Obesity

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

The authors declared no conflicts of interest.
 

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

The authors declared no conflicts of interest.
 

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

The authors declared no conflicts of interest.
 

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

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

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

Why the Risks?

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

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

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

Common Errors

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

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

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

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

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

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

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

Why the Risks?

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

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

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

Common Errors

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

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

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

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

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

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

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

Why the Risks?

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

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

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

Common Errors

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

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

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

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

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

TOPLINE:

Higher energy intake and glycemic load in the late morning are associated with a lower risk for type 2 diabetes (T2D) in Hispanic/Latino adults.

METHODOLOGY:

• Glucose tolerance peaks in the morning and declines in the afternoon and evening in individuals without diabetes.
• Researchers conducted a prospective cohort study enrolling 8868 Hispanic/Latino adults (mean age, 38.7 years; 51.5% women) without diabetes across four US communities between 2008 and 2011, with a second clinic examination conducted between 2014 and 2017.
• Meal timing was categorized into five periods: Early morning (6:00-8:59 AM), late morning (9:00-11:59 AM), afternoon (12:00-5:59 PM), evening (6:00-11:59 PM), and night (0:00-5:59 AM).
• Participants’ energy intake and glycemic load for each period were assessed at baseline using two 24-hour dietary recalls.
• Incident diabetes was identified through annual follow-up calls or at the second clinic examination.

TAKEAWAY:

• Each 100-kcal increment in energy intake and 10-unit increment in glycemic load in the late morning was associated with a 6% and 7% lower risk for T2D, respectively (both P = .001), independent of total energy intake, diet quality, and other confounders.
• No such association was found between energy intake and glycemic load in early morning, afternoon, evening, or night meal timings and the risk for diabetes.
• Substituting 100 kcal of energy intake from the early morning, afternoon, or evening with late-morning equivalents was associated with a 5% lower risk for diabetes (all P < .05).
• Similarly, substituting 10 units of energy-adjusted glycemic load from the early morning, afternoon, or evening with late-morning equivalents yielded a 7%-9% lower risk for diabetes (all P < .05).

IN PRACTICE:

“Our findings further enhance the existing literature by demonstrating the potential long-term promise of eating in alignment with the diurnal rhythm of glucose tolerance for diabetes prevention,” the authors wrote.

SOURCE:

The study was led by Jin Dai, PhD, Fielding School of Public Health, University of California, Los Angeles. It was published online in Diabetes Care.

LIMITATIONS:

The study’s reliance on only two 24-hour self-reported dietary recalls may have introduced measurement error. Diabetes was self-reported, which may have led to outcome misclassification. The study’s relatively short follow-up time may have introduced reverse causation bias. As most patients had T2D, the findings predominately apply to this diabetes subtype. 

DISCLOSURES:

The study was supported by grants from the National Heart, Lung, and Blood Institute. The authors reported no conflicts of interest.

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

TOPLINE:

Higher energy intake and glycemic load in the late morning are associated with a lower risk for type 2 diabetes (T2D) in Hispanic/Latino adults.

METHODOLOGY:

• Glucose tolerance peaks in the morning and declines in the afternoon and evening in individuals without diabetes.
• Researchers conducted a prospective cohort study enrolling 8868 Hispanic/Latino adults (mean age, 38.7 years; 51.5% women) without diabetes across four US communities between 2008 and 2011, with a second clinic examination conducted between 2014 and 2017.
• Meal timing was categorized into five periods: Early morning (6:00-8:59 AM), late morning (9:00-11:59 AM), afternoon (12:00-5:59 PM), evening (6:00-11:59 PM), and night (0:00-5:59 AM).
• Participants’ energy intake and glycemic load for each period were assessed at baseline using two 24-hour dietary recalls.
• Incident diabetes was identified through annual follow-up calls or at the second clinic examination.

TAKEAWAY:

• Each 100-kcal increment in energy intake and 10-unit increment in glycemic load in the late morning was associated with a 6% and 7% lower risk for T2D, respectively (both P = .001), independent of total energy intake, diet quality, and other confounders.
• No such association was found between energy intake and glycemic load in early morning, afternoon, evening, or night meal timings and the risk for diabetes.
• Substituting 100 kcal of energy intake from the early morning, afternoon, or evening with late-morning equivalents was associated with a 5% lower risk for diabetes (all P < .05).
• Similarly, substituting 10 units of energy-adjusted glycemic load from the early morning, afternoon, or evening with late-morning equivalents yielded a 7%-9% lower risk for diabetes (all P < .05).

IN PRACTICE:

“Our findings further enhance the existing literature by demonstrating the potential long-term promise of eating in alignment with the diurnal rhythm of glucose tolerance for diabetes prevention,” the authors wrote.

SOURCE:

The study was led by Jin Dai, PhD, Fielding School of Public Health, University of California, Los Angeles. It was published online in Diabetes Care.

LIMITATIONS:

The study’s reliance on only two 24-hour self-reported dietary recalls may have introduced measurement error. Diabetes was self-reported, which may have led to outcome misclassification. The study’s relatively short follow-up time may have introduced reverse causation bias. As most patients had T2D, the findings predominately apply to this diabetes subtype. 

DISCLOSURES:

The study was supported by grants from the National Heart, Lung, and Blood Institute. The authors reported no conflicts of interest.

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

TOPLINE:

Higher energy intake and glycemic load in the late morning are associated with a lower risk for type 2 diabetes (T2D) in Hispanic/Latino adults.

METHODOLOGY:

• Glucose tolerance peaks in the morning and declines in the afternoon and evening in individuals without diabetes.
• Researchers conducted a prospective cohort study enrolling 8868 Hispanic/Latino adults (mean age, 38.7 years; 51.5% women) without diabetes across four US communities between 2008 and 2011, with a second clinic examination conducted between 2014 and 2017.
• Meal timing was categorized into five periods: Early morning (6:00-8:59 AM), late morning (9:00-11:59 AM), afternoon (12:00-5:59 PM), evening (6:00-11:59 PM), and night (0:00-5:59 AM).
• Participants’ energy intake and glycemic load for each period were assessed at baseline using two 24-hour dietary recalls.
• Incident diabetes was identified through annual follow-up calls or at the second clinic examination.

TAKEAWAY:

• Each 100-kcal increment in energy intake and 10-unit increment in glycemic load in the late morning was associated with a 6% and 7% lower risk for T2D, respectively (both P = .001), independent of total energy intake, diet quality, and other confounders.
• No such association was found between energy intake and glycemic load in early morning, afternoon, evening, or night meal timings and the risk for diabetes.
• Substituting 100 kcal of energy intake from the early morning, afternoon, or evening with late-morning equivalents was associated with a 5% lower risk for diabetes (all P < .05).
• Similarly, substituting 10 units of energy-adjusted glycemic load from the early morning, afternoon, or evening with late-morning equivalents yielded a 7%-9% lower risk for diabetes (all P < .05).

IN PRACTICE:

“Our findings further enhance the existing literature by demonstrating the potential long-term promise of eating in alignment with the diurnal rhythm of glucose tolerance for diabetes prevention,” the authors wrote.

SOURCE:

The study was led by Jin Dai, PhD, Fielding School of Public Health, University of California, Los Angeles. It was published online in Diabetes Care.

LIMITATIONS:

The study’s reliance on only two 24-hour self-reported dietary recalls may have introduced measurement error. Diabetes was self-reported, which may have led to outcome misclassification. The study’s relatively short follow-up time may have introduced reverse causation bias. As most patients had T2D, the findings predominately apply to this diabetes subtype. 

DISCLOSURES:

The study was supported by grants from the National Heart, Lung, and Blood Institute. The authors reported no conflicts of interest.

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

Eat as fast as you can whenever you can.

That was the med student mindset around food, as Catherine Harmon Toomer, MD, discovered during her school years. “Without a good system in place to counter that,” she explains, “unhealthy eating can get out of control, and that’s what happened to me.”

After med school, things got worse for Dr. Toomer. By her second year in practice as a family medicine physician, she’d gained a lot of weight and had been diagnosed with type 2 diabetes and cardiomyopathy. At 36, she went into congestive heart failure and was told she likely had 5 years to live.

A moment she described as “a huge wake-up call.”

Dr. Toomer is far from alone in her struggles to balance working in medicine and eating healthfully.

“Physicians face unique stresses because of the ubiquity of junk food in the clinical setting, easy use of food as a reward and stress reliever, and lack of time to create better wellness habits while counseling patients to do exactly that,” said John La Puma, MD, FACP, internist and cofounder of ChefMD and founder of Chef Clinic.

There is also the culture of medicine, which Dr. Toomer said looks down on self-care. “Even with break times, patient needs come before our own.” So, you sit down to eat, and there’s an emergency. Your clinic closes for lunch, but the phones still ring, and patients continue to email questions. Charting is also so time-consuming that “everything else gets put on the back burner.”

Sticking to a nutritious diet in this context can feel hopeless. But it isn’t. Really. Here are some doctor-tested, real-life ways you can nourish yourself while getting it all done.
 

Something Is Always Better Than Nothing

Sure, you might not be able to eat a balanced lunch or dinner while at work, conceded Amy Margulies, RD, LDN, owner of The Rebellious RD. But try to focus on the bigger picture and take small steps.

First, make sure you eat something, Ms. Margulies advised. “Skipping meals can lead to overeating later and negatively impact energy levels and concentration.”

Lisa Andrews, MEd, RD, LD, owner of Sound Bites Nutrition, recalled one of her patients, a gastrointestinal surgeon with reactive hypoglycemia and fatigue. “She was experiencing energy crashes mid-afternoon,” she said. It was only after starting to eat every 4-5 hours that her patient felt better.

Of course, this is easier said than done. “When you are running from one patient to the other and trying to keep on time with your schedule, there is very little time for eating and no time at all for cooking or even heating up food,” recalled Hélène Bertrand, MD, author of Low Back Pain: 3 Steps to Relief in 2 Minutes.

But during her 55 years as a family medicine physician, Dr. Bertrand found ways to improve (if not perfect) the situation. She lunched on nuts or seeds during the day or grabbed a 95% cacao chocolate bar — higher in antioxidants and lower in sugar than a candy bar.

If you don’t have time for breakfast, try drinking a complete protein shake while driving to work, Dr. Toomer recommended. “It’s not ideal, but it’s better than nothing.” Similarly, if the only way you’ll eat a high-protein, lower-carb snack like hummus is with potato chips, go for it, she said.

Basically, don’t be type A striving for perfection. Take good enough when you can and balance the rest when you have time.
 

Torpedo Temptation

From free treats in the break room to always-present pizza for residents, high-fat, high-sugar, low-nutrient fare is a constant temptation. “I worked with a physician who would bring a balanced lunch to work every day, then find whatever sweet was around for his afternoon treat,” recalled Ms. Margulies.“The cookies, cakes, and donuts were starting to add up — and stopping at one wasn’t working for him.”

What did work was Ms. Margulies’ suggestion to bring a single serving of dark chocolate and fruit to savor during a longer break. “Bringing your favorite treats in appropriate portions can help you stick with your plan throughout the day,” she explained, and you’ll have an easier time resisting what’s in the break room. “When you desire a treat, tell yourself you have what you need and don’t need to indulge in the ‘free food’ just because it’s there. You have power over your choices.”

How about tricking yourself into perceiving cherry tomatoes as treats? That might be unusual, but one of Dr. La Puma’s physician patients did just that, displaying the produce in a candy dish on his office counter. Not only did this strategy help remind him to snack healthfully, it also prompted his patients to ask about eating better, he said.
 

Preparation Is Still Underrated

Many people find meal prepping intimidating. But it doesn’t need to be complicated. For instance, try purchasing precut veggies, cooked chicken breasts, or other healthy convenience options. You can then combine them in packable containers to prep a few meals at a time. For less busy weeks, consider cooking the protein yourself and whipping up basic sauces (like pesto and vinaigrette) to jazz up your meals.

“I worked with a resident who was gaining weight each month,” recalled Ms. Margulies. “She would skip lunch, grab a random snack, then wait until she got home to eat anything she could find.”

Encouraged by Ms. Margulies, she prepared and portioned one or two balanced dinners each week, which she’d later reheat. She also bought fresh and dried fruit and high-protein snacks, keeping single servings in her car to eat on the way home.

Similarly, Jess DeGore, RD, LDN, CDCES, CHWC, a diabetes educator and owner of Dietitian Jess Nutrition, recalled an ob.gyn. client who constantly skipped meals and relied on vending machine snacks. To combat her resulting energy crashes, she followed Ms. DeGore’s advice to prep workday lunches (like quinoa salads) over the weekend and bring fruit and nut snacks to work.
 

Automate as Much as You Can

If healthy is already on hand, you’ll eat healthy, said Ms. Andrews. Build up a snack stash focusing on fiber and protein. Tote a lunch bag with a cooler pack if needed. Some suggestions:

• Oatmeal packets
• Individual Greek yogurt cups or drinkable yogurts
• Protein bars
• Protein shakes
• Fresh fruit
• Fresh veggie sticks
• Nuts, dried chickpeas, or edamame
• Trail mix
• Single servings of hummus, nut butter, or guacamole
• Dried seaweed snacks
• Whole grain crackers
• Hard-boiled eggs
• String cheese
• Peanut butter sandwich
• 95% cacao chocolate bar

Try a Meal Delivery Service

Meal delivery services can be pricey, but potentially worth the expense. By bringing meals or having them sent to your office, you won’t have to find time to go to the cafeteria and stand in line, noted Janese S. Laster, MD, an internal medicine, gastroenterology, obesity medicine, and nutrition physician and founder of Gut Theory Total Digestive Care. Instead, “you’ll have something to warm up and eat while writing notes or in between patients,” she said. Plus, “you won’t have an excuse to skip meals.”

Hydration Yes, Junk Drinks No

The following can be filed in the Doctors-Know-It-But-Don’t-Always-Do-It section: “Hunger can be mistaken for thirst,” said Ms. Margulies. “Staying hydrated will help you better assess whether you’re hungry or thirsty.” Choose water over soda or energy drinks, she added, to hydrate your body without unnecessary extra sugars, sugar substitutes, calories, caffeine, or sodium — all of which can affect how you feel.

Advocate for Your Health

Convincing your institution to make changes might be difficult or even impossible, but consider asking your workplace to implement initiatives like these to boost provider nutrition, suggested Jabe Brown, BHSc (Nat), founder of Melbourne Functional Medicine:

• Establish protected break times when doctors can step away from their duties to eat
• Add more nutritious cafeteria options, like salads, whole grains, and lean proteins
• Overhaul vending machine offerings
• Offer educational workshops on nutrition

Be Tenacious About Good Eating

For Dr. Toomer, that meant taking several years off from work to improve her health. After losing more than 100 pounds, she founded TOTAL Weight Care Institute to help other healthcare professionals follow in her footsteps.

For you, the path toward a healthier diet might be gradual — grabbing a more nutritious snack, spending an extra hour per week on food shopping or prep, remembering a water bottle. Whatever it looks like, make realistic lifestyle tweaks that work for you.

Maybe even try that apple-a-day thing.
 

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

Eat as fast as you can whenever you can.

That was the med student mindset around food, as Catherine Harmon Toomer, MD, discovered during her school years. “Without a good system in place to counter that,” she explains, “unhealthy eating can get out of control, and that’s what happened to me.”

After med school, things got worse for Dr. Toomer. By her second year in practice as a family medicine physician, she’d gained a lot of weight and had been diagnosed with type 2 diabetes and cardiomyopathy. At 36, she went into congestive heart failure and was told she likely had 5 years to live.

A moment she described as “a huge wake-up call.”

Dr. Toomer is far from alone in her struggles to balance working in medicine and eating healthfully.

“Physicians face unique stresses because of the ubiquity of junk food in the clinical setting, easy use of food as a reward and stress reliever, and lack of time to create better wellness habits while counseling patients to do exactly that,” said John La Puma, MD, FACP, internist and cofounder of ChefMD and founder of Chef Clinic.

There is also the culture of medicine, which Dr. Toomer said looks down on self-care. “Even with break times, patient needs come before our own.” So, you sit down to eat, and there’s an emergency. Your clinic closes for lunch, but the phones still ring, and patients continue to email questions. Charting is also so time-consuming that “everything else gets put on the back burner.”

Sticking to a nutritious diet in this context can feel hopeless. But it isn’t. Really. Here are some doctor-tested, real-life ways you can nourish yourself while getting it all done.
 

Something Is Always Better Than Nothing

Sure, you might not be able to eat a balanced lunch or dinner while at work, conceded Amy Margulies, RD, LDN, owner of The Rebellious RD. But try to focus on the bigger picture and take small steps.

First, make sure you eat something, Ms. Margulies advised. “Skipping meals can lead to overeating later and negatively impact energy levels and concentration.”

Lisa Andrews, MEd, RD, LD, owner of Sound Bites Nutrition, recalled one of her patients, a gastrointestinal surgeon with reactive hypoglycemia and fatigue. “She was experiencing energy crashes mid-afternoon,” she said. It was only after starting to eat every 4-5 hours that her patient felt better.

Of course, this is easier said than done. “When you are running from one patient to the other and trying to keep on time with your schedule, there is very little time for eating and no time at all for cooking or even heating up food,” recalled Hélène Bertrand, MD, author of Low Back Pain: 3 Steps to Relief in 2 Minutes.

But during her 55 years as a family medicine physician, Dr. Bertrand found ways to improve (if not perfect) the situation. She lunched on nuts or seeds during the day or grabbed a 95% cacao chocolate bar — higher in antioxidants and lower in sugar than a candy bar.

If you don’t have time for breakfast, try drinking a complete protein shake while driving to work, Dr. Toomer recommended. “It’s not ideal, but it’s better than nothing.” Similarly, if the only way you’ll eat a high-protein, lower-carb snack like hummus is with potato chips, go for it, she said.

Basically, don’t be type A striving for perfection. Take good enough when you can and balance the rest when you have time.
 

Torpedo Temptation

From free treats in the break room to always-present pizza for residents, high-fat, high-sugar, low-nutrient fare is a constant temptation. “I worked with a physician who would bring a balanced lunch to work every day, then find whatever sweet was around for his afternoon treat,” recalled Ms. Margulies.“The cookies, cakes, and donuts were starting to add up — and stopping at one wasn’t working for him.”

What did work was Ms. Margulies’ suggestion to bring a single serving of dark chocolate and fruit to savor during a longer break. “Bringing your favorite treats in appropriate portions can help you stick with your plan throughout the day,” she explained, and you’ll have an easier time resisting what’s in the break room. “When you desire a treat, tell yourself you have what you need and don’t need to indulge in the ‘free food’ just because it’s there. You have power over your choices.”

How about tricking yourself into perceiving cherry tomatoes as treats? That might be unusual, but one of Dr. La Puma’s physician patients did just that, displaying the produce in a candy dish on his office counter. Not only did this strategy help remind him to snack healthfully, it also prompted his patients to ask about eating better, he said.
 

Preparation Is Still Underrated

Many people find meal prepping intimidating. But it doesn’t need to be complicated. For instance, try purchasing precut veggies, cooked chicken breasts, or other healthy convenience options. You can then combine them in packable containers to prep a few meals at a time. For less busy weeks, consider cooking the protein yourself and whipping up basic sauces (like pesto and vinaigrette) to jazz up your meals.

“I worked with a resident who was gaining weight each month,” recalled Ms. Margulies. “She would skip lunch, grab a random snack, then wait until she got home to eat anything she could find.”

Encouraged by Ms. Margulies, she prepared and portioned one or two balanced dinners each week, which she’d later reheat. She also bought fresh and dried fruit and high-protein snacks, keeping single servings in her car to eat on the way home.

Similarly, Jess DeGore, RD, LDN, CDCES, CHWC, a diabetes educator and owner of Dietitian Jess Nutrition, recalled an ob.gyn. client who constantly skipped meals and relied on vending machine snacks. To combat her resulting energy crashes, she followed Ms. DeGore’s advice to prep workday lunches (like quinoa salads) over the weekend and bring fruit and nut snacks to work.
 

Automate as Much as You Can

If healthy is already on hand, you’ll eat healthy, said Ms. Andrews. Build up a snack stash focusing on fiber and protein. Tote a lunch bag with a cooler pack if needed. Some suggestions:

• Oatmeal packets
• Individual Greek yogurt cups or drinkable yogurts
• Protein bars
• Protein shakes
• Fresh fruit
• Fresh veggie sticks
• Nuts, dried chickpeas, or edamame
• Trail mix
• Single servings of hummus, nut butter, or guacamole
• Dried seaweed snacks
• Whole grain crackers
• Hard-boiled eggs
• String cheese
• Peanut butter sandwich
• 95% cacao chocolate bar

Try a Meal Delivery Service

Meal delivery services can be pricey, but potentially worth the expense. By bringing meals or having them sent to your office, you won’t have to find time to go to the cafeteria and stand in line, noted Janese S. Laster, MD, an internal medicine, gastroenterology, obesity medicine, and nutrition physician and founder of Gut Theory Total Digestive Care. Instead, “you’ll have something to warm up and eat while writing notes or in between patients,” she said. Plus, “you won’t have an excuse to skip meals.”

Hydration Yes, Junk Drinks No

The following can be filed in the Doctors-Know-It-But-Don’t-Always-Do-It section: “Hunger can be mistaken for thirst,” said Ms. Margulies. “Staying hydrated will help you better assess whether you’re hungry or thirsty.” Choose water over soda or energy drinks, she added, to hydrate your body without unnecessary extra sugars, sugar substitutes, calories, caffeine, or sodium — all of which can affect how you feel.

Advocate for Your Health

Convincing your institution to make changes might be difficult or even impossible, but consider asking your workplace to implement initiatives like these to boost provider nutrition, suggested Jabe Brown, BHSc (Nat), founder of Melbourne Functional Medicine:

• Establish protected break times when doctors can step away from their duties to eat
• Add more nutritious cafeteria options, like salads, whole grains, and lean proteins
• Overhaul vending machine offerings
• Offer educational workshops on nutrition

Be Tenacious About Good Eating

For Dr. Toomer, that meant taking several years off from work to improve her health. After losing more than 100 pounds, she founded TOTAL Weight Care Institute to help other healthcare professionals follow in her footsteps.

For you, the path toward a healthier diet might be gradual — grabbing a more nutritious snack, spending an extra hour per week on food shopping or prep, remembering a water bottle. Whatever it looks like, make realistic lifestyle tweaks that work for you.

Maybe even try that apple-a-day thing.
 

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

Eat as fast as you can whenever you can.

That was the med student mindset around food, as Catherine Harmon Toomer, MD, discovered during her school years. “Without a good system in place to counter that,” she explains, “unhealthy eating can get out of control, and that’s what happened to me.”

After med school, things got worse for Dr. Toomer. By her second year in practice as a family medicine physician, she’d gained a lot of weight and had been diagnosed with type 2 diabetes and cardiomyopathy. At 36, she went into congestive heart failure and was told she likely had 5 years to live.

A moment she described as “a huge wake-up call.”

Dr. Toomer is far from alone in her struggles to balance working in medicine and eating healthfully.

“Physicians face unique stresses because of the ubiquity of junk food in the clinical setting, easy use of food as a reward and stress reliever, and lack of time to create better wellness habits while counseling patients to do exactly that,” said John La Puma, MD, FACP, internist and cofounder of ChefMD and founder of Chef Clinic.

There is also the culture of medicine, which Dr. Toomer said looks down on self-care. “Even with break times, patient needs come before our own.” So, you sit down to eat, and there’s an emergency. Your clinic closes for lunch, but the phones still ring, and patients continue to email questions. Charting is also so time-consuming that “everything else gets put on the back burner.”

Sticking to a nutritious diet in this context can feel hopeless. But it isn’t. Really. Here are some doctor-tested, real-life ways you can nourish yourself while getting it all done.
 

Something Is Always Better Than Nothing

Sure, you might not be able to eat a balanced lunch or dinner while at work, conceded Amy Margulies, RD, LDN, owner of The Rebellious RD. But try to focus on the bigger picture and take small steps.

First, make sure you eat something, Ms. Margulies advised. “Skipping meals can lead to overeating later and negatively impact energy levels and concentration.”

Lisa Andrews, MEd, RD, LD, owner of Sound Bites Nutrition, recalled one of her patients, a gastrointestinal surgeon with reactive hypoglycemia and fatigue. “She was experiencing energy crashes mid-afternoon,” she said. It was only after starting to eat every 4-5 hours that her patient felt better.

Of course, this is easier said than done. “When you are running from one patient to the other and trying to keep on time with your schedule, there is very little time for eating and no time at all for cooking or even heating up food,” recalled Hélène Bertrand, MD, author of Low Back Pain: 3 Steps to Relief in 2 Minutes.

But during her 55 years as a family medicine physician, Dr. Bertrand found ways to improve (if not perfect) the situation. She lunched on nuts or seeds during the day or grabbed a 95% cacao chocolate bar — higher in antioxidants and lower in sugar than a candy bar.

If you don’t have time for breakfast, try drinking a complete protein shake while driving to work, Dr. Toomer recommended. “It’s not ideal, but it’s better than nothing.” Similarly, if the only way you’ll eat a high-protein, lower-carb snack like hummus is with potato chips, go for it, she said.

Basically, don’t be type A striving for perfection. Take good enough when you can and balance the rest when you have time.
 

Torpedo Temptation

From free treats in the break room to always-present pizza for residents, high-fat, high-sugar, low-nutrient fare is a constant temptation. “I worked with a physician who would bring a balanced lunch to work every day, then find whatever sweet was around for his afternoon treat,” recalled Ms. Margulies.“The cookies, cakes, and donuts were starting to add up — and stopping at one wasn’t working for him.”

What did work was Ms. Margulies’ suggestion to bring a single serving of dark chocolate and fruit to savor during a longer break. “Bringing your favorite treats in appropriate portions can help you stick with your plan throughout the day,” she explained, and you’ll have an easier time resisting what’s in the break room. “When you desire a treat, tell yourself you have what you need and don’t need to indulge in the ‘free food’ just because it’s there. You have power over your choices.”

How about tricking yourself into perceiving cherry tomatoes as treats? That might be unusual, but one of Dr. La Puma’s physician patients did just that, displaying the produce in a candy dish on his office counter. Not only did this strategy help remind him to snack healthfully, it also prompted his patients to ask about eating better, he said.
 

Preparation Is Still Underrated

Many people find meal prepping intimidating. But it doesn’t need to be complicated. For instance, try purchasing precut veggies, cooked chicken breasts, or other healthy convenience options. You can then combine them in packable containers to prep a few meals at a time. For less busy weeks, consider cooking the protein yourself and whipping up basic sauces (like pesto and vinaigrette) to jazz up your meals.

“I worked with a resident who was gaining weight each month,” recalled Ms. Margulies. “She would skip lunch, grab a random snack, then wait until she got home to eat anything she could find.”

Encouraged by Ms. Margulies, she prepared and portioned one or two balanced dinners each week, which she’d later reheat. She also bought fresh and dried fruit and high-protein snacks, keeping single servings in her car to eat on the way home.

Similarly, Jess DeGore, RD, LDN, CDCES, CHWC, a diabetes educator and owner of Dietitian Jess Nutrition, recalled an ob.gyn. client who constantly skipped meals and relied on vending machine snacks. To combat her resulting energy crashes, she followed Ms. DeGore’s advice to prep workday lunches (like quinoa salads) over the weekend and bring fruit and nut snacks to work.
 

Automate as Much as You Can

If healthy is already on hand, you’ll eat healthy, said Ms. Andrews. Build up a snack stash focusing on fiber and protein. Tote a lunch bag with a cooler pack if needed. Some suggestions:

• Oatmeal packets
• Individual Greek yogurt cups or drinkable yogurts
• Protein bars
• Protein shakes
• Fresh fruit
• Fresh veggie sticks
• Nuts, dried chickpeas, or edamame
• Trail mix
• Single servings of hummus, nut butter, or guacamole
• Dried seaweed snacks
• Whole grain crackers
• Hard-boiled eggs
• String cheese
• Peanut butter sandwich
• 95% cacao chocolate bar

Try a Meal Delivery Service

Meal delivery services can be pricey, but potentially worth the expense. By bringing meals or having them sent to your office, you won’t have to find time to go to the cafeteria and stand in line, noted Janese S. Laster, MD, an internal medicine, gastroenterology, obesity medicine, and nutrition physician and founder of Gut Theory Total Digestive Care. Instead, “you’ll have something to warm up and eat while writing notes or in between patients,” she said. Plus, “you won’t have an excuse to skip meals.”

Hydration Yes, Junk Drinks No

The following can be filed in the Doctors-Know-It-But-Don’t-Always-Do-It section: “Hunger can be mistaken for thirst,” said Ms. Margulies. “Staying hydrated will help you better assess whether you’re hungry or thirsty.” Choose water over soda or energy drinks, she added, to hydrate your body without unnecessary extra sugars, sugar substitutes, calories, caffeine, or sodium — all of which can affect how you feel.

Advocate for Your Health

Convincing your institution to make changes might be difficult or even impossible, but consider asking your workplace to implement initiatives like these to boost provider nutrition, suggested Jabe Brown, BHSc (Nat), founder of Melbourne Functional Medicine:

• Establish protected break times when doctors can step away from their duties to eat
• Add more nutritious cafeteria options, like salads, whole grains, and lean proteins
• Overhaul vending machine offerings
• Offer educational workshops on nutrition

Be Tenacious About Good Eating

For Dr. Toomer, that meant taking several years off from work to improve her health. After losing more than 100 pounds, she founded TOTAL Weight Care Institute to help other healthcare professionals follow in her footsteps.

For you, the path toward a healthier diet might be gradual — grabbing a more nutritious snack, spending an extra hour per week on food shopping or prep, remembering a water bottle. Whatever it looks like, make realistic lifestyle tweaks that work for you.

Maybe even try that apple-a-day thing.
 

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

An intermittent fasting (IF) diet and a standard healthy living (HL) diet focused on healthy foods both lead to weight loss, reduced insulin resistance (IR), and slowed brain aging in older overweight adults with IR, new research showed. However, neither diet has an effect on Alzheimer’s disease (AD) biomarkers.

Although investigators found both diets were beneficial, some outcomes were more robust with the IF diet.

“The study provides a blueprint for assessing brain effects of dietary interventions and motivates further research on intermittent fasting and continuous diets for brain health optimization,” wrote the investigators, led by Dimitrios Kapogiannis, MD, chief, human neuroscience section, National Institute on Aging, and adjunct associate professor of neurology, the Johns Hopkins University School of Medicine.

The findings were published online in Cell Metabolism.
 

Cognitive Outcomes

The prevalence of IR — reduced cellular sensitivity to insulin that’s a hallmark of type 2 diabetes — increases with age and obesity, adding to an increased risk for accelerated brain aging as well as AD and related dementias (ADRD) in older adults who have overweight.

Studies reported healthy diets promote overall health, but it’s unclear whether, and to what extent, they improve brain health beyond general health enhancement.

Researchers used multiple brain and cognitive measures to assess dietary effects on brain health, including peripherally harvested neuron-derived extracellular vesicles (NDEVs) to probe neuronal insulin signaling; MRI to investigate the pace of brain aging; magnetic resonance spectroscopy (MRS) to measure brain glucose, metabolites, and neurotransmitters; and NDEVs and cerebrospinal fluid to derive biomarkers for AD/ADRD.

The study included 40 cognitively intact overweight participants with IR, mean age 63.2 years, 60% women, and 62.5% White. Their mean body weight was 97.1 kg and mean body mass index (BMI) was 34.4.

Participants were randomly assigned to 8 weeks of an IF diet or a HL diet that emphasizes fruits, vegetables, whole grains, lean proteins, and low-fat dairy and limits added sugars, saturated fats, and sodium.

The IF diet involved following the HL diet for 5 days per week and restricting calories to a quarter of the recommended daily intake for 2 consecutive days.

Both diets reduced neuronal IR and had comparable effects in improving insulin signaling biomarkers in NDEVs, reducing brain glucose on MRS, and improving blood biomarkers of carbohydrate and lipid metabolism.

Using MRI, researchers also assessed brain age, an indication of whether the brain appears older or younger than an individual’s chronological age. There was a decrease of 2.63 years with the IF diet (P = .05) and 2.42 years with the HL diet (P < .001) in the anterior cingulate and ventromedial prefrontal cortex.

Both diets improved executive function and memory, with those following the IF diet benefiting more in strategic planning, switching between two cognitively demanding tasks, cued recall, and other areas.
 

Hypothesis-Generating Research

AD biomarkers including amyloid beta 42 (Aß42), Aß40, and plasma phosphorylated-tau181 did not change with either diet, a finding that investigators speculated may be due to the short duration of the study. Light-chain neurofilaments increased across groups with no differences between the diets.

In other findings, BMI decreased by 1.41 with the IF diet and by 0.80 with the HL diet, and a similar pattern was observed for weight. Waist circumference decreased in both groups with no significant differences between diets.

An exploratory analysis showed executive function improved with the IF diet but not with the HL diet in women, whereas it improved with both diets in men. BMI and apolipoprotein E and SLC16A7 genotypes also modulated diet effects.

Both diets were well tolerated. The most frequent adverse events were gastrointestinal and occurred only with the IF diet.

The authors noted the findings are preliminary and results are hypothesis generating. Study limitations included the study’s short duration and its power to detect anything other than large to moderate effect size changes and differences between the diets. Researchers also didn’t acquire data on dietary intake, so lapses in adherence can’t be excluded. However, the large decreases in BMI, weight, and waist circumference with both diets indicated high adherence.

The study was supported by the National Institutes of Health’s National Institute on Aging. The authors reported no competing interests.
 

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

An intermittent fasting (IF) diet and a standard healthy living (HL) diet focused on healthy foods both lead to weight loss, reduced insulin resistance (IR), and slowed brain aging in older overweight adults with IR, new research showed. However, neither diet has an effect on Alzheimer’s disease (AD) biomarkers.

Although investigators found both diets were beneficial, some outcomes were more robust with the IF diet.

“The study provides a blueprint for assessing brain effects of dietary interventions and motivates further research on intermittent fasting and continuous diets for brain health optimization,” wrote the investigators, led by Dimitrios Kapogiannis, MD, chief, human neuroscience section, National Institute on Aging, and adjunct associate professor of neurology, the Johns Hopkins University School of Medicine.

The findings were published online in Cell Metabolism.
 

Cognitive Outcomes

The prevalence of IR — reduced cellular sensitivity to insulin that’s a hallmark of type 2 diabetes — increases with age and obesity, adding to an increased risk for accelerated brain aging as well as AD and related dementias (ADRD) in older adults who have overweight.

Studies reported healthy diets promote overall health, but it’s unclear whether, and to what extent, they improve brain health beyond general health enhancement.

Researchers used multiple brain and cognitive measures to assess dietary effects on brain health, including peripherally harvested neuron-derived extracellular vesicles (NDEVs) to probe neuronal insulin signaling; MRI to investigate the pace of brain aging; magnetic resonance spectroscopy (MRS) to measure brain glucose, metabolites, and neurotransmitters; and NDEVs and cerebrospinal fluid to derive biomarkers for AD/ADRD.

The study included 40 cognitively intact overweight participants with IR, mean age 63.2 years, 60% women, and 62.5% White. Their mean body weight was 97.1 kg and mean body mass index (BMI) was 34.4.

Participants were randomly assigned to 8 weeks of an IF diet or a HL diet that emphasizes fruits, vegetables, whole grains, lean proteins, and low-fat dairy and limits added sugars, saturated fats, and sodium.

The IF diet involved following the HL diet for 5 days per week and restricting calories to a quarter of the recommended daily intake for 2 consecutive days.

Both diets reduced neuronal IR and had comparable effects in improving insulin signaling biomarkers in NDEVs, reducing brain glucose on MRS, and improving blood biomarkers of carbohydrate and lipid metabolism.

Using MRI, researchers also assessed brain age, an indication of whether the brain appears older or younger than an individual’s chronological age. There was a decrease of 2.63 years with the IF diet (P = .05) and 2.42 years with the HL diet (P < .001) in the anterior cingulate and ventromedial prefrontal cortex.

Both diets improved executive function and memory, with those following the IF diet benefiting more in strategic planning, switching between two cognitively demanding tasks, cued recall, and other areas.
 

Hypothesis-Generating Research

AD biomarkers including amyloid beta 42 (Aß42), Aß40, and plasma phosphorylated-tau181 did not change with either diet, a finding that investigators speculated may be due to the short duration of the study. Light-chain neurofilaments increased across groups with no differences between the diets.

In other findings, BMI decreased by 1.41 with the IF diet and by 0.80 with the HL diet, and a similar pattern was observed for weight. Waist circumference decreased in both groups with no significant differences between diets.

An exploratory analysis showed executive function improved with the IF diet but not with the HL diet in women, whereas it improved with both diets in men. BMI and apolipoprotein E and SLC16A7 genotypes also modulated diet effects.

Both diets were well tolerated. The most frequent adverse events were gastrointestinal and occurred only with the IF diet.

The authors noted the findings are preliminary and results are hypothesis generating. Study limitations included the study’s short duration and its power to detect anything other than large to moderate effect size changes and differences between the diets. Researchers also didn’t acquire data on dietary intake, so lapses in adherence can’t be excluded. However, the large decreases in BMI, weight, and waist circumference with both diets indicated high adherence.

The study was supported by the National Institutes of Health’s National Institute on Aging. The authors reported no competing interests.
 

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

An intermittent fasting (IF) diet and a standard healthy living (HL) diet focused on healthy foods both lead to weight loss, reduced insulin resistance (IR), and slowed brain aging in older overweight adults with IR, new research showed. However, neither diet has an effect on Alzheimer’s disease (AD) biomarkers.

Although investigators found both diets were beneficial, some outcomes were more robust with the IF diet.

“The study provides a blueprint for assessing brain effects of dietary interventions and motivates further research on intermittent fasting and continuous diets for brain health optimization,” wrote the investigators, led by Dimitrios Kapogiannis, MD, chief, human neuroscience section, National Institute on Aging, and adjunct associate professor of neurology, the Johns Hopkins University School of Medicine.

The findings were published online in Cell Metabolism.
 

Cognitive Outcomes

The prevalence of IR — reduced cellular sensitivity to insulin that’s a hallmark of type 2 diabetes — increases with age and obesity, adding to an increased risk for accelerated brain aging as well as AD and related dementias (ADRD) in older adults who have overweight.

Studies reported healthy diets promote overall health, but it’s unclear whether, and to what extent, they improve brain health beyond general health enhancement.

Researchers used multiple brain and cognitive measures to assess dietary effects on brain health, including peripherally harvested neuron-derived extracellular vesicles (NDEVs) to probe neuronal insulin signaling; MRI to investigate the pace of brain aging; magnetic resonance spectroscopy (MRS) to measure brain glucose, metabolites, and neurotransmitters; and NDEVs and cerebrospinal fluid to derive biomarkers for AD/ADRD.

The study included 40 cognitively intact overweight participants with IR, mean age 63.2 years, 60% women, and 62.5% White. Their mean body weight was 97.1 kg and mean body mass index (BMI) was 34.4.

Participants were randomly assigned to 8 weeks of an IF diet or a HL diet that emphasizes fruits, vegetables, whole grains, lean proteins, and low-fat dairy and limits added sugars, saturated fats, and sodium.

The IF diet involved following the HL diet for 5 days per week and restricting calories to a quarter of the recommended daily intake for 2 consecutive days.

Both diets reduced neuronal IR and had comparable effects in improving insulin signaling biomarkers in NDEVs, reducing brain glucose on MRS, and improving blood biomarkers of carbohydrate and lipid metabolism.

Using MRI, researchers also assessed brain age, an indication of whether the brain appears older or younger than an individual’s chronological age. There was a decrease of 2.63 years with the IF diet (P = .05) and 2.42 years with the HL diet (P < .001) in the anterior cingulate and ventromedial prefrontal cortex.

Both diets improved executive function and memory, with those following the IF diet benefiting more in strategic planning, switching between two cognitively demanding tasks, cued recall, and other areas.
 

Hypothesis-Generating Research

AD biomarkers including amyloid beta 42 (Aß42), Aß40, and plasma phosphorylated-tau181 did not change with either diet, a finding that investigators speculated may be due to the short duration of the study. Light-chain neurofilaments increased across groups with no differences between the diets.

In other findings, BMI decreased by 1.41 with the IF diet and by 0.80 with the HL diet, and a similar pattern was observed for weight. Waist circumference decreased in both groups with no significant differences between diets.

An exploratory analysis showed executive function improved with the IF diet but not with the HL diet in women, whereas it improved with both diets in men. BMI and apolipoprotein E and SLC16A7 genotypes also modulated diet effects.

Both diets were well tolerated. The most frequent adverse events were gastrointestinal and occurred only with the IF diet.

The authors noted the findings are preliminary and results are hypothesis generating. Study limitations included the study’s short duration and its power to detect anything other than large to moderate effect size changes and differences between the diets. Researchers also didn’t acquire data on dietary intake, so lapses in adherence can’t be excluded. However, the large decreases in BMI, weight, and waist circumference with both diets indicated high adherence.

The study was supported by the National Institutes of Health’s National Institute on Aging. The authors reported no competing interests.
 

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

TOPLINE:

Mental health disorders increase the likelihood of developing chronic diabetic complications and vice versa across all age groups in patients with type 1 diabetes (T1D) or type 2 diabetes (T2D).

METHODOLOGY:

• Understanding the relative timing and association between chronic diabetic complications and mental health disorders may aid in improving diabetes screening and care.
• Researchers used a US national healthcare claims database (data obtained from 2001 to 2018) to analyze individuals with and without T1D and T2D, who had no prior mental health disorder or chronic diabetic complication.
• The onset and presence of chronic diabetic complications and mental health disorders were identified to determine their possible association.
• Individuals were stratified by age: 0-19, 20-39, 40-59, and ≥ 60 years.

TAKEAWAY:

• Researchers analyzed 44,735 patients with T1D (47.5% women) and 152,187 with T2D (46.0% women), who were matched with 356,630 individuals without diabetes (51.8% women).
• The presence of chronic diabetic complications increased the risk for a mental health disorder across all age groups, with the highest risk seen in patients aged ≥ 60 years (hazard ratio [HR], 2.9).
• Similarly, diagnosis of a mental health disorder increased the risk for chronic diabetic complications across all age groups, with the highest risk seen in patients aged 0-19 years (HR, 2.5).
• Patients with T2D had a significantly higher risk for a mental health disorder and a lower risk for chronic diabetic complications than those with T1D across all age groups, except those aged ≥ 60 years.
• The bidirectional association between mental health disorders and chronic diabetic complications was not affected by the diabetes type (P > .05 for all interactions).

IN PRACTICE:

“Clinicians and healthcare systems likely need to increase their focus on MHDs [mental health disorders], and innovative models of care are required to optimize care for both individuals with type 1 diabetes and those with type 2 diabetes,” the authors wrote.

SOURCE:

The study, led by Maya Watanabe, Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, was published online in Diabetes Care.

LIMITATIONS:

The study relied on International Classification of Diseases 9th and 10th revision codes, which might have led to misclassification of mental health conditions, chronic diabetes complications, and diabetes type. The data did not capture the symptom onset and severity. The findings may not be generalizable to populations outside the United States.

DISCLOSURES:

The study was supported by the Juvenile Diabetes Research Foundation (now Breakthrough T1D). Some authors reported receiving speaker or expert testimony honoraria and research support, and some declared serving on medical or digital advisory boards or as consultants for various pharmaceutical and medical device companies.

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

TOPLINE:

Mental health disorders increase the likelihood of developing chronic diabetic complications and vice versa across all age groups in patients with type 1 diabetes (T1D) or type 2 diabetes (T2D).

METHODOLOGY:

• Understanding the relative timing and association between chronic diabetic complications and mental health disorders may aid in improving diabetes screening and care.
• Researchers used a US national healthcare claims database (data obtained from 2001 to 2018) to analyze individuals with and without T1D and T2D, who had no prior mental health disorder or chronic diabetic complication.
• The onset and presence of chronic diabetic complications and mental health disorders were identified to determine their possible association.
• Individuals were stratified by age: 0-19, 20-39, 40-59, and ≥ 60 years.

TAKEAWAY:

• Researchers analyzed 44,735 patients with T1D (47.5% women) and 152,187 with T2D (46.0% women), who were matched with 356,630 individuals without diabetes (51.8% women).
• The presence of chronic diabetic complications increased the risk for a mental health disorder across all age groups, with the highest risk seen in patients aged ≥ 60 years (hazard ratio [HR], 2.9).
• Similarly, diagnosis of a mental health disorder increased the risk for chronic diabetic complications across all age groups, with the highest risk seen in patients aged 0-19 years (HR, 2.5).
• Patients with T2D had a significantly higher risk for a mental health disorder and a lower risk for chronic diabetic complications than those with T1D across all age groups, except those aged ≥ 60 years.
• The bidirectional association between mental health disorders and chronic diabetic complications was not affected by the diabetes type (P > .05 for all interactions).

IN PRACTICE:

“Clinicians and healthcare systems likely need to increase their focus on MHDs [mental health disorders], and innovative models of care are required to optimize care for both individuals with type 1 diabetes and those with type 2 diabetes,” the authors wrote.

SOURCE:

The study, led by Maya Watanabe, Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, was published online in Diabetes Care.

LIMITATIONS:

The study relied on International Classification of Diseases 9th and 10th revision codes, which might have led to misclassification of mental health conditions, chronic diabetes complications, and diabetes type. The data did not capture the symptom onset and severity. The findings may not be generalizable to populations outside the United States.

DISCLOSURES:

The study was supported by the Juvenile Diabetes Research Foundation (now Breakthrough T1D). Some authors reported receiving speaker or expert testimony honoraria and research support, and some declared serving on medical or digital advisory boards or as consultants for various pharmaceutical and medical device companies.

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

TOPLINE:

Mental health disorders increase the likelihood of developing chronic diabetic complications and vice versa across all age groups in patients with type 1 diabetes (T1D) or type 2 diabetes (T2D).

METHODOLOGY:

• Understanding the relative timing and association between chronic diabetic complications and mental health disorders may aid in improving diabetes screening and care.
• Researchers used a US national healthcare claims database (data obtained from 2001 to 2018) to analyze individuals with and without T1D and T2D, who had no prior mental health disorder or chronic diabetic complication.
• The onset and presence of chronic diabetic complications and mental health disorders were identified to determine their possible association.
• Individuals were stratified by age: 0-19, 20-39, 40-59, and ≥ 60 years.

TAKEAWAY:

• Researchers analyzed 44,735 patients with T1D (47.5% women) and 152,187 with T2D (46.0% women), who were matched with 356,630 individuals without diabetes (51.8% women).
• The presence of chronic diabetic complications increased the risk for a mental health disorder across all age groups, with the highest risk seen in patients aged ≥ 60 years (hazard ratio [HR], 2.9).
• Similarly, diagnosis of a mental health disorder increased the risk for chronic diabetic complications across all age groups, with the highest risk seen in patients aged 0-19 years (HR, 2.5).
• Patients with T2D had a significantly higher risk for a mental health disorder and a lower risk for chronic diabetic complications than those with T1D across all age groups, except those aged ≥ 60 years.
• The bidirectional association between mental health disorders and chronic diabetic complications was not affected by the diabetes type (P > .05 for all interactions).

IN PRACTICE:

“Clinicians and healthcare systems likely need to increase their focus on MHDs [mental health disorders], and innovative models of care are required to optimize care for both individuals with type 1 diabetes and those with type 2 diabetes,” the authors wrote.

SOURCE:

The study, led by Maya Watanabe, Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, was published online in Diabetes Care.

LIMITATIONS:

The study relied on International Classification of Diseases 9th and 10th revision codes, which might have led to misclassification of mental health conditions, chronic diabetes complications, and diabetes type. The data did not capture the symptom onset and severity. The findings may not be generalizable to populations outside the United States.

DISCLOSURES:

The study was supported by the Juvenile Diabetes Research Foundation (now Breakthrough T1D). Some authors reported receiving speaker or expert testimony honoraria and research support, and some declared serving on medical or digital advisory boards or as consultants for various pharmaceutical and medical device companies.

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

The health consequences of excess visceral fat tissue are well known. But there is another type of fat accumulation in the body that increases the risk for type 2 diabetes and cardiovascular diseases. In Molecular Aspects of Medicine, researchers warned that the dangers arising from intramuscular fat tissue are often underestimated.

“Everyone knows the dangers of abdominal fat or that the deposition of fat in the coronary arteries can cause a heart attack,” said lead author Osvaldo Contreras, PhD, from the School of Clinical Medicine at the University of New South Wales in Sydney, Australia. “But hardly anyone has ever heard of fat accumulation in skeletal muscles, even though they are associated with a whole range of life-threatening diseases.” 

“The work emphasizes that muscles are not only good for standing, walking, or lifting a box. They are metabolically active, produce hormones, communicate in the body, and can positively or negatively affect a person’s health,” Yurdagül Zopf, MD, PhD, professor of integrative medicine specializing in nutritional medicine and director of the Hector Center for Nutrition, Exercise, and Sports at the University Hospital Erlangen, Erlangen, Germany, said in an interview.
 

Associated With Diseases

Increased intramuscular fat is found in various conditions where muscle mass is increasingly lost and replaced by fat and connective tissue. Intramuscular fat has been observed, for example, in patients with chronic muscle diseases, sarcopenia, hormonal disorders, and metabolic diseases such as insulin resistance and type 2 diabetes, as well as in patients with cardiovascular problems such as hypertension and heart failure.

Fat accumulation in the muscles, like all fat deposits in the body, can result from an unhealthy lifestyle with excessive calorie intake and, especially, lack of exercise. “If the body has more energy available than it can use, it will initially store it as subcutaneous fat,” said Dr. Zopf. “Once these storage capacities are depleted, more and more visceral fat is deposited, and then more and more fat is stored in the organs and the muscles.”

Movement plays a particularly important role in intramuscular fat. “We know that the less physically active someone is, the higher the risk that fat will be stored in the muscles,” said Dr. Zopf.
 

Arising From Injuries

Unlike other fat tissues in the body, intramuscular fat can also accumulate in higher amounts when there are injuries to the muscles. The group led by Dr. Contreras and lead author Marcelo Flores-Opazo from the Universidad de O’Higgins in Rancagua, Chile, emphasized the role of fibroadipogenic progenitor (FAP) cells in their review. “FAPs play a crucial role in preserving and repairing muscle tissue injuries. They can differentiate into fibroblasts and adipocytes and are responsible for depositing fat and connective tissue in response to muscle injuries.”

Studies suggest that exercise can prevent FAPs from differentiating into fat and connective tissue cells. Metformin can achieve a similar effect in vitro. Dr. Contreras and colleagues hope that drug-based ways to reduce muscle fat will emerge in the future.

But how do you determine whether a patient has too much intramuscular fat? Although MRI and CT can be used for quantification, these are not routine examinations. There is currently no simple way to determine the fat content in muscles, according to the authors. The study authors hope that advances in molecular testing, imaging, and biopsies will improve diagnostic capabilities in the future.
 

Training Crucial

Until then, Dr. Contreras and colleagues advise close monitoring of one’s body weight and the maintenance of a healthy lifestyle. Excessive fat accumulation in the muscles can be prevented and reversed through adequate exercise and healthy nutrition, they emphasized. 

The important message is that these measures are possible. “With healthy nutrition and exercise, excess fat can be reduced. We have observed a reduction in muscle fat in obese individuals with just two sessions of 15-minute high-intensity workouts per week,” Dr. Zopf reported, citing her own research. The more obese a person is and the higher the inflammation in the body, the more likely additional medication may be needed.

Dr. Zopf also pointed out a peculiarity of intramuscular fat tissue. “Muscle fat can only be trained off.” A fatty liver or too much fat under the skin can be combated well with a diet, but muscles are different. “For that, you have to exercise to counteract the inflammatory cascade in the muscles.”

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

The health consequences of excess visceral fat tissue are well known. But there is another type of fat accumulation in the body that increases the risk for type 2 diabetes and cardiovascular diseases. In Molecular Aspects of Medicine, researchers warned that the dangers arising from intramuscular fat tissue are often underestimated.

“Everyone knows the dangers of abdominal fat or that the deposition of fat in the coronary arteries can cause a heart attack,” said lead author Osvaldo Contreras, PhD, from the School of Clinical Medicine at the University of New South Wales in Sydney, Australia. “But hardly anyone has ever heard of fat accumulation in skeletal muscles, even though they are associated with a whole range of life-threatening diseases.” 

“The work emphasizes that muscles are not only good for standing, walking, or lifting a box. They are metabolically active, produce hormones, communicate in the body, and can positively or negatively affect a person’s health,” Yurdagül Zopf, MD, PhD, professor of integrative medicine specializing in nutritional medicine and director of the Hector Center for Nutrition, Exercise, and Sports at the University Hospital Erlangen, Erlangen, Germany, said in an interview.
 

Associated With Diseases

Increased intramuscular fat is found in various conditions where muscle mass is increasingly lost and replaced by fat and connective tissue. Intramuscular fat has been observed, for example, in patients with chronic muscle diseases, sarcopenia, hormonal disorders, and metabolic diseases such as insulin resistance and type 2 diabetes, as well as in patients with cardiovascular problems such as hypertension and heart failure.

Fat accumulation in the muscles, like all fat deposits in the body, can result from an unhealthy lifestyle with excessive calorie intake and, especially, lack of exercise. “If the body has more energy available than it can use, it will initially store it as subcutaneous fat,” said Dr. Zopf. “Once these storage capacities are depleted, more and more visceral fat is deposited, and then more and more fat is stored in the organs and the muscles.”

Movement plays a particularly important role in intramuscular fat. “We know that the less physically active someone is, the higher the risk that fat will be stored in the muscles,” said Dr. Zopf.
 

Arising From Injuries

Unlike other fat tissues in the body, intramuscular fat can also accumulate in higher amounts when there are injuries to the muscles. The group led by Dr. Contreras and lead author Marcelo Flores-Opazo from the Universidad de O’Higgins in Rancagua, Chile, emphasized the role of fibroadipogenic progenitor (FAP) cells in their review. “FAPs play a crucial role in preserving and repairing muscle tissue injuries. They can differentiate into fibroblasts and adipocytes and are responsible for depositing fat and connective tissue in response to muscle injuries.”

Studies suggest that exercise can prevent FAPs from differentiating into fat and connective tissue cells. Metformin can achieve a similar effect in vitro. Dr. Contreras and colleagues hope that drug-based ways to reduce muscle fat will emerge in the future.

But how do you determine whether a patient has too much intramuscular fat? Although MRI and CT can be used for quantification, these are not routine examinations. There is currently no simple way to determine the fat content in muscles, according to the authors. The study authors hope that advances in molecular testing, imaging, and biopsies will improve diagnostic capabilities in the future.
 

Training Crucial

Until then, Dr. Contreras and colleagues advise close monitoring of one’s body weight and the maintenance of a healthy lifestyle. Excessive fat accumulation in the muscles can be prevented and reversed through adequate exercise and healthy nutrition, they emphasized. 

The important message is that these measures are possible. “With healthy nutrition and exercise, excess fat can be reduced. We have observed a reduction in muscle fat in obese individuals with just two sessions of 15-minute high-intensity workouts per week,” Dr. Zopf reported, citing her own research. The more obese a person is and the higher the inflammation in the body, the more likely additional medication may be needed.

Dr. Zopf also pointed out a peculiarity of intramuscular fat tissue. “Muscle fat can only be trained off.” A fatty liver or too much fat under the skin can be combated well with a diet, but muscles are different. “For that, you have to exercise to counteract the inflammatory cascade in the muscles.”

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

The health consequences of excess visceral fat tissue are well known. But there is another type of fat accumulation in the body that increases the risk for type 2 diabetes and cardiovascular diseases. In Molecular Aspects of Medicine, researchers warned that the dangers arising from intramuscular fat tissue are often underestimated.

“Everyone knows the dangers of abdominal fat or that the deposition of fat in the coronary arteries can cause a heart attack,” said lead author Osvaldo Contreras, PhD, from the School of Clinical Medicine at the University of New South Wales in Sydney, Australia. “But hardly anyone has ever heard of fat accumulation in skeletal muscles, even though they are associated with a whole range of life-threatening diseases.” 

“The work emphasizes that muscles are not only good for standing, walking, or lifting a box. They are metabolically active, produce hormones, communicate in the body, and can positively or negatively affect a person’s health,” Yurdagül Zopf, MD, PhD, professor of integrative medicine specializing in nutritional medicine and director of the Hector Center for Nutrition, Exercise, and Sports at the University Hospital Erlangen, Erlangen, Germany, said in an interview.
 

Associated With Diseases

Increased intramuscular fat is found in various conditions where muscle mass is increasingly lost and replaced by fat and connective tissue. Intramuscular fat has been observed, for example, in patients with chronic muscle diseases, sarcopenia, hormonal disorders, and metabolic diseases such as insulin resistance and type 2 diabetes, as well as in patients with cardiovascular problems such as hypertension and heart failure.

Fat accumulation in the muscles, like all fat deposits in the body, can result from an unhealthy lifestyle with excessive calorie intake and, especially, lack of exercise. “If the body has more energy available than it can use, it will initially store it as subcutaneous fat,” said Dr. Zopf. “Once these storage capacities are depleted, more and more visceral fat is deposited, and then more and more fat is stored in the organs and the muscles.”

Movement plays a particularly important role in intramuscular fat. “We know that the less physically active someone is, the higher the risk that fat will be stored in the muscles,” said Dr. Zopf.
 

Arising From Injuries

Unlike other fat tissues in the body, intramuscular fat can also accumulate in higher amounts when there are injuries to the muscles. The group led by Dr. Contreras and lead author Marcelo Flores-Opazo from the Universidad de O’Higgins in Rancagua, Chile, emphasized the role of fibroadipogenic progenitor (FAP) cells in their review. “FAPs play a crucial role in preserving and repairing muscle tissue injuries. They can differentiate into fibroblasts and adipocytes and are responsible for depositing fat and connective tissue in response to muscle injuries.”

Studies suggest that exercise can prevent FAPs from differentiating into fat and connective tissue cells. Metformin can achieve a similar effect in vitro. Dr. Contreras and colleagues hope that drug-based ways to reduce muscle fat will emerge in the future.

But how do you determine whether a patient has too much intramuscular fat? Although MRI and CT can be used for quantification, these are not routine examinations. There is currently no simple way to determine the fat content in muscles, according to the authors. The study authors hope that advances in molecular testing, imaging, and biopsies will improve diagnostic capabilities in the future.
 

Training Crucial

Until then, Dr. Contreras and colleagues advise close monitoring of one’s body weight and the maintenance of a healthy lifestyle. Excessive fat accumulation in the muscles can be prevented and reversed through adequate exercise and healthy nutrition, they emphasized. 

The important message is that these measures are possible. “With healthy nutrition and exercise, excess fat can be reduced. We have observed a reduction in muscle fat in obese individuals with just two sessions of 15-minute high-intensity workouts per week,” Dr. Zopf reported, citing her own research. The more obese a person is and the higher the inflammation in the body, the more likely additional medication may be needed.

Dr. Zopf also pointed out a peculiarity of intramuscular fat tissue. “Muscle fat can only be trained off.” A fatty liver or too much fat under the skin can be combated well with a diet, but muscles are different. “For that, you have to exercise to counteract the inflammatory cascade in the muscles.”

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

TORONTO — With rates of childhood obesity increasing to the point of becoming a public health concern, related skin conditions are also on the rise in the pediatric population, results of new research show.

The retrospective cohort study found markedly higher rates of skin infections, atopic dermatitis (AD), and acanthosis nigricans among children with overweight, compared with children with average weight.

“Many conditions associated with obesity are strong predictors of cardiovascular mortality as these children age, so doctors can play a key role in advocating for weight loss strategies in this population,” lead study author Samantha Epstein, third-year medical student at Case Western Reserve University, Cleveland, Ohio, said in an interview. The findings were presented at the annual meeting of the Society for Pediatric Dermatology.

Previous research has linked obesity, a chronic inflammatory condition, to psoriasis, AD, hidradenitis suppurativa (HS), acne vulgaris, infections, and rosacea in adults. However, there’s scant research exploring the connection between obesity and cutaneous conditions in children.

According to the Cleveland Clinic, childhood obesity is defined as a body mass index, which is weight in kg divided by the square of height in m², at or above the 95th percentile for age and sex in children aged 2 years or older.

For the study, Ms. Epstein and coauthor Sonal D. Shah, MD, associate professor, Department of Dermatology, Case Western Reserve University, and a board-certified pediatric dermatologist accessed a large national research database and used diagnostic codes to identify over 1 million children (mean age, 8.5 years). Most (about 44%) were White; about one-quarter were Black. The groups were propensity matched, so there were about equal numbers of youngsters with and without obesity and of boys and girls.

They collected data on AD, HS, rosacea, psoriasis, and acanthosis nigricans (a thickened purplish discoloration typically found in body folds around the armpits, groin, and neck). They also gathered information on comorbidities.

Acanthosis nigricans, which is linked to metabolic syndrome, type 2 diabetes, and insulin resistance , was more prevalent among children with obesity (20,885 cases in the with-obesity group and 336 in the without-obesity group, for a relative risk [RR] of 62.16 and an odds ratio [OR] of 64.38).

Skin and subcutaneous tissue infections were also more common among those with obesity (14,795 cases) vs 4720 cases among those without obesity (RR, 3.14; OR, 3.2). As for AD, there were 11,892 cases in the with-obesity group and 2983 in the without-obesity group (RR, 3.99; OR, 4.06). There were 1166 cases of psoriasis among those with obesity and 408 among those without obesity (RR, 2.86; OR, 2.88).

HS (587 cases in the with-obesity group and 70 in the without-obesity group; RR, 8.39; OR, 8.39) and rosacea (351 in the with-obesity group and 138 in the without-obesity group; RR, 2.54; OR, 2.55) were the least common skin conditions.

Higher Comorbidity Rates

Compared with their average-weight counterparts, the children with obesity had higher rates of comorbidities, including type 2 diabetes. Ms. Epstein noted that children with diabetes and obesity had increased risks for every skin condition except for infections of the skin and subcutaneous tissue when compared with children without obesity. 

Such infections were the most common skin conditions among children without obesity. “This was expected just due to the fact that children are outside, they’re playing in the grass and the dirt, and they get infected,” said Ms. Epstein. Still, these infections were three times more common in youngsters with obesity.

Although acanthosis nigricans is “highly correlated” with type 2 diabetes, “not as many children as we would expect in this population have developed type 2 diabetes,” said Ms. Epstein. This might make some sense, though, because these children are still quite young. “When dermatologists recognize this skin condition, they can advocate for weight loss management to try to prevent it.”

Other conditions seen more often in the overweight children with overweight included: hypertension, hyperlipidemia, obstructive sleep apnea, polycystic ovarian syndrome, attention-deficit/hyperactivity disorder, major depressive disorder, depressive episodes, and anxiety (all P < .001).

Commenting on the results, Sonia Havele, MD, a pediatrician and dermatology resident at Children’s Mercy Hospital, Kansas City, Missouri, said in an interview that the study reflects trends that she and her colleagues see in clinic: There are more common skin conditions in their patients with obesity.

She agreed that it offers an opening for education. “The results of this study highlight the opportunity we have as pediatric dermatologists to provide additional counseling on obesity and offer referrals to our colleagues in endocrinology, gastroenterology, and nutrition if needed.”

No conflicts of interest were reported.

TORONTO — With rates of childhood obesity increasing to the point of becoming a public health concern, related skin conditions are also on the rise in the pediatric population, results of new research show.

The retrospective cohort study found markedly higher rates of skin infections, atopic dermatitis (AD), and acanthosis nigricans among children with overweight, compared with children with average weight.

“Many conditions associated with obesity are strong predictors of cardiovascular mortality as these children age, so doctors can play a key role in advocating for weight loss strategies in this population,” lead study author Samantha Epstein, third-year medical student at Case Western Reserve University, Cleveland, Ohio, said in an interview. The findings were presented at the annual meeting of the Society for Pediatric Dermatology.

Previous research has linked obesity, a chronic inflammatory condition, to psoriasis, AD, hidradenitis suppurativa (HS), acne vulgaris, infections, and rosacea in adults. However, there’s scant research exploring the connection between obesity and cutaneous conditions in children.

According to the Cleveland Clinic, childhood obesity is defined as a body mass index, which is weight in kg divided by the square of height in m², at or above the 95th percentile for age and sex in children aged 2 years or older.

For the study, Ms. Epstein and coauthor Sonal D. Shah, MD, associate professor, Department of Dermatology, Case Western Reserve University, and a board-certified pediatric dermatologist accessed a large national research database and used diagnostic codes to identify over 1 million children (mean age, 8.5 years). Most (about 44%) were White; about one-quarter were Black. The groups were propensity matched, so there were about equal numbers of youngsters with and without obesity and of boys and girls.

They collected data on AD, HS, rosacea, psoriasis, and acanthosis nigricans (a thickened purplish discoloration typically found in body folds around the armpits, groin, and neck). They also gathered information on comorbidities.

Acanthosis nigricans, which is linked to metabolic syndrome, type 2 diabetes, and insulin resistance , was more prevalent among children with obesity (20,885 cases in the with-obesity group and 336 in the without-obesity group, for a relative risk [RR] of 62.16 and an odds ratio [OR] of 64.38).

Skin and subcutaneous tissue infections were also more common among those with obesity (14,795 cases) vs 4720 cases among those without obesity (RR, 3.14; OR, 3.2). As for AD, there were 11,892 cases in the with-obesity group and 2983 in the without-obesity group (RR, 3.99; OR, 4.06). There were 1166 cases of psoriasis among those with obesity and 408 among those without obesity (RR, 2.86; OR, 2.88).

HS (587 cases in the with-obesity group and 70 in the without-obesity group; RR, 8.39; OR, 8.39) and rosacea (351 in the with-obesity group and 138 in the without-obesity group; RR, 2.54; OR, 2.55) were the least common skin conditions.

Higher Comorbidity Rates

Compared with their average-weight counterparts, the children with obesity had higher rates of comorbidities, including type 2 diabetes. Ms. Epstein noted that children with diabetes and obesity had increased risks for every skin condition except for infections of the skin and subcutaneous tissue when compared with children without obesity. 

Such infections were the most common skin conditions among children without obesity. “This was expected just due to the fact that children are outside, they’re playing in the grass and the dirt, and they get infected,” said Ms. Epstein. Still, these infections were three times more common in youngsters with obesity.

Although acanthosis nigricans is “highly correlated” with type 2 diabetes, “not as many children as we would expect in this population have developed type 2 diabetes,” said Ms. Epstein. This might make some sense, though, because these children are still quite young. “When dermatologists recognize this skin condition, they can advocate for weight loss management to try to prevent it.”

Other conditions seen more often in the overweight children with overweight included: hypertension, hyperlipidemia, obstructive sleep apnea, polycystic ovarian syndrome, attention-deficit/hyperactivity disorder, major depressive disorder, depressive episodes, and anxiety (all P < .001).

Commenting on the results, Sonia Havele, MD, a pediatrician and dermatology resident at Children’s Mercy Hospital, Kansas City, Missouri, said in an interview that the study reflects trends that she and her colleagues see in clinic: There are more common skin conditions in their patients with obesity.

She agreed that it offers an opening for education. “The results of this study highlight the opportunity we have as pediatric dermatologists to provide additional counseling on obesity and offer referrals to our colleagues in endocrinology, gastroenterology, and nutrition if needed.”

No conflicts of interest were reported.

TORONTO — With rates of childhood obesity increasing to the point of becoming a public health concern, related skin conditions are also on the rise in the pediatric population, results of new research show.

The retrospective cohort study found markedly higher rates of skin infections, atopic dermatitis (AD), and acanthosis nigricans among children with overweight, compared with children with average weight.

“Many conditions associated with obesity are strong predictors of cardiovascular mortality as these children age, so doctors can play a key role in advocating for weight loss strategies in this population,” lead study author Samantha Epstein, third-year medical student at Case Western Reserve University, Cleveland, Ohio, said in an interview. The findings were presented at the annual meeting of the Society for Pediatric Dermatology.

Previous research has linked obesity, a chronic inflammatory condition, to psoriasis, AD, hidradenitis suppurativa (HS), acne vulgaris, infections, and rosacea in adults. However, there’s scant research exploring the connection between obesity and cutaneous conditions in children.

According to the Cleveland Clinic, childhood obesity is defined as a body mass index, which is weight in kg divided by the square of height in m², at or above the 95th percentile for age and sex in children aged 2 years or older.

For the study, Ms. Epstein and coauthor Sonal D. Shah, MD, associate professor, Department of Dermatology, Case Western Reserve University, and a board-certified pediatric dermatologist accessed a large national research database and used diagnostic codes to identify over 1 million children (mean age, 8.5 years). Most (about 44%) were White; about one-quarter were Black. The groups were propensity matched, so there were about equal numbers of youngsters with and without obesity and of boys and girls.

They collected data on AD, HS, rosacea, psoriasis, and acanthosis nigricans (a thickened purplish discoloration typically found in body folds around the armpits, groin, and neck). They also gathered information on comorbidities.

Acanthosis nigricans, which is linked to metabolic syndrome, type 2 diabetes, and insulin resistance , was more prevalent among children with obesity (20,885 cases in the with-obesity group and 336 in the without-obesity group, for a relative risk [RR] of 62.16 and an odds ratio [OR] of 64.38).

Skin and subcutaneous tissue infections were also more common among those with obesity (14,795 cases) vs 4720 cases among those without obesity (RR, 3.14; OR, 3.2). As for AD, there were 11,892 cases in the with-obesity group and 2983 in the without-obesity group (RR, 3.99; OR, 4.06). There were 1166 cases of psoriasis among those with obesity and 408 among those without obesity (RR, 2.86; OR, 2.88).

HS (587 cases in the with-obesity group and 70 in the without-obesity group; RR, 8.39; OR, 8.39) and rosacea (351 in the with-obesity group and 138 in the without-obesity group; RR, 2.54; OR, 2.55) were the least common skin conditions.

Higher Comorbidity Rates

Compared with their average-weight counterparts, the children with obesity had higher rates of comorbidities, including type 2 diabetes. Ms. Epstein noted that children with diabetes and obesity had increased risks for every skin condition except for infections of the skin and subcutaneous tissue when compared with children without obesity. 

Such infections were the most common skin conditions among children without obesity. “This was expected just due to the fact that children are outside, they’re playing in the grass and the dirt, and they get infected,” said Ms. Epstein. Still, these infections were three times more common in youngsters with obesity.

Although acanthosis nigricans is “highly correlated” with type 2 diabetes, “not as many children as we would expect in this population have developed type 2 diabetes,” said Ms. Epstein. This might make some sense, though, because these children are still quite young. “When dermatologists recognize this skin condition, they can advocate for weight loss management to try to prevent it.”

Other conditions seen more often in the overweight children with overweight included: hypertension, hyperlipidemia, obstructive sleep apnea, polycystic ovarian syndrome, attention-deficit/hyperactivity disorder, major depressive disorder, depressive episodes, and anxiety (all P < .001).

Commenting on the results, Sonia Havele, MD, a pediatrician and dermatology resident at Children’s Mercy Hospital, Kansas City, Missouri, said in an interview that the study reflects trends that she and her colleagues see in clinic: There are more common skin conditions in their patients with obesity.

She agreed that it offers an opening for education. “The results of this study highlight the opportunity we have as pediatric dermatologists to provide additional counseling on obesity and offer referrals to our colleagues in endocrinology, gastroenterology, and nutrition if needed.”

No conflicts of interest were reported.

Pharmacist Mark Mikhael has lost 50 pounds over the past 12 months. He no longer has diabetes and finds himself “at my ideal body weight,” with his cholesterol below 200 for the first time in 20 years. “I feel fantastic,” he said.

Like millions of others, Mr. Mikhael credits the new class of weight loss drugs. But he isn’t using brand-name Wegovy or Zepbound. Mr. Mikhael, CEO of Orlando, Florida–based Olympia Pharmaceuticals, has been getting by with his own supply: injecting himself with copies of the drugs formulated by his company.

He’s far from alone. Mr. Mikhael and other industry officials estimate that several large compounding pharmacies like his are provisioning up to 2 million American patients with regular doses of semaglutide, the scientific name for Novo Nordisk’s Wegovy, Ozempic, and Rybelsus formulations, or tirzepatide, the active ingredient in Eli Lilly’s Zepbound and Mounjaro.

The drug-making behemoths fiercely oppose that compounding business. Novo Nordisk and Lilly lump the compounders together with Internet cowboys and unregulated medical spas peddling bogus semaglutide, and have high-powered legal teams trying to stop them. Novo Nordisk has filed at least 21 lawsuits nationwide against companies making purported copies of its drugs, said Brianna Kelley, a spokesperson for the company, and urges doctors to avoid them. The Food and Drug Administration (FDA), too, has cautioned about the potential danger of the compounds, and leading obesity medicine groups starkly warn patients against their use.

But this isn’t an illegal black market, though it has shades of gray.

The FDA allows and even encourages compounding pharmacies to produce and sell copycats when a drug is in short supply, and the wildly popular glucagon-like peptide 1 (GLP-1) drugs have enduring shortages — first reported in March 2022 for semaglutide and in December 2022 for tirzepatide. The drugs have registered unprecedented success in weight loss. They are also showing promise against heart, kidney, and liver diseases and are being tested against conditions as diverse as Alzheimer’s disease and drug addiction.

In recent years, the US health care system has come to depend on compounding pharmacies, many of which are run as nonprofits, to plug supply holes of crucial drugs like cancer medicines cisplatin, methotrexate, and 5-fluorouracil.

Most compounded drugs are old, cheap generics. Semaglutide and tirzepatide, on the other hand, are under patent and earn Novo Nordisk and Lilly billions of dollars a year. Sales of the diabetes and weight loss drugs in 2024 made Novo Nordisk Europe’s most valuable company and Lilly the world’s biggest pharmaceutical company.

While the companies can’t keep up with demand, they heatedly dispute the right of compounders to make and sell copies. Lilly spokesperson Kristiane Silva Bello said her company was “deeply concerned” about “serious health risks” from compounded drugs that “should not be on the market.”

Yet marketed they are. Even Hims & Hers Health — the telemedicine prescriber that got its start with erectile dysfunction drugs — is now peddling compounded semaglutide. It ran ads for the drugs during NBA playoff games. (According to a Hunterbrook Media report, Hims & Hers’ semaglutide supplier has faced legal scrutiny.)

The compounded forms are significantly cheaper than the branded drugs. Patients pay about $100-$450 a month, compared with list prices of roughly $1,000-$1,400 for Lilly and Novo Nordisk products.

Five compounders and distributors interviewed for this article said they conduct due diligence on every lot of semaglutide or tirzepatide they buy or produce, upholding standards of purity, sterility, and consistency similar to those practiced in the commercial drug industry. Compounders operate under strict federal and state standards, they noted.

However, the raw materials used in the compounded forms may differ from those produced for Novo Nordisk and Lilly, said GLP-1 coinventor Jens Juul Holst, of the University of Copenhagen, adding that care must be taken in drug production lest it cause potentially harmful immune reactions.

To date, according to FDA spokespeople, reports of side effects from taking compounded versions haven’t raised major alarms. But everyone with knowledge of the industry, including the compounders themselves, worry that a single batch of a poorly made drug could kill or maim people and destroy confidence in their business.

“I liken the compounding industry to the airline industry,” Mr. Mikhael said. “When you have an airline crash, it hurts everybody.”
 

Warnings From the Past

The industry endured just such a catastrophe in 2012, when the New England Compounding Center released a contaminated injectable steroid that killed at least 64 people and harmed hundreds more.

In response, Congress and the FDA had strengthened oversight. Mr. Mikhael’s company is an outsourcing facility, or 503B compounding pharmacy — so-named for a section of the 2013 law that set new requirements for drug compounders. The companies are licensed to make slightly different versions of FDA-approved drugs in response to shortages or a patient’s special needs.

The law created two classes of compounding pharmacies: The FDA regulates the larger 503B compounders with standards like commercial drug companies, while 503A pharmacies make smaller lots of drugs and are largely overseen by state boards of pharmacy.

The 503A facilities also are producing compounded semaglutide and tirzepatide for hundreds of thousands of patients. Like the 503Bs, these operations take the active ingredient, produced as a powder in FDA-registered factories, mostly in China, then reconstitute it with sterile water and an antimicrobial in small glass vials.

Together, the compounding pharmacies may account for up to 30% of the semaglutide sold in the United States, Mr. Mikhael said, although he cautions that is a “wild ballpark figure” since no one, including the FDA, is tracking sales in the industry.

The compounders say the companies should increase production if they’re worried about competition. Like the dozens of other drugs they produce for hospitals and medical practices, the compounders say, the two diet drugs are essential products.

“If you don’t want a 503B facility to make a copy, it’s pretty simple: Don’t go short,” said Lee Rosebush, chair of a trade association for 503B pharmacies. “FDA created this system because these are necessary drugs.”

Novo Nordisk hasn’t specified why it can’t keep up with demand, but the bottleneck apparently lies in the company’s inability to fill and sterilize enough of its special drug auto-injectors, said Evan Seigerman, a managing director at BMO Capital Markets.

The company announced June 24 that it was investing $4.1 billion in new production lines at its Clayton, North Carolina, site. In 2023, the FDA issued a warning over procedural violations at the site and separate cautions at an Indiana facility that Novo Nordisk took over recently.
 

Compounding for Dummies

At least 28 companies, mostly in China, are registered with the FDA to produce or distribute semaglutide. At least half the companies have entered the market in the past 12 months, driving the raw material’s price down by 35%, according to Scott Welch, who runs a 503A pharmacy in Arlington, Virginia.

Compounders can buy powdered semaglutide from some US distributors for less than $4,000 a gram, said Matthew Johnson, president and CEO of distributor Pharma Source Direct. That comes out to as little as $10 per weekly 2.5-microgram dose – not including overhead and other costs.

While Ozempic or Wegovy patients use a Novo Nordisk device to inject the drug, patients using compounded products draw them from a vial with a small needle, like the device diabetics use for insulin.

Some medical practices provide the compounded drug to patients as part of a weight loss package, with markups. In July 2023, Tabitha Ries, a single mother of six who works as a home health care aide in Garfield, Washington, found an online clinic that charged her $1,000 for 3 months of semaglutide along with counseling. She has lost 35 pounds.

She gets the drug from Mindful Weight Loss, a mostly telehealth-based operation led by physician Vivek Gupta, MD, of Manhattan Beach, California. Dr. Gupta said he’s prescribed the weight loss drugs to 1,500 patients, with about 60% using compounded versions from a 503A pharmacy.

He hasn’t seen any essential difference in patients using the branded and compounded forms, although “some people say the compounding is a little less effective,” Dr. Gupta said.

There’s some risk in using the non–FDA-approved product, he acknowledged, and he requires patients to sign an informed consent waiver.

“Nothing in life is without risk, but I would also argue that the status quo is not safe for people who need the medicine and can’t get it,” he said. “They’re constantly triggered by all this food that’s causing their weight to go up and their sugar to go high, increasing their insulin resistance and affecting their limbs and eyes.”

Compounding semaglutide is a helpful sideline for pharmacists like him, Mr. Welch said, especially given the pinch on drug sale revenue that has led many independents to close in recent years. He figures he earns 95% of his revenue from compounding drugs, rather than traditional prescriptions.

It’s important to distinguish compounded semaglutide from unregulated powders sold as “generic Ozempic” and the like, which may be contaminated or counterfeit, said FDA spokesperson Amanda Hils. But since compounded forms of the drug are not FDA approved, those who make, prescribe, or use them also should have “an increased level of responsibility or awareness,” she said.
 

Corporate Battles

Novo Nordisk and Lilly, in lawsuits each company has filed against competitors, say their own testing has found bacteria and other impurities in products made by compounding pharmacies. The companies also report patent infringement, but compounders, pointing to the FDA loophole for drugs in shortage, appear to have defeated that argument for now.

When the FDA removes the drugs from the shortage list, 503B compounders must immediately stop selling them. Smaller compounders may be able to produce their products for a reduced number of patients, said Scott Brunner, CEO of the Alliance for Pharmacy Compounding, which represents 503A compounders.

The evaporation of the compounded drug supply could come as a shock to patients.

“I dread it,” said David Wertheimer, an internist in Franklin Lakes, New Jersey, who prescribes compounded semaglutide to some patients. “People are not going to be able to plunk down a grand every month. A lot of people will go off the drug, and that’s a shame.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

Pharmacist Mark Mikhael has lost 50 pounds over the past 12 months. He no longer has diabetes and finds himself “at my ideal body weight,” with his cholesterol below 200 for the first time in 20 years. “I feel fantastic,” he said.

Like millions of others, Mr. Mikhael credits the new class of weight loss drugs. But he isn’t using brand-name Wegovy or Zepbound. Mr. Mikhael, CEO of Orlando, Florida–based Olympia Pharmaceuticals, has been getting by with his own supply: injecting himself with copies of the drugs formulated by his company.

He’s far from alone. Mr. Mikhael and other industry officials estimate that several large compounding pharmacies like his are provisioning up to 2 million American patients with regular doses of semaglutide, the scientific name for Novo Nordisk’s Wegovy, Ozempic, and Rybelsus formulations, or tirzepatide, the active ingredient in Eli Lilly’s Zepbound and Mounjaro.

The drug-making behemoths fiercely oppose that compounding business. Novo Nordisk and Lilly lump the compounders together with Internet cowboys and unregulated medical spas peddling bogus semaglutide, and have high-powered legal teams trying to stop them. Novo Nordisk has filed at least 21 lawsuits nationwide against companies making purported copies of its drugs, said Brianna Kelley, a spokesperson for the company, and urges doctors to avoid them. The Food and Drug Administration (FDA), too, has cautioned about the potential danger of the compounds, and leading obesity medicine groups starkly warn patients against their use.

But this isn’t an illegal black market, though it has shades of gray.

The FDA allows and even encourages compounding pharmacies to produce and sell copycats when a drug is in short supply, and the wildly popular glucagon-like peptide 1 (GLP-1) drugs have enduring shortages — first reported in March 2022 for semaglutide and in December 2022 for tirzepatide. The drugs have registered unprecedented success in weight loss. They are also showing promise against heart, kidney, and liver diseases and are being tested against conditions as diverse as Alzheimer’s disease and drug addiction.

In recent years, the US health care system has come to depend on compounding pharmacies, many of which are run as nonprofits, to plug supply holes of crucial drugs like cancer medicines cisplatin, methotrexate, and 5-fluorouracil.

Most compounded drugs are old, cheap generics. Semaglutide and tirzepatide, on the other hand, are under patent and earn Novo Nordisk and Lilly billions of dollars a year. Sales of the diabetes and weight loss drugs in 2024 made Novo Nordisk Europe’s most valuable company and Lilly the world’s biggest pharmaceutical company.

While the companies can’t keep up with demand, they heatedly dispute the right of compounders to make and sell copies. Lilly spokesperson Kristiane Silva Bello said her company was “deeply concerned” about “serious health risks” from compounded drugs that “should not be on the market.”

Yet marketed they are. Even Hims & Hers Health — the telemedicine prescriber that got its start with erectile dysfunction drugs — is now peddling compounded semaglutide. It ran ads for the drugs during NBA playoff games. (According to a Hunterbrook Media report, Hims & Hers’ semaglutide supplier has faced legal scrutiny.)

The compounded forms are significantly cheaper than the branded drugs. Patients pay about $100-$450 a month, compared with list prices of roughly $1,000-$1,400 for Lilly and Novo Nordisk products.

Five compounders and distributors interviewed for this article said they conduct due diligence on every lot of semaglutide or tirzepatide they buy or produce, upholding standards of purity, sterility, and consistency similar to those practiced in the commercial drug industry. Compounders operate under strict federal and state standards, they noted.

However, the raw materials used in the compounded forms may differ from those produced for Novo Nordisk and Lilly, said GLP-1 coinventor Jens Juul Holst, of the University of Copenhagen, adding that care must be taken in drug production lest it cause potentially harmful immune reactions.

To date, according to FDA spokespeople, reports of side effects from taking compounded versions haven’t raised major alarms. But everyone with knowledge of the industry, including the compounders themselves, worry that a single batch of a poorly made drug could kill or maim people and destroy confidence in their business.

“I liken the compounding industry to the airline industry,” Mr. Mikhael said. “When you have an airline crash, it hurts everybody.”
 

Warnings From the Past

The industry endured just such a catastrophe in 2012, when the New England Compounding Center released a contaminated injectable steroid that killed at least 64 people and harmed hundreds more.

In response, Congress and the FDA had strengthened oversight. Mr. Mikhael’s company is an outsourcing facility, or 503B compounding pharmacy — so-named for a section of the 2013 law that set new requirements for drug compounders. The companies are licensed to make slightly different versions of FDA-approved drugs in response to shortages or a patient’s special needs.

The law created two classes of compounding pharmacies: The FDA regulates the larger 503B compounders with standards like commercial drug companies, while 503A pharmacies make smaller lots of drugs and are largely overseen by state boards of pharmacy.

The 503A facilities also are producing compounded semaglutide and tirzepatide for hundreds of thousands of patients. Like the 503Bs, these operations take the active ingredient, produced as a powder in FDA-registered factories, mostly in China, then reconstitute it with sterile water and an antimicrobial in small glass vials.

Together, the compounding pharmacies may account for up to 30% of the semaglutide sold in the United States, Mr. Mikhael said, although he cautions that is a “wild ballpark figure” since no one, including the FDA, is tracking sales in the industry.

The compounders say the companies should increase production if they’re worried about competition. Like the dozens of other drugs they produce for hospitals and medical practices, the compounders say, the two diet drugs are essential products.

“If you don’t want a 503B facility to make a copy, it’s pretty simple: Don’t go short,” said Lee Rosebush, chair of a trade association for 503B pharmacies. “FDA created this system because these are necessary drugs.”

Novo Nordisk hasn’t specified why it can’t keep up with demand, but the bottleneck apparently lies in the company’s inability to fill and sterilize enough of its special drug auto-injectors, said Evan Seigerman, a managing director at BMO Capital Markets.

The company announced June 24 that it was investing $4.1 billion in new production lines at its Clayton, North Carolina, site. In 2023, the FDA issued a warning over procedural violations at the site and separate cautions at an Indiana facility that Novo Nordisk took over recently.
 

Compounding for Dummies

At least 28 companies, mostly in China, are registered with the FDA to produce or distribute semaglutide. At least half the companies have entered the market in the past 12 months, driving the raw material’s price down by 35%, according to Scott Welch, who runs a 503A pharmacy in Arlington, Virginia.

Compounders can buy powdered semaglutide from some US distributors for less than $4,000 a gram, said Matthew Johnson, president and CEO of distributor Pharma Source Direct. That comes out to as little as $10 per weekly 2.5-microgram dose – not including overhead and other costs.

While Ozempic or Wegovy patients use a Novo Nordisk device to inject the drug, patients using compounded products draw them from a vial with a small needle, like the device diabetics use for insulin.

Some medical practices provide the compounded drug to patients as part of a weight loss package, with markups. In July 2023, Tabitha Ries, a single mother of six who works as a home health care aide in Garfield, Washington, found an online clinic that charged her $1,000 for 3 months of semaglutide along with counseling. She has lost 35 pounds.

She gets the drug from Mindful Weight Loss, a mostly telehealth-based operation led by physician Vivek Gupta, MD, of Manhattan Beach, California. Dr. Gupta said he’s prescribed the weight loss drugs to 1,500 patients, with about 60% using compounded versions from a 503A pharmacy.

He hasn’t seen any essential difference in patients using the branded and compounded forms, although “some people say the compounding is a little less effective,” Dr. Gupta said.

There’s some risk in using the non–FDA-approved product, he acknowledged, and he requires patients to sign an informed consent waiver.

“Nothing in life is without risk, but I would also argue that the status quo is not safe for people who need the medicine and can’t get it,” he said. “They’re constantly triggered by all this food that’s causing their weight to go up and their sugar to go high, increasing their insulin resistance and affecting their limbs and eyes.”

Compounding semaglutide is a helpful sideline for pharmacists like him, Mr. Welch said, especially given the pinch on drug sale revenue that has led many independents to close in recent years. He figures he earns 95% of his revenue from compounding drugs, rather than traditional prescriptions.

It’s important to distinguish compounded semaglutide from unregulated powders sold as “generic Ozempic” and the like, which may be contaminated or counterfeit, said FDA spokesperson Amanda Hils. But since compounded forms of the drug are not FDA approved, those who make, prescribe, or use them also should have “an increased level of responsibility or awareness,” she said.
 

Corporate Battles

Novo Nordisk and Lilly, in lawsuits each company has filed against competitors, say their own testing has found bacteria and other impurities in products made by compounding pharmacies. The companies also report patent infringement, but compounders, pointing to the FDA loophole for drugs in shortage, appear to have defeated that argument for now.

When the FDA removes the drugs from the shortage list, 503B compounders must immediately stop selling them. Smaller compounders may be able to produce their products for a reduced number of patients, said Scott Brunner, CEO of the Alliance for Pharmacy Compounding, which represents 503A compounders.

The evaporation of the compounded drug supply could come as a shock to patients.

“I dread it,” said David Wertheimer, an internist in Franklin Lakes, New Jersey, who prescribes compounded semaglutide to some patients. “People are not going to be able to plunk down a grand every month. A lot of people will go off the drug, and that’s a shame.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

Pharmacist Mark Mikhael has lost 50 pounds over the past 12 months. He no longer has diabetes and finds himself “at my ideal body weight,” with his cholesterol below 200 for the first time in 20 years. “I feel fantastic,” he said.

Like millions of others, Mr. Mikhael credits the new class of weight loss drugs. But he isn’t using brand-name Wegovy or Zepbound. Mr. Mikhael, CEO of Orlando, Florida–based Olympia Pharmaceuticals, has been getting by with his own supply: injecting himself with copies of the drugs formulated by his company.

He’s far from alone. Mr. Mikhael and other industry officials estimate that several large compounding pharmacies like his are provisioning up to 2 million American patients with regular doses of semaglutide, the scientific name for Novo Nordisk’s Wegovy, Ozempic, and Rybelsus formulations, or tirzepatide, the active ingredient in Eli Lilly’s Zepbound and Mounjaro.

The drug-making behemoths fiercely oppose that compounding business. Novo Nordisk and Lilly lump the compounders together with Internet cowboys and unregulated medical spas peddling bogus semaglutide, and have high-powered legal teams trying to stop them. Novo Nordisk has filed at least 21 lawsuits nationwide against companies making purported copies of its drugs, said Brianna Kelley, a spokesperson for the company, and urges doctors to avoid them. The Food and Drug Administration (FDA), too, has cautioned about the potential danger of the compounds, and leading obesity medicine groups starkly warn patients against their use.

But this isn’t an illegal black market, though it has shades of gray.

The FDA allows and even encourages compounding pharmacies to produce and sell copycats when a drug is in short supply, and the wildly popular glucagon-like peptide 1 (GLP-1) drugs have enduring shortages — first reported in March 2022 for semaglutide and in December 2022 for tirzepatide. The drugs have registered unprecedented success in weight loss. They are also showing promise against heart, kidney, and liver diseases and are being tested against conditions as diverse as Alzheimer’s disease and drug addiction.

In recent years, the US health care system has come to depend on compounding pharmacies, many of which are run as nonprofits, to plug supply holes of crucial drugs like cancer medicines cisplatin, methotrexate, and 5-fluorouracil.

Most compounded drugs are old, cheap generics. Semaglutide and tirzepatide, on the other hand, are under patent and earn Novo Nordisk and Lilly billions of dollars a year. Sales of the diabetes and weight loss drugs in 2024 made Novo Nordisk Europe’s most valuable company and Lilly the world’s biggest pharmaceutical company.

While the companies can’t keep up with demand, they heatedly dispute the right of compounders to make and sell copies. Lilly spokesperson Kristiane Silva Bello said her company was “deeply concerned” about “serious health risks” from compounded drugs that “should not be on the market.”

Yet marketed they are. Even Hims & Hers Health — the telemedicine prescriber that got its start with erectile dysfunction drugs — is now peddling compounded semaglutide. It ran ads for the drugs during NBA playoff games. (According to a Hunterbrook Media report, Hims & Hers’ semaglutide supplier has faced legal scrutiny.)

The compounded forms are significantly cheaper than the branded drugs. Patients pay about $100-$450 a month, compared with list prices of roughly $1,000-$1,400 for Lilly and Novo Nordisk products.

Five compounders and distributors interviewed for this article said they conduct due diligence on every lot of semaglutide or tirzepatide they buy or produce, upholding standards of purity, sterility, and consistency similar to those practiced in the commercial drug industry. Compounders operate under strict federal and state standards, they noted.

However, the raw materials used in the compounded forms may differ from those produced for Novo Nordisk and Lilly, said GLP-1 coinventor Jens Juul Holst, of the University of Copenhagen, adding that care must be taken in drug production lest it cause potentially harmful immune reactions.

To date, according to FDA spokespeople, reports of side effects from taking compounded versions haven’t raised major alarms. But everyone with knowledge of the industry, including the compounders themselves, worry that a single batch of a poorly made drug could kill or maim people and destroy confidence in their business.

“I liken the compounding industry to the airline industry,” Mr. Mikhael said. “When you have an airline crash, it hurts everybody.”
 

Warnings From the Past

The industry endured just such a catastrophe in 2012, when the New England Compounding Center released a contaminated injectable steroid that killed at least 64 people and harmed hundreds more.

In response, Congress and the FDA had strengthened oversight. Mr. Mikhael’s company is an outsourcing facility, or 503B compounding pharmacy — so-named for a section of the 2013 law that set new requirements for drug compounders. The companies are licensed to make slightly different versions of FDA-approved drugs in response to shortages or a patient’s special needs.

The law created two classes of compounding pharmacies: The FDA regulates the larger 503B compounders with standards like commercial drug companies, while 503A pharmacies make smaller lots of drugs and are largely overseen by state boards of pharmacy.

The 503A facilities also are producing compounded semaglutide and tirzepatide for hundreds of thousands of patients. Like the 503Bs, these operations take the active ingredient, produced as a powder in FDA-registered factories, mostly in China, then reconstitute it with sterile water and an antimicrobial in small glass vials.

Together, the compounding pharmacies may account for up to 30% of the semaglutide sold in the United States, Mr. Mikhael said, although he cautions that is a “wild ballpark figure” since no one, including the FDA, is tracking sales in the industry.

The compounders say the companies should increase production if they’re worried about competition. Like the dozens of other drugs they produce for hospitals and medical practices, the compounders say, the two diet drugs are essential products.

“If you don’t want a 503B facility to make a copy, it’s pretty simple: Don’t go short,” said Lee Rosebush, chair of a trade association for 503B pharmacies. “FDA created this system because these are necessary drugs.”

Novo Nordisk hasn’t specified why it can’t keep up with demand, but the bottleneck apparently lies in the company’s inability to fill and sterilize enough of its special drug auto-injectors, said Evan Seigerman, a managing director at BMO Capital Markets.

The company announced June 24 that it was investing $4.1 billion in new production lines at its Clayton, North Carolina, site. In 2023, the FDA issued a warning over procedural violations at the site and separate cautions at an Indiana facility that Novo Nordisk took over recently.
 

Compounding for Dummies

At least 28 companies, mostly in China, are registered with the FDA to produce or distribute semaglutide. At least half the companies have entered the market in the past 12 months, driving the raw material’s price down by 35%, according to Scott Welch, who runs a 503A pharmacy in Arlington, Virginia.

Compounders can buy powdered semaglutide from some US distributors for less than $4,000 a gram, said Matthew Johnson, president and CEO of distributor Pharma Source Direct. That comes out to as little as $10 per weekly 2.5-microgram dose – not including overhead and other costs.

While Ozempic or Wegovy patients use a Novo Nordisk device to inject the drug, patients using compounded products draw them from a vial with a small needle, like the device diabetics use for insulin.

Some medical practices provide the compounded drug to patients as part of a weight loss package, with markups. In July 2023, Tabitha Ries, a single mother of six who works as a home health care aide in Garfield, Washington, found an online clinic that charged her $1,000 for 3 months of semaglutide along with counseling. She has lost 35 pounds.

She gets the drug from Mindful Weight Loss, a mostly telehealth-based operation led by physician Vivek Gupta, MD, of Manhattan Beach, California. Dr. Gupta said he’s prescribed the weight loss drugs to 1,500 patients, with about 60% using compounded versions from a 503A pharmacy.

He hasn’t seen any essential difference in patients using the branded and compounded forms, although “some people say the compounding is a little less effective,” Dr. Gupta said.

There’s some risk in using the non–FDA-approved product, he acknowledged, and he requires patients to sign an informed consent waiver.

“Nothing in life is without risk, but I would also argue that the status quo is not safe for people who need the medicine and can’t get it,” he said. “They’re constantly triggered by all this food that’s causing their weight to go up and their sugar to go high, increasing their insulin resistance and affecting their limbs and eyes.”

Compounding semaglutide is a helpful sideline for pharmacists like him, Mr. Welch said, especially given the pinch on drug sale revenue that has led many independents to close in recent years. He figures he earns 95% of his revenue from compounding drugs, rather than traditional prescriptions.

It’s important to distinguish compounded semaglutide from unregulated powders sold as “generic Ozempic” and the like, which may be contaminated or counterfeit, said FDA spokesperson Amanda Hils. But since compounded forms of the drug are not FDA approved, those who make, prescribe, or use them also should have “an increased level of responsibility or awareness,” she said.
 

Corporate Battles

Novo Nordisk and Lilly, in lawsuits each company has filed against competitors, say their own testing has found bacteria and other impurities in products made by compounding pharmacies. The companies also report patent infringement, but compounders, pointing to the FDA loophole for drugs in shortage, appear to have defeated that argument for now.

When the FDA removes the drugs from the shortage list, 503B compounders must immediately stop selling them. Smaller compounders may be able to produce their products for a reduced number of patients, said Scott Brunner, CEO of the Alliance for Pharmacy Compounding, which represents 503A compounders.

The evaporation of the compounded drug supply could come as a shock to patients.

“I dread it,” said David Wertheimer, an internist in Franklin Lakes, New Jersey, who prescribes compounded semaglutide to some patients. “People are not going to be able to plunk down a grand every month. A lot of people will go off the drug, and that’s a shame.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

This transcript has been edited for clarity.

On today’s edition of Beyond BMI, I’ll be discussing weight plateaus. This is something that our patients are very familiar with. Sometimes, they’re happy with their weight when they plateau; sometimes, they’re not. A weight plateau is simply a state of equilibrium.

There’s a common adage that the last 5 pounds are the hardest. When people decrease their calorie intake and increase their activity — as we instruct our patients to do to lose weight — the body starts to fight back because it believes this is a famine state. Our bodies feel that we are running around the jungle looking for food to help us survive a perceived famine state.

The body does a few things to help us keep weight on, and this is what leads to the frustration of not being able to lose those last 5 pounds. The first thing that happens in this process, which is called metabolic adaptation, is that when someone loses weight, the body naturally increases appetite signals from the brain, so the person becomes hungrier. Satiety signals from the stomach also decrease, so they feel more hungry and less full. And finally, stable fat cells form to allow the person to seek out more food without losing weight. This eventually leads the patient to regain weight, or they may plateau at a weight they’re not happy with.

I’m sure you’ve seen many studies looking at weight plateaus and the amount of weight loss people are able to achieve with diet, exercise, and behavior change alone vs the same lifestyle modifications plus medication. Studies show that patients who are taking anti-obesity medications achieve far more weight loss than do those who are not taking medications. The reason is related to the different mechanisms of action of the anti-obesity medications. Patients taking these medications are able to tolerate a lower caloric intake for a longer period of time, thus they’re able to burn more fat cells and lose more weight. Some medications perform this by decreasing appetite signals, so patients can continue to eat a small number of calories. Some medications affect the stability of fat cells. Some medications also increase satiety signals, so patients can move beyond that degree of metabolic adaptation and get beyond their previous plateau.

What can we do for patients who are frustrated with their weight plateau? I recommend taking a dive into their daily routine. Find out how many calories they are eating. Find out how much exercise they are doing and see whether there’s any room to reorganize the day or change their meals to create a caloric deficit. Are they eating things that are not filling enough, so they can’t get to the next meal without having a snack in between? We are looking at the quality of the meals as well and making sure there’s an adequate amount of protein and fiber in their meals to help with those increased appetite signals. We should also make sure these patients are getting adequate fluid intake.

These are all strategies that can help our patients try to get beyond their weight plateaus.

If the patient meets criteria for anti-obesity medication, which means a body mass index (BMI) of 27-29 with a weight-related comorbidity or BMI ≥ 30 with or without a comorbidity, you may want to consider anti-obesity medication to help that patient get beyond the plateau.

Plateaus will occur as a natural process because of the appetite signaling and hormonal changes that occur when patients lose weight from any modality. It’s important that we work with our patients to determine whether their weight plateau is due to metabolic adaptation. If they aren’t meeting their goals and they have weight-related comorbidities, we can use other available modalities to help those patients continue to lose weight. Of course, whenever we are prescribing a medication, we need to make sure that it is safe for the patient and the patient is on board with the potential side effects and risks. And we should always make sure our patients know we are their advocates in their weight journey.

Holly Lofton, clinical associate professor of surgery and medicine, NYU Langone Health, New York, NY, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity.

On today’s edition of Beyond BMI, I’ll be discussing weight plateaus. This is something that our patients are very familiar with. Sometimes, they’re happy with their weight when they plateau; sometimes, they’re not. A weight plateau is simply a state of equilibrium.

There’s a common adage that the last 5 pounds are the hardest. When people decrease their calorie intake and increase their activity — as we instruct our patients to do to lose weight — the body starts to fight back because it believes this is a famine state. Our bodies feel that we are running around the jungle looking for food to help us survive a perceived famine state.

The body does a few things to help us keep weight on, and this is what leads to the frustration of not being able to lose those last 5 pounds. The first thing that happens in this process, which is called metabolic adaptation, is that when someone loses weight, the body naturally increases appetite signals from the brain, so the person becomes hungrier. Satiety signals from the stomach also decrease, so they feel more hungry and less full. And finally, stable fat cells form to allow the person to seek out more food without losing weight. This eventually leads the patient to regain weight, or they may plateau at a weight they’re not happy with.

I’m sure you’ve seen many studies looking at weight plateaus and the amount of weight loss people are able to achieve with diet, exercise, and behavior change alone vs the same lifestyle modifications plus medication. Studies show that patients who are taking anti-obesity medications achieve far more weight loss than do those who are not taking medications. The reason is related to the different mechanisms of action of the anti-obesity medications. Patients taking these medications are able to tolerate a lower caloric intake for a longer period of time, thus they’re able to burn more fat cells and lose more weight. Some medications perform this by decreasing appetite signals, so patients can continue to eat a small number of calories. Some medications affect the stability of fat cells. Some medications also increase satiety signals, so patients can move beyond that degree of metabolic adaptation and get beyond their previous plateau.

What can we do for patients who are frustrated with their weight plateau? I recommend taking a dive into their daily routine. Find out how many calories they are eating. Find out how much exercise they are doing and see whether there’s any room to reorganize the day or change their meals to create a caloric deficit. Are they eating things that are not filling enough, so they can’t get to the next meal without having a snack in between? We are looking at the quality of the meals as well and making sure there’s an adequate amount of protein and fiber in their meals to help with those increased appetite signals. We should also make sure these patients are getting adequate fluid intake.

These are all strategies that can help our patients try to get beyond their weight plateaus.

If the patient meets criteria for anti-obesity medication, which means a body mass index (BMI) of 27-29 with a weight-related comorbidity or BMI ≥ 30 with or without a comorbidity, you may want to consider anti-obesity medication to help that patient get beyond the plateau.

Plateaus will occur as a natural process because of the appetite signaling and hormonal changes that occur when patients lose weight from any modality. It’s important that we work with our patients to determine whether their weight plateau is due to metabolic adaptation. If they aren’t meeting their goals and they have weight-related comorbidities, we can use other available modalities to help those patients continue to lose weight. Of course, whenever we are prescribing a medication, we need to make sure that it is safe for the patient and the patient is on board with the potential side effects and risks. And we should always make sure our patients know we are their advocates in their weight journey.

Holly Lofton, clinical associate professor of surgery and medicine, NYU Langone Health, New York, NY, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity.

On today’s edition of Beyond BMI, I’ll be discussing weight plateaus. This is something that our patients are very familiar with. Sometimes, they’re happy with their weight when they plateau; sometimes, they’re not. A weight plateau is simply a state of equilibrium.

There’s a common adage that the last 5 pounds are the hardest. When people decrease their calorie intake and increase their activity — as we instruct our patients to do to lose weight — the body starts to fight back because it believes this is a famine state. Our bodies feel that we are running around the jungle looking for food to help us survive a perceived famine state.

The body does a few things to help us keep weight on, and this is what leads to the frustration of not being able to lose those last 5 pounds. The first thing that happens in this process, which is called metabolic adaptation, is that when someone loses weight, the body naturally increases appetite signals from the brain, so the person becomes hungrier. Satiety signals from the stomach also decrease, so they feel more hungry and less full. And finally, stable fat cells form to allow the person to seek out more food without losing weight. This eventually leads the patient to regain weight, or they may plateau at a weight they’re not happy with.

I’m sure you’ve seen many studies looking at weight plateaus and the amount of weight loss people are able to achieve with diet, exercise, and behavior change alone vs the same lifestyle modifications plus medication. Studies show that patients who are taking anti-obesity medications achieve far more weight loss than do those who are not taking medications. The reason is related to the different mechanisms of action of the anti-obesity medications. Patients taking these medications are able to tolerate a lower caloric intake for a longer period of time, thus they’re able to burn more fat cells and lose more weight. Some medications perform this by decreasing appetite signals, so patients can continue to eat a small number of calories. Some medications affect the stability of fat cells. Some medications also increase satiety signals, so patients can move beyond that degree of metabolic adaptation and get beyond their previous plateau.

What can we do for patients who are frustrated with their weight plateau? I recommend taking a dive into their daily routine. Find out how many calories they are eating. Find out how much exercise they are doing and see whether there’s any room to reorganize the day or change their meals to create a caloric deficit. Are they eating things that are not filling enough, so they can’t get to the next meal without having a snack in between? We are looking at the quality of the meals as well and making sure there’s an adequate amount of protein and fiber in their meals to help with those increased appetite signals. We should also make sure these patients are getting adequate fluid intake.

These are all strategies that can help our patients try to get beyond their weight plateaus.

If the patient meets criteria for anti-obesity medication, which means a body mass index (BMI) of 27-29 with a weight-related comorbidity or BMI ≥ 30 with or without a comorbidity, you may want to consider anti-obesity medication to help that patient get beyond the plateau.

Plateaus will occur as a natural process because of the appetite signaling and hormonal changes that occur when patients lose weight from any modality. It’s important that we work with our patients to determine whether their weight plateau is due to metabolic adaptation. If they aren’t meeting their goals and they have weight-related comorbidities, we can use other available modalities to help those patients continue to lose weight. Of course, whenever we are prescribing a medication, we need to make sure that it is safe for the patient and the patient is on board with the potential side effects and risks. And we should always make sure our patients know we are their advocates in their weight journey.

Holly Lofton, clinical associate professor of surgery and medicine, NYU Langone Health, New York, NY, has disclosed no relevant financial relationships.

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