Diabetes

The US Food and Drug Administration (FDA) has announced a voluntary manufacturer-initiated recall of more than 7000 bottles of duloxetine delayed-release capsules due to unacceptable levels of a potential carcinogen.

Duloxetine (Cymbalta) is a serotonin-norepinephrine reuptake inhibitor used to treat major depressive disorder, generalized anxiety disorder, fibromyalgia, chronic musculoskeletal pain, and neuropathic pain associated with diabetic peripheral neuropathy.

The recall is due to the detection of the nitrosamine impurity, N-nitroso duloxetine, above the proposed interim limit.

Nitrosamines are common in water and foods, and exposure to some levels of the chemical is common. Exposure to nitrosamine impurities above acceptable levels and over long periods may increase cancer risk, the FDA reported.

“If drugs contain levels of nitrosamines above the acceptable daily intake limits, FDA recommends these drugs be recalled by the manufacturer as appropriate,” the agency noted on its website.

The recall was initiated by Breckenridge Pharmaceutical and covers 7107 bottles of 500-count, 20 mg duloxetine delayed-release capsules. The drug is manufactured by Towa Pharmaceutical Europe and distributed nationwide by BPI.

The affected bottles are from lot number 220128 with an expiration date of 12/2024 and NDC of 51991-746-05.

The recall was initiated on October 10 and is ongoing.

“Healthcare professionals can educate patients about alternative treatment options to medications with potential nitrosamine impurities if available and clinically appropriate,” the FDA advises. “If a medication has been recalled, pharmacists may be able to dispense the same medication from a manufacturing lot that has not been recalled. Prescribers may also determine whether there is an alternative treatment option for patients.”

The FDA has labeled this a “class II” recall, which the agency defines as “a situation in which use of or exposure to a violative product may cause temporary or medically reversible adverse health consequences or where the probability of serious adverse health consequences is remote.”

Nitrosamine impurities have prompted a number of drug recalls in recent years, including oral anticoagulants, metformin, and skeletal muscle relaxants.

The impurities may be found in drugs for a number of reasons, the agency reported. The source may be from a drug’s manufacturing process, chemical structure, or the conditions under which it is stored or packaged.
 

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has announced a voluntary manufacturer-initiated recall of more than 7000 bottles of duloxetine delayed-release capsules due to unacceptable levels of a potential carcinogen.

Duloxetine (Cymbalta) is a serotonin-norepinephrine reuptake inhibitor used to treat major depressive disorder, generalized anxiety disorder, fibromyalgia, chronic musculoskeletal pain, and neuropathic pain associated with diabetic peripheral neuropathy.

The recall is due to the detection of the nitrosamine impurity, N-nitroso duloxetine, above the proposed interim limit.

Nitrosamines are common in water and foods, and exposure to some levels of the chemical is common. Exposure to nitrosamine impurities above acceptable levels and over long periods may increase cancer risk, the FDA reported.

“If drugs contain levels of nitrosamines above the acceptable daily intake limits, FDA recommends these drugs be recalled by the manufacturer as appropriate,” the agency noted on its website.

The recall was initiated by Breckenridge Pharmaceutical and covers 7107 bottles of 500-count, 20 mg duloxetine delayed-release capsules. The drug is manufactured by Towa Pharmaceutical Europe and distributed nationwide by BPI.

The affected bottles are from lot number 220128 with an expiration date of 12/2024 and NDC of 51991-746-05.

The recall was initiated on October 10 and is ongoing.

“Healthcare professionals can educate patients about alternative treatment options to medications with potential nitrosamine impurities if available and clinically appropriate,” the FDA advises. “If a medication has been recalled, pharmacists may be able to dispense the same medication from a manufacturing lot that has not been recalled. Prescribers may also determine whether there is an alternative treatment option for patients.”

The FDA has labeled this a “class II” recall, which the agency defines as “a situation in which use of or exposure to a violative product may cause temporary or medically reversible adverse health consequences or where the probability of serious adverse health consequences is remote.”

Nitrosamine impurities have prompted a number of drug recalls in recent years, including oral anticoagulants, metformin, and skeletal muscle relaxants.

The impurities may be found in drugs for a number of reasons, the agency reported. The source may be from a drug’s manufacturing process, chemical structure, or the conditions under which it is stored or packaged.
 

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has announced a voluntary manufacturer-initiated recall of more than 7000 bottles of duloxetine delayed-release capsules due to unacceptable levels of a potential carcinogen.

Duloxetine (Cymbalta) is a serotonin-norepinephrine reuptake inhibitor used to treat major depressive disorder, generalized anxiety disorder, fibromyalgia, chronic musculoskeletal pain, and neuropathic pain associated with diabetic peripheral neuropathy.

The recall is due to the detection of the nitrosamine impurity, N-nitroso duloxetine, above the proposed interim limit.

Nitrosamines are common in water and foods, and exposure to some levels of the chemical is common. Exposure to nitrosamine impurities above acceptable levels and over long periods may increase cancer risk, the FDA reported.

“If drugs contain levels of nitrosamines above the acceptable daily intake limits, FDA recommends these drugs be recalled by the manufacturer as appropriate,” the agency noted on its website.

The recall was initiated by Breckenridge Pharmaceutical and covers 7107 bottles of 500-count, 20 mg duloxetine delayed-release capsules. The drug is manufactured by Towa Pharmaceutical Europe and distributed nationwide by BPI.

The affected bottles are from lot number 220128 with an expiration date of 12/2024 and NDC of 51991-746-05.

The recall was initiated on October 10 and is ongoing.

“Healthcare professionals can educate patients about alternative treatment options to medications with potential nitrosamine impurities if available and clinically appropriate,” the FDA advises. “If a medication has been recalled, pharmacists may be able to dispense the same medication from a manufacturing lot that has not been recalled. Prescribers may also determine whether there is an alternative treatment option for patients.”

The FDA has labeled this a “class II” recall, which the agency defines as “a situation in which use of or exposure to a violative product may cause temporary or medically reversible adverse health consequences or where the probability of serious adverse health consequences is remote.”

Nitrosamine impurities have prompted a number of drug recalls in recent years, including oral anticoagulants, metformin, and skeletal muscle relaxants.

The impurities may be found in drugs for a number of reasons, the agency reported. The source may be from a drug’s manufacturing process, chemical structure, or the conditions under which it is stored or packaged.
 

A version of this article appeared on Medscape.com.

Plant-based diets have become increasingly popular over the last decade as the evidence supporting their health benefits becomes stronger. 

Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets. 

Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet. 
 

Inflammation and Obesity

Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.

Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1. 

If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
 

Plant-Based Diet for Type 2 Diabetes

According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group. 

Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss. 

It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups. 
 

Plant-Based Diet for Chronic Kidney Disease (CKD)

Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.

However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought. 

Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
 

Realistic Options for Patients on Medical Diets

There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t. 

I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities. 

Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.

Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation? 

This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ 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.

Plant-based diets have become increasingly popular over the last decade as the evidence supporting their health benefits becomes stronger. 

Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets. 

Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet. 
 

Inflammation and Obesity

Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.

Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1. 

If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
 

Plant-Based Diet for Type 2 Diabetes

According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group. 

Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss. 

It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups. 
 

Plant-Based Diet for Chronic Kidney Disease (CKD)

Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.

However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought. 

Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
 

Realistic Options for Patients on Medical Diets

There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t. 

I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities. 

Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.

Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation? 

This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ 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.

Plant-based diets have become increasingly popular over the last decade as the evidence supporting their health benefits becomes stronger. 

Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets. 

Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet. 
 

Inflammation and Obesity

Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.

Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1. 

If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
 

Plant-Based Diet for Type 2 Diabetes

According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group. 

Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss. 

It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups. 
 

Plant-Based Diet for Chronic Kidney Disease (CKD)

Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.

However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought. 

Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
 

Realistic Options for Patients on Medical Diets

There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t. 

I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities. 

Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.

Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation? 

This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.

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

A version of this article appeared on Medscape.com.

This October, millions of Americans missed out on two of the most spectacular shows in the universe: the northern lights and a rare comet. Even if you were aware of them, light pollution made them difficult to see, unless you went to a dark area and let your eyes adjust.

It’s not getting any easier — the night sky over North America has been growing brighter by about 10% per year since 2011. More and more research is linking all that light pollution to a surprising range of health consequences: cancer, heart disease, diabetes, Alzheimer’s disease, and even low sperm quality, though the reasons for these troubling associations are not always clear. 

“We’ve lost the contrast between light and dark, and we are confusing our physiology on a regular basis,” said John Hanifin, PhD, associate director of Thomas Jefferson University’s Light Research Program. 

Our own galaxy is invisible to nearly 80% of people in North America. In 1994, an earthquake-triggered blackout in Los Angeles led to calls to the Griffith Observatory from people wondering about that hazy blob of light in the night sky. It was the Milky Way.

Glaring headlights, illuminated buildings, blazing billboards, and streetlights fill our urban skies with a glow that even affects rural residents. Inside, since the invention of the lightbulb, we’ve kept our homes bright at night. Now, we’ve also added blue light-emitting devices — smartphones, television screens, tablets — which have been linked to sleep problems.

But outdoor light may matter for our health, too. “Every photon counts,” Hanifin said. 
 

Bright Lights, Big Problems

For one 2024 study researchers used satellite data to measure light pollution at residential addresses of over 13,000 people. They found that those who lived in places with the brightest skies at night had a 31% higher risk of high blood pressure. Another study out of Hong Kong showed a 29% higher risk of death from coronary heart disease. And yet another found a 17%higher risk of cerebrovascular disease, such as strokes or brain aneurysms. 

Of course, urban areas also have air pollution, noise, and a lack of greenery. So, for some studies, scientists controlled for these factors, and the correlation remained strong (although air pollution with fine particulate matter appeared to be worse for heart health than outdoor light). 

Research has found links between the nighttime glow outside and other diseases:

Breast cancer. “It’s a very strong correlation,” said Randy Nelson, PhD, a neuroscientist at West Virginia University. A study of over 100,000 teachers in California revealed that women living in areas with the most light pollution had a 12%higher risk. That effect is comparable to increasing your intake of ultra-processed foods by 10%. 

Alzheimer’s disease. In a study published this fall, outdoor light at night was more strongly linked to the disease than even alcohol misuse or obesity.

Diabetes. In one recent study, people living in the most illuminated areas had a 28% higher risk of diabetes than those residing in much darker places. In a country like China, scientists concluded that 9 million cases of diabetes could be linked to light pollution. 
 

What Happens in Your Body When You’re Exposed to Light at Night

Research has revealed that light at night (indoors or out) disrupts circadian clocks, increases inflammation, affects cell division, and suppresses melatonin, the “hormone of darkness.” “Darkness is very important,” Hanifin said. When he and his colleagues decades ago started studying the effects of light on human physiology, “people thought we were borderline crazy,” he said.

Nighttime illumination affects the health and behavior of species as diverse as Siberian hamsters, zebra finches, mice, crickets, and mosquitoes. Like most creatures on Earth, humans have internal clocks that are synced to the 24-hour cycle of day and night. The master clock is in your hypothalamus, a diamond-shaped part of the brain, but every cell in your body has its own clock, too. Many physiological processes run on circadian rhythms (a term derived from a Latin phrase meaning “about a day”), from sleep-wake cycle to hormone secretion, as well as processes involved in cancer progression, such as cell division.

“There are special photoreceptors in the eye that don’t deal with visual information. They just send light information,” Nelson said. “If you get light at the wrong time, you’re resetting the clocks.” 

This internal clock “prepares the body for various recurrent challenges, such as eating,” said Christian Benedict, PhD, a sleep researcher at Uppsala University, Sweden. “Light exposure [at night] can mess up this very important system.” This could mean, for instance, that your insulin is released at the wrong time, Benedict said, causing “a jet lag-ish condition that will then impair the ability to handle blood sugar.” Animal studies confirm that exposure to light at night can reduce glucose tolerance and alter insulin secretion – potential pathways to diabetes.

The hormone melatonin, produced when it’s dark by the pineal gland in the brain, is a key player in this modern struggle. Melatonin helps you sleep, synchronizes the body’s circadian rhythms, protects neurons from damage, regulates the immune system, and fights inflammation. But even a sliver of light at night can suppress its secretion. Less than 30 lux of light, about the level of a pedestrian street at night, can slash melatonin by half. 

When lab animals are exposed to nighttime light, they “show enormous neuroinflammation” — that is, inflammation of nervous tissue, Nelson said. In one experiment on humans, those who slept immersed in weak light had higher levels of C-reactive protein in their blood, a marker of inflammation.

Low melatonin has also been linked to cancer. It “allows the metabolic machinery of the cancer cells to be active,” Hanifin said. One of melatonin’s effects is stimulation of natural killer cells, which can recognize and destroy cancer cells. What’s more, when melatonin plunges, estrogen may go up, which could explain the link between light at night and breast cancer (estrogen fuels tumor growth in breast cancers). 

Researchers concede that satellite data might be too coarse to estimate how much light people are actually exposed to while they sleep. Plus, many of us are staring at bright screens. “But the studies keep coming,” Nelson said, suggesting that outdoor light pollution does have an impact. 

When researchers put wrist-worn light sensors on over 80,000 British people, they found that the more light the device registered between half-past midnight and 6 a.m., the more its wearer was at risk of having diabetes several years down the road — no matter how long they’ve actually slept. This, according to the study’s authors, supports the findings of satellite data.

A similar study that used actigraphy with built-in light sensors, measuring whether people had been sleeping in complete darkness for at least five hours, found that light pollution upped the risk of heart disease by 74%.
 

What Can You Do About This?

Not everyone’s melatonin is affected by nighttime light to the same degree. “Some people are very much sensitive to very dim light, whereas others are not as sensitive and need far, far more light stimulation [to impact melatonin],” Benedict said. In one study, some volunteers needed 350 lux to lower their melatonin by half. For such people, flipping on the light in the bathroom at night wouldn’t matter; for others, though, a mere 6 lux was already as harmful – which is darker than twilight. 

You can protect yourself by keeping your bedroom lights off and your screens stashed away, but avoiding outdoor light pollution may be harder. You can invest in high-quality blackout curtains, of course, although some light may still seep inside. You can plant trees in front of your windows, reorient any motion-detector lights, and even petition your local government to reduce over-illumination of buildings and to choose better streetlights. You can support organizations, such as the International Dark-Sky Association, that work to preserve darkness.

Last but not least, you might want to change your habits. If you live in a particularly light-polluted area, such as the District of Columbia, America’s top place for urban blaze, you might reconsider late-night walks or drives around the neighborhood. Instead, Hanifin said, read a book in bed, while keeping the light “as dim as you can.” It’s “a much better idea versus being outside in midtown Manhattan,” he said. According to recent recommendations published by Hanifin and his colleagues, when you sleep, there should be no more than 1 lux of illumination at the level of your eyes — about as much as you’d get from having a lit candle 1 meter away. 

And if we manage to preserve outdoor darkness, and the stars reappear (including the breathtaking Milky Way), we could reap more benefits — some research suggests that stargazing can elicit positive emotions, a sense of personal growth, and “a variety of transcendent thoughts and experiences.” 
 

A version of this article appeared on WebMD.com.

This October, millions of Americans missed out on two of the most spectacular shows in the universe: the northern lights and a rare comet. Even if you were aware of them, light pollution made them difficult to see, unless you went to a dark area and let your eyes adjust.

It’s not getting any easier — the night sky over North America has been growing brighter by about 10% per year since 2011. More and more research is linking all that light pollution to a surprising range of health consequences: cancer, heart disease, diabetes, Alzheimer’s disease, and even low sperm quality, though the reasons for these troubling associations are not always clear. 

“We’ve lost the contrast between light and dark, and we are confusing our physiology on a regular basis,” said John Hanifin, PhD, associate director of Thomas Jefferson University’s Light Research Program. 

Our own galaxy is invisible to nearly 80% of people in North America. In 1994, an earthquake-triggered blackout in Los Angeles led to calls to the Griffith Observatory from people wondering about that hazy blob of light in the night sky. It was the Milky Way.

Glaring headlights, illuminated buildings, blazing billboards, and streetlights fill our urban skies with a glow that even affects rural residents. Inside, since the invention of the lightbulb, we’ve kept our homes bright at night. Now, we’ve also added blue light-emitting devices — smartphones, television screens, tablets — which have been linked to sleep problems.

But outdoor light may matter for our health, too. “Every photon counts,” Hanifin said. 
 

Bright Lights, Big Problems

For one 2024 study researchers used satellite data to measure light pollution at residential addresses of over 13,000 people. They found that those who lived in places with the brightest skies at night had a 31% higher risk of high blood pressure. Another study out of Hong Kong showed a 29% higher risk of death from coronary heart disease. And yet another found a 17%higher risk of cerebrovascular disease, such as strokes or brain aneurysms. 

Of course, urban areas also have air pollution, noise, and a lack of greenery. So, for some studies, scientists controlled for these factors, and the correlation remained strong (although air pollution with fine particulate matter appeared to be worse for heart health than outdoor light). 

Research has found links between the nighttime glow outside and other diseases:

Breast cancer. “It’s a very strong correlation,” said Randy Nelson, PhD, a neuroscientist at West Virginia University. A study of over 100,000 teachers in California revealed that women living in areas with the most light pollution had a 12%higher risk. That effect is comparable to increasing your intake of ultra-processed foods by 10%. 

Alzheimer’s disease. In a study published this fall, outdoor light at night was more strongly linked to the disease than even alcohol misuse or obesity.

Diabetes. In one recent study, people living in the most illuminated areas had a 28% higher risk of diabetes than those residing in much darker places. In a country like China, scientists concluded that 9 million cases of diabetes could be linked to light pollution. 
 

What Happens in Your Body When You’re Exposed to Light at Night

Research has revealed that light at night (indoors or out) disrupts circadian clocks, increases inflammation, affects cell division, and suppresses melatonin, the “hormone of darkness.” “Darkness is very important,” Hanifin said. When he and his colleagues decades ago started studying the effects of light on human physiology, “people thought we were borderline crazy,” he said.

Nighttime illumination affects the health and behavior of species as diverse as Siberian hamsters, zebra finches, mice, crickets, and mosquitoes. Like most creatures on Earth, humans have internal clocks that are synced to the 24-hour cycle of day and night. The master clock is in your hypothalamus, a diamond-shaped part of the brain, but every cell in your body has its own clock, too. Many physiological processes run on circadian rhythms (a term derived from a Latin phrase meaning “about a day”), from sleep-wake cycle to hormone secretion, as well as processes involved in cancer progression, such as cell division.

“There are special photoreceptors in the eye that don’t deal with visual information. They just send light information,” Nelson said. “If you get light at the wrong time, you’re resetting the clocks.” 

This internal clock “prepares the body for various recurrent challenges, such as eating,” said Christian Benedict, PhD, a sleep researcher at Uppsala University, Sweden. “Light exposure [at night] can mess up this very important system.” This could mean, for instance, that your insulin is released at the wrong time, Benedict said, causing “a jet lag-ish condition that will then impair the ability to handle blood sugar.” Animal studies confirm that exposure to light at night can reduce glucose tolerance and alter insulin secretion – potential pathways to diabetes.

The hormone melatonin, produced when it’s dark by the pineal gland in the brain, is a key player in this modern struggle. Melatonin helps you sleep, synchronizes the body’s circadian rhythms, protects neurons from damage, regulates the immune system, and fights inflammation. But even a sliver of light at night can suppress its secretion. Less than 30 lux of light, about the level of a pedestrian street at night, can slash melatonin by half. 

When lab animals are exposed to nighttime light, they “show enormous neuroinflammation” — that is, inflammation of nervous tissue, Nelson said. In one experiment on humans, those who slept immersed in weak light had higher levels of C-reactive protein in their blood, a marker of inflammation.

Low melatonin has also been linked to cancer. It “allows the metabolic machinery of the cancer cells to be active,” Hanifin said. One of melatonin’s effects is stimulation of natural killer cells, which can recognize and destroy cancer cells. What’s more, when melatonin plunges, estrogen may go up, which could explain the link between light at night and breast cancer (estrogen fuels tumor growth in breast cancers). 

Researchers concede that satellite data might be too coarse to estimate how much light people are actually exposed to while they sleep. Plus, many of us are staring at bright screens. “But the studies keep coming,” Nelson said, suggesting that outdoor light pollution does have an impact. 

When researchers put wrist-worn light sensors on over 80,000 British people, they found that the more light the device registered between half-past midnight and 6 a.m., the more its wearer was at risk of having diabetes several years down the road — no matter how long they’ve actually slept. This, according to the study’s authors, supports the findings of satellite data.

A similar study that used actigraphy with built-in light sensors, measuring whether people had been sleeping in complete darkness for at least five hours, found that light pollution upped the risk of heart disease by 74%.
 

What Can You Do About This?

Not everyone’s melatonin is affected by nighttime light to the same degree. “Some people are very much sensitive to very dim light, whereas others are not as sensitive and need far, far more light stimulation [to impact melatonin],” Benedict said. In one study, some volunteers needed 350 lux to lower their melatonin by half. For such people, flipping on the light in the bathroom at night wouldn’t matter; for others, though, a mere 6 lux was already as harmful – which is darker than twilight. 

You can protect yourself by keeping your bedroom lights off and your screens stashed away, but avoiding outdoor light pollution may be harder. You can invest in high-quality blackout curtains, of course, although some light may still seep inside. You can plant trees in front of your windows, reorient any motion-detector lights, and even petition your local government to reduce over-illumination of buildings and to choose better streetlights. You can support organizations, such as the International Dark-Sky Association, that work to preserve darkness.

Last but not least, you might want to change your habits. If you live in a particularly light-polluted area, such as the District of Columbia, America’s top place for urban blaze, you might reconsider late-night walks or drives around the neighborhood. Instead, Hanifin said, read a book in bed, while keeping the light “as dim as you can.” It’s “a much better idea versus being outside in midtown Manhattan,” he said. According to recent recommendations published by Hanifin and his colleagues, when you sleep, there should be no more than 1 lux of illumination at the level of your eyes — about as much as you’d get from having a lit candle 1 meter away. 

And if we manage to preserve outdoor darkness, and the stars reappear (including the breathtaking Milky Way), we could reap more benefits — some research suggests that stargazing can elicit positive emotions, a sense of personal growth, and “a variety of transcendent thoughts and experiences.” 
 

A version of this article appeared on WebMD.com.

This October, millions of Americans missed out on two of the most spectacular shows in the universe: the northern lights and a rare comet. Even if you were aware of them, light pollution made them difficult to see, unless you went to a dark area and let your eyes adjust.

It’s not getting any easier — the night sky over North America has been growing brighter by about 10% per year since 2011. More and more research is linking all that light pollution to a surprising range of health consequences: cancer, heart disease, diabetes, Alzheimer’s disease, and even low sperm quality, though the reasons for these troubling associations are not always clear. 

“We’ve lost the contrast between light and dark, and we are confusing our physiology on a regular basis,” said John Hanifin, PhD, associate director of Thomas Jefferson University’s Light Research Program. 

Our own galaxy is invisible to nearly 80% of people in North America. In 1994, an earthquake-triggered blackout in Los Angeles led to calls to the Griffith Observatory from people wondering about that hazy blob of light in the night sky. It was the Milky Way.

Glaring headlights, illuminated buildings, blazing billboards, and streetlights fill our urban skies with a glow that even affects rural residents. Inside, since the invention of the lightbulb, we’ve kept our homes bright at night. Now, we’ve also added blue light-emitting devices — smartphones, television screens, tablets — which have been linked to sleep problems.

But outdoor light may matter for our health, too. “Every photon counts,” Hanifin said. 
 

Bright Lights, Big Problems

For one 2024 study researchers used satellite data to measure light pollution at residential addresses of over 13,000 people. They found that those who lived in places with the brightest skies at night had a 31% higher risk of high blood pressure. Another study out of Hong Kong showed a 29% higher risk of death from coronary heart disease. And yet another found a 17%higher risk of cerebrovascular disease, such as strokes or brain aneurysms. 

Of course, urban areas also have air pollution, noise, and a lack of greenery. So, for some studies, scientists controlled for these factors, and the correlation remained strong (although air pollution with fine particulate matter appeared to be worse for heart health than outdoor light). 

Research has found links between the nighttime glow outside and other diseases:

Breast cancer. “It’s a very strong correlation,” said Randy Nelson, PhD, a neuroscientist at West Virginia University. A study of over 100,000 teachers in California revealed that women living in areas with the most light pollution had a 12%higher risk. That effect is comparable to increasing your intake of ultra-processed foods by 10%. 

Alzheimer’s disease. In a study published this fall, outdoor light at night was more strongly linked to the disease than even alcohol misuse or obesity.

Diabetes. In one recent study, people living in the most illuminated areas had a 28% higher risk of diabetes than those residing in much darker places. In a country like China, scientists concluded that 9 million cases of diabetes could be linked to light pollution. 
 

What Happens in Your Body When You’re Exposed to Light at Night

Research has revealed that light at night (indoors or out) disrupts circadian clocks, increases inflammation, affects cell division, and suppresses melatonin, the “hormone of darkness.” “Darkness is very important,” Hanifin said. When he and his colleagues decades ago started studying the effects of light on human physiology, “people thought we were borderline crazy,” he said.

Nighttime illumination affects the health and behavior of species as diverse as Siberian hamsters, zebra finches, mice, crickets, and mosquitoes. Like most creatures on Earth, humans have internal clocks that are synced to the 24-hour cycle of day and night. The master clock is in your hypothalamus, a diamond-shaped part of the brain, but every cell in your body has its own clock, too. Many physiological processes run on circadian rhythms (a term derived from a Latin phrase meaning “about a day”), from sleep-wake cycle to hormone secretion, as well as processes involved in cancer progression, such as cell division.

“There are special photoreceptors in the eye that don’t deal with visual information. They just send light information,” Nelson said. “If you get light at the wrong time, you’re resetting the clocks.” 

This internal clock “prepares the body for various recurrent challenges, such as eating,” said Christian Benedict, PhD, a sleep researcher at Uppsala University, Sweden. “Light exposure [at night] can mess up this very important system.” This could mean, for instance, that your insulin is released at the wrong time, Benedict said, causing “a jet lag-ish condition that will then impair the ability to handle blood sugar.” Animal studies confirm that exposure to light at night can reduce glucose tolerance and alter insulin secretion – potential pathways to diabetes.

The hormone melatonin, produced when it’s dark by the pineal gland in the brain, is a key player in this modern struggle. Melatonin helps you sleep, synchronizes the body’s circadian rhythms, protects neurons from damage, regulates the immune system, and fights inflammation. But even a sliver of light at night can suppress its secretion. Less than 30 lux of light, about the level of a pedestrian street at night, can slash melatonin by half. 

When lab animals are exposed to nighttime light, they “show enormous neuroinflammation” — that is, inflammation of nervous tissue, Nelson said. In one experiment on humans, those who slept immersed in weak light had higher levels of C-reactive protein in their blood, a marker of inflammation.

Low melatonin has also been linked to cancer. It “allows the metabolic machinery of the cancer cells to be active,” Hanifin said. One of melatonin’s effects is stimulation of natural killer cells, which can recognize and destroy cancer cells. What’s more, when melatonin plunges, estrogen may go up, which could explain the link between light at night and breast cancer (estrogen fuels tumor growth in breast cancers). 

Researchers concede that satellite data might be too coarse to estimate how much light people are actually exposed to while they sleep. Plus, many of us are staring at bright screens. “But the studies keep coming,” Nelson said, suggesting that outdoor light pollution does have an impact. 

When researchers put wrist-worn light sensors on over 80,000 British people, they found that the more light the device registered between half-past midnight and 6 a.m., the more its wearer was at risk of having diabetes several years down the road — no matter how long they’ve actually slept. This, according to the study’s authors, supports the findings of satellite data.

A similar study that used actigraphy with built-in light sensors, measuring whether people had been sleeping in complete darkness for at least five hours, found that light pollution upped the risk of heart disease by 74%.
 

What Can You Do About This?

Not everyone’s melatonin is affected by nighttime light to the same degree. “Some people are very much sensitive to very dim light, whereas others are not as sensitive and need far, far more light stimulation [to impact melatonin],” Benedict said. In one study, some volunteers needed 350 lux to lower their melatonin by half. For such people, flipping on the light in the bathroom at night wouldn’t matter; for others, though, a mere 6 lux was already as harmful – which is darker than twilight. 

You can protect yourself by keeping your bedroom lights off and your screens stashed away, but avoiding outdoor light pollution may be harder. You can invest in high-quality blackout curtains, of course, although some light may still seep inside. You can plant trees in front of your windows, reorient any motion-detector lights, and even petition your local government to reduce over-illumination of buildings and to choose better streetlights. You can support organizations, such as the International Dark-Sky Association, that work to preserve darkness.

Last but not least, you might want to change your habits. If you live in a particularly light-polluted area, such as the District of Columbia, America’s top place for urban blaze, you might reconsider late-night walks or drives around the neighborhood. Instead, Hanifin said, read a book in bed, while keeping the light “as dim as you can.” It’s “a much better idea versus being outside in midtown Manhattan,” he said. According to recent recommendations published by Hanifin and his colleagues, when you sleep, there should be no more than 1 lux of illumination at the level of your eyes — about as much as you’d get from having a lit candle 1 meter away. 

And if we manage to preserve outdoor darkness, and the stars reappear (including the breathtaking Milky Way), we could reap more benefits — some research suggests that stargazing can elicit positive emotions, a sense of personal growth, and “a variety of transcendent thoughts and experiences.” 
 

A version of this article appeared on WebMD.com.

A low-carbohydrate diet can help preserve beta-cell function in people with mild type 2 diabetes (T2D), potentially allowing some to achieve target glucose levels without medication, new research suggests.

In the 12-week study of 57 people with T2D who were not using insulin, C-peptide levels were significantly higher among those randomized to receive a low-carbohydrate diet (~9% of total calories) vs a higher-carbohydrate diet (~55%). The results were published online on October 22, 2024, in The Journal of Clinical Endocrinology & Metabolism.

“While other studies have demonstrated metabolic health benefits of low-carb diets, our results are the first to show that dietary carbohydrate restriction can improve beta-cell function ... Furthermore, the carbohydrate-restricted diet improved insulin secretion in African American patients to a much greater extent than in Caucasian Americans,” study author Marian L. Yurchishin, MS, Department of Nutrition Sciences, The University of Alabama, Birmingham, Alabama, told Medscape Medical News.

Yurchishin added, “Our data suggests that a carbohydrate-restricted diet provides the opportunity to improve beta-cell function without the need for medication use or weight loss. This approach may be more appealing and effective for some persons with T2D, particularly in patients of African descent.”

At the same time, she clarified, “Our research should not be interpreted to mean that a carbohydrate-restricted diet can replace medical therapy in those who need it, especially patients at risk of cardiovascular disease, heart failure, or chronic kidney disease…or when medications are needed to achieve A1c targets.”

Asked to comment, Alison B. Evert, RDN, CDCES, former (now retired) manager of the Nutrition and Diabetes Education Programs at the University of Washington Medicine Primary Care, Kirkland, Washington, expressed some caveats about the findings, noting “I doubt this approach would be sustainable for the average person.” 

Evert also pointed out that the amount of fat in the carbohydrate-restricted diet — 65% of energy vs just 20% of energy with the higher-carbohydrate diet — was “extremely high ... essentially a keto diet,” and that in the real-world people might not receive education on heart-healthy fat intake. Moreover, she noted that the study’s use of grocery delivery to the participants with instructions for food preparation “is not a real-world situation either.”
 

Low-Carbohydrate Diet Increased C-Peptide Levels

The study participants were all either African American or European American. All had been diagnosed with T2D within the past 10 years, with average 4.9 years in the carbohydrate-restricted group vs 3.0 years in the higher-carbohydrate group. The two diets contained approximately the same number of calories.

All their medications were discontinued 1-2 weeks prior to baseline testing.

A hyperglycemic clamp was used to assess the acute (first-phase) and maximal (arginine-stimulated) C-peptide response to glucose at baseline and after 12 weeks of following the diets. First-phase beta-cell response to glucose was assessed at 30 minutes, insulin sensitivity was evaluated at 2 hours, and maximal beta-cell response to arginine was evaluated after another 30 minutes.

Oral glucose tolerance tests were also conducted at baseline and at 12 weeks to determine the disposition index (DI), a marker of beta-cell function that factors in both C-peptide and insulin sensitivity.

Of 65 participants enrolled, eight discontinued the study, most due to non-adherence. At 12 weeks, the acute C-peptide response from baseline was twice as high with the carbohydrate-restricted diet than with the higher-carbohydrate diet (P < .05). This difference was significant among the 37 African Americans (110% greater; P < .01) but not for the 20 European Americans.

Evert said that because people have typically lost at least 50% of their beta-cell function at the time of T2D diagnosis, “it is helpful to have return of first phase response, but long-term discontinuation of medications that also have cardioprotective function seems short sighted in this patient population.”

The overall maximal C-peptide response was 22% greater with the carbohydrate-restricted diet (P < .05), this time only significant in the European Americans (48%; P < .01) but not the African Americans.

In the combined group, the DI was 32% greater with the carbohydrate-restricted diet (P < .05) but only significantly so in the African American participants (48%; P < .01); however, no DI changes were seen with the higher-carbohydrate diet in the European American participants.

Regarding the racial differences, Yurchishin explained “Research supports the contention that the pathophysiology of T2D differs can differ among races based on genetic factors and environmental interactions that affect beta-cell function. For example, T2D onset in African Americans may be less related to obesity and insulin resistance than it is in European Americans and depend on alterations in beta-cell function to a larger degree. While sociocultural factors do influence T2D risk, other studies have also shown that there are inherent biological differences in the mechanisms that lead to beta-cell failure between races that warrant further investigation.” 

In their paper, Yurchishin and colleagues concluded, “With the caveat that carbohydrate restriction may be difficult for some patients, such a diet may allow patients with mild T2D to discontinue medication and enjoy eating meals and snacks that meet their energy needs while improving beta-cell function, an outcome that cannot be achieved with medication.” 

Evert commented, “I think it is a bit subjective to say that people following a 9% carb intake ‘will enjoy eating their meals and snacks that meet their energy needs.’ Guess they would enjoy as long as they choose very high fat, low carb foods.”

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the UAB Nutrition Obesity Research Center, and the UAB Diabetes Research Center. Yurchishin was supported by the National Heart, Lung, and Blood Institute. Evert had no disclosures.
 

A version of this article appeared on Medscape.com.

A low-carbohydrate diet can help preserve beta-cell function in people with mild type 2 diabetes (T2D), potentially allowing some to achieve target glucose levels without medication, new research suggests.

In the 12-week study of 57 people with T2D who were not using insulin, C-peptide levels were significantly higher among those randomized to receive a low-carbohydrate diet (~9% of total calories) vs a higher-carbohydrate diet (~55%). The results were published online on October 22, 2024, in The Journal of Clinical Endocrinology & Metabolism.

“While other studies have demonstrated metabolic health benefits of low-carb diets, our results are the first to show that dietary carbohydrate restriction can improve beta-cell function ... Furthermore, the carbohydrate-restricted diet improved insulin secretion in African American patients to a much greater extent than in Caucasian Americans,” study author Marian L. Yurchishin, MS, Department of Nutrition Sciences, The University of Alabama, Birmingham, Alabama, told Medscape Medical News.

Yurchishin added, “Our data suggests that a carbohydrate-restricted diet provides the opportunity to improve beta-cell function without the need for medication use or weight loss. This approach may be more appealing and effective for some persons with T2D, particularly in patients of African descent.”

At the same time, she clarified, “Our research should not be interpreted to mean that a carbohydrate-restricted diet can replace medical therapy in those who need it, especially patients at risk of cardiovascular disease, heart failure, or chronic kidney disease…or when medications are needed to achieve A1c targets.”

Asked to comment, Alison B. Evert, RDN, CDCES, former (now retired) manager of the Nutrition and Diabetes Education Programs at the University of Washington Medicine Primary Care, Kirkland, Washington, expressed some caveats about the findings, noting “I doubt this approach would be sustainable for the average person.” 

Evert also pointed out that the amount of fat in the carbohydrate-restricted diet — 65% of energy vs just 20% of energy with the higher-carbohydrate diet — was “extremely high ... essentially a keto diet,” and that in the real-world people might not receive education on heart-healthy fat intake. Moreover, she noted that the study’s use of grocery delivery to the participants with instructions for food preparation “is not a real-world situation either.”
 

Low-Carbohydrate Diet Increased C-Peptide Levels

The study participants were all either African American or European American. All had been diagnosed with T2D within the past 10 years, with average 4.9 years in the carbohydrate-restricted group vs 3.0 years in the higher-carbohydrate group. The two diets contained approximately the same number of calories.

All their medications were discontinued 1-2 weeks prior to baseline testing.

A hyperglycemic clamp was used to assess the acute (first-phase) and maximal (arginine-stimulated) C-peptide response to glucose at baseline and after 12 weeks of following the diets. First-phase beta-cell response to glucose was assessed at 30 minutes, insulin sensitivity was evaluated at 2 hours, and maximal beta-cell response to arginine was evaluated after another 30 minutes.

Oral glucose tolerance tests were also conducted at baseline and at 12 weeks to determine the disposition index (DI), a marker of beta-cell function that factors in both C-peptide and insulin sensitivity.

Of 65 participants enrolled, eight discontinued the study, most due to non-adherence. At 12 weeks, the acute C-peptide response from baseline was twice as high with the carbohydrate-restricted diet than with the higher-carbohydrate diet (P < .05). This difference was significant among the 37 African Americans (110% greater; P < .01) but not for the 20 European Americans.

Evert said that because people have typically lost at least 50% of their beta-cell function at the time of T2D diagnosis, “it is helpful to have return of first phase response, but long-term discontinuation of medications that also have cardioprotective function seems short sighted in this patient population.”

The overall maximal C-peptide response was 22% greater with the carbohydrate-restricted diet (P < .05), this time only significant in the European Americans (48%; P < .01) but not the African Americans.

In the combined group, the DI was 32% greater with the carbohydrate-restricted diet (P < .05) but only significantly so in the African American participants (48%; P < .01); however, no DI changes were seen with the higher-carbohydrate diet in the European American participants.

Regarding the racial differences, Yurchishin explained “Research supports the contention that the pathophysiology of T2D differs can differ among races based on genetic factors and environmental interactions that affect beta-cell function. For example, T2D onset in African Americans may be less related to obesity and insulin resistance than it is in European Americans and depend on alterations in beta-cell function to a larger degree. While sociocultural factors do influence T2D risk, other studies have also shown that there are inherent biological differences in the mechanisms that lead to beta-cell failure between races that warrant further investigation.” 

In their paper, Yurchishin and colleagues concluded, “With the caveat that carbohydrate restriction may be difficult for some patients, such a diet may allow patients with mild T2D to discontinue medication and enjoy eating meals and snacks that meet their energy needs while improving beta-cell function, an outcome that cannot be achieved with medication.” 

Evert commented, “I think it is a bit subjective to say that people following a 9% carb intake ‘will enjoy eating their meals and snacks that meet their energy needs.’ Guess they would enjoy as long as they choose very high fat, low carb foods.”

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the UAB Nutrition Obesity Research Center, and the UAB Diabetes Research Center. Yurchishin was supported by the National Heart, Lung, and Blood Institute. Evert had no disclosures.
 

A version of this article appeared on Medscape.com.

A low-carbohydrate diet can help preserve beta-cell function in people with mild type 2 diabetes (T2D), potentially allowing some to achieve target glucose levels without medication, new research suggests.

In the 12-week study of 57 people with T2D who were not using insulin, C-peptide levels were significantly higher among those randomized to receive a low-carbohydrate diet (~9% of total calories) vs a higher-carbohydrate diet (~55%). The results were published online on October 22, 2024, in The Journal of Clinical Endocrinology & Metabolism.

“While other studies have demonstrated metabolic health benefits of low-carb diets, our results are the first to show that dietary carbohydrate restriction can improve beta-cell function ... Furthermore, the carbohydrate-restricted diet improved insulin secretion in African American patients to a much greater extent than in Caucasian Americans,” study author Marian L. Yurchishin, MS, Department of Nutrition Sciences, The University of Alabama, Birmingham, Alabama, told Medscape Medical News.

Yurchishin added, “Our data suggests that a carbohydrate-restricted diet provides the opportunity to improve beta-cell function without the need for medication use or weight loss. This approach may be more appealing and effective for some persons with T2D, particularly in patients of African descent.”

At the same time, she clarified, “Our research should not be interpreted to mean that a carbohydrate-restricted diet can replace medical therapy in those who need it, especially patients at risk of cardiovascular disease, heart failure, or chronic kidney disease…or when medications are needed to achieve A1c targets.”

Asked to comment, Alison B. Evert, RDN, CDCES, former (now retired) manager of the Nutrition and Diabetes Education Programs at the University of Washington Medicine Primary Care, Kirkland, Washington, expressed some caveats about the findings, noting “I doubt this approach would be sustainable for the average person.” 

Evert also pointed out that the amount of fat in the carbohydrate-restricted diet — 65% of energy vs just 20% of energy with the higher-carbohydrate diet — was “extremely high ... essentially a keto diet,” and that in the real-world people might not receive education on heart-healthy fat intake. Moreover, she noted that the study’s use of grocery delivery to the participants with instructions for food preparation “is not a real-world situation either.”
 

Low-Carbohydrate Diet Increased C-Peptide Levels

The study participants were all either African American or European American. All had been diagnosed with T2D within the past 10 years, with average 4.9 years in the carbohydrate-restricted group vs 3.0 years in the higher-carbohydrate group. The two diets contained approximately the same number of calories.

All their medications were discontinued 1-2 weeks prior to baseline testing.

A hyperglycemic clamp was used to assess the acute (first-phase) and maximal (arginine-stimulated) C-peptide response to glucose at baseline and after 12 weeks of following the diets. First-phase beta-cell response to glucose was assessed at 30 minutes, insulin sensitivity was evaluated at 2 hours, and maximal beta-cell response to arginine was evaluated after another 30 minutes.

Oral glucose tolerance tests were also conducted at baseline and at 12 weeks to determine the disposition index (DI), a marker of beta-cell function that factors in both C-peptide and insulin sensitivity.

Of 65 participants enrolled, eight discontinued the study, most due to non-adherence. At 12 weeks, the acute C-peptide response from baseline was twice as high with the carbohydrate-restricted diet than with the higher-carbohydrate diet (P < .05). This difference was significant among the 37 African Americans (110% greater; P < .01) but not for the 20 European Americans.

Evert said that because people have typically lost at least 50% of their beta-cell function at the time of T2D diagnosis, “it is helpful to have return of first phase response, but long-term discontinuation of medications that also have cardioprotective function seems short sighted in this patient population.”

The overall maximal C-peptide response was 22% greater with the carbohydrate-restricted diet (P < .05), this time only significant in the European Americans (48%; P < .01) but not the African Americans.

In the combined group, the DI was 32% greater with the carbohydrate-restricted diet (P < .05) but only significantly so in the African American participants (48%; P < .01); however, no DI changes were seen with the higher-carbohydrate diet in the European American participants.

Regarding the racial differences, Yurchishin explained “Research supports the contention that the pathophysiology of T2D differs can differ among races based on genetic factors and environmental interactions that affect beta-cell function. For example, T2D onset in African Americans may be less related to obesity and insulin resistance than it is in European Americans and depend on alterations in beta-cell function to a larger degree. While sociocultural factors do influence T2D risk, other studies have also shown that there are inherent biological differences in the mechanisms that lead to beta-cell failure between races that warrant further investigation.” 

In their paper, Yurchishin and colleagues concluded, “With the caveat that carbohydrate restriction may be difficult for some patients, such a diet may allow patients with mild T2D to discontinue medication and enjoy eating meals and snacks that meet their energy needs while improving beta-cell function, an outcome that cannot be achieved with medication.” 

Evert commented, “I think it is a bit subjective to say that people following a 9% carb intake ‘will enjoy eating their meals and snacks that meet their energy needs.’ Guess they would enjoy as long as they choose very high fat, low carb foods.”

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the UAB Nutrition Obesity Research Center, and the UAB Diabetes Research Center. Yurchishin was supported by the National Heart, Lung, and Blood Institute. Evert had no disclosures.
 

A version of this article appeared on Medscape.com.

Recent reports suggest diabetic retinopathy is more common in younger people than previously thought, leading to a call for more frequent screening for this condition and more attention to follow-up after diagnosis.

The increased incidence of diabetic retinopathy is “a potentially unappreciated public health catastrophe,” Julie Rosenthal, MD, MS, of the University of Michigan, Ann Arbor, Michigan, and her coauthors wrote in a recent viewpoint in JAMA Ophthalmology.

Rosenthal, an ophthalmologist, said she has been treating each year several young people with diabetes with symptoms of retinopathy that might have been prevented through earlier detection and treatment.

Some patients with retinopathy seek out eye specialists for issues such as seeing floaters, vision loss, or feeling of having cobwebs in their vision, which can be symptoms of bleeding. Other patients may have no symptoms with their retinopathy discovered only in screening.

“It would be wonderful to never need to treat any 20-year-olds with proliferative diabetic retinopathy who are losing vision,” Rosenthal said.

Diabetic retinopathy once was considered rare in young people, with earlier research suggesting an age-adjusted prevalence of 4%-13% in youths with type 2 diabetes, roughly in line with that for type 1 diabetes.

But an analysis of more recent data drawn from two major federally funded studies of diabetes in young people shows what Rosenthal and her colleagues called “alarming rates” of retinopathy. Data from these studies suggest more than half (52%) of youths with type 1 diabetes may have some retinopathy, and as many as 55% of those with youth-onset type 2 diabetes.

Other research suggests young people with type 2 diabetes may have almost twice the risk of developing retinopathy, develop it sooner after diabetes diagnosis, and are more likely to have vision-threatening retinopathy, Rosenthal and coauthors wrote.

Elizabeth Jensen, PhD, of Wake Forest University, Winston-Salem, North Carolina, the lead author of a 2023 study cited by Rosenthal and coauthors in their JAMA Ophthalmology viewpoint, told Medscape Medical News she also supports a call for more screening of young people.

“What many people don’t realize is that there is evidence of retinal changes consistent with development of diabetic retinopathy early in disease,” Jensen said.

The proportion of people with diabetic retinopathy varied according to a range of modifiable factors, including A1c levels and blood pressure, she added.

This fact underscores the need to not only screen for diabetic retinopathy early but also consider addressing those modifiable factors that may mitigate risk for the development and progression of diabetic retinopathy, Jensen said.

Rosenthal said some patients have the false impression of sight loss being inevitable with diabetes. Their primary care physicians can help make them aware that there are treatments for retinopathy in cases where it can’t be avoided.

These interventions include laser treatments and injecting medicines into the eye. “It sounds a lot scarier than it is,” Rosenthal said.

“We do know that keeping good control over not only glucose but also blood pressure, cholesterol, and lipids is all important for decreasing the risk. But even if those are under control, sometimes people can still get diabetes in their eyes,” Rosenthal said. “The longer you have diabetes, the higher your risk of having problems in your eye.”
 

‘Stagnant Guidelines’

Guidelines from major medical groups have “remained largely stagnant in the face of new evidence of increasing diabetes prevalence,” making it difficult to know when to screen younger people, according to Rosenthal and her colleagues.

Medical associations, including the American Diabetes Association (ADA) and the American Academy of Ophthalmology, now recommend ocular screening for youths with type 1 diabetes 3-5 years after diagnosis in those who are at least 11 years old or are experiencing puberty, and for youths with type 2 diabetes from the time of diagnosis.

Follow-up diabetic eye examinations can be performed every 2 years, with some groups advocating for even more infrequent follow-up examinations.

“These guidelines are rooted in evidence from prior studies showing that it is rare to have advanced retinopathy prior to this age,” Rosenthal and coauthors wrote. “However, these guidelines have remained largely stagnant in the face of new evidence of increasing diabetes prevalence.”

The American Academy of Ophthalmology told Medscape Medical News it has no immediate plans to update its recommendations. These include directing people with type 1 diabetes without known diabetic retinopathy to have annual dilated eye examinations beginning 5 years after the onset of diabetes. Individuals with type 2 diabetes without diabetic retinopathy should have annual dilated eye examinations to detect the onset of diabetic retinopathy.

The group also said clinicians should make sure patients understand that even if they may have good vision and no ocular symptoms, they may still have significant disease that needs treatment.
 

More Opportunities for Screening Tools

The current standards of care for retinopathy from the ADA note new products on the market are increasing the options for screening.

“Retinal photography with remote reading by experts has great potential to provide screening services in areas where qualified eye care professionals are not readily available,” according to standards.

“However, the benefits and optimal utilization of this type of screening have yet to be fully determined,” the group stated. “Results of all screening eye examinations should be documented and transmitted to the referring healthcare professionals.”

The approach has promise, despite some significant challenges, according to Rithwick Rajagopal, MD, PhD, an associate professor of ophthalmology and visual sciences at Washington University in St. Louis, St. Louis, Missouri.

Rajagopal and colleagues in 2022 published results of a test of retinopathy screening during appointments at the primary care medicine clinic of Barnes-Jewish Hospital in St. Louis, Missouri. They found the system used worked well in ruling out retinopathy and appeared to help more patients receive care for the condition. Among patients referred for follow-up eye exams, the adherence rate was 55.4% at 1-year compared with the historical adherence rate of 18.7%, Rajagopal and his colleagues reported.

In an email exchange with Medscape Medical News, Rajagopal highlighted several barriers to wider adoption of retinopathy screenings in primary care.

“First is unfamiliarity with eye anatomy and physiology, which is associated with low level of comfort in capturing the photographs and interpreting the results (even though the cameras are increasingly easy to use and that the AI software generates the diagnosis),” Rajagopal said.

In addition, questions about reimbursement and liability remain unresolved.

But Rajagopal said he still expects more use of products such as the EyeArt 2.0 automated DR screening software (Eyenuk, Inc.).

“Despite the above concerns, point-of-care screening offers a powerful solution to a long-standing problem: People with diabetes in this country are generally not adherent to recommended retinal screening guidelines,” Rajagopal told Medscape Medical News. “There are multiple causes of such poor adherence, but point-of-care screening solves several of them: No need to take time off for an additional medical visit, no additional co-pay for eye doctor visits, and no need for dilation in many cases.”

Aiding in the adoption of this service is likely the special Current Procedural Terminology (billing) code — 92229 — the American Medical Association introduced in 2021 for diabetic eye exams when ordered by a physician who is not an ophthalmologist. Many commercial health plans and many state Medicaid programs now cover this service, which is still off-label, Michael Abramoff, MD, PhD, of the University of Iowa, Iowa City, Iowa, and founder of Digital Diagnostics, maker of the AI-assisted LumineticsCore diagnostic system, told Medscape Medical News. A representative for Eyenuk also told Medscape Medical News many insurers now cover the screening service.

LumineticsCore has been used in a study done in conjunction with appointments for regular care at the Johns Hopkins Pediatric Diabetes Center in Baltimore.

Abramoff and coauthors, including Risa Wolf, MD, a pediatric endocrinologist at Johns Hopkins University School of Medicine in Baltimore, reported this year in Nature Communications that 100% of patients in the group offered the autonomous AI screening completed their eye exam that day, while only 22% of a comparison group followed through within 6 months to complete an eye exam with an optometrist or ophthalmologist.

Wolf, who is also a coauthor with Rosenthal of the commentary in JAMA Ophthalmology, said she agrees these tools have the potential to expand the pool of clinicians who can screen patients for retinopathy.
 

Make Screening Easier

The critical issue is to make it easier for young adults with diabetes to get checked for retinopathy, Wolf said. People in their late teens and early 20s face many challenges in getting needed medical screenings. They often are shifting away from living with parents, who likely managed their care for them in their childhood.

These young adults tend to be busy with college and the demands of starting out in careers while living on their own. And they may not want to address the potential consequences of diabetes, which can seem remote to people not feeling effects of the illness.

“It’s just not always a priority, especially when you’re in this time of life where you’re generally feeling very healthy,” Wolf said. “But we want to make sure that they are getting screened.”

Rosenthal reported receiving research grant support from MediBeacon, outside the submitted work. Other coauthors reported receiving grants from Breakthrough T1D, Physical Sciences, Novartis, Genentech/Roche, Novo Nordisk, and Boehringer Ingelheim, and receiving nonfinancial support from Optovue, Boston Micromachines, Novo Nordisk, Adaptive Sensory Technology, Genentech/Roche, Novartis, and Alcon outside the submitted work. Jensen reported no relevant financial disclosures.

Eyenuk Inc. provided the camera and automated screening software used in the study reported by Rajagopal and coauthors and was involved in the data collection and management, but otherwise had no role in the design or conduct of this research. Rajagopal had no personal financial disclosures.
 

A version of this article appeared on Medscape.com.

Recent reports suggest diabetic retinopathy is more common in younger people than previously thought, leading to a call for more frequent screening for this condition and more attention to follow-up after diagnosis.

The increased incidence of diabetic retinopathy is “a potentially unappreciated public health catastrophe,” Julie Rosenthal, MD, MS, of the University of Michigan, Ann Arbor, Michigan, and her coauthors wrote in a recent viewpoint in JAMA Ophthalmology.

Rosenthal, an ophthalmologist, said she has been treating each year several young people with diabetes with symptoms of retinopathy that might have been prevented through earlier detection and treatment.

Some patients with retinopathy seek out eye specialists for issues such as seeing floaters, vision loss, or feeling of having cobwebs in their vision, which can be symptoms of bleeding. Other patients may have no symptoms with their retinopathy discovered only in screening.

“It would be wonderful to never need to treat any 20-year-olds with proliferative diabetic retinopathy who are losing vision,” Rosenthal said.

Diabetic retinopathy once was considered rare in young people, with earlier research suggesting an age-adjusted prevalence of 4%-13% in youths with type 2 diabetes, roughly in line with that for type 1 diabetes.

But an analysis of more recent data drawn from two major federally funded studies of diabetes in young people shows what Rosenthal and her colleagues called “alarming rates” of retinopathy. Data from these studies suggest more than half (52%) of youths with type 1 diabetes may have some retinopathy, and as many as 55% of those with youth-onset type 2 diabetes.

Other research suggests young people with type 2 diabetes may have almost twice the risk of developing retinopathy, develop it sooner after diabetes diagnosis, and are more likely to have vision-threatening retinopathy, Rosenthal and coauthors wrote.

Elizabeth Jensen, PhD, of Wake Forest University, Winston-Salem, North Carolina, the lead author of a 2023 study cited by Rosenthal and coauthors in their JAMA Ophthalmology viewpoint, told Medscape Medical News she also supports a call for more screening of young people.

“What many people don’t realize is that there is evidence of retinal changes consistent with development of diabetic retinopathy early in disease,” Jensen said.

The proportion of people with diabetic retinopathy varied according to a range of modifiable factors, including A1c levels and blood pressure, she added.

This fact underscores the need to not only screen for diabetic retinopathy early but also consider addressing those modifiable factors that may mitigate risk for the development and progression of diabetic retinopathy, Jensen said.

Rosenthal said some patients have the false impression of sight loss being inevitable with diabetes. Their primary care physicians can help make them aware that there are treatments for retinopathy in cases where it can’t be avoided.

These interventions include laser treatments and injecting medicines into the eye. “It sounds a lot scarier than it is,” Rosenthal said.

“We do know that keeping good control over not only glucose but also blood pressure, cholesterol, and lipids is all important for decreasing the risk. But even if those are under control, sometimes people can still get diabetes in their eyes,” Rosenthal said. “The longer you have diabetes, the higher your risk of having problems in your eye.”
 

‘Stagnant Guidelines’

Guidelines from major medical groups have “remained largely stagnant in the face of new evidence of increasing diabetes prevalence,” making it difficult to know when to screen younger people, according to Rosenthal and her colleagues.

Medical associations, including the American Diabetes Association (ADA) and the American Academy of Ophthalmology, now recommend ocular screening for youths with type 1 diabetes 3-5 years after diagnosis in those who are at least 11 years old or are experiencing puberty, and for youths with type 2 diabetes from the time of diagnosis.

Follow-up diabetic eye examinations can be performed every 2 years, with some groups advocating for even more infrequent follow-up examinations.

“These guidelines are rooted in evidence from prior studies showing that it is rare to have advanced retinopathy prior to this age,” Rosenthal and coauthors wrote. “However, these guidelines have remained largely stagnant in the face of new evidence of increasing diabetes prevalence.”

The American Academy of Ophthalmology told Medscape Medical News it has no immediate plans to update its recommendations. These include directing people with type 1 diabetes without known diabetic retinopathy to have annual dilated eye examinations beginning 5 years after the onset of diabetes. Individuals with type 2 diabetes without diabetic retinopathy should have annual dilated eye examinations to detect the onset of diabetic retinopathy.

The group also said clinicians should make sure patients understand that even if they may have good vision and no ocular symptoms, they may still have significant disease that needs treatment.
 

More Opportunities for Screening Tools

The current standards of care for retinopathy from the ADA note new products on the market are increasing the options for screening.

“Retinal photography with remote reading by experts has great potential to provide screening services in areas where qualified eye care professionals are not readily available,” according to standards.

“However, the benefits and optimal utilization of this type of screening have yet to be fully determined,” the group stated. “Results of all screening eye examinations should be documented and transmitted to the referring healthcare professionals.”

The approach has promise, despite some significant challenges, according to Rithwick Rajagopal, MD, PhD, an associate professor of ophthalmology and visual sciences at Washington University in St. Louis, St. Louis, Missouri.

Rajagopal and colleagues in 2022 published results of a test of retinopathy screening during appointments at the primary care medicine clinic of Barnes-Jewish Hospital in St. Louis, Missouri. They found the system used worked well in ruling out retinopathy and appeared to help more patients receive care for the condition. Among patients referred for follow-up eye exams, the adherence rate was 55.4% at 1-year compared with the historical adherence rate of 18.7%, Rajagopal and his colleagues reported.

In an email exchange with Medscape Medical News, Rajagopal highlighted several barriers to wider adoption of retinopathy screenings in primary care.

“First is unfamiliarity with eye anatomy and physiology, which is associated with low level of comfort in capturing the photographs and interpreting the results (even though the cameras are increasingly easy to use and that the AI software generates the diagnosis),” Rajagopal said.

In addition, questions about reimbursement and liability remain unresolved.

But Rajagopal said he still expects more use of products such as the EyeArt 2.0 automated DR screening software (Eyenuk, Inc.).

“Despite the above concerns, point-of-care screening offers a powerful solution to a long-standing problem: People with diabetes in this country are generally not adherent to recommended retinal screening guidelines,” Rajagopal told Medscape Medical News. “There are multiple causes of such poor adherence, but point-of-care screening solves several of them: No need to take time off for an additional medical visit, no additional co-pay for eye doctor visits, and no need for dilation in many cases.”

Aiding in the adoption of this service is likely the special Current Procedural Terminology (billing) code — 92229 — the American Medical Association introduced in 2021 for diabetic eye exams when ordered by a physician who is not an ophthalmologist. Many commercial health plans and many state Medicaid programs now cover this service, which is still off-label, Michael Abramoff, MD, PhD, of the University of Iowa, Iowa City, Iowa, and founder of Digital Diagnostics, maker of the AI-assisted LumineticsCore diagnostic system, told Medscape Medical News. A representative for Eyenuk also told Medscape Medical News many insurers now cover the screening service.

LumineticsCore has been used in a study done in conjunction with appointments for regular care at the Johns Hopkins Pediatric Diabetes Center in Baltimore.

Abramoff and coauthors, including Risa Wolf, MD, a pediatric endocrinologist at Johns Hopkins University School of Medicine in Baltimore, reported this year in Nature Communications that 100% of patients in the group offered the autonomous AI screening completed their eye exam that day, while only 22% of a comparison group followed through within 6 months to complete an eye exam with an optometrist or ophthalmologist.

Wolf, who is also a coauthor with Rosenthal of the commentary in JAMA Ophthalmology, said she agrees these tools have the potential to expand the pool of clinicians who can screen patients for retinopathy.
 

Make Screening Easier

The critical issue is to make it easier for young adults with diabetes to get checked for retinopathy, Wolf said. People in their late teens and early 20s face many challenges in getting needed medical screenings. They often are shifting away from living with parents, who likely managed their care for them in their childhood.

These young adults tend to be busy with college and the demands of starting out in careers while living on their own. And they may not want to address the potential consequences of diabetes, which can seem remote to people not feeling effects of the illness.

“It’s just not always a priority, especially when you’re in this time of life where you’re generally feeling very healthy,” Wolf said. “But we want to make sure that they are getting screened.”

Rosenthal reported receiving research grant support from MediBeacon, outside the submitted work. Other coauthors reported receiving grants from Breakthrough T1D, Physical Sciences, Novartis, Genentech/Roche, Novo Nordisk, and Boehringer Ingelheim, and receiving nonfinancial support from Optovue, Boston Micromachines, Novo Nordisk, Adaptive Sensory Technology, Genentech/Roche, Novartis, and Alcon outside the submitted work. Jensen reported no relevant financial disclosures.

Eyenuk Inc. provided the camera and automated screening software used in the study reported by Rajagopal and coauthors and was involved in the data collection and management, but otherwise had no role in the design or conduct of this research. Rajagopal had no personal financial disclosures.
 

A version of this article appeared on Medscape.com.

Recent reports suggest diabetic retinopathy is more common in younger people than previously thought, leading to a call for more frequent screening for this condition and more attention to follow-up after diagnosis.

The increased incidence of diabetic retinopathy is “a potentially unappreciated public health catastrophe,” Julie Rosenthal, MD, MS, of the University of Michigan, Ann Arbor, Michigan, and her coauthors wrote in a recent viewpoint in JAMA Ophthalmology.

Rosenthal, an ophthalmologist, said she has been treating each year several young people with diabetes with symptoms of retinopathy that might have been prevented through earlier detection and treatment.

Some patients with retinopathy seek out eye specialists for issues such as seeing floaters, vision loss, or feeling of having cobwebs in their vision, which can be symptoms of bleeding. Other patients may have no symptoms with their retinopathy discovered only in screening.

“It would be wonderful to never need to treat any 20-year-olds with proliferative diabetic retinopathy who are losing vision,” Rosenthal said.

Diabetic retinopathy once was considered rare in young people, with earlier research suggesting an age-adjusted prevalence of 4%-13% in youths with type 2 diabetes, roughly in line with that for type 1 diabetes.

But an analysis of more recent data drawn from two major federally funded studies of diabetes in young people shows what Rosenthal and her colleagues called “alarming rates” of retinopathy. Data from these studies suggest more than half (52%) of youths with type 1 diabetes may have some retinopathy, and as many as 55% of those with youth-onset type 2 diabetes.

Other research suggests young people with type 2 diabetes may have almost twice the risk of developing retinopathy, develop it sooner after diabetes diagnosis, and are more likely to have vision-threatening retinopathy, Rosenthal and coauthors wrote.

Elizabeth Jensen, PhD, of Wake Forest University, Winston-Salem, North Carolina, the lead author of a 2023 study cited by Rosenthal and coauthors in their JAMA Ophthalmology viewpoint, told Medscape Medical News she also supports a call for more screening of young people.

“What many people don’t realize is that there is evidence of retinal changes consistent with development of diabetic retinopathy early in disease,” Jensen said.

The proportion of people with diabetic retinopathy varied according to a range of modifiable factors, including A1c levels and blood pressure, she added.

This fact underscores the need to not only screen for diabetic retinopathy early but also consider addressing those modifiable factors that may mitigate risk for the development and progression of diabetic retinopathy, Jensen said.

Rosenthal said some patients have the false impression of sight loss being inevitable with diabetes. Their primary care physicians can help make them aware that there are treatments for retinopathy in cases where it can’t be avoided.

These interventions include laser treatments and injecting medicines into the eye. “It sounds a lot scarier than it is,” Rosenthal said.

“We do know that keeping good control over not only glucose but also blood pressure, cholesterol, and lipids is all important for decreasing the risk. But even if those are under control, sometimes people can still get diabetes in their eyes,” Rosenthal said. “The longer you have diabetes, the higher your risk of having problems in your eye.”
 

‘Stagnant Guidelines’

Guidelines from major medical groups have “remained largely stagnant in the face of new evidence of increasing diabetes prevalence,” making it difficult to know when to screen younger people, according to Rosenthal and her colleagues.

Medical associations, including the American Diabetes Association (ADA) and the American Academy of Ophthalmology, now recommend ocular screening for youths with type 1 diabetes 3-5 years after diagnosis in those who are at least 11 years old or are experiencing puberty, and for youths with type 2 diabetes from the time of diagnosis.

Follow-up diabetic eye examinations can be performed every 2 years, with some groups advocating for even more infrequent follow-up examinations.

“These guidelines are rooted in evidence from prior studies showing that it is rare to have advanced retinopathy prior to this age,” Rosenthal and coauthors wrote. “However, these guidelines have remained largely stagnant in the face of new evidence of increasing diabetes prevalence.”

The American Academy of Ophthalmology told Medscape Medical News it has no immediate plans to update its recommendations. These include directing people with type 1 diabetes without known diabetic retinopathy to have annual dilated eye examinations beginning 5 years after the onset of diabetes. Individuals with type 2 diabetes without diabetic retinopathy should have annual dilated eye examinations to detect the onset of diabetic retinopathy.

The group also said clinicians should make sure patients understand that even if they may have good vision and no ocular symptoms, they may still have significant disease that needs treatment.
 

More Opportunities for Screening Tools

The current standards of care for retinopathy from the ADA note new products on the market are increasing the options for screening.

“Retinal photography with remote reading by experts has great potential to provide screening services in areas where qualified eye care professionals are not readily available,” according to standards.

“However, the benefits and optimal utilization of this type of screening have yet to be fully determined,” the group stated. “Results of all screening eye examinations should be documented and transmitted to the referring healthcare professionals.”

The approach has promise, despite some significant challenges, according to Rithwick Rajagopal, MD, PhD, an associate professor of ophthalmology and visual sciences at Washington University in St. Louis, St. Louis, Missouri.

Rajagopal and colleagues in 2022 published results of a test of retinopathy screening during appointments at the primary care medicine clinic of Barnes-Jewish Hospital in St. Louis, Missouri. They found the system used worked well in ruling out retinopathy and appeared to help more patients receive care for the condition. Among patients referred for follow-up eye exams, the adherence rate was 55.4% at 1-year compared with the historical adherence rate of 18.7%, Rajagopal and his colleagues reported.

In an email exchange with Medscape Medical News, Rajagopal highlighted several barriers to wider adoption of retinopathy screenings in primary care.

“First is unfamiliarity with eye anatomy and physiology, which is associated with low level of comfort in capturing the photographs and interpreting the results (even though the cameras are increasingly easy to use and that the AI software generates the diagnosis),” Rajagopal said.

In addition, questions about reimbursement and liability remain unresolved.

But Rajagopal said he still expects more use of products such as the EyeArt 2.0 automated DR screening software (Eyenuk, Inc.).

“Despite the above concerns, point-of-care screening offers a powerful solution to a long-standing problem: People with diabetes in this country are generally not adherent to recommended retinal screening guidelines,” Rajagopal told Medscape Medical News. “There are multiple causes of such poor adherence, but point-of-care screening solves several of them: No need to take time off for an additional medical visit, no additional co-pay for eye doctor visits, and no need for dilation in many cases.”

Aiding in the adoption of this service is likely the special Current Procedural Terminology (billing) code — 92229 — the American Medical Association introduced in 2021 for diabetic eye exams when ordered by a physician who is not an ophthalmologist. Many commercial health plans and many state Medicaid programs now cover this service, which is still off-label, Michael Abramoff, MD, PhD, of the University of Iowa, Iowa City, Iowa, and founder of Digital Diagnostics, maker of the AI-assisted LumineticsCore diagnostic system, told Medscape Medical News. A representative for Eyenuk also told Medscape Medical News many insurers now cover the screening service.

LumineticsCore has been used in a study done in conjunction with appointments for regular care at the Johns Hopkins Pediatric Diabetes Center in Baltimore.

Abramoff and coauthors, including Risa Wolf, MD, a pediatric endocrinologist at Johns Hopkins University School of Medicine in Baltimore, reported this year in Nature Communications that 100% of patients in the group offered the autonomous AI screening completed their eye exam that day, while only 22% of a comparison group followed through within 6 months to complete an eye exam with an optometrist or ophthalmologist.

Wolf, who is also a coauthor with Rosenthal of the commentary in JAMA Ophthalmology, said she agrees these tools have the potential to expand the pool of clinicians who can screen patients for retinopathy.
 

Make Screening Easier

The critical issue is to make it easier for young adults with diabetes to get checked for retinopathy, Wolf said. People in their late teens and early 20s face many challenges in getting needed medical screenings. They often are shifting away from living with parents, who likely managed their care for them in their childhood.

These young adults tend to be busy with college and the demands of starting out in careers while living on their own. And they may not want to address the potential consequences of diabetes, which can seem remote to people not feeling effects of the illness.

“It’s just not always a priority, especially when you’re in this time of life where you’re generally feeling very healthy,” Wolf said. “But we want to make sure that they are getting screened.”

Rosenthal reported receiving research grant support from MediBeacon, outside the submitted work. Other coauthors reported receiving grants from Breakthrough T1D, Physical Sciences, Novartis, Genentech/Roche, Novo Nordisk, and Boehringer Ingelheim, and receiving nonfinancial support from Optovue, Boston Micromachines, Novo Nordisk, Adaptive Sensory Technology, Genentech/Roche, Novartis, and Alcon outside the submitted work. Jensen reported no relevant financial disclosures.

Eyenuk Inc. provided the camera and automated screening software used in the study reported by Rajagopal and coauthors and was involved in the data collection and management, but otherwise had no role in the design or conduct of this research. Rajagopal had no personal financial disclosures.
 

A version of this article appeared on Medscape.com.

Lauren is a 45-year-old corporate lawyer who managed to excel in every aspect of her life, including parenting her three children while working full-time as a corporate lawyer. A math major at Harvard, she loves data.

Suffice it to say, given that I was treating her for a thyroid condition rather than diabetes, I was a little surprised when she requested I prescribe her a FreeStyle Libre (Abbott) monitor. She explained she was struggling to lose 10 pounds, and she thought continuous glucose monitoring (CGM) would help her determine which foods were impeding her weight loss journey. 

While I didn’t see much downside to acquiescing, I felt she had probably been spending too much time on Reddit. What information could CGM give someone without diabetes that couldn’t be gleaned from a food label? Nevertheless, Lauren filled the prescription and began her foray into this relatively uncharted world. When she returned for a follow-up visit several months later, I was shocked to see that she had lost her intended weight. With my tail between my legs, I decided to review the theories and science behind the use of CGM in patients without insulin resistance. 

Although it’s not rocket science, CGM can help patients through a “carrot and stick” approach to dieting. Lean proteins, nonstarchy vegetables, and monounsaturated fats such as nuts and avocado all support weight loss and tend to keep blood glucose levels stable. In contrast, foods known to cause weight gain (eg, sugary foods, refined starches, and processed foods) cause sugar spikes in real time. Similarly, large portion sizes are more likely to result in sugar spikes, and pairing proteins with carbohydrates minimizes blood glucose excursions. 

Though all of this is basic common sense, the constant feedback from a CGM device holds patients accountable for their food choices and helps with behavioral change. And because blood glucose is influenced by myriad factors including stress, genetics and metabolism, CGM can also potentially help create personal guidance for food choices. 

In addition, CGM can reveal the effect of poor sleep and stress on blood glucose levels, thereby encouraging healthier lifestyle choices. The data collected also may provide information on how different modalities of physical activity affect blood glucose levels. A recent study compared the effect of high-intensity interval training (HIIT) and continuous moderate-intensity exercise on postmeal blood glucose in overweight individuals without diabetes. CGM revealed that HIIT is more advantageous for preventing postmeal spikes. 

Although CGM appears to be a sophisticated form of cognitive-behavioral therapy, I do worry that the incessant stream of information can lead to worsening anxiety, obsessive compulsive behaviors, or restrictive eating tendencies. Still, thanks to Lauren, I now believe that real-time CGM may lead to behavior modification in food selection and physical activity. 
 

Dr. Messer, Clinical Assistant Professor, Mount Sinai School of Medicine; Associate Professor, Hofstra School of Medicine, New York, NY, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Lauren is a 45-year-old corporate lawyer who managed to excel in every aspect of her life, including parenting her three children while working full-time as a corporate lawyer. A math major at Harvard, she loves data.

Suffice it to say, given that I was treating her for a thyroid condition rather than diabetes, I was a little surprised when she requested I prescribe her a FreeStyle Libre (Abbott) monitor. She explained she was struggling to lose 10 pounds, and she thought continuous glucose monitoring (CGM) would help her determine which foods were impeding her weight loss journey. 

While I didn’t see much downside to acquiescing, I felt she had probably been spending too much time on Reddit. What information could CGM give someone without diabetes that couldn’t be gleaned from a food label? Nevertheless, Lauren filled the prescription and began her foray into this relatively uncharted world. When she returned for a follow-up visit several months later, I was shocked to see that she had lost her intended weight. With my tail between my legs, I decided to review the theories and science behind the use of CGM in patients without insulin resistance. 

Although it’s not rocket science, CGM can help patients through a “carrot and stick” approach to dieting. Lean proteins, nonstarchy vegetables, and monounsaturated fats such as nuts and avocado all support weight loss and tend to keep blood glucose levels stable. In contrast, foods known to cause weight gain (eg, sugary foods, refined starches, and processed foods) cause sugar spikes in real time. Similarly, large portion sizes are more likely to result in sugar spikes, and pairing proteins with carbohydrates minimizes blood glucose excursions. 

Though all of this is basic common sense, the constant feedback from a CGM device holds patients accountable for their food choices and helps with behavioral change. And because blood glucose is influenced by myriad factors including stress, genetics and metabolism, CGM can also potentially help create personal guidance for food choices. 

In addition, CGM can reveal the effect of poor sleep and stress on blood glucose levels, thereby encouraging healthier lifestyle choices. The data collected also may provide information on how different modalities of physical activity affect blood glucose levels. A recent study compared the effect of high-intensity interval training (HIIT) and continuous moderate-intensity exercise on postmeal blood glucose in overweight individuals without diabetes. CGM revealed that HIIT is more advantageous for preventing postmeal spikes. 

Although CGM appears to be a sophisticated form of cognitive-behavioral therapy, I do worry that the incessant stream of information can lead to worsening anxiety, obsessive compulsive behaviors, or restrictive eating tendencies. Still, thanks to Lauren, I now believe that real-time CGM may lead to behavior modification in food selection and physical activity. 
 

Dr. Messer, Clinical Assistant Professor, Mount Sinai School of Medicine; Associate Professor, Hofstra School of Medicine, New York, NY, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Lauren is a 45-year-old corporate lawyer who managed to excel in every aspect of her life, including parenting her three children while working full-time as a corporate lawyer. A math major at Harvard, she loves data.

Suffice it to say, given that I was treating her for a thyroid condition rather than diabetes, I was a little surprised when she requested I prescribe her a FreeStyle Libre (Abbott) monitor. She explained she was struggling to lose 10 pounds, and she thought continuous glucose monitoring (CGM) would help her determine which foods were impeding her weight loss journey. 

While I didn’t see much downside to acquiescing, I felt she had probably been spending too much time on Reddit. What information could CGM give someone without diabetes that couldn’t be gleaned from a food label? Nevertheless, Lauren filled the prescription and began her foray into this relatively uncharted world. When she returned for a follow-up visit several months later, I was shocked to see that she had lost her intended weight. With my tail between my legs, I decided to review the theories and science behind the use of CGM in patients without insulin resistance. 

Although it’s not rocket science, CGM can help patients through a “carrot and stick” approach to dieting. Lean proteins, nonstarchy vegetables, and monounsaturated fats such as nuts and avocado all support weight loss and tend to keep blood glucose levels stable. In contrast, foods known to cause weight gain (eg, sugary foods, refined starches, and processed foods) cause sugar spikes in real time. Similarly, large portion sizes are more likely to result in sugar spikes, and pairing proteins with carbohydrates minimizes blood glucose excursions. 

Though all of this is basic common sense, the constant feedback from a CGM device holds patients accountable for their food choices and helps with behavioral change. And because blood glucose is influenced by myriad factors including stress, genetics and metabolism, CGM can also potentially help create personal guidance for food choices. 

In addition, CGM can reveal the effect of poor sleep and stress on blood glucose levels, thereby encouraging healthier lifestyle choices. The data collected also may provide information on how different modalities of physical activity affect blood glucose levels. A recent study compared the effect of high-intensity interval training (HIIT) and continuous moderate-intensity exercise on postmeal blood glucose in overweight individuals without diabetes. CGM revealed that HIIT is more advantageous for preventing postmeal spikes. 

Although CGM appears to be a sophisticated form of cognitive-behavioral therapy, I do worry that the incessant stream of information can lead to worsening anxiety, obsessive compulsive behaviors, or restrictive eating tendencies. Still, thanks to Lauren, I now believe that real-time CGM may lead to behavior modification in food selection and physical activity. 
 

Dr. Messer, Clinical Assistant Professor, Mount Sinai School of Medicine; Associate Professor, Hofstra School of Medicine, New York, NY, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

When prescribing glucagon-like peptide 1 (GLP-1) medications, many physicians prefer tirzepatide over the more well-known semaglutide due to its superior efficacy in weight loss and A1c reduction. Studies indicated that tirzepatide can lead to greater weight loss than semaglutide.

Factors like insurance coverage, drug availability, and side effects also influence physicians’ choices, with some patients benefiting from the broader dosing options that tirzepatide offers.

In this Q&A, Medscape Medical News explored how physicians can make the best decisions with their patients when choosing between GLP-1 medications tirzepatide and semaglutide for the treatment for type 2 diabetes and obesity.

We spoke to physicians who specialize in medical weight loss on things to consider when choosing between these two medications, such as patient profiles, drug access and availability, and financial considerations. We also discussed the side effect profiles of the medications based on current data in the literature.
 

Medscape Medical News: How are you deciding which of the two drugs to prescribe?

Caroline Messer, MD, endocrinologist at Lenox Hill Hospital, Northwell, New York City: To some degree, it’s based on insurance. But in general, I’m pushing most patients toward tirzepatide just because the data show that there’s more weight loss and more A1c reduction on tirzepatide. But the research shows that there are more side effects. But I think every practicing clinician who uses these medications knows that there are actually fewer side effects despite what the trial showed.

Sue Decotiis, MD, weight loss doctor, New York City: I think that many doctors that are prescribing these drugs are not really weight loss specialists. It’s just like one of many drugs that they prescribe. And semaglutide (Ozempic) is more well known. I think it’s because they don’t really know that it’s not as good as the other drugs. There are still massive shortages of these drugs. So that’s another reason why a doctor may choose one drug over another. Also, if a patient’s reliant on insurance to cover it, they may go with whatever the insurance company is willing to cover.

Kathleen Dungan, MD, professor of internal medicine, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center and College of Medicine: Some patients may have preferences with the delivery device. In the past year, in particular, availability of these drugs was limited and varied from time to time and geographically, and therefore, patients needed to substitute one drug for another in order to maintain treatment.

Maria Teresa Anton, MD, endocrinologist and educator, Pritikin Longevity Center, Miami: While I do not prescribe these medications, I do focus on integrating them into a comprehensive lifestyle program that empowers patients to make sustainable changes. By fostering an environment of education and support, we enhance their well-being and promote long-term health outcomes. In my practice, I’ve found that the most successful outcomes occur when these medications are combined with a comprehensive approach, including dietary changes, physical activity, and behavioral support.
 

Medscape Medical News: How do you make the decision of tirzepatide vs semaglutide?

Messer: There’s no guideline per se. Sometimes when I don’t want a patient to lose too much weight, I might consider Ozempic or Wegovy if you know they only have 5 lb to lose. If diabetes, then I might go for the Ozempic instead, just because the weight loss is so drastic with tirzepatide with any kind of appetite.

Decotiis: If somebody has a lot of weight to lose and they’re highly insulin resistant, as most people are when they start these drugs, I really prefer tirzepatide ... because I think patients are going to lose more weight, they’re going to lose more fat. I also see that patients have less side effects because before tirzepatide came out, I was prescribing mostly semaglutide, and there were a lot of side effects. But semaglutide is fine. I mean, it’s a good drug. Maybe it’s better for people that don’t have as much weight to lose. So I don’t have to worry about them hitting that wall after a certain period of time. But it’s a good drug. I mean, I certainly still use it.
 

Medscape Medical News: What of the data and the literature on the differences in the outcomes and the side effect profile?

Messer: In terms of outcomes, the weight loss is almost double [with tirzepatide]. It depends what trial you’re looking at, but we tend to see like about 15% of your body weight you lose with the semaglutide and 25%-30% with the tirzepatide. The big difference, I suppose…is semaglutide now has a cardiovascular indication and the tirzepatide doesn’t, but I’m very confident that tirzepatide is going to get the same indication.

Decotiis: When that first Lilly study came out in June of 2022, it really blew everybody away. I mean, some patients lost up to 25% of their weight on tirzepatide, whereas on Ozempic, it was really like 15%. Now, in my practice, I really monitor everyone with a body composition scale. I’m not just looking at somebody’s weight or body mass index, I am looking at how much body fat they have, how much muscle mass they have, how much water they have, and how much bone they have.

The golden rule here is make sure the patient loses fat, and you want to make sure they’re not losing muscle or too much water. The patient really needs to be adequately hydrated. So what I’m saying is a lot of people who have lost weight have not reached the promised land because they haven’t lost enough body fat to get them into that healthy zone. But once they reduce the body fat to a certain percentage, let’s say for a woman about 20%, or a man in the low teens, they’re less likely to regain that weight because they haven’t really lost fat. And that’s how we gain health.
 

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

When prescribing glucagon-like peptide 1 (GLP-1) medications, many physicians prefer tirzepatide over the more well-known semaglutide due to its superior efficacy in weight loss and A1c reduction. Studies indicated that tirzepatide can lead to greater weight loss than semaglutide.

Factors like insurance coverage, drug availability, and side effects also influence physicians’ choices, with some patients benefiting from the broader dosing options that tirzepatide offers.

In this Q&A, Medscape Medical News explored how physicians can make the best decisions with their patients when choosing between GLP-1 medications tirzepatide and semaglutide for the treatment for type 2 diabetes and obesity.

We spoke to physicians who specialize in medical weight loss on things to consider when choosing between these two medications, such as patient profiles, drug access and availability, and financial considerations. We also discussed the side effect profiles of the medications based on current data in the literature.
 

Medscape Medical News: How are you deciding which of the two drugs to prescribe?

Caroline Messer, MD, endocrinologist at Lenox Hill Hospital, Northwell, New York City: To some degree, it’s based on insurance. But in general, I’m pushing most patients toward tirzepatide just because the data show that there’s more weight loss and more A1c reduction on tirzepatide. But the research shows that there are more side effects. But I think every practicing clinician who uses these medications knows that there are actually fewer side effects despite what the trial showed.

Sue Decotiis, MD, weight loss doctor, New York City: I think that many doctors that are prescribing these drugs are not really weight loss specialists. It’s just like one of many drugs that they prescribe. And semaglutide (Ozempic) is more well known. I think it’s because they don’t really know that it’s not as good as the other drugs. There are still massive shortages of these drugs. So that’s another reason why a doctor may choose one drug over another. Also, if a patient’s reliant on insurance to cover it, they may go with whatever the insurance company is willing to cover.

Kathleen Dungan, MD, professor of internal medicine, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center and College of Medicine: Some patients may have preferences with the delivery device. In the past year, in particular, availability of these drugs was limited and varied from time to time and geographically, and therefore, patients needed to substitute one drug for another in order to maintain treatment.

Maria Teresa Anton, MD, endocrinologist and educator, Pritikin Longevity Center, Miami: While I do not prescribe these medications, I do focus on integrating them into a comprehensive lifestyle program that empowers patients to make sustainable changes. By fostering an environment of education and support, we enhance their well-being and promote long-term health outcomes. In my practice, I’ve found that the most successful outcomes occur when these medications are combined with a comprehensive approach, including dietary changes, physical activity, and behavioral support.
 

Medscape Medical News: How do you make the decision of tirzepatide vs semaglutide?

Messer: There’s no guideline per se. Sometimes when I don’t want a patient to lose too much weight, I might consider Ozempic or Wegovy if you know they only have 5 lb to lose. If diabetes, then I might go for the Ozempic instead, just because the weight loss is so drastic with tirzepatide with any kind of appetite.

Decotiis: If somebody has a lot of weight to lose and they’re highly insulin resistant, as most people are when they start these drugs, I really prefer tirzepatide ... because I think patients are going to lose more weight, they’re going to lose more fat. I also see that patients have less side effects because before tirzepatide came out, I was prescribing mostly semaglutide, and there were a lot of side effects. But semaglutide is fine. I mean, it’s a good drug. Maybe it’s better for people that don’t have as much weight to lose. So I don’t have to worry about them hitting that wall after a certain period of time. But it’s a good drug. I mean, I certainly still use it.
 

Medscape Medical News: What of the data and the literature on the differences in the outcomes and the side effect profile?

Messer: In terms of outcomes, the weight loss is almost double [with tirzepatide]. It depends what trial you’re looking at, but we tend to see like about 15% of your body weight you lose with the semaglutide and 25%-30% with the tirzepatide. The big difference, I suppose…is semaglutide now has a cardiovascular indication and the tirzepatide doesn’t, but I’m very confident that tirzepatide is going to get the same indication.

Decotiis: When that first Lilly study came out in June of 2022, it really blew everybody away. I mean, some patients lost up to 25% of their weight on tirzepatide, whereas on Ozempic, it was really like 15%. Now, in my practice, I really monitor everyone with a body composition scale. I’m not just looking at somebody’s weight or body mass index, I am looking at how much body fat they have, how much muscle mass they have, how much water they have, and how much bone they have.

The golden rule here is make sure the patient loses fat, and you want to make sure they’re not losing muscle or too much water. The patient really needs to be adequately hydrated. So what I’m saying is a lot of people who have lost weight have not reached the promised land because they haven’t lost enough body fat to get them into that healthy zone. But once they reduce the body fat to a certain percentage, let’s say for a woman about 20%, or a man in the low teens, they’re less likely to regain that weight because they haven’t really lost fat. And that’s how we gain health.
 

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

When prescribing glucagon-like peptide 1 (GLP-1) medications, many physicians prefer tirzepatide over the more well-known semaglutide due to its superior efficacy in weight loss and A1c reduction. Studies indicated that tirzepatide can lead to greater weight loss than semaglutide.

Factors like insurance coverage, drug availability, and side effects also influence physicians’ choices, with some patients benefiting from the broader dosing options that tirzepatide offers.

In this Q&A, Medscape Medical News explored how physicians can make the best decisions with their patients when choosing between GLP-1 medications tirzepatide and semaglutide for the treatment for type 2 diabetes and obesity.

We spoke to physicians who specialize in medical weight loss on things to consider when choosing between these two medications, such as patient profiles, drug access and availability, and financial considerations. We also discussed the side effect profiles of the medications based on current data in the literature.
 

Medscape Medical News: How are you deciding which of the two drugs to prescribe?

Caroline Messer, MD, endocrinologist at Lenox Hill Hospital, Northwell, New York City: To some degree, it’s based on insurance. But in general, I’m pushing most patients toward tirzepatide just because the data show that there’s more weight loss and more A1c reduction on tirzepatide. But the research shows that there are more side effects. But I think every practicing clinician who uses these medications knows that there are actually fewer side effects despite what the trial showed.

Sue Decotiis, MD, weight loss doctor, New York City: I think that many doctors that are prescribing these drugs are not really weight loss specialists. It’s just like one of many drugs that they prescribe. And semaglutide (Ozempic) is more well known. I think it’s because they don’t really know that it’s not as good as the other drugs. There are still massive shortages of these drugs. So that’s another reason why a doctor may choose one drug over another. Also, if a patient’s reliant on insurance to cover it, they may go with whatever the insurance company is willing to cover.

Kathleen Dungan, MD, professor of internal medicine, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center and College of Medicine: Some patients may have preferences with the delivery device. In the past year, in particular, availability of these drugs was limited and varied from time to time and geographically, and therefore, patients needed to substitute one drug for another in order to maintain treatment.

Maria Teresa Anton, MD, endocrinologist and educator, Pritikin Longevity Center, Miami: While I do not prescribe these medications, I do focus on integrating them into a comprehensive lifestyle program that empowers patients to make sustainable changes. By fostering an environment of education and support, we enhance their well-being and promote long-term health outcomes. In my practice, I’ve found that the most successful outcomes occur when these medications are combined with a comprehensive approach, including dietary changes, physical activity, and behavioral support.
 

Medscape Medical News: How do you make the decision of tirzepatide vs semaglutide?

Messer: There’s no guideline per se. Sometimes when I don’t want a patient to lose too much weight, I might consider Ozempic or Wegovy if you know they only have 5 lb to lose. If diabetes, then I might go for the Ozempic instead, just because the weight loss is so drastic with tirzepatide with any kind of appetite.

Decotiis: If somebody has a lot of weight to lose and they’re highly insulin resistant, as most people are when they start these drugs, I really prefer tirzepatide ... because I think patients are going to lose more weight, they’re going to lose more fat. I also see that patients have less side effects because before tirzepatide came out, I was prescribing mostly semaglutide, and there were a lot of side effects. But semaglutide is fine. I mean, it’s a good drug. Maybe it’s better for people that don’t have as much weight to lose. So I don’t have to worry about them hitting that wall after a certain period of time. But it’s a good drug. I mean, I certainly still use it.
 

Medscape Medical News: What of the data and the literature on the differences in the outcomes and the side effect profile?

Messer: In terms of outcomes, the weight loss is almost double [with tirzepatide]. It depends what trial you’re looking at, but we tend to see like about 15% of your body weight you lose with the semaglutide and 25%-30% with the tirzepatide. The big difference, I suppose…is semaglutide now has a cardiovascular indication and the tirzepatide doesn’t, but I’m very confident that tirzepatide is going to get the same indication.

Decotiis: When that first Lilly study came out in June of 2022, it really blew everybody away. I mean, some patients lost up to 25% of their weight on tirzepatide, whereas on Ozempic, it was really like 15%. Now, in my practice, I really monitor everyone with a body composition scale. I’m not just looking at somebody’s weight or body mass index, I am looking at how much body fat they have, how much muscle mass they have, how much water they have, and how much bone they have.

The golden rule here is make sure the patient loses fat, and you want to make sure they’re not losing muscle or too much water. The patient really needs to be adequately hydrated. So what I’m saying is a lot of people who have lost weight have not reached the promised land because they haven’t lost enough body fat to get them into that healthy zone. But once they reduce the body fat to a certain percentage, let’s say for a woman about 20%, or a man in the low teens, they’re less likely to regain that weight because they haven’t really lost fat. And that’s how we gain health.
 

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

TOPLINE:

In healthy young adults, a single 30-minute bout of outdoor aerobic exercise significantly reduces fasting and 1-hour glucose levels during an oral glucose tolerance test (OGTT) the next day and improves insulin sensitivity.

METHODOLOGY:

• Recent studies have identified 1-hour post-load glucose concentration during an OGTT as a specific and early predictor of diabetes, and exercise has long been known for its metabolic benefits in people with and without diabetes.
• The researchers investigated the effect of a single bout of aerobic exercise on 1-hour post-load glucose levels during an OGTT in 32 young, healthy, normal-weight or marginally overweight individuals (mean age, 35 years; 14 women and 18 men) with a sedentary or moderately active lifestyle.
• The participants underwent an initial OGTT after at least 4 days of physical inactivity, followed by a second OGTT the day after a single 30-minute bout of aerobic exercise.
• The exercise session consisted of a light jog for 30 minutes, monitored using a metabolic holter to quantify energy expenditure and exercise intensity. The participants did not undertake any exercise outside the lab sessions.
• Blood glucose levels were measured, and insulin sensitivity and secretion were estimated using surrogate indices derived from OGTT glucose and insulin assays, including the Matsuda index, oral glucose insulin sensitivity (OGIS) index, and quantitative insulin sensitivity check index, as well as the homeostasis model assessment (HOMA) of insulin resistance and of beta-cell function (HOMA-B).

TAKEAWAY:

•  
• Postexercise insulin levels also were significantly lower 1 hour after glucose load, decreasing from 57.4 IU/mL at baseline to 43.5 IU/mL the day after exercise (P = .01).
• Insulin sensitivity improved significantly after exercise, as indicated by increases in the Matsuda index (P = .02) and OGIS index (P = .04), along with a reduction in insulin resistance (P = .04).
• The study found a trend toward increased beta-cell function the day after an exercise bout, as indicated by a nonsignificant increase in HOMA-B from 144.7 at baseline to 167.1 after exercise.

IN PRACTICE:

“Improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D [type 2 diabetes] risk and cardiovascular risk,” the authors wrote.

SOURCE:

The study was led by Simona Moffa, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, and Gian Pio Sorice, Università Degli Studi di Bari “Aldo Moro,” Bari, Italy. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

The study had a limited sample size, which may affect the generalizability of the findings. C-peptide levels, which could have provided additional insights into insulin secretion, were not assessed in the study.

DISCLOSURES:

The study was supported by grants from Università Cattolica del Sacro Cuore. The authors declared no conflicts of interest.
 

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

TOPLINE:

In healthy young adults, a single 30-minute bout of outdoor aerobic exercise significantly reduces fasting and 1-hour glucose levels during an oral glucose tolerance test (OGTT) the next day and improves insulin sensitivity.

METHODOLOGY:

• Recent studies have identified 1-hour post-load glucose concentration during an OGTT as a specific and early predictor of diabetes, and exercise has long been known for its metabolic benefits in people with and without diabetes.
• The researchers investigated the effect of a single bout of aerobic exercise on 1-hour post-load glucose levels during an OGTT in 32 young, healthy, normal-weight or marginally overweight individuals (mean age, 35 years; 14 women and 18 men) with a sedentary or moderately active lifestyle.
• The participants underwent an initial OGTT after at least 4 days of physical inactivity, followed by a second OGTT the day after a single 30-minute bout of aerobic exercise.
• The exercise session consisted of a light jog for 30 minutes, monitored using a metabolic holter to quantify energy expenditure and exercise intensity. The participants did not undertake any exercise outside the lab sessions.
• Blood glucose levels were measured, and insulin sensitivity and secretion were estimated using surrogate indices derived from OGTT glucose and insulin assays, including the Matsuda index, oral glucose insulin sensitivity (OGIS) index, and quantitative insulin sensitivity check index, as well as the homeostasis model assessment (HOMA) of insulin resistance and of beta-cell function (HOMA-B).

TAKEAWAY:

•  
• Postexercise insulin levels also were significantly lower 1 hour after glucose load, decreasing from 57.4 IU/mL at baseline to 43.5 IU/mL the day after exercise (P = .01).
• Insulin sensitivity improved significantly after exercise, as indicated by increases in the Matsuda index (P = .02) and OGIS index (P = .04), along with a reduction in insulin resistance (P = .04).
• The study found a trend toward increased beta-cell function the day after an exercise bout, as indicated by a nonsignificant increase in HOMA-B from 144.7 at baseline to 167.1 after exercise.

IN PRACTICE:

“Improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D [type 2 diabetes] risk and cardiovascular risk,” the authors wrote.

SOURCE:

The study was led by Simona Moffa, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, and Gian Pio Sorice, Università Degli Studi di Bari “Aldo Moro,” Bari, Italy. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

The study had a limited sample size, which may affect the generalizability of the findings. C-peptide levels, which could have provided additional insights into insulin secretion, were not assessed in the study.

DISCLOSURES:

The study was supported by grants from Università Cattolica del Sacro Cuore. The authors declared no conflicts of interest.
 

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

TOPLINE:

In healthy young adults, a single 30-minute bout of outdoor aerobic exercise significantly reduces fasting and 1-hour glucose levels during an oral glucose tolerance test (OGTT) the next day and improves insulin sensitivity.

METHODOLOGY:

• Recent studies have identified 1-hour post-load glucose concentration during an OGTT as a specific and early predictor of diabetes, and exercise has long been known for its metabolic benefits in people with and without diabetes.
• The researchers investigated the effect of a single bout of aerobic exercise on 1-hour post-load glucose levels during an OGTT in 32 young, healthy, normal-weight or marginally overweight individuals (mean age, 35 years; 14 women and 18 men) with a sedentary or moderately active lifestyle.
• The participants underwent an initial OGTT after at least 4 days of physical inactivity, followed by a second OGTT the day after a single 30-minute bout of aerobic exercise.
• The exercise session consisted of a light jog for 30 minutes, monitored using a metabolic holter to quantify energy expenditure and exercise intensity. The participants did not undertake any exercise outside the lab sessions.
• Blood glucose levels were measured, and insulin sensitivity and secretion were estimated using surrogate indices derived from OGTT glucose and insulin assays, including the Matsuda index, oral glucose insulin sensitivity (OGIS) index, and quantitative insulin sensitivity check index, as well as the homeostasis model assessment (HOMA) of insulin resistance and of beta-cell function (HOMA-B).

TAKEAWAY:

•  
• Postexercise insulin levels also were significantly lower 1 hour after glucose load, decreasing from 57.4 IU/mL at baseline to 43.5 IU/mL the day after exercise (P = .01).
• Insulin sensitivity improved significantly after exercise, as indicated by increases in the Matsuda index (P = .02) and OGIS index (P = .04), along with a reduction in insulin resistance (P = .04).
• The study found a trend toward increased beta-cell function the day after an exercise bout, as indicated by a nonsignificant increase in HOMA-B from 144.7 at baseline to 167.1 after exercise.

IN PRACTICE:

“Improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D [type 2 diabetes] risk and cardiovascular risk,” the authors wrote.

SOURCE:

The study was led by Simona Moffa, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, and Gian Pio Sorice, Università Degli Studi di Bari “Aldo Moro,” Bari, Italy. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

The study had a limited sample size, which may affect the generalizability of the findings. C-peptide levels, which could have provided additional insights into insulin secretion, were not assessed in the study.

DISCLOSURES:

The study was supported by grants from Università Cattolica del Sacro Cuore. The authors declared no conflicts of interest.
 

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

TOPLINE:

Patients who achieved an A1c level < 6.5% after metabolic bariatric surgery (MBS) maintained this target in the short and long terms, regardless of whether they continued or discontinued metformin after the procedure.

METHODOLOGY:

• MBS is effective in individuals with type 2 diabetes (T2D) and obesity, but the recommendations for managing patients who achieve diabetes remission after bariatric surgery are not clear.
• Researchers conducted a retrospective cohort study using electronic health records from Clalit Health Services in Israel to assess the association between metformin continuation after MBS and the short- and long-term relapse of diabetes (2 and 5 years after surgery, respectively).
• They included 366 patients (aged ≥ 24 years; body mass index [BMI], ≥ 30) with obesity and T2D who received metformin and achieved A1c levels < 6.5% for up to 6 months after MBS.
• Patients who continued metformin (n = 122; ≥ 3 filled prescriptions; mean follow-up, 5.3 years) were matched and compared with those who discontinued it (n = 244; 0 prescriptions; mean follow-up, 5.8 years) after MBS.
• The primary outcome was the long-term relapse of diabetes, defined by an A1c level ≥ 6.5% during the follow-up period, and the secondary outcomes were short- and long-term A1c levels, changes in BMI, and all-cause mortality.

TAKEAWAY:

• After adjustment for patient variables, no significant association was found between metformin continuation after MBS and risk for relapse of diabetes (adjusted hazard ratio, 1.65).
• Patients in both groups maintained mean A1c levels < 6.5% during the short- and long-term follow-up periods, showing that discontinuing metformin did not impede glycemic control.
• No significant differences were noted between patients who continued or discontinued metformin in terms of weight loss.
• The mortality rate was low in both the groups, with no substantial difference noted between the groups that continued metformin (4.1%) or discontinued metformin (2.5%).

IN PRACTICE:

“The lack of a significant association of metformin continuation with A1c level observed in the current study supports the notion that metformin may not have an additional benefit after MBS,” the authors wrote.

SOURCE:

This study was led by Dror Dicker, MD, Internal Medicine Department D and Obesity Clinic, Hasharon Hospital, Rabin Medical Center, Petah Tikva, Israel, and published online in Diabetes, Obesity and Metabolism.

LIMITATIONS: 

The observational nature of the study and the lack of randomization may have introduced residual confounding. The small number of patients remaining in the final study population limited the generalizability of the findings. The follow-up period of approximately 5 years may not have been sufficient to observe the long-term effects of metformin continuation.

DISCLOSURES:

The study received funding from Ariel University. Two authors disclosed receiving grants, personal fees, or nonfinancial support from various sources unrelated to this study.

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:

Patients who achieved an A1c level < 6.5% after metabolic bariatric surgery (MBS) maintained this target in the short and long terms, regardless of whether they continued or discontinued metformin after the procedure.

METHODOLOGY:

• MBS is effective in individuals with type 2 diabetes (T2D) and obesity, but the recommendations for managing patients who achieve diabetes remission after bariatric surgery are not clear.
• Researchers conducted a retrospective cohort study using electronic health records from Clalit Health Services in Israel to assess the association between metformin continuation after MBS and the short- and long-term relapse of diabetes (2 and 5 years after surgery, respectively).
• They included 366 patients (aged ≥ 24 years; body mass index [BMI], ≥ 30) with obesity and T2D who received metformin and achieved A1c levels < 6.5% for up to 6 months after MBS.
• Patients who continued metformin (n = 122; ≥ 3 filled prescriptions; mean follow-up, 5.3 years) were matched and compared with those who discontinued it (n = 244; 0 prescriptions; mean follow-up, 5.8 years) after MBS.
• The primary outcome was the long-term relapse of diabetes, defined by an A1c level ≥ 6.5% during the follow-up period, and the secondary outcomes were short- and long-term A1c levels, changes in BMI, and all-cause mortality.

TAKEAWAY:

• After adjustment for patient variables, no significant association was found between metformin continuation after MBS and risk for relapse of diabetes (adjusted hazard ratio, 1.65).
• Patients in both groups maintained mean A1c levels < 6.5% during the short- and long-term follow-up periods, showing that discontinuing metformin did not impede glycemic control.
• No significant differences were noted between patients who continued or discontinued metformin in terms of weight loss.
• The mortality rate was low in both the groups, with no substantial difference noted between the groups that continued metformin (4.1%) or discontinued metformin (2.5%).

IN PRACTICE:

“The lack of a significant association of metformin continuation with A1c level observed in the current study supports the notion that metformin may not have an additional benefit after MBS,” the authors wrote.

SOURCE:

This study was led by Dror Dicker, MD, Internal Medicine Department D and Obesity Clinic, Hasharon Hospital, Rabin Medical Center, Petah Tikva, Israel, and published online in Diabetes, Obesity and Metabolism.

LIMITATIONS: 

The observational nature of the study and the lack of randomization may have introduced residual confounding. The small number of patients remaining in the final study population limited the generalizability of the findings. The follow-up period of approximately 5 years may not have been sufficient to observe the long-term effects of metformin continuation.

DISCLOSURES:

The study received funding from Ariel University. Two authors disclosed receiving grants, personal fees, or nonfinancial support from various sources unrelated to this study.

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:

Patients who achieved an A1c level < 6.5% after metabolic bariatric surgery (MBS) maintained this target in the short and long terms, regardless of whether they continued or discontinued metformin after the procedure.

METHODOLOGY:

• MBS is effective in individuals with type 2 diabetes (T2D) and obesity, but the recommendations for managing patients who achieve diabetes remission after bariatric surgery are not clear.
• Researchers conducted a retrospective cohort study using electronic health records from Clalit Health Services in Israel to assess the association between metformin continuation after MBS and the short- and long-term relapse of diabetes (2 and 5 years after surgery, respectively).
• They included 366 patients (aged ≥ 24 years; body mass index [BMI], ≥ 30) with obesity and T2D who received metformin and achieved A1c levels < 6.5% for up to 6 months after MBS.
• Patients who continued metformin (n = 122; ≥ 3 filled prescriptions; mean follow-up, 5.3 years) were matched and compared with those who discontinued it (n = 244; 0 prescriptions; mean follow-up, 5.8 years) after MBS.
• The primary outcome was the long-term relapse of diabetes, defined by an A1c level ≥ 6.5% during the follow-up period, and the secondary outcomes were short- and long-term A1c levels, changes in BMI, and all-cause mortality.

TAKEAWAY:

• After adjustment for patient variables, no significant association was found between metformin continuation after MBS and risk for relapse of diabetes (adjusted hazard ratio, 1.65).
• Patients in both groups maintained mean A1c levels < 6.5% during the short- and long-term follow-up periods, showing that discontinuing metformin did not impede glycemic control.
• No significant differences were noted between patients who continued or discontinued metformin in terms of weight loss.
• The mortality rate was low in both the groups, with no substantial difference noted between the groups that continued metformin (4.1%) or discontinued metformin (2.5%).

IN PRACTICE:

“The lack of a significant association of metformin continuation with A1c level observed in the current study supports the notion that metformin may not have an additional benefit after MBS,” the authors wrote.

SOURCE:

This study was led by Dror Dicker, MD, Internal Medicine Department D and Obesity Clinic, Hasharon Hospital, Rabin Medical Center, Petah Tikva, Israel, and published online in Diabetes, Obesity and Metabolism.

LIMITATIONS: 

The observational nature of the study and the lack of randomization may have introduced residual confounding. The small number of patients remaining in the final study population limited the generalizability of the findings. The follow-up period of approximately 5 years may not have been sufficient to observe the long-term effects of metformin continuation.

DISCLOSURES:

The study received funding from Ariel University. Two authors disclosed receiving grants, personal fees, or nonfinancial support from various sources unrelated to this study.

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.