong relationship, in work I’ve done a decade ago now, showing that calcium supplementation (in the form of phosphate binders) in patients on dialysis or with advanced renal disease is linked to much higher coronary calcium progression. 

We did prospective, randomized trials showing that calcium intake as binders to reduce phosphorus led to more coronary calcium. We always thought that was just relegated to the renal population, and there might be an overlap here with the diabetes and more renal disease. I have a feeling that it has to do with more of that. It might be regulation of parathyroid hormone as well, which might be more abnormal in patients with diabetes. 
 

Avoid Supratherapeutic Vitamin D Levels

Ms. Ward:: What are you telling your patients? 

Dr. Budoff: I tell patients with normal kidney function that the bone will modulate 99.9% of the calcium uptake. If they have osteopenia or osteoporosis, regardless of their calcium score, I’m very comfortable putting them on supplements. 

I’m a little more cautious with the vitamin D levels, and I keep an eye on that and regulate how much vitamin D they get based on their levels. I get them into the normal range, but I don’t want them supratherapeutic. You can even follow their calcium score. Again, we’ve shown that if you’re taking too much calcium, your calcium score will go up. I can just check it again in a couple of years to make sure that it’s safe. 

Ms. Ward:: In terms of vitamin D levels, when you’re saying “supratherapeutic,” what levels do you consider a safe amount to take?

Dr. Budoff: I’d like them under 100 ng/mL as far as their upper level. Normal is around 70 ng/mL at most labs. I try to keep them in the normal range. I don’t even want them to be high-normal if I’m going to be concomitantly giving them calcium supplements. Of course, if they have renal insufficiency, then I’m much more cautious. We’ve even seen calcium supplements raise the serum calcium, which you never see with dietary calcium. That’s another potential proof that it might be too much too fast. 

For renal patients, even in mild renal insufficiency, maybe even in diabetes where we’ve seen a signal, maybe aim lower in the amount of calcium supplementation if diet is insufficient, and aim a little lower in vitamin D targets, and I think you’ll be in a safer place. 

Ms. Ward: Is there anything else you want to add? 

Dr. Budoff: The evidence is still evolving. I’d say that it’s interesting and maybe a little frustrating that we don’t have a final answer on all of this. I would stay tuned for more data because we’re looking at many of the epidemiologic studies to try to see what happens in the real world, with both dietary intake of calcium and calcium supplementation. 

Ms. Ward: Thank you very much for joining me today. 

Dr. Budoff: It’s a pleasure. Thanks for having me. 

Dr. Budoff disclosed being a speaker for Amarin Pharma.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Tricia Ward: Hi. I’m Tricia Ward, from theheart.org/Medscape Cardiology. I’m joined today by Dr Matthew Budoff. He is professor of medicine at UCLA and the endowed chair of preventive cardiology at the Lundquist Institute. Welcome, Dr Budoff. 

Matthew J. Budoff, MD: Thank you. 

Dietary Calcium vs Coronary Calcium

Ms. Ward: The reason I wanted to talk to you today is because there have been some recent studies linking calcium supplements to an increased risk for cardiovascular disease. I’m old enough to remember when we used to tell people that dietary calcium and coronary calcium weren’t connected and weren’t the same. Were we wrong?

Dr. Budoff: I think there’s a large amount of mixed data out there still. The US Preventive Services Task Force looked into this a number of years ago and said there’s no association between calcium supplementation and increased risk for cardiovascular disease. 

As you mentioned, there are a couple of newer studies that point us toward a relationship. I think that we still have a little bit of a mixed bag, but we need to dive a little deeper into that to figure out what’s going on. 

Ms. Ward: Does it appear to be connected to calcium in the form of supplements vs calcium from foods? 

Dr. Budoff: We looked very carefully at dietary calcium in the MESA study, the multiethnic study of atherosclerosis. There is no relationship between dietary calcium intake and coronary calcium or cardiovascular events. We’re talking mostly about supplements now when we talk about this increased risk that we’re seeing.
 

Does Vitamin D Exacerbate Risk? 

Ms. Ward: Because it’s seen with supplements, is that likely because that’s a much higher concentration of calcium coming in or do you think it’s something inherent in its being in the form of a supplement?

Dr. Budoff: I think there are two things. One, it’s definitely a higher concentration all at once. You get many more milligrams at a time when you take a supplement than if you had a high-calcium food or drink.

Also, most supplements have vitamin D as well. I think vitamin D and calcium work synergistically. When you give them both together simultaneously, I think that may have more of a potentiating effect that might exacerbate any potential risk. 

Ms. Ward: Is there any reason to think there might be a difference in type of calcium supplement? I always think of the chalky tablet form vs calcium chews. 

Dr. Budoff: I’m not aware of a difference in the supplement type. I think the vitamin D issue is a big problem because we all have patients who take thousands of units of vitamin D — just crazy numbers. People advocate really high numbers and that stays in the system. 

Personally, I think part of the explanation is that with very high levels of vitamin D on top of calcium supplementation, you now absorb it better. You now get it into the bone, but maybe also into the coronary arteries. If you’re very high in vitamin D and then are taking a large calcium supplement, it might be the calcium/vitamin D combination that’s giving us some trouble. I think people on vitamin D supplements really need to watch their levels and not get supratherapeutic. 

Ms. Ward: With the vitamin D? 

Dr. Budoff: With the vitamin D.
 

Diabetes and Renal Function

Ms. Ward: In some of the studies, there seems to be a higher risk in patients with diabetes. Is there any reason why that would be?

Dr. Budoff: I can’t think of a reason exactly why with diabetes per se, except for renal disease. Patients with diabetes have more intrinsic renal disease, proteinuria, and even a reduced eGFR. We’ve seen that the kidney is very strongly tied to this. We have a very strong relationship, in work I’ve done a decade ago now, showing that calcium supplementation (in the form of phosphate binders) in patients on dialysis or with advanced renal disease is linked to much higher coronary calcium progression. 

We did prospective, randomized trials showing that calcium intake as binders to reduce phosphorus led to more coronary calcium. We always thought that was just relegated to the renal population, and there might be an overlap here with the diabetes and more renal disease. I have a feeling that it has to do with more of that. It might be regulation of parathyroid hormone as well, which might be more abnormal in patients with diabetes. 
 

Avoid Supratherapeutic Vitamin D Levels

Ms. Ward:: What are you telling your patients? 

Dr. Budoff: I tell patients with normal kidney function that the bone will modulate 99.9% of the calcium uptake. If they have osteopenia or osteoporosis, regardless of their calcium score, I’m very comfortable putting them on supplements. 

I’m a little more cautious with the vitamin D levels, and I keep an eye on that and regulate how much vitamin D they get based on their levels. I get them into the normal range, but I don’t want them supratherapeutic. You can even follow their calcium score. Again, we’ve shown that if you’re taking too much calcium, your calcium score will go up. I can just check it again in a couple of years to make sure that it’s safe. 

Ms. Ward:: In terms of vitamin D levels, when you’re saying “supratherapeutic,” what levels do you consider a safe amount to take?

Dr. Budoff: I’d like them under 100 ng/mL as far as their upper level. Normal is around 70 ng/mL at most labs. I try to keep them in the normal range. I don’t even want them to be high-normal if I’m going to be concomitantly giving them calcium supplements. Of course, if they have renal insufficiency, then I’m much more cautious. We’ve even seen calcium supplements raise the serum calcium, which you never see with dietary calcium. That’s another potential proof that it might be too much too fast. 

For renal patients, even in mild renal insufficiency, maybe even in diabetes where we’ve seen a signal, maybe aim lower in the amount of calcium supplementation if diet is insufficient, and aim a little lower in vitamin D targets, and I think you’ll be in a safer place. 

Ms. Ward: Is there anything else you want to add? 

Dr. Budoff: The evidence is still evolving. I’d say that it’s interesting and maybe a little frustrating that we don’t have a final answer on all of this. I would stay tuned for more data because we’re looking at many of the epidemiologic studies to try to see what happens in the real world, with both dietary intake of calcium and calcium supplementation. 

Ms. Ward: Thank you very much for joining me today. 

Dr. Budoff: It’s a pleasure. Thanks for having me. 

Dr. Budoff disclosed being a speaker for Amarin Pharma.

A version of this article appeared on Medscape.com.

LYON, FRANCE — High levels of lipoprotein(a) [Lp(a)] in the blood are associated with a significantly increased risk for chronic kidney disease, report investigators who are studying the link in a two-part study of more than 100,000 people.

There is already genetic evidence showing that Lp(a) can cause cardiovascular conditions, including myocardial infarction, aortic valve stenosis, peripheral artery disease, and ischemic stroke.

Now, researchers presenting at the European Atherosclerosis Society (EAS) 2024 Congress are adding new organs – the kidneys – to the list of those that can be damaged by elevated Lp(a).

“This is very important,” said lead investigator Anne Langsted, MD, PhD, DMSc, from the Department of Clinical Biochemistry at the Rigshospitalet in Denmark. And “hopefully, we’ll have a treatment for Lp(a) on the market very soon. Until then, I think individuals who have kidney disease would benefit a lot from reducing other risk factors, if they also have high levels” of Lp(a).

Using data gathered from the Copenhagen General Population Study, the study involved 108,439 individuals who had a range of tests including estimated glomerular filtration rate (eGFR), plasma Lp(a) levels, and LPA genotyping. The patients were then linked to a series of national registries to study outcomes. 

The researchers conducted two separate analyses: an observational study of Lp(a) levels in 70,040 individuals and a Mendelian randomization study of LPA kringle IV–type 2 domain repeats in 106,624 individuals. The number of those repeats is inversely associated with median Lp(a) plasma levels.

The observational study showed that eGFR decreased with increasing median plasma Lp(a) levels; the Mendelian randomization study indicated that eGFR decreased KIV-2 repeat numbers dropped.

Across both parts of the study, it was found that each 50 mg/dL increase in plasma Lp(a) levels was associated with an increased risk of at least 25% for chronic kidney disease.
 

Lp(a) and Chronic Kidney Disease

When high plasma levels of Lp(a) have been spotted before in patients with kidney disease, “we’ve kind of assumed that it was probably the kidney disease that caused the higher levels,” Dr. Langsted said. But her team hypothesized that the opposite was at play and that Lp(a) levels are genetically determined, and increased plasma Lp(a) levels may be causally associated with rising risk for chronic kidney disease.

Gerald F. Watts, MD, PhD, DSc, Winthrop Professor of cardiometabolic and internal medicine at the University of Western Australia in Perth, and co-chair of the study, said in an interview that “although Mendelian randomization is a technique that allows you to infer causality, it’s probably a little bit more complex than that in reality,” adding that there is likely a bidirectional relationship between Lp(a) and chronic kidney disease.

Having increased Lp(a) levels on their own is not sufficient to trigger chronic kidney disease. “You probably need another event and then you get into a vicious cycle,” Dr. Watts said.

The mechanism linking Lp(a) with chronic kidney disease remains unclear, but Dr. Watts explained that the lipoprotein probably damages the renal tubes when it is reabsorbed after it dissociates from low-density lipoprotein cholesterol.

The next step will be to identify the people who are most susceptible to this and figure out what treatment might help. Dr. Watts suggested that gene silencing, in which Lp(a) is “completely obliterated,” will lead to an improvement in renal function.

A version of this article appeared on Medscape.com.

LYON, FRANCE — High levels of lipoprotein(a) [Lp(a)] in the blood are associated with a significantly increased risk for chronic kidney disease, report investigators who are studying the link in a two-part study of more than 100,000 people.

There is already genetic evidence showing that Lp(a) can cause cardiovascular conditions, including myocardial infarction, aortic valve stenosis, peripheral artery disease, and ischemic stroke.

Now, researchers presenting at the European Atherosclerosis Society (EAS) 2024 Congress are adding new organs – the kidneys – to the list of those that can be damaged by elevated Lp(a).

“This is very important,” said lead investigator Anne Langsted, MD, PhD, DMSc, from the Department of Clinical Biochemistry at the Rigshospitalet in Denmark. And “hopefully, we’ll have a treatment for Lp(a) on the market very soon. Until then, I think individuals who have kidney disease would benefit a lot from reducing other risk factors, if they also have high levels” of Lp(a).

Using data gathered from the Copenhagen General Population Study, the study involved 108,439 individuals who had a range of tests including estimated glomerular filtration rate (eGFR), plasma Lp(a) levels, and LPA genotyping. The patients were then linked to a series of national registries to study outcomes. 

The researchers conducted two separate analyses: an observational study of Lp(a) levels in 70,040 individuals and a Mendelian randomization study of LPA kringle IV–type 2 domain repeats in 106,624 individuals. The number of those repeats is inversely associated with median Lp(a) plasma levels.

The observational study showed that eGFR decreased with increasing median plasma Lp(a) levels; the Mendelian randomization study indicated that eGFR decreased KIV-2 repeat numbers dropped.

Across both parts of the study, it was found that each 50 mg/dL increase in plasma Lp(a) levels was associated with an increased risk of at least 25% for chronic kidney disease.
 

Lp(a) and Chronic Kidney Disease

When high plasma levels of Lp(a) have been spotted before in patients with kidney disease, “we’ve kind of assumed that it was probably the kidney disease that caused the higher levels,” Dr. Langsted said. But her team hypothesized that the opposite was at play and that Lp(a) levels are genetically determined, and increased plasma Lp(a) levels may be causally associated with rising risk for chronic kidney disease.

Gerald F. Watts, MD, PhD, DSc, Winthrop Professor of cardiometabolic and internal medicine at the University of Western Australia in Perth, and co-chair of the study, said in an interview that “although Mendelian randomization is a technique that allows you to infer causality, it’s probably a little bit more complex than that in reality,” adding that there is likely a bidirectional relationship between Lp(a) and chronic kidney disease.

Having increased Lp(a) levels on their own is not sufficient to trigger chronic kidney disease. “You probably need another event and then you get into a vicious cycle,” Dr. Watts said.

The mechanism linking Lp(a) with chronic kidney disease remains unclear, but Dr. Watts explained that the lipoprotein probably damages the renal tubes when it is reabsorbed after it dissociates from low-density lipoprotein cholesterol.

The next step will be to identify the people who are most susceptible to this and figure out what treatment might help. Dr. Watts suggested that gene silencing, in which Lp(a) is “completely obliterated,” will lead to an improvement in renal function.

A version of this article appeared on Medscape.com.

LYON, FRANCE — High levels of lipoprotein(a) [Lp(a)] in the blood are associated with a significantly increased risk for chronic kidney disease, report investigators who are studying the link in a two-part study of more than 100,000 people.

There is already genetic evidence showing that Lp(a) can cause cardiovascular conditions, including myocardial infarction, aortic valve stenosis, peripheral artery disease, and ischemic stroke.

Now, researchers presenting at the European Atherosclerosis Society (EAS) 2024 Congress are adding new organs – the kidneys – to the list of those that can be damaged by elevated Lp(a).

“This is very important,” said lead investigator Anne Langsted, MD, PhD, DMSc, from the Department of Clinical Biochemistry at the Rigshospitalet in Denmark. And “hopefully, we’ll have a treatment for Lp(a) on the market very soon. Until then, I think individuals who have kidney disease would benefit a lot from reducing other risk factors, if they also have high levels” of Lp(a).

Using data gathered from the Copenhagen General Population Study, the study involved 108,439 individuals who had a range of tests including estimated glomerular filtration rate (eGFR), plasma Lp(a) levels, and LPA genotyping. The patients were then linked to a series of national registries to study outcomes. 

The researchers conducted two separate analyses: an observational study of Lp(a) levels in 70,040 individuals and a Mendelian randomization study of LPA kringle IV–type 2 domain repeats in 106,624 individuals. The number of those repeats is inversely associated with median Lp(a) plasma levels.

The observational study showed that eGFR decreased with increasing median plasma Lp(a) levels; the Mendelian randomization study indicated that eGFR decreased KIV-2 repeat numbers dropped.

Across both parts of the study, it was found that each 50 mg/dL increase in plasma Lp(a) levels was associated with an increased risk of at least 25% for chronic kidney disease.
 

Lp(a) and Chronic Kidney Disease

When high plasma levels of Lp(a) have been spotted before in patients with kidney disease, “we’ve kind of assumed that it was probably the kidney disease that caused the higher levels,” Dr. Langsted said. But her team hypothesized that the opposite was at play and that Lp(a) levels are genetically determined, and increased plasma Lp(a) levels may be causally associated with rising risk for chronic kidney disease.

Gerald F. Watts, MD, PhD, DSc, Winthrop Professor of cardiometabolic and internal medicine at the University of Western Australia in Perth, and co-chair of the study, said in an interview that “although Mendelian randomization is a technique that allows you to infer causality, it’s probably a little bit more complex than that in reality,” adding that there is likely a bidirectional relationship between Lp(a) and chronic kidney disease.

Having increased Lp(a) levels on their own is not sufficient to trigger chronic kidney disease. “You probably need another event and then you get into a vicious cycle,” Dr. Watts said.

The mechanism linking Lp(a) with chronic kidney disease remains unclear, but Dr. Watts explained that the lipoprotein probably damages the renal tubes when it is reabsorbed after it dissociates from low-density lipoprotein cholesterol.

The next step will be to identify the people who are most susceptible to this and figure out what treatment might help. Dr. Watts suggested that gene silencing, in which Lp(a) is “completely obliterated,” will lead to an improvement in renal function.

A version of this article appeared on Medscape.com.

BOSTON — An investigational male contraceptive gel suppresses sperm more rapidly than previous products in development, new data suggested.

The product, 8 mg segesterone acetate (Nestorone) combined with 74 mg testosterone (“NesT”) is a gel that a man applies daily to both shoulders. The progesterone blocks spermatogenesis, and the testosterone restores blood levels to maintain sexual function. It is under development by the National Institute of Child Health and Human Development (NICHD) in collaboration with the Population Council, the Los Angeles Biomedical Research Institute, and the University of Washington School of Medicine.

Currently, the only available male contraceptives are vasectomy, which isn’t easily reversible, and condoms, which have a high failure rate. Previous attempts to develop a “male pill” have been unsuccessful for a variety of reasons, but so far, this product appears effective and safe, Diana Blithe, PhD, chief of the Contraceptive Development Program at NICHD, said at a press briefing held on June 2, 2024, during the annual meeting of the Endocrine Society.

“It’s been a long time coming. … Men need and want more contraceptive options such as an effective reversible method,” she told this news organization.

New phase 2b data show that among 222 couples in which the man initially had normal (> 15 million/mL) sperm counts, the median time to suppression (< 1 million/mL) was less than 8 weeks with NesT compared with 9-15 weeks seen in previous trials of injected male hormonal contraceptives. Nearly all (86%) had achieved suppression by 15 weeks.

After two consecutive counts of < 1 million/mL, the couples entered the trial’s ongoing 2-year efficacy phase. There have been no major safety concerns thus far, but “we need more data,” Dr. Blithe noted.

Asked to comment, session moderator Frances Hayes, MBBCh, associate clinical chief of the Division of Reproductive Endocrinology at Massachusetts General Hospital, Boston, said, “certainly, I think it’s a big advance on what we have so far. … I think it’s showing great promise.”

Dr. Hayes did caution, though, that “with real-world use, daily application of a gel might be a bit more challenging than taking an injection…an injection is more consistent. With a gel, patients might forget or shower it off. But I don’t think 1 day of interruption would be a significant thing.”

Transference of the topical to a partner or a child is another potential concern, Dr. Hayes noted, although this is true of current testosterone gel products as well. During the briefing, Dr. Blithe said that this issue is why the product is recommended to be placed on the upper arms rather than the abdomen or another spot more likely to come into contact with another person. Also, in the trial, men were instructed to wear shirts during intercourse.

Regarding the rapidity of sperm suppression, Dr. Hayes said, “It’s surprising. It looks great as a reversible contraceptive. … Normally, you think of the life cycle of the sperm being about 72 days. So to see 50% suppression by 8 weeks, and then 85%-90% by 15 weeks, that’s very rapid. It may be that the progesterone that they’re using is very potent. Progestins can have some negative effects on lipids and mood. We didn’t really see the safety data in this presentation. So that will be interesting to see.”

During the briefing, Dr. Blithe said that the phase 2b trial is expected to finish by the end of this year, and in the meantime, the researchers are communicating with the US Food and Drug Administration about the design of a phase 3 trial because this is an unprecedented area. “They don’t have guidelines yet. They’ll need to develop them first.”

Dr. Blithe has been the NICHD principal investigator on cooperative research and development agreements with HRA Pharma and Daré Bioscience. Dr. Hayes had no disclosures.

A version of this article appeared on Medscape.com .

BOSTON — An investigational male contraceptive gel suppresses sperm more rapidly than previous products in development, new data suggested.

The product, 8 mg segesterone acetate (Nestorone) combined with 74 mg testosterone (“NesT”) is a gel that a man applies daily to both shoulders. The progesterone blocks spermatogenesis, and the testosterone restores blood levels to maintain sexual function. It is under development by the National Institute of Child Health and Human Development (NICHD) in collaboration with the Population Council, the Los Angeles Biomedical Research Institute, and the University of Washington School of Medicine.

Currently, the only available male contraceptives are vasectomy, which isn’t easily reversible, and condoms, which have a high failure rate. Previous attempts to develop a “male pill” have been unsuccessful for a variety of reasons, but so far, this product appears effective and safe, Diana Blithe, PhD, chief of the Contraceptive Development Program at NICHD, said at a press briefing held on June 2, 2024, during the annual meeting of the Endocrine Society.

“It’s been a long time coming. … Men need and want more contraceptive options such as an effective reversible method,” she told this news organization.

New phase 2b data show that among 222 couples in which the man initially had normal (> 15 million/mL) sperm counts, the median time to suppression (< 1 million/mL) was less than 8 weeks with NesT compared with 9-15 weeks seen in previous trials of injected male hormonal contraceptives. Nearly all (86%) had achieved suppression by 15 weeks.

After two consecutive counts of < 1 million/mL, the couples entered the trial’s ongoing 2-year efficacy phase. There have been no major safety concerns thus far, but “we need more data,” Dr. Blithe noted.

Asked to comment, session moderator Frances Hayes, MBBCh, associate clinical chief of the Division of Reproductive Endocrinology at Massachusetts General Hospital, Boston, said, “certainly, I think it’s a big advance on what we have so far. … I think it’s showing great promise.”

Dr. Hayes did caution, though, that “with real-world use, daily application of a gel might be a bit more challenging than taking an injection…an injection is more consistent. With a gel, patients might forget or shower it off. But I don’t think 1 day of interruption would be a significant thing.”

Transference of the topical to a partner or a child is another potential concern, Dr. Hayes noted, although this is true of current testosterone gel products as well. During the briefing, Dr. Blithe said that this issue is why the product is recommended to be placed on the upper arms rather than the abdomen or another spot more likely to come into contact with another person. Also, in the trial, men were instructed to wear shirts during intercourse.

Regarding the rapidity of sperm suppression, Dr. Hayes said, “It’s surprising. It looks great as a reversible contraceptive. … Normally, you think of the life cycle of the sperm being about 72 days. So to see 50% suppression by 8 weeks, and then 85%-90% by 15 weeks, that’s very rapid. It may be that the progesterone that they’re using is very potent. Progestins can have some negative effects on lipids and mood. We didn’t really see the safety data in this presentation. So that will be interesting to see.”

During the briefing, Dr. Blithe said that the phase 2b trial is expected to finish by the end of this year, and in the meantime, the researchers are communicating with the US Food and Drug Administration about the design of a phase 3 trial because this is an unprecedented area. “They don’t have guidelines yet. They’ll need to develop them first.”

Dr. Blithe has been the NICHD principal investigator on cooperative research and development agreements with HRA Pharma and Daré Bioscience. Dr. Hayes had no disclosures.

A version of this article appeared on Medscape.com .

BOSTON — An investigational male contraceptive gel suppresses sperm more rapidly than previous products in development, new data suggested.

The product, 8 mg segesterone acetate (Nestorone) combined with 74 mg testosterone (“NesT”) is a gel that a man applies daily to both shoulders. The progesterone blocks spermatogenesis, and the testosterone restores blood levels to maintain sexual function. It is under development by the National Institute of Child Health and Human Development (NICHD) in collaboration with the Population Council, the Los Angeles Biomedical Research Institute, and the University of Washington School of Medicine.

Currently, the only available male contraceptives are vasectomy, which isn’t easily reversible, and condoms, which have a high failure rate. Previous attempts to develop a “male pill” have been unsuccessful for a variety of reasons, but so far, this product appears effective and safe, Diana Blithe, PhD, chief of the Contraceptive Development Program at NICHD, said at a press briefing held on June 2, 2024, during the annual meeting of the Endocrine Society.

“It’s been a long time coming. … Men need and want more contraceptive options such as an effective reversible method,” she told this news organization.

New phase 2b data show that among 222 couples in which the man initially had normal (> 15 million/mL) sperm counts, the median time to suppression (< 1 million/mL) was less than 8 weeks with NesT compared with 9-15 weeks seen in previous trials of injected male hormonal contraceptives. Nearly all (86%) had achieved suppression by 15 weeks.

After two consecutive counts of < 1 million/mL, the couples entered the trial’s ongoing 2-year efficacy phase. There have been no major safety concerns thus far, but “we need more data,” Dr. Blithe noted.

Asked to comment, session moderator Frances Hayes, MBBCh, associate clinical chief of the Division of Reproductive Endocrinology at Massachusetts General Hospital, Boston, said, “certainly, I think it’s a big advance on what we have so far. … I think it’s showing great promise.”

Dr. Hayes did caution, though, that “with real-world use, daily application of a gel might be a bit more challenging than taking an injection…an injection is more consistent. With a gel, patients might forget or shower it off. But I don’t think 1 day of interruption would be a significant thing.”

Transference of the topical to a partner or a child is another potential concern, Dr. Hayes noted, although this is true of current testosterone gel products as well. During the briefing, Dr. Blithe said that this issue is why the product is recommended to be placed on the upper arms rather than the abdomen or another spot more likely to come into contact with another person. Also, in the trial, men were instructed to wear shirts during intercourse.

Regarding the rapidity of sperm suppression, Dr. Hayes said, “It’s surprising. It looks great as a reversible contraceptive. … Normally, you think of the life cycle of the sperm being about 72 days. So to see 50% suppression by 8 weeks, and then 85%-90% by 15 weeks, that’s very rapid. It may be that the progesterone that they’re using is very potent. Progestins can have some negative effects on lipids and mood. We didn’t really see the safety data in this presentation. So that will be interesting to see.”

During the briefing, Dr. Blithe said that the phase 2b trial is expected to finish by the end of this year, and in the meantime, the researchers are communicating with the US Food and Drug Administration about the design of a phase 3 trial because this is an unprecedented area. “They don’t have guidelines yet. They’ll need to develop them first.”

Dr. Blithe has been the NICHD principal investigator on cooperative research and development agreements with HRA Pharma and Daré Bioscience. Dr. Hayes had no disclosures.

A version of this article appeared on Medscape.com .

TOPLINE:

A diet rich in green, leafy, cruciferous, and colorful vegetables may improve glucose tolerance and insulin sensitivity, whereas a high intake of potato fries or chips may worsen these outcomes, an Australian study shows.

METHODOLOGY:

• Researchers assessed the association between the intake of vegetables and potatoes with markers of type 2 diabetes (T2D) in 8009 participants (median age, 52 years; 55% women) from the Australian Diabetes, Obesity, and Lifestyle Study.
• A self-administered 74-item food frequency questionnaire was used to assess participants’ eating habits over 12 months prior to baseline.
• Participants were categorized into four quartiles of vegetable intake, from the highest intake (Q4) to the lowest intake (Q1).
• The association between vegetable intake and various metabolic markers such as fasting plasma glucose (FPG), 2-hour post-load plasma glucose, updated homeostasis model assessment of beta cell function (HOMA2-%beta), HOMA2 of insulin sensitivity (HOMA2-%S), and fasting insulin were evaluated over a 12-year follow-up period.

TAKEAWAY:

• The post-load glucose was 3% lower in participants in the highest vs lowest quartile of total vegetable intake (ratio of means [RoM], 0.97; 95% CI, 0.96-0.99).
• Post-load glucose was 4% lower (RoM, 0.96; 95% CI, 0.95-0.98), HOMA2-%beta was 3% lower (RoM, 0.97; 95% CI, 0.96-0.99), and serum insulin was 5% lower (RoM, 0.95; 95% CI, 0.93-0.98) in those in the highest vs lowest quartile of green leafy vegetable intake.
• Those in the highest vs lowest quartile of potato fries or chips intake had 1% higher FPG, 3% higher HOMA2-%beta, and 8% higher serum insulin but 6% lower HOMA2-%S, revealing a negative impact on glucose tolerance and insulin sensitivity.
• The risk for T2D over 12 years was 26% and 25% lower among those in the highest and moderate quartiles of cruciferous vegetable intake, respectively, than among those in the lowest quartile of cruciferous vegetable intake.

IN PRACTICE:

The authors wrote that their study “sheds light on the physiological alterations in insulin regulation and glucose tolerance resulting from higher vegetable and subgroups of vegetable intake and supports the notion that vegetable subgroups may act differently in regulating insulin and blood glucose levels.”

SOURCE:

The study was led by Pratik Pokharel, MPH, Nutrition & Health Innovation Research Institute, School of Medical and Health Sciences, Edith Cowan University, Perth, Australia, and was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study’s observational nature precluded the inference of causality. Potential measurement errors in dietary exposures and recall bias linked to the food frequency questionnaire could have affected the findings. The overrepresentation of participants from higher education and socioeconomic subgroups and loss to follow-up could limit the generalizability of the findings.

DISCLOSURES:

The study was funded by the National Health and Medical Research Council, National Heart Foundation of Australia, and Royal Perth Hospital Medical Research Foundation. Several authors reported receiving grants from various sources during the conduct of this study. The other authors reported no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

A diet rich in green, leafy, cruciferous, and colorful vegetables may improve glucose tolerance and insulin sensitivity, whereas a high intake of potato fries or chips may worsen these outcomes, an Australian study shows.

METHODOLOGY:

• Researchers assessed the association between the intake of vegetables and potatoes with markers of type 2 diabetes (T2D) in 8009 participants (median age, 52 years; 55% women) from the Australian Diabetes, Obesity, and Lifestyle Study.
• A self-administered 74-item food frequency questionnaire was used to assess participants’ eating habits over 12 months prior to baseline.
• Participants were categorized into four quartiles of vegetable intake, from the highest intake (Q4) to the lowest intake (Q1).
• The association between vegetable intake and various metabolic markers such as fasting plasma glucose (FPG), 2-hour post-load plasma glucose, updated homeostasis model assessment of beta cell function (HOMA2-%beta), HOMA2 of insulin sensitivity (HOMA2-%S), and fasting insulin were evaluated over a 12-year follow-up period.

TAKEAWAY:

• The post-load glucose was 3% lower in participants in the highest vs lowest quartile of total vegetable intake (ratio of means [RoM], 0.97; 95% CI, 0.96-0.99).
• Post-load glucose was 4% lower (RoM, 0.96; 95% CI, 0.95-0.98), HOMA2-%beta was 3% lower (RoM, 0.97; 95% CI, 0.96-0.99), and serum insulin was 5% lower (RoM, 0.95; 95% CI, 0.93-0.98) in those in the highest vs lowest quartile of green leafy vegetable intake.
• Those in the highest vs lowest quartile of potato fries or chips intake had 1% higher FPG, 3% higher HOMA2-%beta, and 8% higher serum insulin but 6% lower HOMA2-%S, revealing a negative impact on glucose tolerance and insulin sensitivity.
• The risk for T2D over 12 years was 26% and 25% lower among those in the highest and moderate quartiles of cruciferous vegetable intake, respectively, than among those in the lowest quartile of cruciferous vegetable intake.

IN PRACTICE:

The authors wrote that their study “sheds light on the physiological alterations in insulin regulation and glucose tolerance resulting from higher vegetable and subgroups of vegetable intake and supports the notion that vegetable subgroups may act differently in regulating insulin and blood glucose levels.”

SOURCE:

The study was led by Pratik Pokharel, MPH, Nutrition & Health Innovation Research Institute, School of Medical and Health Sciences, Edith Cowan University, Perth, Australia, and was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study’s observational nature precluded the inference of causality. Potential measurement errors in dietary exposures and recall bias linked to the food frequency questionnaire could have affected the findings. The overrepresentation of participants from higher education and socioeconomic subgroups and loss to follow-up could limit the generalizability of the findings.

DISCLOSURES:

The study was funded by the National Health and Medical Research Council, National Heart Foundation of Australia, and Royal Perth Hospital Medical Research Foundation. Several authors reported receiving grants from various sources during the conduct of this study. The other authors reported no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

A diet rich in green, leafy, cruciferous, and colorful vegetables may improve glucose tolerance and insulin sensitivity, whereas a high intake of potato fries or chips may worsen these outcomes, an Australian study shows.

METHODOLOGY:

• Researchers assessed the association between the intake of vegetables and potatoes with markers of type 2 diabetes (T2D) in 8009 participants (median age, 52 years; 55% women) from the Australian Diabetes, Obesity, and Lifestyle Study.
• A self-administered 74-item food frequency questionnaire was used to assess participants’ eating habits over 12 months prior to baseline.
• Participants were categorized into four quartiles of vegetable intake, from the highest intake (Q4) to the lowest intake (Q1).
• The association between vegetable intake and various metabolic markers such as fasting plasma glucose (FPG), 2-hour post-load plasma glucose, updated homeostasis model assessment of beta cell function (HOMA2-%beta), HOMA2 of insulin sensitivity (HOMA2-%S), and fasting insulin were evaluated over a 12-year follow-up period.

TAKEAWAY:

• The post-load glucose was 3% lower in participants in the highest vs lowest quartile of total vegetable intake (ratio of means [RoM], 0.97; 95% CI, 0.96-0.99).
• Post-load glucose was 4% lower (RoM, 0.96; 95% CI, 0.95-0.98), HOMA2-%beta was 3% lower (RoM, 0.97; 95% CI, 0.96-0.99), and serum insulin was 5% lower (RoM, 0.95; 95% CI, 0.93-0.98) in those in the highest vs lowest quartile of green leafy vegetable intake.
• Those in the highest vs lowest quartile of potato fries or chips intake had 1% higher FPG, 3% higher HOMA2-%beta, and 8% higher serum insulin but 6% lower HOMA2-%S, revealing a negative impact on glucose tolerance and insulin sensitivity.
• The risk for T2D over 12 years was 26% and 25% lower among those in the highest and moderate quartiles of cruciferous vegetable intake, respectively, than among those in the lowest quartile of cruciferous vegetable intake.

IN PRACTICE:

The authors wrote that their study “sheds light on the physiological alterations in insulin regulation and glucose tolerance resulting from higher vegetable and subgroups of vegetable intake and supports the notion that vegetable subgroups may act differently in regulating insulin and blood glucose levels.”

SOURCE:

The study was led by Pratik Pokharel, MPH, Nutrition & Health Innovation Research Institute, School of Medical and Health Sciences, Edith Cowan University, Perth, Australia, and was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study’s observational nature precluded the inference of causality. Potential measurement errors in dietary exposures and recall bias linked to the food frequency questionnaire could have affected the findings. The overrepresentation of participants from higher education and socioeconomic subgroups and loss to follow-up could limit the generalizability of the findings.

DISCLOSURES:

The study was funded by the National Health and Medical Research Council, National Heart Foundation of Australia, and Royal Perth Hospital Medical Research Foundation. Several authors reported receiving grants from various sources during the conduct of this study. The other authors reported no conflicts of interest.

A version of this article appeared on Medscape.com.