Diabetes

TOPLINE:

Consuming five or more servings per week of dark chocolate is associated with a lower risk for type 2 diabetes (T2D), compared with infrequent or no consumption. Conversely, a higher consumption of milk chocolate does not significantly affect the risk for diabetes and may contribute to greater weight gain.

METHODOLOGY:

• Chocolate is rich in flavanols, natural compounds known to support heart health and lower the risk for T2D. However, the link between chocolate consumption and the risk for T2D is uncertain, with inconsistent research findings that don’t distinguish between dark or milk chocolate.
• Researchers conducted a prospective cohort study to investigate the associations between dark, milk, and total chocolate consumption and the risk for T2D in three long-term US studies of female nurses and male healthcare professionals with no history of diabetes, cardiovascular disease, or cancer at baseline.
• The relationship between total chocolate consumption and the risk for diabetes was investigated in 192,208 individuals who reported their chocolate consumption using validated food frequency questionnaires every 4 years from 1986 onward.
• Information on chocolate subtypes was assessed from 2006/2007 onward in 111,654 participants.
• Participants self-reported T2D through biennial questionnaires, which was confirmed via supplementary questionnaires collecting data on glucose levels, hemoglobin A1c concentration, symptoms, and treatments; they also self-reported their body weight at baseline and during follow-ups.

TAKEAWAY:

• During 4,829,175 person-years of follow-up, researchers identified 18,862 individuals with incident T2D in the total chocolate analysis cohort.
• In the chocolate subtype cohort, 4771 incident T2D cases were identified during 1,270,348 person-years of follow-up. Having at least five servings per week of dark chocolate was associated with a 21% lower risk for T2D (adjusted hazard ratio, 0.79; P for trend = .006), while milk chocolate consumption showed no significant link (P for trend = .75).
• The risk for T2D decreased by 3% for each additional serving of dark chocolate consumed weekly, indicating a dose-response effect.
• Compared with individuals who did not change their chocolate intake, those who had an increased milk chocolate intake had greater weight gain over 4-year periods (mean difference, 0.35 kg; 95% CI, 0.27-0.43); dark chocolate showed no significant association with weight change.

IN PRACTICE:

“Even though dark and milk chocolate have similar levels of calories and saturated fat, it appears that the rich polyphenols in dark chocolate might offset the effects of saturated fat and sugar on weight gain and diabetes. It’s an intriguing difference that’s worth exploring more,” corresponding author Qi Sun from the Departments of Nutrition and Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts, said in a press release.

SOURCE:

This study was led by Binkai Liu, Harvard TH Chan School of Public Health. It was published online in The BMJ.

LIMITATIONS:

The relatively limited number of participants in the higher chocolate consumption groups may have reduced the statistical power for detecting modest associations between dark chocolate consumption and the risk for T2D. Additionally, the study population primarily consisted of non-Hispanic White adults older than 50 years at baseline, which, along with their professional backgrounds, may have limited the generalizability of the study findings to other populations with different socioeconomic or personal characteristics. Chocolate consumption in this study was lower than the national average of three servings per week, which may have limited the ability to assess the dose-response relationship at higher intake levels.

DISCLOSURES:

This study was supported by grants from the National Institutes of Health. Some authors reported receiving investigator-initiated grants, being on scientific advisory boards, and receiving research funding from certain institutions.

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:

Consuming five or more servings per week of dark chocolate is associated with a lower risk for type 2 diabetes (T2D), compared with infrequent or no consumption. Conversely, a higher consumption of milk chocolate does not significantly affect the risk for diabetes and may contribute to greater weight gain.

METHODOLOGY:

• Chocolate is rich in flavanols, natural compounds known to support heart health and lower the risk for T2D. However, the link between chocolate consumption and the risk for T2D is uncertain, with inconsistent research findings that don’t distinguish between dark or milk chocolate.
• Researchers conducted a prospective cohort study to investigate the associations between dark, milk, and total chocolate consumption and the risk for T2D in three long-term US studies of female nurses and male healthcare professionals with no history of diabetes, cardiovascular disease, or cancer at baseline.
• The relationship between total chocolate consumption and the risk for diabetes was investigated in 192,208 individuals who reported their chocolate consumption using validated food frequency questionnaires every 4 years from 1986 onward.
• Information on chocolate subtypes was assessed from 2006/2007 onward in 111,654 participants.
• Participants self-reported T2D through biennial questionnaires, which was confirmed via supplementary questionnaires collecting data on glucose levels, hemoglobin A1c concentration, symptoms, and treatments; they also self-reported their body weight at baseline and during follow-ups.

TAKEAWAY:

• During 4,829,175 person-years of follow-up, researchers identified 18,862 individuals with incident T2D in the total chocolate analysis cohort.
• In the chocolate subtype cohort, 4771 incident T2D cases were identified during 1,270,348 person-years of follow-up. Having at least five servings per week of dark chocolate was associated with a 21% lower risk for T2D (adjusted hazard ratio, 0.79; P for trend = .006), while milk chocolate consumption showed no significant link (P for trend = .75).
• The risk for T2D decreased by 3% for each additional serving of dark chocolate consumed weekly, indicating a dose-response effect.
• Compared with individuals who did not change their chocolate intake, those who had an increased milk chocolate intake had greater weight gain over 4-year periods (mean difference, 0.35 kg; 95% CI, 0.27-0.43); dark chocolate showed no significant association with weight change.

IN PRACTICE:

“Even though dark and milk chocolate have similar levels of calories and saturated fat, it appears that the rich polyphenols in dark chocolate might offset the effects of saturated fat and sugar on weight gain and diabetes. It’s an intriguing difference that’s worth exploring more,” corresponding author Qi Sun from the Departments of Nutrition and Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts, said in a press release.

SOURCE:

This study was led by Binkai Liu, Harvard TH Chan School of Public Health. It was published online in The BMJ.

LIMITATIONS:

The relatively limited number of participants in the higher chocolate consumption groups may have reduced the statistical power for detecting modest associations between dark chocolate consumption and the risk for T2D. Additionally, the study population primarily consisted of non-Hispanic White adults older than 50 years at baseline, which, along with their professional backgrounds, may have limited the generalizability of the study findings to other populations with different socioeconomic or personal characteristics. Chocolate consumption in this study was lower than the national average of three servings per week, which may have limited the ability to assess the dose-response relationship at higher intake levels.

DISCLOSURES:

This study was supported by grants from the National Institutes of Health. Some authors reported receiving investigator-initiated grants, being on scientific advisory boards, and receiving research funding from certain institutions.

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:

Consuming five or more servings per week of dark chocolate is associated with a lower risk for type 2 diabetes (T2D), compared with infrequent or no consumption. Conversely, a higher consumption of milk chocolate does not significantly affect the risk for diabetes and may contribute to greater weight gain.

METHODOLOGY:

• Chocolate is rich in flavanols, natural compounds known to support heart health and lower the risk for T2D. However, the link between chocolate consumption and the risk for T2D is uncertain, with inconsistent research findings that don’t distinguish between dark or milk chocolate.
• Researchers conducted a prospective cohort study to investigate the associations between dark, milk, and total chocolate consumption and the risk for T2D in three long-term US studies of female nurses and male healthcare professionals with no history of diabetes, cardiovascular disease, or cancer at baseline.
• The relationship between total chocolate consumption and the risk for diabetes was investigated in 192,208 individuals who reported their chocolate consumption using validated food frequency questionnaires every 4 years from 1986 onward.
• Information on chocolate subtypes was assessed from 2006/2007 onward in 111,654 participants.
• Participants self-reported T2D through biennial questionnaires, which was confirmed via supplementary questionnaires collecting data on glucose levels, hemoglobin A1c concentration, symptoms, and treatments; they also self-reported their body weight at baseline and during follow-ups.

TAKEAWAY:

• During 4,829,175 person-years of follow-up, researchers identified 18,862 individuals with incident T2D in the total chocolate analysis cohort.
• In the chocolate subtype cohort, 4771 incident T2D cases were identified during 1,270,348 person-years of follow-up. Having at least five servings per week of dark chocolate was associated with a 21% lower risk for T2D (adjusted hazard ratio, 0.79; P for trend = .006), while milk chocolate consumption showed no significant link (P for trend = .75).
• The risk for T2D decreased by 3% for each additional serving of dark chocolate consumed weekly, indicating a dose-response effect.
• Compared with individuals who did not change their chocolate intake, those who had an increased milk chocolate intake had greater weight gain over 4-year periods (mean difference, 0.35 kg; 95% CI, 0.27-0.43); dark chocolate showed no significant association with weight change.

IN PRACTICE:

“Even though dark and milk chocolate have similar levels of calories and saturated fat, it appears that the rich polyphenols in dark chocolate might offset the effects of saturated fat and sugar on weight gain and diabetes. It’s an intriguing difference that’s worth exploring more,” corresponding author Qi Sun from the Departments of Nutrition and Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts, said in a press release.

SOURCE:

This study was led by Binkai Liu, Harvard TH Chan School of Public Health. It was published online in The BMJ.

LIMITATIONS:

The relatively limited number of participants in the higher chocolate consumption groups may have reduced the statistical power for detecting modest associations between dark chocolate consumption and the risk for T2D. Additionally, the study population primarily consisted of non-Hispanic White adults older than 50 years at baseline, which, along with their professional backgrounds, may have limited the generalizability of the study findings to other populations with different socioeconomic or personal characteristics. Chocolate consumption in this study was lower than the national average of three servings per week, which may have limited the ability to assess the dose-response relationship at higher intake levels.

DISCLOSURES:

This study was supported by grants from the National Institutes of Health. Some authors reported receiving investigator-initiated grants, being on scientific advisory boards, and receiving research funding from certain institutions.

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

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

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

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

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

 

Diet Education Is Vital in Chronic Disease Management

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

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

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

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

 

How to Work Nutrient Density into the Conversation

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

 

Diet Education Is Vital in Chronic Disease Management

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

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

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

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

 

How to Work Nutrient Density into the Conversation

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

 

Diet Education Is Vital in Chronic Disease Management

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

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

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

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

 

How to Work Nutrient Density into the Conversation

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

When a patient signs on to a telehealth portal, there’s little more a provider can do than ask questions. But a new artificial intelligence (AI) technology could allow providers to get feedback about the patient’s blood pressure and diabetes risk just from a video call or a smartphone app.

Researchers at the University of Tokyo in Japan are using AI to determine whether people might have high blood pressure or diabetes based on video data collected with a special sensor. 

The technology relies on photoplethysmography (PPG), which measures changes in blood volume by detecting the amount of light absorbed by blood just below the skin. 

This technology is already used for things like finger pulse oximetry to determine oxygen saturation and heart rate. Wearable devices like Apple Watches and Fitbits also use PPG technologies to detect heart rate and atrial fibrillation.

“If we could detect and accurately measure your blood pressure, heart rate, and oxygen saturation non-invasively that would be fantastic,” said Eugene Yang, MD, professor of medicine in the division of cardiology at the University of Washington School of Medicine in Seattle who was not involved in the study.

 

How Does PPG Work — and Is This New Tech Accurate?

Using PPG, “you’re detecting these small, little blood vessels that sit underneath the surface of your skin,” explained Yang.

“Since both hypertension and diabetes are diseases that damage blood vessels, we thought these diseases might affect blood flow and pulse wave transit times,” said Ryoko Uchida, a project researcher in the cardiology department at the University of Tokyo and one of the leaders of the study.

PPG devices primarily use green light to detect blood flow, as hemoglobin, the oxygen-carrying molecule in blood, absorbs green light most effectively, Yang said. “So, if you extract and remove all the other channels of light and only focus on the green channel, then that’s when you’ll be able to potentially see blood flow and pulsatile blood flow activity,” he noted.

The University of Tokyo researchers used remote or contactless PPG, which requires a short video recording of someone’s face and palms, as the person holds as still as possible. A special sensor collects the video and detects only certain wavelengths of light. Then the researchers developed an AI algorithm to extract data from participants’ skin, such as changes in pulse transit time — the time it takes for the pulse to travel from the palm to the face.

To correlate the video algorithm to blood pressure and diabetes risk, the researchers measured blood participants’ pressure with a continuous sphygmomanometer (an automatic blood pressure cuff) at the same time as they collected the video. They also did a blood A1c test to detect diabetes.

So far, they’ve tested their video algorithm on 215 people. The algorithm applied to a 30-second video was 86% accurate in detecting if blood pressure was above normal, and a 5-second video was 81% accurate in detecting higher blood pressure.

Compared with using hemoglobin A1c blood test results to screen for diabetes, the video algorithm was 75% accurate in identifying people who had subtle blood changes that correlated to diabetes.

“Most of this focus has been on wearable devices, patches, rings, wrist devices,” Yang said, “the facial video stuff is great because you can imagine that there are other ways of applying it.”

Yang, who is also doing research on facial video processing, pointed out it could be helpful not only in telehealth visits, but also for patients in the hospital with highly contagious diseases who need to be in isolation, or just for people using their smartphones. 

“People are tied to their smartphones, so you could imagine that that would be great as a way for people to have awareness about their blood pressure or their diabetes status,” Yang noted.

 

More Work to Do

The study has a few caveats. The special sensor they used in this study isn’t yet integrated into smartphone cameras or other common video recording devices. But Uchida is hopeful that it could be mass-produced and inexpensive to someday add.

Also, the study was done in a Japanese population, and lighter skin may be easier to capture changes in blood flow, Uchida noted. Pulse oximeters, which use the same technology, tend to overestimate blood oxygen in people with darker skin tones.

“It is necessary to test whether the same results are obtained in a variety of subjects other than Japanese and Asians,” Uchida said, in addition to validating the tool with more participants.

The study has also not yet undergone peer review.

And Yang pointed out that this new AI technology provides more of a screening tool to predict who is at high risk for high blood pressure or diabetes, rather than precise measurements for either disease.

There are already some devices that claim to measure blood pressure using PPG technology, like blood pressure monitoring watches. But Yang warns that these kinds of devices aren’t validated, meaning we don’t really know how well they work.

One difficulty in getting any kind of PPG blood pressure monitoring device to market is that the organizations involved in setting medical device standards (like the International Organization for Standards) doesn’t yet have a validation standard for this technology, Yang said, so there’s really no way to consistently verify the technology’s accuracy.

“I am optimistic that we are capable of figuring out how to validate these things. I just think we have so many things we have to iron out before that happens,” Yang explained, noting that it will be at least 3 years before a remote blood monitoring system is widely available.

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

When a patient signs on to a telehealth portal, there’s little more a provider can do than ask questions. But a new artificial intelligence (AI) technology could allow providers to get feedback about the patient’s blood pressure and diabetes risk just from a video call or a smartphone app.

Researchers at the University of Tokyo in Japan are using AI to determine whether people might have high blood pressure or diabetes based on video data collected with a special sensor. 

The technology relies on photoplethysmography (PPG), which measures changes in blood volume by detecting the amount of light absorbed by blood just below the skin. 

This technology is already used for things like finger pulse oximetry to determine oxygen saturation and heart rate. Wearable devices like Apple Watches and Fitbits also use PPG technologies to detect heart rate and atrial fibrillation.

“If we could detect and accurately measure your blood pressure, heart rate, and oxygen saturation non-invasively that would be fantastic,” said Eugene Yang, MD, professor of medicine in the division of cardiology at the University of Washington School of Medicine in Seattle who was not involved in the study.

 

How Does PPG Work — and Is This New Tech Accurate?

Using PPG, “you’re detecting these small, little blood vessels that sit underneath the surface of your skin,” explained Yang.

“Since both hypertension and diabetes are diseases that damage blood vessels, we thought these diseases might affect blood flow and pulse wave transit times,” said Ryoko Uchida, a project researcher in the cardiology department at the University of Tokyo and one of the leaders of the study.

PPG devices primarily use green light to detect blood flow, as hemoglobin, the oxygen-carrying molecule in blood, absorbs green light most effectively, Yang said. “So, if you extract and remove all the other channels of light and only focus on the green channel, then that’s when you’ll be able to potentially see blood flow and pulsatile blood flow activity,” he noted.

The University of Tokyo researchers used remote or contactless PPG, which requires a short video recording of someone’s face and palms, as the person holds as still as possible. A special sensor collects the video and detects only certain wavelengths of light. Then the researchers developed an AI algorithm to extract data from participants’ skin, such as changes in pulse transit time — the time it takes for the pulse to travel from the palm to the face.

To correlate the video algorithm to blood pressure and diabetes risk, the researchers measured blood participants’ pressure with a continuous sphygmomanometer (an automatic blood pressure cuff) at the same time as they collected the video. They also did a blood A1c test to detect diabetes.

So far, they’ve tested their video algorithm on 215 people. The algorithm applied to a 30-second video was 86% accurate in detecting if blood pressure was above normal, and a 5-second video was 81% accurate in detecting higher blood pressure.

Compared with using hemoglobin A1c blood test results to screen for diabetes, the video algorithm was 75% accurate in identifying people who had subtle blood changes that correlated to diabetes.

“Most of this focus has been on wearable devices, patches, rings, wrist devices,” Yang said, “the facial video stuff is great because you can imagine that there are other ways of applying it.”

Yang, who is also doing research on facial video processing, pointed out it could be helpful not only in telehealth visits, but also for patients in the hospital with highly contagious diseases who need to be in isolation, or just for people using their smartphones. 

“People are tied to their smartphones, so you could imagine that that would be great as a way for people to have awareness about their blood pressure or their diabetes status,” Yang noted.

 

More Work to Do

The study has a few caveats. The special sensor they used in this study isn’t yet integrated into smartphone cameras or other common video recording devices. But Uchida is hopeful that it could be mass-produced and inexpensive to someday add.

Also, the study was done in a Japanese population, and lighter skin may be easier to capture changes in blood flow, Uchida noted. Pulse oximeters, which use the same technology, tend to overestimate blood oxygen in people with darker skin tones.

“It is necessary to test whether the same results are obtained in a variety of subjects other than Japanese and Asians,” Uchida said, in addition to validating the tool with more participants.

The study has also not yet undergone peer review.

And Yang pointed out that this new AI technology provides more of a screening tool to predict who is at high risk for high blood pressure or diabetes, rather than precise measurements for either disease.

There are already some devices that claim to measure blood pressure using PPG technology, like blood pressure monitoring watches. But Yang warns that these kinds of devices aren’t validated, meaning we don’t really know how well they work.

One difficulty in getting any kind of PPG blood pressure monitoring device to market is that the organizations involved in setting medical device standards (like the International Organization for Standards) doesn’t yet have a validation standard for this technology, Yang said, so there’s really no way to consistently verify the technology’s accuracy.

“I am optimistic that we are capable of figuring out how to validate these things. I just think we have so many things we have to iron out before that happens,” Yang explained, noting that it will be at least 3 years before a remote blood monitoring system is widely available.

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

When a patient signs on to a telehealth portal, there’s little more a provider can do than ask questions. But a new artificial intelligence (AI) technology could allow providers to get feedback about the patient’s blood pressure and diabetes risk just from a video call or a smartphone app.

Researchers at the University of Tokyo in Japan are using AI to determine whether people might have high blood pressure or diabetes based on video data collected with a special sensor. 

The technology relies on photoplethysmography (PPG), which measures changes in blood volume by detecting the amount of light absorbed by blood just below the skin. 

This technology is already used for things like finger pulse oximetry to determine oxygen saturation and heart rate. Wearable devices like Apple Watches and Fitbits also use PPG technologies to detect heart rate and atrial fibrillation.

“If we could detect and accurately measure your blood pressure, heart rate, and oxygen saturation non-invasively that would be fantastic,” said Eugene Yang, MD, professor of medicine in the division of cardiology at the University of Washington School of Medicine in Seattle who was not involved in the study.

 

How Does PPG Work — and Is This New Tech Accurate?

Using PPG, “you’re detecting these small, little blood vessels that sit underneath the surface of your skin,” explained Yang.

“Since both hypertension and diabetes are diseases that damage blood vessels, we thought these diseases might affect blood flow and pulse wave transit times,” said Ryoko Uchida, a project researcher in the cardiology department at the University of Tokyo and one of the leaders of the study.

PPG devices primarily use green light to detect blood flow, as hemoglobin, the oxygen-carrying molecule in blood, absorbs green light most effectively, Yang said. “So, if you extract and remove all the other channels of light and only focus on the green channel, then that’s when you’ll be able to potentially see blood flow and pulsatile blood flow activity,” he noted.

The University of Tokyo researchers used remote or contactless PPG, which requires a short video recording of someone’s face and palms, as the person holds as still as possible. A special sensor collects the video and detects only certain wavelengths of light. Then the researchers developed an AI algorithm to extract data from participants’ skin, such as changes in pulse transit time — the time it takes for the pulse to travel from the palm to the face.

To correlate the video algorithm to blood pressure and diabetes risk, the researchers measured blood participants’ pressure with a continuous sphygmomanometer (an automatic blood pressure cuff) at the same time as they collected the video. They also did a blood A1c test to detect diabetes.

So far, they’ve tested their video algorithm on 215 people. The algorithm applied to a 30-second video was 86% accurate in detecting if blood pressure was above normal, and a 5-second video was 81% accurate in detecting higher blood pressure.

Compared with using hemoglobin A1c blood test results to screen for diabetes, the video algorithm was 75% accurate in identifying people who had subtle blood changes that correlated to diabetes.

“Most of this focus has been on wearable devices, patches, rings, wrist devices,” Yang said, “the facial video stuff is great because you can imagine that there are other ways of applying it.”

Yang, who is also doing research on facial video processing, pointed out it could be helpful not only in telehealth visits, but also for patients in the hospital with highly contagious diseases who need to be in isolation, or just for people using their smartphones. 

“People are tied to their smartphones, so you could imagine that that would be great as a way for people to have awareness about their blood pressure or their diabetes status,” Yang noted.

 

More Work to Do

The study has a few caveats. The special sensor they used in this study isn’t yet integrated into smartphone cameras or other common video recording devices. But Uchida is hopeful that it could be mass-produced and inexpensive to someday add.

Also, the study was done in a Japanese population, and lighter skin may be easier to capture changes in blood flow, Uchida noted. Pulse oximeters, which use the same technology, tend to overestimate blood oxygen in people with darker skin tones.

“It is necessary to test whether the same results are obtained in a variety of subjects other than Japanese and Asians,” Uchida said, in addition to validating the tool with more participants.

The study has also not yet undergone peer review.

And Yang pointed out that this new AI technology provides more of a screening tool to predict who is at high risk for high blood pressure or diabetes, rather than precise measurements for either disease.

There are already some devices that claim to measure blood pressure using PPG technology, like blood pressure monitoring watches. But Yang warns that these kinds of devices aren’t validated, meaning we don’t really know how well they work.

One difficulty in getting any kind of PPG blood pressure monitoring device to market is that the organizations involved in setting medical device standards (like the International Organization for Standards) doesn’t yet have a validation standard for this technology, Yang said, so there’s really no way to consistently verify the technology’s accuracy.

“I am optimistic that we are capable of figuring out how to validate these things. I just think we have so many things we have to iron out before that happens,” Yang explained, noting that it will be at least 3 years before a remote blood monitoring system is widely available.

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

TOPLINE:

Use of the glucagon-like peptide 1 (GLP-1) receptor agonists semaglutide and liraglutide is linked to a lower risk for alcohol use disorder (AUD)–related hospitalizations, compared with traditional AUD medications, a new study suggested.

METHODOLOGY:

• Researchers conducted a nationwide cohort study from 2006 to 2023 in Sweden that included more than 220,000 individuals with AUD (mean age, 40 years; 64% men).
• Data were obtained from registers of inpatient and specialized outpatient care, sickness absence, and disability pension, with a median follow-up period of 8.8 years.
• The primary exposure measured was the use of individual GLP-1 receptor agonists — commonly used to treat type 2 diabetes and obesity — compared with nonuse.
• The secondary exposure examined was the use of medications indicated for AUD.
• The primary outcome was AUD-related hospitalization; secondary outcomes included hospitalization due to substance use disorder (SUD), somatic hospitalization, and suicide attempts.

TAKEAWAY:

• About 59% of participants experienced AUD-related hospitalization.
• Semaglutide users (n = 4321) had the lowest risk for hospitalization related to AUD (adjusted hazard ratio [aHR], 0.64; 95% CI, 0.50-0.83) and to any SUD (aHR, 0.68; 95% CI, 0.54-0.85).
• Liraglutide users (n = 2509) had the second lowest risk for both AUD-related (aHR, 0.72; 95% CI, 0.57-0.92) and SUD-related (aHR, 0.78; 95% CI, 0.64-0.97) hospitalizations.
• The use of both semaglutide (aHR, 0.78; 95% CI, 0.68-0.90) and liraglutide (aHR, 0.79; 95% CI, 0.69-0.91) was linked to a reduced risk for hospitalization because of somatic reasons but was not associated with the risk of suicide attempts.
• Traditional AUD medications showed modest effectiveness with a slightly decreased but nonsignificant risk for AUD-related hospitalization (aHR, 0.98).

IN PRACTICE:

“AUDs and SUDs are undertreated pharmacologically, despite the availability of effective treatments. However, novel treatments are also needed because existing treatments may not be suitable for all patients. Semaglutide and liraglutide may be effective in the treatment of AUD, and clinical trials are urgently needed to confirm these findings,” the investigators wrote.

SOURCE:

This study was led by Markku Lähteenvuo, MD, PhD, University of Eastern Finland, Niuvanniemi Hospital, Kuopio. It was published online on November 13 in JAMA Psychiatry.

LIMITATIONS:

The observational nature of this study limited causal inferences.

DISCLOSURES:

The data used in this study were obtained from the REWHARD consortium, supported by the Swedish Research Council. Four of the six authors reported receiving grants or personal fees from various sources outside the submitted work, which are fully listed in the original article.

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

TOPLINE:

Use of the glucagon-like peptide 1 (GLP-1) receptor agonists semaglutide and liraglutide is linked to a lower risk for alcohol use disorder (AUD)–related hospitalizations, compared with traditional AUD medications, a new study suggested.

METHODOLOGY:

• Researchers conducted a nationwide cohort study from 2006 to 2023 in Sweden that included more than 220,000 individuals with AUD (mean age, 40 years; 64% men).
• Data were obtained from registers of inpatient and specialized outpatient care, sickness absence, and disability pension, with a median follow-up period of 8.8 years.
• The primary exposure measured was the use of individual GLP-1 receptor agonists — commonly used to treat type 2 diabetes and obesity — compared with nonuse.
• The secondary exposure examined was the use of medications indicated for AUD.
• The primary outcome was AUD-related hospitalization; secondary outcomes included hospitalization due to substance use disorder (SUD), somatic hospitalization, and suicide attempts.

TAKEAWAY:

• About 59% of participants experienced AUD-related hospitalization.
• Semaglutide users (n = 4321) had the lowest risk for hospitalization related to AUD (adjusted hazard ratio [aHR], 0.64; 95% CI, 0.50-0.83) and to any SUD (aHR, 0.68; 95% CI, 0.54-0.85).
• Liraglutide users (n = 2509) had the second lowest risk for both AUD-related (aHR, 0.72; 95% CI, 0.57-0.92) and SUD-related (aHR, 0.78; 95% CI, 0.64-0.97) hospitalizations.
• The use of both semaglutide (aHR, 0.78; 95% CI, 0.68-0.90) and liraglutide (aHR, 0.79; 95% CI, 0.69-0.91) was linked to a reduced risk for hospitalization because of somatic reasons but was not associated with the risk of suicide attempts.
• Traditional AUD medications showed modest effectiveness with a slightly decreased but nonsignificant risk for AUD-related hospitalization (aHR, 0.98).

IN PRACTICE:

“AUDs and SUDs are undertreated pharmacologically, despite the availability of effective treatments. However, novel treatments are also needed because existing treatments may not be suitable for all patients. Semaglutide and liraglutide may be effective in the treatment of AUD, and clinical trials are urgently needed to confirm these findings,” the investigators wrote.

SOURCE:

This study was led by Markku Lähteenvuo, MD, PhD, University of Eastern Finland, Niuvanniemi Hospital, Kuopio. It was published online on November 13 in JAMA Psychiatry.

LIMITATIONS:

The observational nature of this study limited causal inferences.

DISCLOSURES:

The data used in this study were obtained from the REWHARD consortium, supported by the Swedish Research Council. Four of the six authors reported receiving grants or personal fees from various sources outside the submitted work, which are fully listed in the original article.

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

TOPLINE:

Use of the glucagon-like peptide 1 (GLP-1) receptor agonists semaglutide and liraglutide is linked to a lower risk for alcohol use disorder (AUD)–related hospitalizations, compared with traditional AUD medications, a new study suggested.

METHODOLOGY:

• Researchers conducted a nationwide cohort study from 2006 to 2023 in Sweden that included more than 220,000 individuals with AUD (mean age, 40 years; 64% men).
• Data were obtained from registers of inpatient and specialized outpatient care, sickness absence, and disability pension, with a median follow-up period of 8.8 years.
• The primary exposure measured was the use of individual GLP-1 receptor agonists — commonly used to treat type 2 diabetes and obesity — compared with nonuse.
• The secondary exposure examined was the use of medications indicated for AUD.
• The primary outcome was AUD-related hospitalization; secondary outcomes included hospitalization due to substance use disorder (SUD), somatic hospitalization, and suicide attempts.

TAKEAWAY:

• About 59% of participants experienced AUD-related hospitalization.
• Semaglutide users (n = 4321) had the lowest risk for hospitalization related to AUD (adjusted hazard ratio [aHR], 0.64; 95% CI, 0.50-0.83) and to any SUD (aHR, 0.68; 95% CI, 0.54-0.85).
• Liraglutide users (n = 2509) had the second lowest risk for both AUD-related (aHR, 0.72; 95% CI, 0.57-0.92) and SUD-related (aHR, 0.78; 95% CI, 0.64-0.97) hospitalizations.
• The use of both semaglutide (aHR, 0.78; 95% CI, 0.68-0.90) and liraglutide (aHR, 0.79; 95% CI, 0.69-0.91) was linked to a reduced risk for hospitalization because of somatic reasons but was not associated with the risk of suicide attempts.
• Traditional AUD medications showed modest effectiveness with a slightly decreased but nonsignificant risk for AUD-related hospitalization (aHR, 0.98).

IN PRACTICE:

“AUDs and SUDs are undertreated pharmacologically, despite the availability of effective treatments. However, novel treatments are also needed because existing treatments may not be suitable for all patients. Semaglutide and liraglutide may be effective in the treatment of AUD, and clinical trials are urgently needed to confirm these findings,” the investigators wrote.

SOURCE:

This study was led by Markku Lähteenvuo, MD, PhD, University of Eastern Finland, Niuvanniemi Hospital, Kuopio. It was published online on November 13 in JAMA Psychiatry.

LIMITATIONS:

The observational nature of this study limited causal inferences.

DISCLOSURES:

The data used in this study were obtained from the REWHARD consortium, supported by the Swedish Research Council. Four of the six authors reported receiving grants or personal fees from various sources outside the submitted work, which are fully listed in the original article.

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

WASHINGTON — Glucagon-like peptide 1 receptor agonist (GLP-1 RA) medications appear beneficial for people with systemic lupus erythematosus (SLE) and lupus nephritis, two new studies suggest. 

“The risk of cardiovascular disease is thought to be at least double that for people with lupus ... and we know the risk of progressing to end-stage renal disease [ESKD] for patients with lupus nephritis can be as high as 10%-30%, so there’s clearly a major unmet need for new treatments and approaches to improve these outcomes, perhaps with adjunctive treatment beyond our typical immunosuppressive therapy,” April Jorge, MD, of Massachusetts General Hospital, Boston, said at the annual meeting of the American College of Rheumatology (ACR). 

The GLP-1 RAs are approved for the treatment of type 2 diabetes (T2D) and obesity. They also have proven cardiovascular benefit, along with emerging data suggesting kidney protection independent of glucose lowering. Jorge presented findings from a study using data from the US multicenter electronic health record database TriNetX, showing that, among patients who had both T2D and SLE, those using GLP-1 RAs had lower risks for major adverse cardiac events (MACE), venous thrombosis, kidney disease progression, and all-cause mortality, compared with those using a different class of T2D medication. 

A second study using TriNetX, presented at the same ACR meeting session by Anna-Kay Palmer, MD, a third-year internal medicine resident at Jefferson Einstein Hospital, Philadelphia, Pennsylvania, showed that GLP-1 RAs reduced the risk of progression to ESKD in patients with lupus nephritis, possibly caused by reductions in pro-inflammatory mediators.

Asked to comment, session moderator Diane L. Kamen, MD, professor of medicine at the Medical University of South Carolina Division of Rheumatology, Charleston, said in an interview that she definitely supports the use of GLP-1 RAs for patients who have SLE and/or lupus nephritis and also a drug label indication, either T2D or obesity. “[The GLP-1 RA prescriber] will usually run it by rheumatology to make sure that it doesn’t conflict with any of their other medical treatment, and it’s very reassuring to know that they could actually get a win-win.” 

But as far as prescribing off-label for those with SLE/lupus nephritis who don’t have other GLP-1 RA indications, Kamen said, “that’s a black hole at this point. We need to do those prospective studies. But if they have another indication, yes.”

 

Cardiovascular, Kidney Benefits of GLP-1 RAs

Jorge noted that patients with lupus were excluded from the randomized clinical trials of GLP-1 RAs, so the current study was designed to investigate the potential impact of these medications on cardiovascular and kidney outcomes in patients with SLE and lupus nephritis. 

From TriNetX data for 46 healthcare organizations nationwide, a total of 96,511 patients with both SLE and T2D but not ESKD had initiated either a GLP-1 RA or another diabetes drug class, dipeptidyl peptidase 4 inhibitors (DPP4i), between October 2006 and August 2021. Of those, 29,177 had lupus nephritis. 

Propensity score matching for factors such as demographics, lupus severity, comorbidities, and medication use was used to emulate a randomized trial. This yielded 25,838 with SLE and T2D, of whom 910 initiated a GLP-1 RA and 1004 started a DPP4i, and 12,387 with lupus nephritis and T2D, including 267 on a GLP-1 RA and 324 on a DPP4i. After matching, the mean age was 55 years, more than 90% were women, and just under half were White individuals. About one third had chronic kidney disease stages ≥ 3, and about 15% had heart failure. 

Over an average follow-up time of 1.2-1.4 years among those with SLE, the hazard ratio (HR) for MACE (a composite of myocardial infarction, stroke, and heart failure) for those taking a GLP-1 RA vs a DPP4i was 0.66, a significant difference. And for venous thrombosis, the HR was also significant at 0.49.

Kidney disease progression, defined as an estimated glomerular filtration rate decline of 30% or more or new ESKD, was significantly less likely in the GLP-1 RA group, with a HR of 0.77. All-cause mortality also was dramatically reduced (HR, 0.26). As expected, there was no difference in control outcome, genital infections (HR, 1.02). 

In the subgroup with lupus nephritis, there were also lower risks for both MACE (HR, 0.64) and for renal progression (HR, 0.70). “The findings suggest similar cardiac and kidney benefits among patients with SLE and lupus nephritis as have been observed in other populations,” Jorge concluded. 

Kamen commented that the study design “was pretty brilliant, because you wouldn’t be able to do a placebo-controlled trial since the indication was diabetes ... but the fact is you do see that the GLP-1 RA gets the benefit whereas the other drug does not.”

Next steps, Jorge said, will be mechanistic studies to better understand the effects of GLP-1 RAs in lupus and other rheumatic diseases, prospective studies of GLP-1 RAs in SLE and lupus nephritis without diabetes, and clarification of ideal timing for GLP-1 RA use in SLE and lupus nephritis. 

“Ideally, with our prospective studies with these patients we can try to isolate the effect on patients with lupus and also better understand whether there might be an impact on disease activity through the anti-inflammatory effects of these medications, rather than just the cardioprotective and nephroprotective benefits,” she said. 

 

In Those With Lupus Nephritis, Kidney Protection Seen

In her presentation, Palmer noted that, despite immunosuppressive therapies for SLE, 10%-20% of patients who develop lupus nephritis will progress to ESKD within 5 years of diagnosis. 

She added that GLP-1 RAs have been shown to reduce albuminuria in people with diabetes and have been hypothesized to reduce inflammation through multiple pathways, thereby potentially reducing kidney disease independently of the presence of diabetes or weight loss. These pathways include modulating immune cell signaling and reducing pro-inflammatory cytokines. 

Based on all this, Palmer and colleagues used International Classification of Diseases – 10th edition diagnostic codes in TriNetX to identify 839 patients who had been diagnosed with lupus nephritis between 2014 and 2024 and who were prescribed liraglutide, dulaglutide, semaglutide, or exenatide for any time after the lupus nephritis diagnosis. Another 29,840 patients with lupus nephritis had not used GLP-1 RAs. 

After 1:1 propensity score matching for age, sex, race, ethnicity, presence of hypertension, diabetes, use of immunosuppressive and diabetes medication, smoking, obesity, and statin use, there were 735 individuals in each group. About two thirds in each had diabetes, whereas the rest had been prescribed the GLP-1 RAs for other indications. 

Patients who were not on GLP-1 RAs were twice as likely to develop ESKD or dialysis (8.88% vs 3.971%; odds ratio, 2.35; P = .001). 

Kamen pointed out that not including the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers was a study flaw. On the other hand, the fact that not everyone in this study had diabetes was an advantage.

Jorge received grant/research support from Bristol-Myers Squibb, Cabaletta Bio, and the Lupus Clinical Investigator Network. Kamen is an adviser/review panel member for Alpine Immune Sciences. Palmer had no disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Glucagon-like peptide 1 receptor agonist (GLP-1 RA) medications appear beneficial for people with systemic lupus erythematosus (SLE) and lupus nephritis, two new studies suggest. 

“The risk of cardiovascular disease is thought to be at least double that for people with lupus ... and we know the risk of progressing to end-stage renal disease [ESKD] for patients with lupus nephritis can be as high as 10%-30%, so there’s clearly a major unmet need for new treatments and approaches to improve these outcomes, perhaps with adjunctive treatment beyond our typical immunosuppressive therapy,” April Jorge, MD, of Massachusetts General Hospital, Boston, said at the annual meeting of the American College of Rheumatology (ACR). 

The GLP-1 RAs are approved for the treatment of type 2 diabetes (T2D) and obesity. They also have proven cardiovascular benefit, along with emerging data suggesting kidney protection independent of glucose lowering. Jorge presented findings from a study using data from the US multicenter electronic health record database TriNetX, showing that, among patients who had both T2D and SLE, those using GLP-1 RAs had lower risks for major adverse cardiac events (MACE), venous thrombosis, kidney disease progression, and all-cause mortality, compared with those using a different class of T2D medication. 

A second study using TriNetX, presented at the same ACR meeting session by Anna-Kay Palmer, MD, a third-year internal medicine resident at Jefferson Einstein Hospital, Philadelphia, Pennsylvania, showed that GLP-1 RAs reduced the risk of progression to ESKD in patients with lupus nephritis, possibly caused by reductions in pro-inflammatory mediators.

Asked to comment, session moderator Diane L. Kamen, MD, professor of medicine at the Medical University of South Carolina Division of Rheumatology, Charleston, said in an interview that she definitely supports the use of GLP-1 RAs for patients who have SLE and/or lupus nephritis and also a drug label indication, either T2D or obesity. “[The GLP-1 RA prescriber] will usually run it by rheumatology to make sure that it doesn’t conflict with any of their other medical treatment, and it’s very reassuring to know that they could actually get a win-win.” 

But as far as prescribing off-label for those with SLE/lupus nephritis who don’t have other GLP-1 RA indications, Kamen said, “that’s a black hole at this point. We need to do those prospective studies. But if they have another indication, yes.”

 

Cardiovascular, Kidney Benefits of GLP-1 RAs

Jorge noted that patients with lupus were excluded from the randomized clinical trials of GLP-1 RAs, so the current study was designed to investigate the potential impact of these medications on cardiovascular and kidney outcomes in patients with SLE and lupus nephritis. 

From TriNetX data for 46 healthcare organizations nationwide, a total of 96,511 patients with both SLE and T2D but not ESKD had initiated either a GLP-1 RA or another diabetes drug class, dipeptidyl peptidase 4 inhibitors (DPP4i), between October 2006 and August 2021. Of those, 29,177 had lupus nephritis. 

Propensity score matching for factors such as demographics, lupus severity, comorbidities, and medication use was used to emulate a randomized trial. This yielded 25,838 with SLE and T2D, of whom 910 initiated a GLP-1 RA and 1004 started a DPP4i, and 12,387 with lupus nephritis and T2D, including 267 on a GLP-1 RA and 324 on a DPP4i. After matching, the mean age was 55 years, more than 90% were women, and just under half were White individuals. About one third had chronic kidney disease stages ≥ 3, and about 15% had heart failure. 

Over an average follow-up time of 1.2-1.4 years among those with SLE, the hazard ratio (HR) for MACE (a composite of myocardial infarction, stroke, and heart failure) for those taking a GLP-1 RA vs a DPP4i was 0.66, a significant difference. And for venous thrombosis, the HR was also significant at 0.49.

Kidney disease progression, defined as an estimated glomerular filtration rate decline of 30% or more or new ESKD, was significantly less likely in the GLP-1 RA group, with a HR of 0.77. All-cause mortality also was dramatically reduced (HR, 0.26). As expected, there was no difference in control outcome, genital infections (HR, 1.02). 

In the subgroup with lupus nephritis, there were also lower risks for both MACE (HR, 0.64) and for renal progression (HR, 0.70). “The findings suggest similar cardiac and kidney benefits among patients with SLE and lupus nephritis as have been observed in other populations,” Jorge concluded. 

Kamen commented that the study design “was pretty brilliant, because you wouldn’t be able to do a placebo-controlled trial since the indication was diabetes ... but the fact is you do see that the GLP-1 RA gets the benefit whereas the other drug does not.”

Next steps, Jorge said, will be mechanistic studies to better understand the effects of GLP-1 RAs in lupus and other rheumatic diseases, prospective studies of GLP-1 RAs in SLE and lupus nephritis without diabetes, and clarification of ideal timing for GLP-1 RA use in SLE and lupus nephritis. 

“Ideally, with our prospective studies with these patients we can try to isolate the effect on patients with lupus and also better understand whether there might be an impact on disease activity through the anti-inflammatory effects of these medications, rather than just the cardioprotective and nephroprotective benefits,” she said. 

 

In Those With Lupus Nephritis, Kidney Protection Seen

In her presentation, Palmer noted that, despite immunosuppressive therapies for SLE, 10%-20% of patients who develop lupus nephritis will progress to ESKD within 5 years of diagnosis. 

She added that GLP-1 RAs have been shown to reduce albuminuria in people with diabetes and have been hypothesized to reduce inflammation through multiple pathways, thereby potentially reducing kidney disease independently of the presence of diabetes or weight loss. These pathways include modulating immune cell signaling and reducing pro-inflammatory cytokines. 

Based on all this, Palmer and colleagues used International Classification of Diseases – 10th edition diagnostic codes in TriNetX to identify 839 patients who had been diagnosed with lupus nephritis between 2014 and 2024 and who were prescribed liraglutide, dulaglutide, semaglutide, or exenatide for any time after the lupus nephritis diagnosis. Another 29,840 patients with lupus nephritis had not used GLP-1 RAs. 

After 1:1 propensity score matching for age, sex, race, ethnicity, presence of hypertension, diabetes, use of immunosuppressive and diabetes medication, smoking, obesity, and statin use, there were 735 individuals in each group. About two thirds in each had diabetes, whereas the rest had been prescribed the GLP-1 RAs for other indications. 

Patients who were not on GLP-1 RAs were twice as likely to develop ESKD or dialysis (8.88% vs 3.971%; odds ratio, 2.35; P = .001). 

Kamen pointed out that not including the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers was a study flaw. On the other hand, the fact that not everyone in this study had diabetes was an advantage.

Jorge received grant/research support from Bristol-Myers Squibb, Cabaletta Bio, and the Lupus Clinical Investigator Network. Kamen is an adviser/review panel member for Alpine Immune Sciences. Palmer had no disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON — Glucagon-like peptide 1 receptor agonist (GLP-1 RA) medications appear beneficial for people with systemic lupus erythematosus (SLE) and lupus nephritis, two new studies suggest. 

“The risk of cardiovascular disease is thought to be at least double that for people with lupus ... and we know the risk of progressing to end-stage renal disease [ESKD] for patients with lupus nephritis can be as high as 10%-30%, so there’s clearly a major unmet need for new treatments and approaches to improve these outcomes, perhaps with adjunctive treatment beyond our typical immunosuppressive therapy,” April Jorge, MD, of Massachusetts General Hospital, Boston, said at the annual meeting of the American College of Rheumatology (ACR). 

The GLP-1 RAs are approved for the treatment of type 2 diabetes (T2D) and obesity. They also have proven cardiovascular benefit, along with emerging data suggesting kidney protection independent of glucose lowering. Jorge presented findings from a study using data from the US multicenter electronic health record database TriNetX, showing that, among patients who had both T2D and SLE, those using GLP-1 RAs had lower risks for major adverse cardiac events (MACE), venous thrombosis, kidney disease progression, and all-cause mortality, compared with those using a different class of T2D medication. 

A second study using TriNetX, presented at the same ACR meeting session by Anna-Kay Palmer, MD, a third-year internal medicine resident at Jefferson Einstein Hospital, Philadelphia, Pennsylvania, showed that GLP-1 RAs reduced the risk of progression to ESKD in patients with lupus nephritis, possibly caused by reductions in pro-inflammatory mediators.

Asked to comment, session moderator Diane L. Kamen, MD, professor of medicine at the Medical University of South Carolina Division of Rheumatology, Charleston, said in an interview that she definitely supports the use of GLP-1 RAs for patients who have SLE and/or lupus nephritis and also a drug label indication, either T2D or obesity. “[The GLP-1 RA prescriber] will usually run it by rheumatology to make sure that it doesn’t conflict with any of their other medical treatment, and it’s very reassuring to know that they could actually get a win-win.” 

But as far as prescribing off-label for those with SLE/lupus nephritis who don’t have other GLP-1 RA indications, Kamen said, “that’s a black hole at this point. We need to do those prospective studies. But if they have another indication, yes.”

 

Cardiovascular, Kidney Benefits of GLP-1 RAs

Jorge noted that patients with lupus were excluded from the randomized clinical trials of GLP-1 RAs, so the current study was designed to investigate the potential impact of these medications on cardiovascular and kidney outcomes in patients with SLE and lupus nephritis. 

From TriNetX data for 46 healthcare organizations nationwide, a total of 96,511 patients with both SLE and T2D but not ESKD had initiated either a GLP-1 RA or another diabetes drug class, dipeptidyl peptidase 4 inhibitors (DPP4i), between October 2006 and August 2021. Of those, 29,177 had lupus nephritis. 

Propensity score matching for factors such as demographics, lupus severity, comorbidities, and medication use was used to emulate a randomized trial. This yielded 25,838 with SLE and T2D, of whom 910 initiated a GLP-1 RA and 1004 started a DPP4i, and 12,387 with lupus nephritis and T2D, including 267 on a GLP-1 RA and 324 on a DPP4i. After matching, the mean age was 55 years, more than 90% were women, and just under half were White individuals. About one third had chronic kidney disease stages ≥ 3, and about 15% had heart failure. 

Over an average follow-up time of 1.2-1.4 years among those with SLE, the hazard ratio (HR) for MACE (a composite of myocardial infarction, stroke, and heart failure) for those taking a GLP-1 RA vs a DPP4i was 0.66, a significant difference. And for venous thrombosis, the HR was also significant at 0.49.

Kidney disease progression, defined as an estimated glomerular filtration rate decline of 30% or more or new ESKD, was significantly less likely in the GLP-1 RA group, with a HR of 0.77. All-cause mortality also was dramatically reduced (HR, 0.26). As expected, there was no difference in control outcome, genital infections (HR, 1.02). 

In the subgroup with lupus nephritis, there were also lower risks for both MACE (HR, 0.64) and for renal progression (HR, 0.70). “The findings suggest similar cardiac and kidney benefits among patients with SLE and lupus nephritis as have been observed in other populations,” Jorge concluded. 

Kamen commented that the study design “was pretty brilliant, because you wouldn’t be able to do a placebo-controlled trial since the indication was diabetes ... but the fact is you do see that the GLP-1 RA gets the benefit whereas the other drug does not.”

Next steps, Jorge said, will be mechanistic studies to better understand the effects of GLP-1 RAs in lupus and other rheumatic diseases, prospective studies of GLP-1 RAs in SLE and lupus nephritis without diabetes, and clarification of ideal timing for GLP-1 RA use in SLE and lupus nephritis. 

“Ideally, with our prospective studies with these patients we can try to isolate the effect on patients with lupus and also better understand whether there might be an impact on disease activity through the anti-inflammatory effects of these medications, rather than just the cardioprotective and nephroprotective benefits,” she said. 

 

In Those With Lupus Nephritis, Kidney Protection Seen

In her presentation, Palmer noted that, despite immunosuppressive therapies for SLE, 10%-20% of patients who develop lupus nephritis will progress to ESKD within 5 years of diagnosis. 

She added that GLP-1 RAs have been shown to reduce albuminuria in people with diabetes and have been hypothesized to reduce inflammation through multiple pathways, thereby potentially reducing kidney disease independently of the presence of diabetes or weight loss. These pathways include modulating immune cell signaling and reducing pro-inflammatory cytokines. 

Based on all this, Palmer and colleagues used International Classification of Diseases – 10th edition diagnostic codes in TriNetX to identify 839 patients who had been diagnosed with lupus nephritis between 2014 and 2024 and who were prescribed liraglutide, dulaglutide, semaglutide, or exenatide for any time after the lupus nephritis diagnosis. Another 29,840 patients with lupus nephritis had not used GLP-1 RAs. 

After 1:1 propensity score matching for age, sex, race, ethnicity, presence of hypertension, diabetes, use of immunosuppressive and diabetes medication, smoking, obesity, and statin use, there were 735 individuals in each group. About two thirds in each had diabetes, whereas the rest had been prescribed the GLP-1 RAs for other indications. 

Patients who were not on GLP-1 RAs were twice as likely to develop ESKD or dialysis (8.88% vs 3.971%; odds ratio, 2.35; P = .001). 

Kamen pointed out that not including the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers was a study flaw. On the other hand, the fact that not everyone in this study had diabetes was an advantage.

Jorge received grant/research support from Bristol-Myers Squibb, Cabaletta Bio, and the Lupus Clinical Investigator Network. Kamen is an adviser/review panel member for Alpine Immune Sciences. Palmer had no disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

In older postmenopausal women with type 2 diabetes (T2D), pyridoxamine treatment has potential to prevent fractures and protect bone tissue by targeting advanced glycation end products and also lowers levels of A1c, an early glycation product.

METHODOLOGY:

• Despite greater bone density and low bone turnover, people with T2D have increased fractures risk and higher associated mortality, but previous research linking advanced glycation end products (AGEs) to bone fragility suggests an AGE inhibitor could be a novel therapeutic strategy to prevent the accumulation of AGE in bone tissue.
• This randomized clinical trial, conducted at the Metabolic Bone Disease Unit of Columbia University Irving Medical Center, New York City, from December 2017 to February 2021, assessed the efficacy of the vitamin B6 metabolite pyridoxamine, an AGE inhibitor, in promoting bone formation in 55 older postmenopausal women with T2D.
• The participants received either 200 mg of oral pyridoxamine dihydrochloride (n = 27; mean age, 75.6 years) or matching placebo tablets (n = 28; mean age, 73.1 years) twice daily for 1 year.
• The primary outcome was the change in the levels of the bone formation marker Procollagen Type I Intact N-terminal Propeptide (P1NP) from baseline to after 12 months of treatment.
• Other outcomes included changes in bone mineral density measured at the lumbar spine, total hip, femoral neck, and 1/3 radius using dual energy x-ray absorptiometry; A1c levels; and skin autofluorescence at 12 months, a surrogate for bone AGEs. The safety of pyridoxamine was evaluated by monitoring neurologic findings and adverse events because high doses of the parent vitamin B6 have been reported to cause neurotoxicity.

TAKEAWAY:

• At 12 months, pyridoxamine treatment increased P1NP levels by 23% (P = .028) compared with 4.1% with placebo (P = .576), a “nearly significant difference.”
• Bone mineral density at the femoral neck increased by 2.64% with pyridoxamine but decreased by 0.91% with placebo (P = .007), with no changes at the lumbar spine, total hip, or 1/3 radius. The levels of bone resorption markers or skin autofluorescence were not significantly different between the groups.
• A1c levels decreased by 0.38% in the pyridoxamine group and correlated with increased P1NP levels, compared with a 0.05% increase in the placebo group (P = .04).
• Pyridoxamine was well tolerated. Four serious adverse events were reported in the pyridoxamine group and seven in the placebo group; none of these were related to the trial treatment.

IN PRACTICE:

“[The study] findings suggest that AGE inhibition might clinically improve the low bone formation state of T2D, and that PM [pyridoxamine] might warrant further investigation as a potential disease mechanism-directed approach for the therapy of T2D bone fragility,” the authors wrote.

SOURCE:

The study was led by Aiden V. Brossfield, Metabolic Bone Disease Unit, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study findings were preliminary. The study’s small sample size and individual variability led to a lack of statistical significance. The exclusion of men may have limited the generalizability of the findings. The short duration of 1 year may have been insufficient for detecting changes in skin AGEs. The levels of circulating AGEs or pyridoxamine were not measured, which could have provided additional insights.

DISCLOSURES:

The study was supported by a grant from the US National Institute on Aging. The authors declared no conflicts of interest.

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

TOPLINE:

In older postmenopausal women with type 2 diabetes (T2D), pyridoxamine treatment has potential to prevent fractures and protect bone tissue by targeting advanced glycation end products and also lowers levels of A1c, an early glycation product.

METHODOLOGY:

• Despite greater bone density and low bone turnover, people with T2D have increased fractures risk and higher associated mortality, but previous research linking advanced glycation end products (AGEs) to bone fragility suggests an AGE inhibitor could be a novel therapeutic strategy to prevent the accumulation of AGE in bone tissue.
• This randomized clinical trial, conducted at the Metabolic Bone Disease Unit of Columbia University Irving Medical Center, New York City, from December 2017 to February 2021, assessed the efficacy of the vitamin B6 metabolite pyridoxamine, an AGE inhibitor, in promoting bone formation in 55 older postmenopausal women with T2D.
• The participants received either 200 mg of oral pyridoxamine dihydrochloride (n = 27; mean age, 75.6 years) or matching placebo tablets (n = 28; mean age, 73.1 years) twice daily for 1 year.
• The primary outcome was the change in the levels of the bone formation marker Procollagen Type I Intact N-terminal Propeptide (P1NP) from baseline to after 12 months of treatment.
• Other outcomes included changes in bone mineral density measured at the lumbar spine, total hip, femoral neck, and 1/3 radius using dual energy x-ray absorptiometry; A1c levels; and skin autofluorescence at 12 months, a surrogate for bone AGEs. The safety of pyridoxamine was evaluated by monitoring neurologic findings and adverse events because high doses of the parent vitamin B6 have been reported to cause neurotoxicity.

TAKEAWAY:

• At 12 months, pyridoxamine treatment increased P1NP levels by 23% (P = .028) compared with 4.1% with placebo (P = .576), a “nearly significant difference.”
• Bone mineral density at the femoral neck increased by 2.64% with pyridoxamine but decreased by 0.91% with placebo (P = .007), with no changes at the lumbar spine, total hip, or 1/3 radius. The levels of bone resorption markers or skin autofluorescence were not significantly different between the groups.
• A1c levels decreased by 0.38% in the pyridoxamine group and correlated with increased P1NP levels, compared with a 0.05% increase in the placebo group (P = .04).
• Pyridoxamine was well tolerated. Four serious adverse events were reported in the pyridoxamine group and seven in the placebo group; none of these were related to the trial treatment.

IN PRACTICE:

“[The study] findings suggest that AGE inhibition might clinically improve the low bone formation state of T2D, and that PM [pyridoxamine] might warrant further investigation as a potential disease mechanism-directed approach for the therapy of T2D bone fragility,” the authors wrote.

SOURCE:

The study was led by Aiden V. Brossfield, Metabolic Bone Disease Unit, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study findings were preliminary. The study’s small sample size and individual variability led to a lack of statistical significance. The exclusion of men may have limited the generalizability of the findings. The short duration of 1 year may have been insufficient for detecting changes in skin AGEs. The levels of circulating AGEs or pyridoxamine were not measured, which could have provided additional insights.

DISCLOSURES:

The study was supported by a grant from the US National Institute on Aging. The authors declared no conflicts of interest.

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

TOPLINE:

In older postmenopausal women with type 2 diabetes (T2D), pyridoxamine treatment has potential to prevent fractures and protect bone tissue by targeting advanced glycation end products and also lowers levels of A1c, an early glycation product.

METHODOLOGY:

• Despite greater bone density and low bone turnover, people with T2D have increased fractures risk and higher associated mortality, but previous research linking advanced glycation end products (AGEs) to bone fragility suggests an AGE inhibitor could be a novel therapeutic strategy to prevent the accumulation of AGE in bone tissue.
• This randomized clinical trial, conducted at the Metabolic Bone Disease Unit of Columbia University Irving Medical Center, New York City, from December 2017 to February 2021, assessed the efficacy of the vitamin B6 metabolite pyridoxamine, an AGE inhibitor, in promoting bone formation in 55 older postmenopausal women with T2D.
• The participants received either 200 mg of oral pyridoxamine dihydrochloride (n = 27; mean age, 75.6 years) or matching placebo tablets (n = 28; mean age, 73.1 years) twice daily for 1 year.
• The primary outcome was the change in the levels of the bone formation marker Procollagen Type I Intact N-terminal Propeptide (P1NP) from baseline to after 12 months of treatment.
• Other outcomes included changes in bone mineral density measured at the lumbar spine, total hip, femoral neck, and 1/3 radius using dual energy x-ray absorptiometry; A1c levels; and skin autofluorescence at 12 months, a surrogate for bone AGEs. The safety of pyridoxamine was evaluated by monitoring neurologic findings and adverse events because high doses of the parent vitamin B6 have been reported to cause neurotoxicity.

TAKEAWAY:

• At 12 months, pyridoxamine treatment increased P1NP levels by 23% (P = .028) compared with 4.1% with placebo (P = .576), a “nearly significant difference.”
• Bone mineral density at the femoral neck increased by 2.64% with pyridoxamine but decreased by 0.91% with placebo (P = .007), with no changes at the lumbar spine, total hip, or 1/3 radius. The levels of bone resorption markers or skin autofluorescence were not significantly different between the groups.
• A1c levels decreased by 0.38% in the pyridoxamine group and correlated with increased P1NP levels, compared with a 0.05% increase in the placebo group (P = .04).
• Pyridoxamine was well tolerated. Four serious adverse events were reported in the pyridoxamine group and seven in the placebo group; none of these were related to the trial treatment.

IN PRACTICE:

“[The study] findings suggest that AGE inhibition might clinically improve the low bone formation state of T2D, and that PM [pyridoxamine] might warrant further investigation as a potential disease mechanism-directed approach for the therapy of T2D bone fragility,” the authors wrote.

SOURCE:

The study was led by Aiden V. Brossfield, Metabolic Bone Disease Unit, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The study findings were preliminary. The study’s small sample size and individual variability led to a lack of statistical significance. The exclusion of men may have limited the generalizability of the findings. The short duration of 1 year may have been insufficient for detecting changes in skin AGEs. The levels of circulating AGEs or pyridoxamine were not measured, which could have provided additional insights.

DISCLOSURES:

The study was supported by a grant from the US National Institute on Aging. The authors declared no conflicts of interest.

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

TOPLINE:

Up to one in seven young adults with obesity and type 2 diabetes (T2D) have clinically significant hepatic fibrosis, signaling the crucial need for screening in this population to aid early detection and intervention.

METHODOLOGY:

• Researchers aimed to assess the prevalence of hepatic steatosis and clinically significant fibrosis (stage ≥ 2) in young adults without a history of metabolic dysfunction–associated steatotic liver disease (MASLD), hypothesizing that the rates would be comparable with those in older adults, especially in the presence of cardiometabolic risk factors.
• Overall, 1420 participants aged 21-79 years with or without T2D (63% or 37%, respectively) were included from outpatient clinics at the University of Florida, Gainesville, Florida, and divided into two age groups: < 45 years (n = 243) and ≥ 45 years (n = 1177).
• All the participants underwent assessment of liver stiffness via transient elastography, with magnetic resonance elastography (MRE) or liver biopsy recommended when indicated.
• Participants also underwent a medical history review, physical examination, and fasting blood tests to rule out secondary causes of liver disease.

TAKEAWAY:

• Overall, 52% of participants had hepatic steatosis, and 9.5% had clinically significant fibrosis.
• There were no significant differences in the frequencies of hepatic steatosis (50.2% vs 52.7%; P = .6) or clinically significant hepatic fibrosis (7.5% vs 9.9%; P = .2) observed between young and older adults.
• The presence of either T2D or obesity was linked to an increased prevalence of both hepatic steatosis and fibrosis in both the age groups (P < .01).
• In young and older adults, the presence of both T2D and obesity led to the highest rates of both hepatic steatosis and clinically significant fibrosis, with the latter rate being statistically similar between the groups (15.7% vs 17.3%; P = .2).
• The presence of T2D and obesity was the strongest risk factors for hepatic fibrosis in young adults (odds ratios, 4.33 and 1.16, respectively; P < .05 for both).

IN PRACTICE:

“The clinical implication is that young adults with obesity and T2D carry a high risk of future cirrhosis, possibly as high as older adults, and must be aggressively screened at the first visit and carefully followed,” the authors wrote.

SOURCE:

This study, led by Anu Sharma, University of Florida College of Medicine, Gainesville, was published online in Obesity.

LIMITATIONS:

The diagnosis of clinically significant hepatic fibrosis was confirmed via MRE and/or liver biopsy in only 30% of all participants. The study population included a slightly higher proportion of young adults with obesity, T2D, and other cardiometabolic risk factors than that in national averages, which may have limited its generalizability. Genetic variants associated with MASLD were not included in this study.

DISCLOSURES:

This study was funded partly by grants from the National Institutes of Health and Echosens. One author disclosed receiving research support and serving as a consultant for various pharmaceutical companies.

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

TOPLINE:

Up to one in seven young adults with obesity and type 2 diabetes (T2D) have clinically significant hepatic fibrosis, signaling the crucial need for screening in this population to aid early detection and intervention.

METHODOLOGY:

• Researchers aimed to assess the prevalence of hepatic steatosis and clinically significant fibrosis (stage ≥ 2) in young adults without a history of metabolic dysfunction–associated steatotic liver disease (MASLD), hypothesizing that the rates would be comparable with those in older adults, especially in the presence of cardiometabolic risk factors.
• Overall, 1420 participants aged 21-79 years with or without T2D (63% or 37%, respectively) were included from outpatient clinics at the University of Florida, Gainesville, Florida, and divided into two age groups: < 45 years (n = 243) and ≥ 45 years (n = 1177).
• All the participants underwent assessment of liver stiffness via transient elastography, with magnetic resonance elastography (MRE) or liver biopsy recommended when indicated.
• Participants also underwent a medical history review, physical examination, and fasting blood tests to rule out secondary causes of liver disease.

TAKEAWAY:

• Overall, 52% of participants had hepatic steatosis, and 9.5% had clinically significant fibrosis.
• There were no significant differences in the frequencies of hepatic steatosis (50.2% vs 52.7%; P = .6) or clinically significant hepatic fibrosis (7.5% vs 9.9%; P = .2) observed between young and older adults.
• The presence of either T2D or obesity was linked to an increased prevalence of both hepatic steatosis and fibrosis in both the age groups (P < .01).
• In young and older adults, the presence of both T2D and obesity led to the highest rates of both hepatic steatosis and clinically significant fibrosis, with the latter rate being statistically similar between the groups (15.7% vs 17.3%; P = .2).
• The presence of T2D and obesity was the strongest risk factors for hepatic fibrosis in young adults (odds ratios, 4.33 and 1.16, respectively; P < .05 for both).

IN PRACTICE:

“The clinical implication is that young adults with obesity and T2D carry a high risk of future cirrhosis, possibly as high as older adults, and must be aggressively screened at the first visit and carefully followed,” the authors wrote.

SOURCE:

This study, led by Anu Sharma, University of Florida College of Medicine, Gainesville, was published online in Obesity.

LIMITATIONS:

The diagnosis of clinically significant hepatic fibrosis was confirmed via MRE and/or liver biopsy in only 30% of all participants. The study population included a slightly higher proportion of young adults with obesity, T2D, and other cardiometabolic risk factors than that in national averages, which may have limited its generalizability. Genetic variants associated with MASLD were not included in this study.

DISCLOSURES:

This study was funded partly by grants from the National Institutes of Health and Echosens. One author disclosed receiving research support and serving as a consultant for various pharmaceutical companies.

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

TOPLINE:

Up to one in seven young adults with obesity and type 2 diabetes (T2D) have clinically significant hepatic fibrosis, signaling the crucial need for screening in this population to aid early detection and intervention.

METHODOLOGY:

• Researchers aimed to assess the prevalence of hepatic steatosis and clinically significant fibrosis (stage ≥ 2) in young adults without a history of metabolic dysfunction–associated steatotic liver disease (MASLD), hypothesizing that the rates would be comparable with those in older adults, especially in the presence of cardiometabolic risk factors.
• Overall, 1420 participants aged 21-79 years with or without T2D (63% or 37%, respectively) were included from outpatient clinics at the University of Florida, Gainesville, Florida, and divided into two age groups: < 45 years (n = 243) and ≥ 45 years (n = 1177).
• All the participants underwent assessment of liver stiffness via transient elastography, with magnetic resonance elastography (MRE) or liver biopsy recommended when indicated.
• Participants also underwent a medical history review, physical examination, and fasting blood tests to rule out secondary causes of liver disease.

TAKEAWAY:

• Overall, 52% of participants had hepatic steatosis, and 9.5% had clinically significant fibrosis.
• There were no significant differences in the frequencies of hepatic steatosis (50.2% vs 52.7%; P = .6) or clinically significant hepatic fibrosis (7.5% vs 9.9%; P = .2) observed between young and older adults.
• The presence of either T2D or obesity was linked to an increased prevalence of both hepatic steatosis and fibrosis in both the age groups (P < .01).
• In young and older adults, the presence of both T2D and obesity led to the highest rates of both hepatic steatosis and clinically significant fibrosis, with the latter rate being statistically similar between the groups (15.7% vs 17.3%; P = .2).
• The presence of T2D and obesity was the strongest risk factors for hepatic fibrosis in young adults (odds ratios, 4.33 and 1.16, respectively; P < .05 for both).

IN PRACTICE:

“The clinical implication is that young adults with obesity and T2D carry a high risk of future cirrhosis, possibly as high as older adults, and must be aggressively screened at the first visit and carefully followed,” the authors wrote.

SOURCE:

This study, led by Anu Sharma, University of Florida College of Medicine, Gainesville, was published online in Obesity.

LIMITATIONS:

The diagnosis of clinically significant hepatic fibrosis was confirmed via MRE and/or liver biopsy in only 30% of all participants. The study population included a slightly higher proportion of young adults with obesity, T2D, and other cardiometabolic risk factors than that in national averages, which may have limited its generalizability. Genetic variants associated with MASLD were not included in this study.

DISCLOSURES:

This study was funded partly by grants from the National Institutes of Health and Echosens. One author disclosed receiving research support and serving as a consultant for various pharmaceutical companies.

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

TOPLINE:

Elevated levels of plasma F2-isoprostanes, a reliable marker of oxidative stress, are associated with an increased risk for fractures in older ambulatory patients with type 2 diabetes (T2D) independently of bone density.

METHODOLOGY:

• Patients with T2D face an increased risk for fractures at any given bone mineral density; oxidative stress levels (reflected in circulating F2-isoprostanes), which are elevated in T2D, are associated with other T2D complications, and may weaken bone integrity.
• Researchers analyzed data from an observational cohort study to investigate the association between the levels of circulating F2-isoprostanes and the risk for clinical fractures in older patients with T2D.
• The data included 703 older ambulatory adults (baseline age, 70-79 years; about half White individuals and half Black individuals ; about half men and half women) from the Health, Aging and Body Composition Study, of whom 132 had T2D.
• Plasma F2-isoprostane levels were measured using baseline serum samples; bone turnover markers were also measured including procollagen type 1 N-terminal propeptide, osteocalcin, and C-terminal telopeptide of type 1 collagen.
• Incident clinical fractures were tracked over a follow-up period of up to 17.3 years, with fractures verified through radiology reports.

TAKEAWAY:

• Overall, 25.8% patients in the T2D group and 23.5% adults in the non-diabetes group reported an incident clinical fracture during a mean follow-up period of 6.2 and 8.0 years, respectively.
• In patients with T2D, the risk for incident clinical fracture increased by 93% for every standard deviation increase in the log F2-isoprostane serum levels (hazard ratio [HR], 1.93; 95% CI, 1.26-2.95; P = .002) independently of baseline bone density, medication use, and other risk factors, with no such association reported in individuals without T2D (HR, 0.98; 95% CI, 0.81-1.18; P = .79).
• In the T2D group, elevated plasma F2-isoprostane levels were also associated with a decrease in total hip bone mineral density over 4 years (r = −0.28; P = .008), but not in the non-diabetes group.
• No correlation was found between plasma F2-isoprostane levels and circulating advanced glycoxidation end-products, bone turnover markers, or A1c levels in either group.
•  

IN PRACTICE:

“Oxidative stress in T2D may play an important role in the decline of bone quality and not just bone quantity,” the authors wrote.

SOURCE:

This study was led by Bowen Wang, PhD, Rensselaer Polytechnic Institute, Troy, New York. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

This study was conducted in a well-functioning elderly population with only White and Black participants, which may limit the generalizability of the findings to other age groups or less healthy populations. Additionally, the study did not assess prevalent vertebral fracture risk due to the small sample size. 

DISCLOSURES:

This study was supported by the US National Institute on Aging and the Intramural Research Program of the US National Institutes of Health and the Dr and Ms Sands and Sands Family for Orthopaedic Research. The authors reported no relevant conflicts of interest.

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

TOPLINE:

Elevated levels of plasma F2-isoprostanes, a reliable marker of oxidative stress, are associated with an increased risk for fractures in older ambulatory patients with type 2 diabetes (T2D) independently of bone density.

METHODOLOGY:

• Patients with T2D face an increased risk for fractures at any given bone mineral density; oxidative stress levels (reflected in circulating F2-isoprostanes), which are elevated in T2D, are associated with other T2D complications, and may weaken bone integrity.
• Researchers analyzed data from an observational cohort study to investigate the association between the levels of circulating F2-isoprostanes and the risk for clinical fractures in older patients with T2D.
• The data included 703 older ambulatory adults (baseline age, 70-79 years; about half White individuals and half Black individuals ; about half men and half women) from the Health, Aging and Body Composition Study, of whom 132 had T2D.
• Plasma F2-isoprostane levels were measured using baseline serum samples; bone turnover markers were also measured including procollagen type 1 N-terminal propeptide, osteocalcin, and C-terminal telopeptide of type 1 collagen.
• Incident clinical fractures were tracked over a follow-up period of up to 17.3 years, with fractures verified through radiology reports.

TAKEAWAY:

• Overall, 25.8% patients in the T2D group and 23.5% adults in the non-diabetes group reported an incident clinical fracture during a mean follow-up period of 6.2 and 8.0 years, respectively.
• In patients with T2D, the risk for incident clinical fracture increased by 93% for every standard deviation increase in the log F2-isoprostane serum levels (hazard ratio [HR], 1.93; 95% CI, 1.26-2.95; P = .002) independently of baseline bone density, medication use, and other risk factors, with no such association reported in individuals without T2D (HR, 0.98; 95% CI, 0.81-1.18; P = .79).
• In the T2D group, elevated plasma F2-isoprostane levels were also associated with a decrease in total hip bone mineral density over 4 years (r = −0.28; P = .008), but not in the non-diabetes group.
• No correlation was found between plasma F2-isoprostane levels and circulating advanced glycoxidation end-products, bone turnover markers, or A1c levels in either group.
•  

IN PRACTICE:

“Oxidative stress in T2D may play an important role in the decline of bone quality and not just bone quantity,” the authors wrote.

SOURCE:

This study was led by Bowen Wang, PhD, Rensselaer Polytechnic Institute, Troy, New York. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

This study was conducted in a well-functioning elderly population with only White and Black participants, which may limit the generalizability of the findings to other age groups or less healthy populations. Additionally, the study did not assess prevalent vertebral fracture risk due to the small sample size. 

DISCLOSURES:

This study was supported by the US National Institute on Aging and the Intramural Research Program of the US National Institutes of Health and the Dr and Ms Sands and Sands Family for Orthopaedic Research. The authors reported no relevant conflicts of interest.

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

TOPLINE:

Elevated levels of plasma F2-isoprostanes, a reliable marker of oxidative stress, are associated with an increased risk for fractures in older ambulatory patients with type 2 diabetes (T2D) independently of bone density.

METHODOLOGY:

• Patients with T2D face an increased risk for fractures at any given bone mineral density; oxidative stress levels (reflected in circulating F2-isoprostanes), which are elevated in T2D, are associated with other T2D complications, and may weaken bone integrity.
• Researchers analyzed data from an observational cohort study to investigate the association between the levels of circulating F2-isoprostanes and the risk for clinical fractures in older patients with T2D.
• The data included 703 older ambulatory adults (baseline age, 70-79 years; about half White individuals and half Black individuals ; about half men and half women) from the Health, Aging and Body Composition Study, of whom 132 had T2D.
• Plasma F2-isoprostane levels were measured using baseline serum samples; bone turnover markers were also measured including procollagen type 1 N-terminal propeptide, osteocalcin, and C-terminal telopeptide of type 1 collagen.
• Incident clinical fractures were tracked over a follow-up period of up to 17.3 years, with fractures verified through radiology reports.

TAKEAWAY:

• Overall, 25.8% patients in the T2D group and 23.5% adults in the non-diabetes group reported an incident clinical fracture during a mean follow-up period of 6.2 and 8.0 years, respectively.
• In patients with T2D, the risk for incident clinical fracture increased by 93% for every standard deviation increase in the log F2-isoprostane serum levels (hazard ratio [HR], 1.93; 95% CI, 1.26-2.95; P = .002) independently of baseline bone density, medication use, and other risk factors, with no such association reported in individuals without T2D (HR, 0.98; 95% CI, 0.81-1.18; P = .79).
• In the T2D group, elevated plasma F2-isoprostane levels were also associated with a decrease in total hip bone mineral density over 4 years (r = −0.28; P = .008), but not in the non-diabetes group.
• No correlation was found between plasma F2-isoprostane levels and circulating advanced glycoxidation end-products, bone turnover markers, or A1c levels in either group.
•  

IN PRACTICE:

“Oxidative stress in T2D may play an important role in the decline of bone quality and not just bone quantity,” the authors wrote.

SOURCE:

This study was led by Bowen Wang, PhD, Rensselaer Polytechnic Institute, Troy, New York. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

This study was conducted in a well-functioning elderly population with only White and Black participants, which may limit the generalizability of the findings to other age groups or less healthy populations. Additionally, the study did not assess prevalent vertebral fracture risk due to the small sample size. 

DISCLOSURES:

This study was supported by the US National Institute on Aging and the Intramural Research Program of the US National Institutes of Health and the Dr and Ms Sands and Sands Family for Orthopaedic Research. The authors reported no relevant conflicts of interest.

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

TOPLINE:

US alcohol-related mortality rates increased from 10.7 to 21.6 per 100,000 between 1999 and 2020, with the largest rise of 3.8-fold observed in adults aged 25-34 years. Women experienced a 2.5-fold increase, while the Midwest region showed a similar rise in mortality rates.

METHODOLOGY:

• Analysis utilized the US Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research to examine alcohol-related mortality trends from 1999 to 2020.
• Researchers analyzed data from a total US population of 180,408,769 people aged 25 to 85+ years in 1999 and 226,635,013 people in 2020.
• International Classification of Diseases, Tenth Revision, codes were used to identify deaths with alcohol attribution, including mental and behavioral disorders, alcoholic organ damage, and alcohol-related poisoning.

TAKEAWAY:

• Overall mortality rates increased from 10.7 (95% CI, 10.6-10.8) per 100,000 in 1999 to 21.6 (95% CI, 21.4-21.8) per 100,000 in 2020, representing a significant twofold increase.
• Adults aged 55-64 years demonstrated both the steepest increase and highest absolute rates in both 1999 and 2020.
• American Indian and Alaska Native individuals experienced the steepest increase and highest absolute rates among all racial groups.
• The West region maintained the highest absolute rates in both 1999 and 2020, despite the Midwest showing the largest increase.

IN PRACTICE:

“Individuals who consume large amounts of alcohol tend to have the highest risks of total mortality as well as deaths from cardiovascular disease. Cardiovascular disease deaths are predominantly due to myocardial infarction and stroke. To mitigate these risks, health providers may wish to implement screening for alcohol use in primary care and other healthcare settings. By providing brief interventions and referrals to treatment, healthcare providers would be able to achieve the early identification of individuals at risk of alcohol-related harm and offer them the support and resources they need to reduce their alcohol consumption,” wrote the authors of the study.

SOURCE:

The study was led by Alexandra Matarazzo, BS, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton. It was published online in The American Journal of Medicine.

LIMITATIONS:

According to the authors, the cross-sectional nature of the data limits the study to descriptive analysis only, making it suitable for hypothesis generation but not hypothesis testing. While the validity and generalizability within the United States are secure because of the use of complete population data, potential bias and uncontrolled confounding may exist because of different population mixes between the two time points.

DISCLOSURES:

The authors reported no relevant conflicts of interest. One coauthor disclosed serving as an independent scientist in an advisory role to investigators and sponsors as Chair of Data Monitoring Committees for Amgen and UBC, to the Food and Drug Administration, and to Up to Date. Additional disclosures are noted in the original article.

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

TOPLINE:

US alcohol-related mortality rates increased from 10.7 to 21.6 per 100,000 between 1999 and 2020, with the largest rise of 3.8-fold observed in adults aged 25-34 years. Women experienced a 2.5-fold increase, while the Midwest region showed a similar rise in mortality rates.

METHODOLOGY:

• Analysis utilized the US Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research to examine alcohol-related mortality trends from 1999 to 2020.
• Researchers analyzed data from a total US population of 180,408,769 people aged 25 to 85+ years in 1999 and 226,635,013 people in 2020.
• International Classification of Diseases, Tenth Revision, codes were used to identify deaths with alcohol attribution, including mental and behavioral disorders, alcoholic organ damage, and alcohol-related poisoning.

TAKEAWAY:

• Overall mortality rates increased from 10.7 (95% CI, 10.6-10.8) per 100,000 in 1999 to 21.6 (95% CI, 21.4-21.8) per 100,000 in 2020, representing a significant twofold increase.
• Adults aged 55-64 years demonstrated both the steepest increase and highest absolute rates in both 1999 and 2020.
• American Indian and Alaska Native individuals experienced the steepest increase and highest absolute rates among all racial groups.
• The West region maintained the highest absolute rates in both 1999 and 2020, despite the Midwest showing the largest increase.

IN PRACTICE:

“Individuals who consume large amounts of alcohol tend to have the highest risks of total mortality as well as deaths from cardiovascular disease. Cardiovascular disease deaths are predominantly due to myocardial infarction and stroke. To mitigate these risks, health providers may wish to implement screening for alcohol use in primary care and other healthcare settings. By providing brief interventions and referrals to treatment, healthcare providers would be able to achieve the early identification of individuals at risk of alcohol-related harm and offer them the support and resources they need to reduce their alcohol consumption,” wrote the authors of the study.

SOURCE:

The study was led by Alexandra Matarazzo, BS, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton. It was published online in The American Journal of Medicine.

LIMITATIONS:

According to the authors, the cross-sectional nature of the data limits the study to descriptive analysis only, making it suitable for hypothesis generation but not hypothesis testing. While the validity and generalizability within the United States are secure because of the use of complete population data, potential bias and uncontrolled confounding may exist because of different population mixes between the two time points.

DISCLOSURES:

The authors reported no relevant conflicts of interest. One coauthor disclosed serving as an independent scientist in an advisory role to investigators and sponsors as Chair of Data Monitoring Committees for Amgen and UBC, to the Food and Drug Administration, and to Up to Date. Additional disclosures are noted in the original article.

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

TOPLINE:

US alcohol-related mortality rates increased from 10.7 to 21.6 per 100,000 between 1999 and 2020, with the largest rise of 3.8-fold observed in adults aged 25-34 years. Women experienced a 2.5-fold increase, while the Midwest region showed a similar rise in mortality rates.

METHODOLOGY:

• Analysis utilized the US Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research to examine alcohol-related mortality trends from 1999 to 2020.
• Researchers analyzed data from a total US population of 180,408,769 people aged 25 to 85+ years in 1999 and 226,635,013 people in 2020.
• International Classification of Diseases, Tenth Revision, codes were used to identify deaths with alcohol attribution, including mental and behavioral disorders, alcoholic organ damage, and alcohol-related poisoning.

TAKEAWAY:

• Overall mortality rates increased from 10.7 (95% CI, 10.6-10.8) per 100,000 in 1999 to 21.6 (95% CI, 21.4-21.8) per 100,000 in 2020, representing a significant twofold increase.
• Adults aged 55-64 years demonstrated both the steepest increase and highest absolute rates in both 1999 and 2020.
• American Indian and Alaska Native individuals experienced the steepest increase and highest absolute rates among all racial groups.
• The West region maintained the highest absolute rates in both 1999 and 2020, despite the Midwest showing the largest increase.

IN PRACTICE:

“Individuals who consume large amounts of alcohol tend to have the highest risks of total mortality as well as deaths from cardiovascular disease. Cardiovascular disease deaths are predominantly due to myocardial infarction and stroke. To mitigate these risks, health providers may wish to implement screening for alcohol use in primary care and other healthcare settings. By providing brief interventions and referrals to treatment, healthcare providers would be able to achieve the early identification of individuals at risk of alcohol-related harm and offer them the support and resources they need to reduce their alcohol consumption,” wrote the authors of the study.

SOURCE:

The study was led by Alexandra Matarazzo, BS, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton. It was published online in The American Journal of Medicine.

LIMITATIONS:

According to the authors, the cross-sectional nature of the data limits the study to descriptive analysis only, making it suitable for hypothesis generation but not hypothesis testing. While the validity and generalizability within the United States are secure because of the use of complete population data, potential bias and uncontrolled confounding may exist because of different population mixes between the two time points.

DISCLOSURES:

The authors reported no relevant conflicts of interest. One coauthor disclosed serving as an independent scientist in an advisory role to investigators and sponsors as Chair of Data Monitoring Committees for Amgen and UBC, to the Food and Drug Administration, and to Up to Date. Additional disclosures are noted in the original article.

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