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New antiobesity drugs will benefit many. Is that bad?
where some economists opined that their coverage would be disastrous for Medicare.
Among their concerns? The drugs need to be taken long term (just like drugs for any other chronic condition). The new drugs are more expensive than the old drugs (just like new drugs for any other chronic condition). Lots of people will want to take them (just like highly effective drugs for any other chronic condition that has a significant quality-of-life or clinical impact). The U.K. recommended that they be covered only for 2 years (unlike drugs for any other chronic condition). And the Institute for Clinical and Economic Review (ICER) on which they lean heavily decided that $13,618 annually was too expensive for a medication that leads to sustained 15%-20% weight losses and those losses’ consequential benefits.
As a clinician working with patients who sustain those levels of weight loss, I find that conclusion confusing. Whether by way of lifestyle alone, or more often by way of lifestyle efforts plus medication or lifestyle efforts plus surgery, the benefits reported and seen with 15%-20% weight losses are almost uniformly huge. Patients are regularly seen discontinuing or reducing the dosage of multiple medications as a result of improvements to multiple weight-responsive comorbidities, and they also report objective benefits to mood, sleep, mobility, pain, and energy. Losing that much weight changes lives. Not to mention the impact that that degree of loss has on the primary prevention of so many diseases, including plausible reductions in many common cancers – reductions that have been shown to occur after surgery-related weight losses and for which there’s no plausible reason to imagine that they wouldn’t occur with pharmaceutical-related losses.
Are those discussions found in the NEJM op-ed or in the ICER report? Well, yes, sort of. However, in the NEJM op-ed, the word “prevention” isn’t used once, and unlike with oral hypoglycemics or antihypertensives, the authors state that with antiobesity medications, additional research is needed to determine whether medication-induced changes to A1c, blood pressure, and waist circumference would have clinical benefits: “Antiobesity medications have been shown to improve the surrogate end points of weight, glycated hemoglobin levels, systolic blood pressure, and waist circumference. Long-term studies are needed, however, to clarify how medication-induced changes in these surrogate markers translate to health outcomes.”
Primary prevention is mentioned in the ICER review, but in the “limitations” section where the authors explain that they didn’t include it in their modeling: “The long-term benefits of preventing other comorbidities including cancer, chronic kidney disease, osteoarthritis, and sleep apnea were not explicitly modeled in the base case.”
And they pretended that the impact on existing weight-responsive comorbidities mostly didn’t exist, too: “To limit the complexity of the cost-effectiveness model and to prevent double-counting of treatment benefits, we limited the long-term effects of treatments for weight management to cardiovascular risk and delays in the onset and/or diagnosis of diabetes mellitus.”
As far as cardiovascular disease (CVD) benefits go, you might have thought that it would be a slam dunk on that basis alone, at least according to a recent simple back-of-the-envelope math exercise presented at a recent American College of Cardiology conference, which applied the semaglutide treatment group weight changes in the STEP 1 trial to estimate the population impact on weight and obesity in 30- to 74-year-olds without prior CVD, and estimated 10-year CVD risks utilizing the BMI-based Framingham CVD risk scores. By their accounting, semaglutide treatment in eligible American patients has the potential to prevent over 1.6 million CVD events over 10 years.
Finally, even putting aside ICER’s admittedly and exceedingly narrow base case, what lifestyle-alone studies could ICER possibly be comparing with drug efficacy? And what does “alone” mean? Does “alone” mean with a months- or years long interprofessional behavioral program? Does “alone” mean by way of diet books? Does “alone” mean by way of simply “moving more and eating less”? I’m not aware of robust studies demonstrating any long-term meaningful, predictable, reproducible, durable weight loss outcomes for any lifestyle-only approach, intensive or otherwise.
It’s difficult for me to imagine a situation in which a drug other than an antiobesity drug would be found to have too many benefits to include in your cost-effectiveness analysis but where you’d be comfortable to run that analysis anyhow, and then come out against the drug’s recommendation and fearmonger about its use.
But then again, systemic weight bias is a hell of a drug.
Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa. He disclosed ties with Constant Health and Novo Nordisk, and has shared opinions via Weighty Matters and social media.
A version of this article originally appeared on Medscape.com.
where some economists opined that their coverage would be disastrous for Medicare.
Among their concerns? The drugs need to be taken long term (just like drugs for any other chronic condition). The new drugs are more expensive than the old drugs (just like new drugs for any other chronic condition). Lots of people will want to take them (just like highly effective drugs for any other chronic condition that has a significant quality-of-life or clinical impact). The U.K. recommended that they be covered only for 2 years (unlike drugs for any other chronic condition). And the Institute for Clinical and Economic Review (ICER) on which they lean heavily decided that $13,618 annually was too expensive for a medication that leads to sustained 15%-20% weight losses and those losses’ consequential benefits.
As a clinician working with patients who sustain those levels of weight loss, I find that conclusion confusing. Whether by way of lifestyle alone, or more often by way of lifestyle efforts plus medication or lifestyle efforts plus surgery, the benefits reported and seen with 15%-20% weight losses are almost uniformly huge. Patients are regularly seen discontinuing or reducing the dosage of multiple medications as a result of improvements to multiple weight-responsive comorbidities, and they also report objective benefits to mood, sleep, mobility, pain, and energy. Losing that much weight changes lives. Not to mention the impact that that degree of loss has on the primary prevention of so many diseases, including plausible reductions in many common cancers – reductions that have been shown to occur after surgery-related weight losses and for which there’s no plausible reason to imagine that they wouldn’t occur with pharmaceutical-related losses.
Are those discussions found in the NEJM op-ed or in the ICER report? Well, yes, sort of. However, in the NEJM op-ed, the word “prevention” isn’t used once, and unlike with oral hypoglycemics or antihypertensives, the authors state that with antiobesity medications, additional research is needed to determine whether medication-induced changes to A1c, blood pressure, and waist circumference would have clinical benefits: “Antiobesity medications have been shown to improve the surrogate end points of weight, glycated hemoglobin levels, systolic blood pressure, and waist circumference. Long-term studies are needed, however, to clarify how medication-induced changes in these surrogate markers translate to health outcomes.”
Primary prevention is mentioned in the ICER review, but in the “limitations” section where the authors explain that they didn’t include it in their modeling: “The long-term benefits of preventing other comorbidities including cancer, chronic kidney disease, osteoarthritis, and sleep apnea were not explicitly modeled in the base case.”
And they pretended that the impact on existing weight-responsive comorbidities mostly didn’t exist, too: “To limit the complexity of the cost-effectiveness model and to prevent double-counting of treatment benefits, we limited the long-term effects of treatments for weight management to cardiovascular risk and delays in the onset and/or diagnosis of diabetes mellitus.”
As far as cardiovascular disease (CVD) benefits go, you might have thought that it would be a slam dunk on that basis alone, at least according to a recent simple back-of-the-envelope math exercise presented at a recent American College of Cardiology conference, which applied the semaglutide treatment group weight changes in the STEP 1 trial to estimate the population impact on weight and obesity in 30- to 74-year-olds without prior CVD, and estimated 10-year CVD risks utilizing the BMI-based Framingham CVD risk scores. By their accounting, semaglutide treatment in eligible American patients has the potential to prevent over 1.6 million CVD events over 10 years.
Finally, even putting aside ICER’s admittedly and exceedingly narrow base case, what lifestyle-alone studies could ICER possibly be comparing with drug efficacy? And what does “alone” mean? Does “alone” mean with a months- or years long interprofessional behavioral program? Does “alone” mean by way of diet books? Does “alone” mean by way of simply “moving more and eating less”? I’m not aware of robust studies demonstrating any long-term meaningful, predictable, reproducible, durable weight loss outcomes for any lifestyle-only approach, intensive or otherwise.
It’s difficult for me to imagine a situation in which a drug other than an antiobesity drug would be found to have too many benefits to include in your cost-effectiveness analysis but where you’d be comfortable to run that analysis anyhow, and then come out against the drug’s recommendation and fearmonger about its use.
But then again, systemic weight bias is a hell of a drug.
Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa. He disclosed ties with Constant Health and Novo Nordisk, and has shared opinions via Weighty Matters and social media.
A version of this article originally appeared on Medscape.com.
where some economists opined that their coverage would be disastrous for Medicare.
Among their concerns? The drugs need to be taken long term (just like drugs for any other chronic condition). The new drugs are more expensive than the old drugs (just like new drugs for any other chronic condition). Lots of people will want to take them (just like highly effective drugs for any other chronic condition that has a significant quality-of-life or clinical impact). The U.K. recommended that they be covered only for 2 years (unlike drugs for any other chronic condition). And the Institute for Clinical and Economic Review (ICER) on which they lean heavily decided that $13,618 annually was too expensive for a medication that leads to sustained 15%-20% weight losses and those losses’ consequential benefits.
As a clinician working with patients who sustain those levels of weight loss, I find that conclusion confusing. Whether by way of lifestyle alone, or more often by way of lifestyle efforts plus medication or lifestyle efforts plus surgery, the benefits reported and seen with 15%-20% weight losses are almost uniformly huge. Patients are regularly seen discontinuing or reducing the dosage of multiple medications as a result of improvements to multiple weight-responsive comorbidities, and they also report objective benefits to mood, sleep, mobility, pain, and energy. Losing that much weight changes lives. Not to mention the impact that that degree of loss has on the primary prevention of so many diseases, including plausible reductions in many common cancers – reductions that have been shown to occur after surgery-related weight losses and for which there’s no plausible reason to imagine that they wouldn’t occur with pharmaceutical-related losses.
Are those discussions found in the NEJM op-ed or in the ICER report? Well, yes, sort of. However, in the NEJM op-ed, the word “prevention” isn’t used once, and unlike with oral hypoglycemics or antihypertensives, the authors state that with antiobesity medications, additional research is needed to determine whether medication-induced changes to A1c, blood pressure, and waist circumference would have clinical benefits: “Antiobesity medications have been shown to improve the surrogate end points of weight, glycated hemoglobin levels, systolic blood pressure, and waist circumference. Long-term studies are needed, however, to clarify how medication-induced changes in these surrogate markers translate to health outcomes.”
Primary prevention is mentioned in the ICER review, but in the “limitations” section where the authors explain that they didn’t include it in their modeling: “The long-term benefits of preventing other comorbidities including cancer, chronic kidney disease, osteoarthritis, and sleep apnea were not explicitly modeled in the base case.”
And they pretended that the impact on existing weight-responsive comorbidities mostly didn’t exist, too: “To limit the complexity of the cost-effectiveness model and to prevent double-counting of treatment benefits, we limited the long-term effects of treatments for weight management to cardiovascular risk and delays in the onset and/or diagnosis of diabetes mellitus.”
As far as cardiovascular disease (CVD) benefits go, you might have thought that it would be a slam dunk on that basis alone, at least according to a recent simple back-of-the-envelope math exercise presented at a recent American College of Cardiology conference, which applied the semaglutide treatment group weight changes in the STEP 1 trial to estimate the population impact on weight and obesity in 30- to 74-year-olds without prior CVD, and estimated 10-year CVD risks utilizing the BMI-based Framingham CVD risk scores. By their accounting, semaglutide treatment in eligible American patients has the potential to prevent over 1.6 million CVD events over 10 years.
Finally, even putting aside ICER’s admittedly and exceedingly narrow base case, what lifestyle-alone studies could ICER possibly be comparing with drug efficacy? And what does “alone” mean? Does “alone” mean with a months- or years long interprofessional behavioral program? Does “alone” mean by way of diet books? Does “alone” mean by way of simply “moving more and eating less”? I’m not aware of robust studies demonstrating any long-term meaningful, predictable, reproducible, durable weight loss outcomes for any lifestyle-only approach, intensive or otherwise.
It’s difficult for me to imagine a situation in which a drug other than an antiobesity drug would be found to have too many benefits to include in your cost-effectiveness analysis but where you’d be comfortable to run that analysis anyhow, and then come out against the drug’s recommendation and fearmonger about its use.
But then again, systemic weight bias is a hell of a drug.
Dr. Freedhoff is associate professor, department of family medicine, University of Ottawa, and medical director, Bariatric Medical Institute, Ottawa. He disclosed ties with Constant Health and Novo Nordisk, and has shared opinions via Weighty Matters and social media.
A version of this article originally appeared on Medscape.com.
Forceps may help moms with obesity avoid cesareans
Among patients who undergo forceps-assisted vaginal delivery, obesity does not appear to be associated with increased risk for complications such as injuries to the anal sphincter or the need for their babies to be admitted to the neonatal intensive care unit, researchers have found.
But obesity does appear to increase the chances that when physicians attempt operative vaginal delivery with either forceps or a vacuum, patients will wind up undergoing cesarean delivery, another study found.
Taken together, the new data may help inform physicians’ decisions about when to consider operative vaginal delivery as an alternative to emergency cesarean births.
A prospective study showed that failed operative vaginal delivery – that is, a cesarean delivery after an attempted operative vaginal delivery – occurred for 10.1% of patients with obesity and 4.2% of those without obesity.
Researchers presented the findings at the meeting sponsored by the Society for Maternal-Fetal Medicine.
“We want to really try to reduce the rate of C-sections and primary cesarean deliveries. One of the ways to do that is to attempt operative vaginal delivery,” said Marissa Platner, MD, assistant professor of maternal-fetal medicine at Emory University School of Medicine, Atlanta, who was not involved in the new research.
Data on how obesity influences risks with operative vaginal delivery have been limited and mixed, the researchers said.
To examine how often attempted operative vaginal delivery fails in patients with obesity, Jennifer Grasch, MD, a maternal-fetal medicine fellow at the Ohio State University Wexner Medical Center, Columbus, and her colleagues conducted a secondary analysis of data from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be, which included more than 10,000 participants.
“We know that cesarean sections among people with obesity are associated with increased complications, such as higher rates of infection and wound complications, than for people with lower BMI,” Dr. Grasch said. “Operative vaginal delivery can be an alternative to cesarean delivery in some situations, so we were interested in whether attempted operative vaginal delivery was also associated with higher rates of complications in individuals with obesity than those without obesity.”
The researchers focused on 791 patients with an attempted operative vaginal delivery. About 40% had a BMI of 30 or greater. Clinicians used a vacuum in approximately 60% of the attempts.
After an attempted vacuum-assisted delivery, neonatal morbidity was more common for infants whose mothers had obesity than for those whose mothers did not (32.7% vs. 22.3%; adjusted odds ratio, 1.61 [1.07-2.43]). Neonatal morbidity did not differ by obesity status following forceps-attempted delivery. Other adverse outcomes, including measures of maternal morbidity, did not significantly differ by obesity status, according to the researchers.
Choice may come down to experience
Several factors influence whether a clinician chooses forceps- or vacuum-assisted delivery or cesarean delivery, “but one of the most important is experience,” Dr. Grasch said. “Complication rates with both forms of operative vaginal delivery are low, yet there has been a trend toward lower rates of both in the last few decades.”
Elizabeth Cochrane, MD, a maternal-fetal medicine fellow at Mount Sinai Hospital, New York, and her colleagues investigated the relationship between obesity and adverse outcomes among patients with forceps-assisted vaginal deliveries.
The researchers analyzed data from 897 patients who underwent a forceps-assisted vaginal delivery between 2017 and 2021; 29% had a BMI of 30 or greater.
Injuries to the anal sphincter – which can lead to fecal incontinence – occurred in 18.7% of patients without obesity and in 17.7% of those with obesity. Admission to the neonatal intensive care unit occurred in 11.5% of patients without obesity and in 12.3% of patients with obesity. The differences were not statistically significant.
The bottom line: For forceps-assisted vaginal delivery, “obesity does not appear to be associated with increased rates” of adverse outcomes for mothers or newborns, the researchers concluded.
Reassuring data
The study by Dr. Cochrane’s group “provides helpful information for providers to be reassured when they are performing forceps deliveries” for patients with obesity, Dr. Platner said.
Rates of obesity have risen in the United States, and physicians often wonder whether a patient with obesity could be a candidate for forceps-assisted delivery, Dr. Cochrane said. In 2019, 29% of women had obesity before becoming pregnant.
“It all really comes down to how comfortable the provider is in that skill set and also the overall clinical scenario,” she said. “Sometimes an operative delivery with forceps or a vacuum can be the fastest way to deliver a baby when there is acute concern for maternal decompensation or fetal decompensation.”
The alternative is an emergency cesarean delivery. Given that those operations can be riskier and more difficult for patients with higher BMIs, a forceps-assisted delivery may be “an interesting alternative to emergency caesarean sections, as long as it is in an appropriate clinical setting with providers who feel very confident and comfortable using those devices,” Dr. Cochrane said.
A version of this article first appeared on Medscape.com.
Among patients who undergo forceps-assisted vaginal delivery, obesity does not appear to be associated with increased risk for complications such as injuries to the anal sphincter or the need for their babies to be admitted to the neonatal intensive care unit, researchers have found.
But obesity does appear to increase the chances that when physicians attempt operative vaginal delivery with either forceps or a vacuum, patients will wind up undergoing cesarean delivery, another study found.
Taken together, the new data may help inform physicians’ decisions about when to consider operative vaginal delivery as an alternative to emergency cesarean births.
A prospective study showed that failed operative vaginal delivery – that is, a cesarean delivery after an attempted operative vaginal delivery – occurred for 10.1% of patients with obesity and 4.2% of those without obesity.
Researchers presented the findings at the meeting sponsored by the Society for Maternal-Fetal Medicine.
“We want to really try to reduce the rate of C-sections and primary cesarean deliveries. One of the ways to do that is to attempt operative vaginal delivery,” said Marissa Platner, MD, assistant professor of maternal-fetal medicine at Emory University School of Medicine, Atlanta, who was not involved in the new research.
Data on how obesity influences risks with operative vaginal delivery have been limited and mixed, the researchers said.
To examine how often attempted operative vaginal delivery fails in patients with obesity, Jennifer Grasch, MD, a maternal-fetal medicine fellow at the Ohio State University Wexner Medical Center, Columbus, and her colleagues conducted a secondary analysis of data from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be, which included more than 10,000 participants.
“We know that cesarean sections among people with obesity are associated with increased complications, such as higher rates of infection and wound complications, than for people with lower BMI,” Dr. Grasch said. “Operative vaginal delivery can be an alternative to cesarean delivery in some situations, so we were interested in whether attempted operative vaginal delivery was also associated with higher rates of complications in individuals with obesity than those without obesity.”
The researchers focused on 791 patients with an attempted operative vaginal delivery. About 40% had a BMI of 30 or greater. Clinicians used a vacuum in approximately 60% of the attempts.
After an attempted vacuum-assisted delivery, neonatal morbidity was more common for infants whose mothers had obesity than for those whose mothers did not (32.7% vs. 22.3%; adjusted odds ratio, 1.61 [1.07-2.43]). Neonatal morbidity did not differ by obesity status following forceps-attempted delivery. Other adverse outcomes, including measures of maternal morbidity, did not significantly differ by obesity status, according to the researchers.
Choice may come down to experience
Several factors influence whether a clinician chooses forceps- or vacuum-assisted delivery or cesarean delivery, “but one of the most important is experience,” Dr. Grasch said. “Complication rates with both forms of operative vaginal delivery are low, yet there has been a trend toward lower rates of both in the last few decades.”
Elizabeth Cochrane, MD, a maternal-fetal medicine fellow at Mount Sinai Hospital, New York, and her colleagues investigated the relationship between obesity and adverse outcomes among patients with forceps-assisted vaginal deliveries.
The researchers analyzed data from 897 patients who underwent a forceps-assisted vaginal delivery between 2017 and 2021; 29% had a BMI of 30 or greater.
Injuries to the anal sphincter – which can lead to fecal incontinence – occurred in 18.7% of patients without obesity and in 17.7% of those with obesity. Admission to the neonatal intensive care unit occurred in 11.5% of patients without obesity and in 12.3% of patients with obesity. The differences were not statistically significant.
The bottom line: For forceps-assisted vaginal delivery, “obesity does not appear to be associated with increased rates” of adverse outcomes for mothers or newborns, the researchers concluded.
Reassuring data
The study by Dr. Cochrane’s group “provides helpful information for providers to be reassured when they are performing forceps deliveries” for patients with obesity, Dr. Platner said.
Rates of obesity have risen in the United States, and physicians often wonder whether a patient with obesity could be a candidate for forceps-assisted delivery, Dr. Cochrane said. In 2019, 29% of women had obesity before becoming pregnant.
“It all really comes down to how comfortable the provider is in that skill set and also the overall clinical scenario,” she said. “Sometimes an operative delivery with forceps or a vacuum can be the fastest way to deliver a baby when there is acute concern for maternal decompensation or fetal decompensation.”
The alternative is an emergency cesarean delivery. Given that those operations can be riskier and more difficult for patients with higher BMIs, a forceps-assisted delivery may be “an interesting alternative to emergency caesarean sections, as long as it is in an appropriate clinical setting with providers who feel very confident and comfortable using those devices,” Dr. Cochrane said.
A version of this article first appeared on Medscape.com.
Among patients who undergo forceps-assisted vaginal delivery, obesity does not appear to be associated with increased risk for complications such as injuries to the anal sphincter or the need for their babies to be admitted to the neonatal intensive care unit, researchers have found.
But obesity does appear to increase the chances that when physicians attempt operative vaginal delivery with either forceps or a vacuum, patients will wind up undergoing cesarean delivery, another study found.
Taken together, the new data may help inform physicians’ decisions about when to consider operative vaginal delivery as an alternative to emergency cesarean births.
A prospective study showed that failed operative vaginal delivery – that is, a cesarean delivery after an attempted operative vaginal delivery – occurred for 10.1% of patients with obesity and 4.2% of those without obesity.
Researchers presented the findings at the meeting sponsored by the Society for Maternal-Fetal Medicine.
“We want to really try to reduce the rate of C-sections and primary cesarean deliveries. One of the ways to do that is to attempt operative vaginal delivery,” said Marissa Platner, MD, assistant professor of maternal-fetal medicine at Emory University School of Medicine, Atlanta, who was not involved in the new research.
Data on how obesity influences risks with operative vaginal delivery have been limited and mixed, the researchers said.
To examine how often attempted operative vaginal delivery fails in patients with obesity, Jennifer Grasch, MD, a maternal-fetal medicine fellow at the Ohio State University Wexner Medical Center, Columbus, and her colleagues conducted a secondary analysis of data from the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be, which included more than 10,000 participants.
“We know that cesarean sections among people with obesity are associated with increased complications, such as higher rates of infection and wound complications, than for people with lower BMI,” Dr. Grasch said. “Operative vaginal delivery can be an alternative to cesarean delivery in some situations, so we were interested in whether attempted operative vaginal delivery was also associated with higher rates of complications in individuals with obesity than those without obesity.”
The researchers focused on 791 patients with an attempted operative vaginal delivery. About 40% had a BMI of 30 or greater. Clinicians used a vacuum in approximately 60% of the attempts.
After an attempted vacuum-assisted delivery, neonatal morbidity was more common for infants whose mothers had obesity than for those whose mothers did not (32.7% vs. 22.3%; adjusted odds ratio, 1.61 [1.07-2.43]). Neonatal morbidity did not differ by obesity status following forceps-attempted delivery. Other adverse outcomes, including measures of maternal morbidity, did not significantly differ by obesity status, according to the researchers.
Choice may come down to experience
Several factors influence whether a clinician chooses forceps- or vacuum-assisted delivery or cesarean delivery, “but one of the most important is experience,” Dr. Grasch said. “Complication rates with both forms of operative vaginal delivery are low, yet there has been a trend toward lower rates of both in the last few decades.”
Elizabeth Cochrane, MD, a maternal-fetal medicine fellow at Mount Sinai Hospital, New York, and her colleagues investigated the relationship between obesity and adverse outcomes among patients with forceps-assisted vaginal deliveries.
The researchers analyzed data from 897 patients who underwent a forceps-assisted vaginal delivery between 2017 and 2021; 29% had a BMI of 30 or greater.
Injuries to the anal sphincter – which can lead to fecal incontinence – occurred in 18.7% of patients without obesity and in 17.7% of those with obesity. Admission to the neonatal intensive care unit occurred in 11.5% of patients without obesity and in 12.3% of patients with obesity. The differences were not statistically significant.
The bottom line: For forceps-assisted vaginal delivery, “obesity does not appear to be associated with increased rates” of adverse outcomes for mothers or newborns, the researchers concluded.
Reassuring data
The study by Dr. Cochrane’s group “provides helpful information for providers to be reassured when they are performing forceps deliveries” for patients with obesity, Dr. Platner said.
Rates of obesity have risen in the United States, and physicians often wonder whether a patient with obesity could be a candidate for forceps-assisted delivery, Dr. Cochrane said. In 2019, 29% of women had obesity before becoming pregnant.
“It all really comes down to how comfortable the provider is in that skill set and also the overall clinical scenario,” she said. “Sometimes an operative delivery with forceps or a vacuum can be the fastest way to deliver a baby when there is acute concern for maternal decompensation or fetal decompensation.”
The alternative is an emergency cesarean delivery. Given that those operations can be riskier and more difficult for patients with higher BMIs, a forceps-assisted delivery may be “an interesting alternative to emergency caesarean sections, as long as it is in an appropriate clinical setting with providers who feel very confident and comfortable using those devices,” Dr. Cochrane said.
A version of this article first appeared on Medscape.com.
FROM SMFM 2023
What happens when newer weight loss meds are stopped?
Some of these medicines are approved for treating obesity (Wegovy), whereas others are approved for type 2 diabetes (Ozempic and Mounjaro). Tirzepatide (Mounjaro) has been fast-tracked for approval for weight loss by the U.S. Food and Drug Administration this year, and in the first of the series of studies looking at its effect on obesity, the SURMOUNT-1 trial, tirzepatide demonstrated a mean weight loss of around 22% in people without diabetes, spurring significant off-label use.
Our offices are full of patients who have taken these medications, with unprecedented improvements in their weight, cardiometabolic health, and quality of life. What happens when patients stop taking these medications? Or more importantly, why stop them?
Although these drugs are very effective for weight loss and treating diabetes, there can be adverse effects, primarily gastrointestinal, that limit treatment continuation. Nausea is the most common side effect and usually diminishes over time. Slow dose titration and dietary modification can minimize unwanted gastrointestinal side effects.
Drug-induced acute pancreatitis, a rare adverse event requiring patients to stop therapy, was seen in approximately 0.2% of people in clinical trials.
Medications effective but cost prohibitive?
Beyond adverse effects, patients may be forced to stop treatment because of medication cost, changes in insurance coverage, or issues with drug availability.
Two incretin therapies currently approved for treating obesity – liraglutide (Saxenda) and semaglutide (Wegovy) – cost around $1,400 per month. Insurance coverage and manufacturer discounts can make treatment affordable, but anti-obesity medicines aren’t covered by Medicare or by many employer-sponsored commercial plans.
Changes in employment or insurance coverage, or expiration of manufacturer copay cards, may require patients to stop or change therapies. The increased prescribing and overall expense of these drugs have prompted insurance plans and self-insured groups to consider whether providing coverage for these medications is sustainable.
Limited coverage has led to significant off-label prescribing of incretin therapies that aren’t approved for treating obesity (for instance, Ozempic and Mounjaro) and compounding pharmacies selling peptides that allegedly contain the active pharmaceutical ingredients. High demand for these medications has created significant supply shortages over the past year, causing many people to be without treatment for significant periods of time, as reported by this news organization.
Recently, I saw a patient who lost more than 30 pounds with semaglutide (Wegovy). She then changed employers and the medication was no longer covered. She gained back almost 10 pounds over 3 months and was prescribed tirzepatide (Mounjaro) off-label for weight loss by another provider, using a manufacturer discount card to make the medication affordable. The patient did well with the new regimen and lost about 20 pounds, but the pharmacy stopped filling the prescription when changes were made to the discount card. Afraid of regaining the weight, she came to see us as a new patient to discuss her options with her lack of coverage for anti-obesity medications.
Stopping equals weight regain
Obesity is a chronic disease like hypertension. It responds to treatment and when people stop taking these anti-obesity medications, this is generally associated with increased appetite and less satiety, and there is subsequent weight regain and a recurrence in excess weight-related complications.
The STEP-1 trial extension showed an initial mean body weight reduction of 17.3% with weekly semaglutide 2.4 mg over 1 year. On average, two-thirds of the weight lost was regained by participants within 1 year of stopping semaglutide and the study’s lifestyle intervention. Many of the improvements seen in cardiometabolic variables, like blood glucose and blood pressure, similarly reverted to baseline.
There are also 2-year data from the STEP-5 trial with semaglutide; 3-year data from the SCALE trial with liraglutide; and 5-year nonrandomized data with multiple agents that show durable, clinically significant weight loss from medical therapies for obesity.
These data together demonstrate that medications are effective for durable weight loss if they are continued. However, this is not how obesity is currently treated. Anti-obesity medications are prescribed to less than 3% of eligible people in the United States, and the average duration of therapy is less than 90 days. This treatment length isn’t sufficient to see the full benefits most medications offer and certainly doesn’t support long-term weight maintenance.
A recent study showed that, in addition to maintaining weight loss from medical therapies, incretin-containing anti-obesity medication regimens were effective for treating weight regain and facilitating healthier weight after bariatric surgery.
Chronic therapy is needed for weight maintenance because several neurohormonal changes occur owing to weight loss. Metabolic adaptation is the relative reduction in energy expenditure, below what would be expected, in people after weight loss. When this is combined with physiologic changes that increase appetite and decrease satiety, many people create a positive energy balance that results in weight regain. This has been observed in reality TV shows such as “The Biggest Loser”: It’s biology, not willpower.
Unfortunately, many people – including health care providers – don’t understand how these changes promote weight regain and patients are too often blamed when their weight goes back up after medications are stopped. This blame is greatly misinformed by weight-biased beliefs that people with obesity are lazy and lack self-control for weight loss or maintenance. Nobody would be surprised if someone’s blood pressure went up if their antihypertensive medications were stopped. Why do we think so differently when treating obesity?
The prevalence of obesity in the United States is over 40% and growing. We are fortunate to have new medications that on average lead to 15% or greater weight loss when combined with lifestyle modification.
However, these medications are expensive and the limited insurance coverage currently available may not improve. From a patient experience perspective, it’s distressing to have to discontinue treatments that have helped to achieve a healthier weight and then experience regain.
People need better access to evidence-based treatments for obesity, which include lifestyle interventions, anti-obesity medications, and bariatric procedures. Successful treatment of obesity should include a personalized, patient-centered approach that may require a combination of therapies, such as medications and surgery, for lasting weight control.
Dr. Almandoz is associate professor, department of internal medicine, division of endocrinology; medical director, weight wellness program, University of Texas Southwestern, Dallas. He disclosed ties with Novo Nordisk and Eli Lilly. Follow Dr. Almandoz on Twitter: @JaimeAlmandoz.
A version of this article originally appeared on Medscape.com.
Some of these medicines are approved for treating obesity (Wegovy), whereas others are approved for type 2 diabetes (Ozempic and Mounjaro). Tirzepatide (Mounjaro) has been fast-tracked for approval for weight loss by the U.S. Food and Drug Administration this year, and in the first of the series of studies looking at its effect on obesity, the SURMOUNT-1 trial, tirzepatide demonstrated a mean weight loss of around 22% in people without diabetes, spurring significant off-label use.
Our offices are full of patients who have taken these medications, with unprecedented improvements in their weight, cardiometabolic health, and quality of life. What happens when patients stop taking these medications? Or more importantly, why stop them?
Although these drugs are very effective for weight loss and treating diabetes, there can be adverse effects, primarily gastrointestinal, that limit treatment continuation. Nausea is the most common side effect and usually diminishes over time. Slow dose titration and dietary modification can minimize unwanted gastrointestinal side effects.
Drug-induced acute pancreatitis, a rare adverse event requiring patients to stop therapy, was seen in approximately 0.2% of people in clinical trials.
Medications effective but cost prohibitive?
Beyond adverse effects, patients may be forced to stop treatment because of medication cost, changes in insurance coverage, or issues with drug availability.
Two incretin therapies currently approved for treating obesity – liraglutide (Saxenda) and semaglutide (Wegovy) – cost around $1,400 per month. Insurance coverage and manufacturer discounts can make treatment affordable, but anti-obesity medicines aren’t covered by Medicare or by many employer-sponsored commercial plans.
Changes in employment or insurance coverage, or expiration of manufacturer copay cards, may require patients to stop or change therapies. The increased prescribing and overall expense of these drugs have prompted insurance plans and self-insured groups to consider whether providing coverage for these medications is sustainable.
Limited coverage has led to significant off-label prescribing of incretin therapies that aren’t approved for treating obesity (for instance, Ozempic and Mounjaro) and compounding pharmacies selling peptides that allegedly contain the active pharmaceutical ingredients. High demand for these medications has created significant supply shortages over the past year, causing many people to be without treatment for significant periods of time, as reported by this news organization.
Recently, I saw a patient who lost more than 30 pounds with semaglutide (Wegovy). She then changed employers and the medication was no longer covered. She gained back almost 10 pounds over 3 months and was prescribed tirzepatide (Mounjaro) off-label for weight loss by another provider, using a manufacturer discount card to make the medication affordable. The patient did well with the new regimen and lost about 20 pounds, but the pharmacy stopped filling the prescription when changes were made to the discount card. Afraid of regaining the weight, she came to see us as a new patient to discuss her options with her lack of coverage for anti-obesity medications.
Stopping equals weight regain
Obesity is a chronic disease like hypertension. It responds to treatment and when people stop taking these anti-obesity medications, this is generally associated with increased appetite and less satiety, and there is subsequent weight regain and a recurrence in excess weight-related complications.
The STEP-1 trial extension showed an initial mean body weight reduction of 17.3% with weekly semaglutide 2.4 mg over 1 year. On average, two-thirds of the weight lost was regained by participants within 1 year of stopping semaglutide and the study’s lifestyle intervention. Many of the improvements seen in cardiometabolic variables, like blood glucose and blood pressure, similarly reverted to baseline.
There are also 2-year data from the STEP-5 trial with semaglutide; 3-year data from the SCALE trial with liraglutide; and 5-year nonrandomized data with multiple agents that show durable, clinically significant weight loss from medical therapies for obesity.
These data together demonstrate that medications are effective for durable weight loss if they are continued. However, this is not how obesity is currently treated. Anti-obesity medications are prescribed to less than 3% of eligible people in the United States, and the average duration of therapy is less than 90 days. This treatment length isn’t sufficient to see the full benefits most medications offer and certainly doesn’t support long-term weight maintenance.
A recent study showed that, in addition to maintaining weight loss from medical therapies, incretin-containing anti-obesity medication regimens were effective for treating weight regain and facilitating healthier weight after bariatric surgery.
Chronic therapy is needed for weight maintenance because several neurohormonal changes occur owing to weight loss. Metabolic adaptation is the relative reduction in energy expenditure, below what would be expected, in people after weight loss. When this is combined with physiologic changes that increase appetite and decrease satiety, many people create a positive energy balance that results in weight regain. This has been observed in reality TV shows such as “The Biggest Loser”: It’s biology, not willpower.
Unfortunately, many people – including health care providers – don’t understand how these changes promote weight regain and patients are too often blamed when their weight goes back up after medications are stopped. This blame is greatly misinformed by weight-biased beliefs that people with obesity are lazy and lack self-control for weight loss or maintenance. Nobody would be surprised if someone’s blood pressure went up if their antihypertensive medications were stopped. Why do we think so differently when treating obesity?
The prevalence of obesity in the United States is over 40% and growing. We are fortunate to have new medications that on average lead to 15% or greater weight loss when combined with lifestyle modification.
However, these medications are expensive and the limited insurance coverage currently available may not improve. From a patient experience perspective, it’s distressing to have to discontinue treatments that have helped to achieve a healthier weight and then experience regain.
People need better access to evidence-based treatments for obesity, which include lifestyle interventions, anti-obesity medications, and bariatric procedures. Successful treatment of obesity should include a personalized, patient-centered approach that may require a combination of therapies, such as medications and surgery, for lasting weight control.
Dr. Almandoz is associate professor, department of internal medicine, division of endocrinology; medical director, weight wellness program, University of Texas Southwestern, Dallas. He disclosed ties with Novo Nordisk and Eli Lilly. Follow Dr. Almandoz on Twitter: @JaimeAlmandoz.
A version of this article originally appeared on Medscape.com.
Some of these medicines are approved for treating obesity (Wegovy), whereas others are approved for type 2 diabetes (Ozempic and Mounjaro). Tirzepatide (Mounjaro) has been fast-tracked for approval for weight loss by the U.S. Food and Drug Administration this year, and in the first of the series of studies looking at its effect on obesity, the SURMOUNT-1 trial, tirzepatide demonstrated a mean weight loss of around 22% in people without diabetes, spurring significant off-label use.
Our offices are full of patients who have taken these medications, with unprecedented improvements in their weight, cardiometabolic health, and quality of life. What happens when patients stop taking these medications? Or more importantly, why stop them?
Although these drugs are very effective for weight loss and treating diabetes, there can be adverse effects, primarily gastrointestinal, that limit treatment continuation. Nausea is the most common side effect and usually diminishes over time. Slow dose titration and dietary modification can minimize unwanted gastrointestinal side effects.
Drug-induced acute pancreatitis, a rare adverse event requiring patients to stop therapy, was seen in approximately 0.2% of people in clinical trials.
Medications effective but cost prohibitive?
Beyond adverse effects, patients may be forced to stop treatment because of medication cost, changes in insurance coverage, or issues with drug availability.
Two incretin therapies currently approved for treating obesity – liraglutide (Saxenda) and semaglutide (Wegovy) – cost around $1,400 per month. Insurance coverage and manufacturer discounts can make treatment affordable, but anti-obesity medicines aren’t covered by Medicare or by many employer-sponsored commercial plans.
Changes in employment or insurance coverage, or expiration of manufacturer copay cards, may require patients to stop or change therapies. The increased prescribing and overall expense of these drugs have prompted insurance plans and self-insured groups to consider whether providing coverage for these medications is sustainable.
Limited coverage has led to significant off-label prescribing of incretin therapies that aren’t approved for treating obesity (for instance, Ozempic and Mounjaro) and compounding pharmacies selling peptides that allegedly contain the active pharmaceutical ingredients. High demand for these medications has created significant supply shortages over the past year, causing many people to be without treatment for significant periods of time, as reported by this news organization.
Recently, I saw a patient who lost more than 30 pounds with semaglutide (Wegovy). She then changed employers and the medication was no longer covered. She gained back almost 10 pounds over 3 months and was prescribed tirzepatide (Mounjaro) off-label for weight loss by another provider, using a manufacturer discount card to make the medication affordable. The patient did well with the new regimen and lost about 20 pounds, but the pharmacy stopped filling the prescription when changes were made to the discount card. Afraid of regaining the weight, she came to see us as a new patient to discuss her options with her lack of coverage for anti-obesity medications.
Stopping equals weight regain
Obesity is a chronic disease like hypertension. It responds to treatment and when people stop taking these anti-obesity medications, this is generally associated with increased appetite and less satiety, and there is subsequent weight regain and a recurrence in excess weight-related complications.
The STEP-1 trial extension showed an initial mean body weight reduction of 17.3% with weekly semaglutide 2.4 mg over 1 year. On average, two-thirds of the weight lost was regained by participants within 1 year of stopping semaglutide and the study’s lifestyle intervention. Many of the improvements seen in cardiometabolic variables, like blood glucose and blood pressure, similarly reverted to baseline.
There are also 2-year data from the STEP-5 trial with semaglutide; 3-year data from the SCALE trial with liraglutide; and 5-year nonrandomized data with multiple agents that show durable, clinically significant weight loss from medical therapies for obesity.
These data together demonstrate that medications are effective for durable weight loss if they are continued. However, this is not how obesity is currently treated. Anti-obesity medications are prescribed to less than 3% of eligible people in the United States, and the average duration of therapy is less than 90 days. This treatment length isn’t sufficient to see the full benefits most medications offer and certainly doesn’t support long-term weight maintenance.
A recent study showed that, in addition to maintaining weight loss from medical therapies, incretin-containing anti-obesity medication regimens were effective for treating weight regain and facilitating healthier weight after bariatric surgery.
Chronic therapy is needed for weight maintenance because several neurohormonal changes occur owing to weight loss. Metabolic adaptation is the relative reduction in energy expenditure, below what would be expected, in people after weight loss. When this is combined with physiologic changes that increase appetite and decrease satiety, many people create a positive energy balance that results in weight regain. This has been observed in reality TV shows such as “The Biggest Loser”: It’s biology, not willpower.
Unfortunately, many people – including health care providers – don’t understand how these changes promote weight regain and patients are too often blamed when their weight goes back up after medications are stopped. This blame is greatly misinformed by weight-biased beliefs that people with obesity are lazy and lack self-control for weight loss or maintenance. Nobody would be surprised if someone’s blood pressure went up if their antihypertensive medications were stopped. Why do we think so differently when treating obesity?
The prevalence of obesity in the United States is over 40% and growing. We are fortunate to have new medications that on average lead to 15% or greater weight loss when combined with lifestyle modification.
However, these medications are expensive and the limited insurance coverage currently available may not improve. From a patient experience perspective, it’s distressing to have to discontinue treatments that have helped to achieve a healthier weight and then experience regain.
People need better access to evidence-based treatments for obesity, which include lifestyle interventions, anti-obesity medications, and bariatric procedures. Successful treatment of obesity should include a personalized, patient-centered approach that may require a combination of therapies, such as medications and surgery, for lasting weight control.
Dr. Almandoz is associate professor, department of internal medicine, division of endocrinology; medical director, weight wellness program, University of Texas Southwestern, Dallas. He disclosed ties with Novo Nordisk and Eli Lilly. Follow Dr. Almandoz on Twitter: @JaimeAlmandoz.
A version of this article originally appeared on Medscape.com.
Should GI own the obesity field?
SAN FRANCISCO –
“We see this as a field that GI should own,” said Naresh T. Gunaratnam, MD, a gastroenterologist at Huron Gastro in Ypsilanti, Mich., who has made obesity treatment an important part of his practice.
Gastroenterologists are uniquely qualified in endoscopic sleeve gastroplasty and in the placement of intragastric balloons and can also bring their internal medicine training to bear in patient education and medical prescription, Dr. Gunaratnam said in an interview.
He and three colleagues spoke about innovation in obesity and metabolism at the 2023 AGA Tech Summit sponsored by the AGA Center for GI Innovation and Technology.
Significant hurdles remain to launching new endoscopic devices for treating obesity, but evidence shows that the existing treatments are effective when combined with medication and other treatments, said panelist Reem Z. Sharaiha, MD, MSc, a gastroenterologist with expertise in obesity at Weill Cornell Medicine in New York. “You can never find just one cure for obesity, you should always think about a combination.”
Obesity rates continue to spiral worldwide, with over 100 million adults in the United States weighing in at over 30 kg/m2, said Dr. Sharaiha, but less than 5% per year receive adequate treatment. The condition is driving upticks in diabetes and nonalcoholic fatty liver disease and contributing to cancer, heart disease, stroke, and COVID-19 infections.
Even small reductions in body weight can significantly improve these conditions, she said. Less than a 5% in total body weight on average results in significant reductions in HbA1c, triglycerides, blood pressure and steatosis.
In recent years, the Food and Drug Administration has several devices that gastroenterologists can use to treat obesity, Dr. Sharaiha said, including three brands of intragastric balloon used to reduce appetite by filling the stomach. The AGA now recommends such an intragastric balloon for people with obesity who have “failed a trial of conventional weight-loss strategies.”
But many devices have been withdrawn from the market, including two of the balloon systems. Why do so many devices fail? Sometimes the FDA demands trials that are too expensive, Dr. Sharaiha said. The COVID-19 pandemic put financial pressure on some companies that have already secured FDA approval. Some insurance companies are not willing to pay for the devices, even after the FDA has approved them. Some are not cost effective.
And sometimes patients don’t accept them. That may have been one challenge with Aspire’s AspireAssist, which allowed patients to empty their stomachs into the toilet using a surgically implanted tube, though the company cited “the financial impact of the COVID-19 pandemic” when it withdrew the device from the market last year.
More devices are in the pipeline, but they face an uncertain path forward, Dr. Sharaiha said. “Device companies are usually startups that need funding. With the economic downturn, venture capital funding is hard to get.”
In the meantime, patients with class 3 obesity in particular may benefit from surgery, she said.
For others, medications are playing a more important role in the obesity epidemic, with an average 10%-15% body weight loss, Dr. Sharaiha said. Injections with semaglutide (Ozempic), a glucagon-like peptide 1 (GLP-1) receptor agonist that is approved to improve glycemic control in adults with type 2 diabetes mellitus, is leading the charge.
Tirzepatide (Mounjaro) may be even more effective, Dr. Sharaiha said. The FDA approved the drug last year to improve blood sugar control in adults with type 2 diabetes and was fast-tracked in October for the treatment of adults with obesity, or who are overweight with weight-related comorbidities.
Medications provide add-on benefits to many patients who have been treated with intragastric balloons or endoscopic sleeve gastroplasty, Dr. Sharaiha said.
Also lifestyle and education should not be neglected, said Dr. Gunaratnam, who lost 50 pounds by changing his diet. He urged gastroenterologists to take on the challenge of treating obesity. It’s not the part of his practice with the best reimbursement, but it is the most satisfying. “I get more hugs, cards, and tears by doing this because when you change weight, you’re impacting every part of their lives,” he said.
Dr. Gunaratnam is the founder of Lean Medical LLC and Satya Health Sciences. Dr. Sharaiha has served as a consultant for Boston Scientific Corporation and Cook Medical Inc.
SAN FRANCISCO –
“We see this as a field that GI should own,” said Naresh T. Gunaratnam, MD, a gastroenterologist at Huron Gastro in Ypsilanti, Mich., who has made obesity treatment an important part of his practice.
Gastroenterologists are uniquely qualified in endoscopic sleeve gastroplasty and in the placement of intragastric balloons and can also bring their internal medicine training to bear in patient education and medical prescription, Dr. Gunaratnam said in an interview.
He and three colleagues spoke about innovation in obesity and metabolism at the 2023 AGA Tech Summit sponsored by the AGA Center for GI Innovation and Technology.
Significant hurdles remain to launching new endoscopic devices for treating obesity, but evidence shows that the existing treatments are effective when combined with medication and other treatments, said panelist Reem Z. Sharaiha, MD, MSc, a gastroenterologist with expertise in obesity at Weill Cornell Medicine in New York. “You can never find just one cure for obesity, you should always think about a combination.”
Obesity rates continue to spiral worldwide, with over 100 million adults in the United States weighing in at over 30 kg/m2, said Dr. Sharaiha, but less than 5% per year receive adequate treatment. The condition is driving upticks in diabetes and nonalcoholic fatty liver disease and contributing to cancer, heart disease, stroke, and COVID-19 infections.
Even small reductions in body weight can significantly improve these conditions, she said. Less than a 5% in total body weight on average results in significant reductions in HbA1c, triglycerides, blood pressure and steatosis.
In recent years, the Food and Drug Administration has several devices that gastroenterologists can use to treat obesity, Dr. Sharaiha said, including three brands of intragastric balloon used to reduce appetite by filling the stomach. The AGA now recommends such an intragastric balloon for people with obesity who have “failed a trial of conventional weight-loss strategies.”
But many devices have been withdrawn from the market, including two of the balloon systems. Why do so many devices fail? Sometimes the FDA demands trials that are too expensive, Dr. Sharaiha said. The COVID-19 pandemic put financial pressure on some companies that have already secured FDA approval. Some insurance companies are not willing to pay for the devices, even after the FDA has approved them. Some are not cost effective.
And sometimes patients don’t accept them. That may have been one challenge with Aspire’s AspireAssist, which allowed patients to empty their stomachs into the toilet using a surgically implanted tube, though the company cited “the financial impact of the COVID-19 pandemic” when it withdrew the device from the market last year.
More devices are in the pipeline, but they face an uncertain path forward, Dr. Sharaiha said. “Device companies are usually startups that need funding. With the economic downturn, venture capital funding is hard to get.”
In the meantime, patients with class 3 obesity in particular may benefit from surgery, she said.
For others, medications are playing a more important role in the obesity epidemic, with an average 10%-15% body weight loss, Dr. Sharaiha said. Injections with semaglutide (Ozempic), a glucagon-like peptide 1 (GLP-1) receptor agonist that is approved to improve glycemic control in adults with type 2 diabetes mellitus, is leading the charge.
Tirzepatide (Mounjaro) may be even more effective, Dr. Sharaiha said. The FDA approved the drug last year to improve blood sugar control in adults with type 2 diabetes and was fast-tracked in October for the treatment of adults with obesity, or who are overweight with weight-related comorbidities.
Medications provide add-on benefits to many patients who have been treated with intragastric balloons or endoscopic sleeve gastroplasty, Dr. Sharaiha said.
Also lifestyle and education should not be neglected, said Dr. Gunaratnam, who lost 50 pounds by changing his diet. He urged gastroenterologists to take on the challenge of treating obesity. It’s not the part of his practice with the best reimbursement, but it is the most satisfying. “I get more hugs, cards, and tears by doing this because when you change weight, you’re impacting every part of their lives,” he said.
Dr. Gunaratnam is the founder of Lean Medical LLC and Satya Health Sciences. Dr. Sharaiha has served as a consultant for Boston Scientific Corporation and Cook Medical Inc.
SAN FRANCISCO –
“We see this as a field that GI should own,” said Naresh T. Gunaratnam, MD, a gastroenterologist at Huron Gastro in Ypsilanti, Mich., who has made obesity treatment an important part of his practice.
Gastroenterologists are uniquely qualified in endoscopic sleeve gastroplasty and in the placement of intragastric balloons and can also bring their internal medicine training to bear in patient education and medical prescription, Dr. Gunaratnam said in an interview.
He and three colleagues spoke about innovation in obesity and metabolism at the 2023 AGA Tech Summit sponsored by the AGA Center for GI Innovation and Technology.
Significant hurdles remain to launching new endoscopic devices for treating obesity, but evidence shows that the existing treatments are effective when combined with medication and other treatments, said panelist Reem Z. Sharaiha, MD, MSc, a gastroenterologist with expertise in obesity at Weill Cornell Medicine in New York. “You can never find just one cure for obesity, you should always think about a combination.”
Obesity rates continue to spiral worldwide, with over 100 million adults in the United States weighing in at over 30 kg/m2, said Dr. Sharaiha, but less than 5% per year receive adequate treatment. The condition is driving upticks in diabetes and nonalcoholic fatty liver disease and contributing to cancer, heart disease, stroke, and COVID-19 infections.
Even small reductions in body weight can significantly improve these conditions, she said. Less than a 5% in total body weight on average results in significant reductions in HbA1c, triglycerides, blood pressure and steatosis.
In recent years, the Food and Drug Administration has several devices that gastroenterologists can use to treat obesity, Dr. Sharaiha said, including three brands of intragastric balloon used to reduce appetite by filling the stomach. The AGA now recommends such an intragastric balloon for people with obesity who have “failed a trial of conventional weight-loss strategies.”
But many devices have been withdrawn from the market, including two of the balloon systems. Why do so many devices fail? Sometimes the FDA demands trials that are too expensive, Dr. Sharaiha said. The COVID-19 pandemic put financial pressure on some companies that have already secured FDA approval. Some insurance companies are not willing to pay for the devices, even after the FDA has approved them. Some are not cost effective.
And sometimes patients don’t accept them. That may have been one challenge with Aspire’s AspireAssist, which allowed patients to empty their stomachs into the toilet using a surgically implanted tube, though the company cited “the financial impact of the COVID-19 pandemic” when it withdrew the device from the market last year.
More devices are in the pipeline, but they face an uncertain path forward, Dr. Sharaiha said. “Device companies are usually startups that need funding. With the economic downturn, venture capital funding is hard to get.”
In the meantime, patients with class 3 obesity in particular may benefit from surgery, she said.
For others, medications are playing a more important role in the obesity epidemic, with an average 10%-15% body weight loss, Dr. Sharaiha said. Injections with semaglutide (Ozempic), a glucagon-like peptide 1 (GLP-1) receptor agonist that is approved to improve glycemic control in adults with type 2 diabetes mellitus, is leading the charge.
Tirzepatide (Mounjaro) may be even more effective, Dr. Sharaiha said. The FDA approved the drug last year to improve blood sugar control in adults with type 2 diabetes and was fast-tracked in October for the treatment of adults with obesity, or who are overweight with weight-related comorbidities.
Medications provide add-on benefits to many patients who have been treated with intragastric balloons or endoscopic sleeve gastroplasty, Dr. Sharaiha said.
Also lifestyle and education should not be neglected, said Dr. Gunaratnam, who lost 50 pounds by changing his diet. He urged gastroenterologists to take on the challenge of treating obesity. It’s not the part of his practice with the best reimbursement, but it is the most satisfying. “I get more hugs, cards, and tears by doing this because when you change weight, you’re impacting every part of their lives,” he said.
Dr. Gunaratnam is the founder of Lean Medical LLC and Satya Health Sciences. Dr. Sharaiha has served as a consultant for Boston Scientific Corporation and Cook Medical Inc.
AT THE 2023 AGA TECH SUMMIT
Like mother, like daughter? Moms pass obesity risk to girls
Girls between 4 and 9 years old were more likely to have high fat mass and a high body mass index if their mothers had excess adiposity – but this relationship was not seen between mothers and sons, or between fathers and sons or daughters, in a new study.
The researchers measured fat mass, lean mass, and BMI in the sons and daughters when they were age 4 (before a phenomenon known as “adiposity rebound”), ages 6-7 (around the adiposity rebound), and ages 8-9 (before or at the onset of puberty).
They also obtained measurements from the mothers and fathers when the offspring were ages 8-9.
The group found “a strong association between the fat mass of mothers and their daughters but not their sons,” Rebecca J. Moon, BM, PhD, and colleagues report.
“It would be important to establish persistence through puberty,” according to the researchers, “but nonetheless, these findings are clinically important, highlighting girls who are born to mothers with high BMI and excess adiposity are at high risk of themselves of becoming overweight/obese or having unfavorable body composition early in childhood.”
The mother-daughter relationship for fat mass appears to be established by age 4 years, note Dr. Moon, of the MRC Lifecourse Epidemiology Centre, University of Southampton (England), and colleagues.
Therefore, “early awareness and intervention is needed in mothers with excess adiposity, and potentially beginning even in the periconception and in utero period.”
Because 97% of the mothers and fathers were White, the findings may not be generalizable to other populations, they caution.
The results, from the Southampton Women’s Survey prospective cohort study, were published online in the Journal of Clinical Endocrinology & Metabolism.
One of the first studies to look at fat mass, not just BMI
Children with overweight or obesity are more likely to have excess weight in adulthood that puts them at risk of developing type 2 diabetes, cardiovascular disease, cancer, and osteoarthritis. Previous research has reported that children with overweight or obesity were more likely to have mothers with adiposity.
However, most prior studies have looked at BMI alone and did not measure fat mass, and it was not known how a father’s obesity might affect offspring or how risk may differ in boy versus girl children.
Researchers analyzed data from a subset of participants in the Southampton Women’s Survey of 3,158 women who were aged 20-34 in 1998-2002 and delivered a liveborn infant.
The current study included 240 mother-father-offspring trios who had data for BMI and dual-energy X-ray absorptiometry (DXA) scans (whole body less head).
Mothers were a mean age of 31 years at delivery and had a median pre-pregnancy BMI of 23.7 kg/m2.
The offspring were 129 boys (54%) and 111 girls.
The offspring had DXA scans at ages 4, 6-7, and 8-9 years, and the mothers and fathers had a DXA scan at the last time point.
At ages 6-7 and ages 8-9, BMI and fat mass of the girls reflected that of their mothers (a significant association).
At age 4, BMI and fat mass of the daughters tended to be associated with that of their mothers, but the 95% confidence interval crossed zero.
There were no significant mother-son, father-son, or father-daughter associations for BMI or fat mass at each of the three studied ages.
The study received funding from the Medical Research Council, the British Heart Foundation, the National Institute for Health and Care Research Southampton Biomedical Research Centre, the NIHR Oxford Biomedical Research Centre, the Seventh Framework Program, the Biotechnology and Biological Sciences Research Council, the Horizon 2020 Framework Program, and the National Institute on Aging. Dr. Moon has reported receiving travel bursaries from Kyowa Kirin unrelated to the current study. Disclosures for the other authors are listed with the article.
A version of this article originally appeared on Medscape.com.
Girls between 4 and 9 years old were more likely to have high fat mass and a high body mass index if their mothers had excess adiposity – but this relationship was not seen between mothers and sons, or between fathers and sons or daughters, in a new study.
The researchers measured fat mass, lean mass, and BMI in the sons and daughters when they were age 4 (before a phenomenon known as “adiposity rebound”), ages 6-7 (around the adiposity rebound), and ages 8-9 (before or at the onset of puberty).
They also obtained measurements from the mothers and fathers when the offspring were ages 8-9.
The group found “a strong association between the fat mass of mothers and their daughters but not their sons,” Rebecca J. Moon, BM, PhD, and colleagues report.
“It would be important to establish persistence through puberty,” according to the researchers, “but nonetheless, these findings are clinically important, highlighting girls who are born to mothers with high BMI and excess adiposity are at high risk of themselves of becoming overweight/obese or having unfavorable body composition early in childhood.”
The mother-daughter relationship for fat mass appears to be established by age 4 years, note Dr. Moon, of the MRC Lifecourse Epidemiology Centre, University of Southampton (England), and colleagues.
Therefore, “early awareness and intervention is needed in mothers with excess adiposity, and potentially beginning even in the periconception and in utero period.”
Because 97% of the mothers and fathers were White, the findings may not be generalizable to other populations, they caution.
The results, from the Southampton Women’s Survey prospective cohort study, were published online in the Journal of Clinical Endocrinology & Metabolism.
One of the first studies to look at fat mass, not just BMI
Children with overweight or obesity are more likely to have excess weight in adulthood that puts them at risk of developing type 2 diabetes, cardiovascular disease, cancer, and osteoarthritis. Previous research has reported that children with overweight or obesity were more likely to have mothers with adiposity.
However, most prior studies have looked at BMI alone and did not measure fat mass, and it was not known how a father’s obesity might affect offspring or how risk may differ in boy versus girl children.
Researchers analyzed data from a subset of participants in the Southampton Women’s Survey of 3,158 women who were aged 20-34 in 1998-2002 and delivered a liveborn infant.
The current study included 240 mother-father-offspring trios who had data for BMI and dual-energy X-ray absorptiometry (DXA) scans (whole body less head).
Mothers were a mean age of 31 years at delivery and had a median pre-pregnancy BMI of 23.7 kg/m2.
The offspring were 129 boys (54%) and 111 girls.
The offspring had DXA scans at ages 4, 6-7, and 8-9 years, and the mothers and fathers had a DXA scan at the last time point.
At ages 6-7 and ages 8-9, BMI and fat mass of the girls reflected that of their mothers (a significant association).
At age 4, BMI and fat mass of the daughters tended to be associated with that of their mothers, but the 95% confidence interval crossed zero.
There were no significant mother-son, father-son, or father-daughter associations for BMI or fat mass at each of the three studied ages.
The study received funding from the Medical Research Council, the British Heart Foundation, the National Institute for Health and Care Research Southampton Biomedical Research Centre, the NIHR Oxford Biomedical Research Centre, the Seventh Framework Program, the Biotechnology and Biological Sciences Research Council, the Horizon 2020 Framework Program, and the National Institute on Aging. Dr. Moon has reported receiving travel bursaries from Kyowa Kirin unrelated to the current study. Disclosures for the other authors are listed with the article.
A version of this article originally appeared on Medscape.com.
Girls between 4 and 9 years old were more likely to have high fat mass and a high body mass index if their mothers had excess adiposity – but this relationship was not seen between mothers and sons, or between fathers and sons or daughters, in a new study.
The researchers measured fat mass, lean mass, and BMI in the sons and daughters when they were age 4 (before a phenomenon known as “adiposity rebound”), ages 6-7 (around the adiposity rebound), and ages 8-9 (before or at the onset of puberty).
They also obtained measurements from the mothers and fathers when the offspring were ages 8-9.
The group found “a strong association between the fat mass of mothers and their daughters but not their sons,” Rebecca J. Moon, BM, PhD, and colleagues report.
“It would be important to establish persistence through puberty,” according to the researchers, “but nonetheless, these findings are clinically important, highlighting girls who are born to mothers with high BMI and excess adiposity are at high risk of themselves of becoming overweight/obese or having unfavorable body composition early in childhood.”
The mother-daughter relationship for fat mass appears to be established by age 4 years, note Dr. Moon, of the MRC Lifecourse Epidemiology Centre, University of Southampton (England), and colleagues.
Therefore, “early awareness and intervention is needed in mothers with excess adiposity, and potentially beginning even in the periconception and in utero period.”
Because 97% of the mothers and fathers were White, the findings may not be generalizable to other populations, they caution.
The results, from the Southampton Women’s Survey prospective cohort study, were published online in the Journal of Clinical Endocrinology & Metabolism.
One of the first studies to look at fat mass, not just BMI
Children with overweight or obesity are more likely to have excess weight in adulthood that puts them at risk of developing type 2 diabetes, cardiovascular disease, cancer, and osteoarthritis. Previous research has reported that children with overweight or obesity were more likely to have mothers with adiposity.
However, most prior studies have looked at BMI alone and did not measure fat mass, and it was not known how a father’s obesity might affect offspring or how risk may differ in boy versus girl children.
Researchers analyzed data from a subset of participants in the Southampton Women’s Survey of 3,158 women who were aged 20-34 in 1998-2002 and delivered a liveborn infant.
The current study included 240 mother-father-offspring trios who had data for BMI and dual-energy X-ray absorptiometry (DXA) scans (whole body less head).
Mothers were a mean age of 31 years at delivery and had a median pre-pregnancy BMI of 23.7 kg/m2.
The offspring were 129 boys (54%) and 111 girls.
The offspring had DXA scans at ages 4, 6-7, and 8-9 years, and the mothers and fathers had a DXA scan at the last time point.
At ages 6-7 and ages 8-9, BMI and fat mass of the girls reflected that of their mothers (a significant association).
At age 4, BMI and fat mass of the daughters tended to be associated with that of their mothers, but the 95% confidence interval crossed zero.
There were no significant mother-son, father-son, or father-daughter associations for BMI or fat mass at each of the three studied ages.
The study received funding from the Medical Research Council, the British Heart Foundation, the National Institute for Health and Care Research Southampton Biomedical Research Centre, the NIHR Oxford Biomedical Research Centre, the Seventh Framework Program, the Biotechnology and Biological Sciences Research Council, the Horizon 2020 Framework Program, and the National Institute on Aging. Dr. Moon has reported receiving travel bursaries from Kyowa Kirin unrelated to the current study. Disclosures for the other authors are listed with the article.
A version of this article originally appeared on Medscape.com.
What’s the ‘secret sauce’ to help patients move more?
“Just Do It” is a cute marketing slogan. But let’s face it: Clinically, it doesn’t work well. Most people just don’t exercise. according to recent data from the Centers for Disease Control and Prevention.
Furthermore, when surveyed about aerobic exercise and strength training, only 24.6% meet these weekly recommendations. These low rates of physical activity are alarming, given the immense benefits of exercise in improving mental and physical health and well-being.
Many people know that exercise is good for them but struggle to go workout consistently. I know firsthand how challenging this can be. In addition to being an integrative obesity specialist, I have gone from 0 minutes of physical activity in 2014 to becoming a fitness enthusiast who’s run more than 5,300 miles over 8 years. I know that as doctors and clinicians, we can profoundly influence our patients’ exercise journey.
Here are five tips to help motivate your patients make the change from “I Won’t Do It” to “I’m Doing It.”
Tip 1: ‘[Clinician], heal thyself’
Data don’t lie. Doctors who move more are more likely to counsel patients on exercise. I’ve been the doctor on both sides of the exercise spectrum. At my heaviest weight and lowest physical activity level, I felt hypocritical counseling patients on exercise.
If and when I counseled my patients on exercise, it was very directive and impersonal. When I started running consistently, I went to the opposite end of the spectrum. In my running zeal, it took a while for me to understand that not everyone wants to run dozens of miles a week. Shocking! Some people can’t handle intense workouts. The “I did it so you can too” perspective wasn’t helpful for long-term change in most patients.
What has been beneficial is recalling the obstacles and emotions I had (and still have) with staying consistent with physical activity. When physicians and clinicians move regularly, we’re more equipped to give our patients genuine counseling based on practicality rather than theory.
Now that self-reflection has been addressed, let’s get to patient counseling.
Tip 2: Motivate, don’t berate
Lectures on why patients should exercise are less helpful than asking, “Why aren›t you able to exercise more often?”
Asking open-ended questions is essential in motivational interviewing. Motivational interviewing promotes behavioral change through collaborative conversation.
Instead of telling the patient what to do, motivational interviewing seeks to establish a person’s why and create an effective plan based on their motivation. Asking open-ended questions is also helpful in determining any challenges to regular exercise, rather than calling these challenges “excuses,” which can be counterproductive.
I encourage patients to embrace challenges as opportunities for improvement. If they say: “I can’t find time to work out,” I suggest that they create time to work out by walking 10-15 minutes during lunch or after dinner. The information gleaned from open-ended questions helps set practical SMARTER goals, which we will discuss next.
Tip 3: Set SMARTER goals
After assessing the patient’s motivation and barriers, use this information to transform their desire to change into an actionable plan through a SMARTER goal. SMARTER stands for Specific, Measurable, Attainable, Relevant, Time-Sensitive, Enjoyable, and Rewarding. Practical goals have each of these components. That’s why “Just Do It” or even “Exercise 150 minutes a week” isn’t a clear path for actionable change. SMARTER goals go beyond what to do and help people personalize how to change.
For example, the SMARTER version of “exercise 150 minutes a week” for a busy person who works 50 hours a week may look like this: “My goal is to incorporate 150 minutes of physical activity through 60 minutes of aerobic exercise Monday through Friday (20-minute lunch walks) and 90 minutes of combination resistance training on the weekend (two 45-minute sessions) while listening to my favorite music. To meet my goal, I will reward myself by calling a friend to catch up or buy myself a new workout outfit.”
Exercise prescriptions are another helpful way to empower patients with a realistic exercise strategy. In my practice, I developed my own exercise prescription which focuses on overcoming time barriers to exercise and finding personally enjoyable exercises. To enhance self-directed physical activity, I›ve found it useful to have patients complete part of the “exercise prescription” on their own before or after their visit.
Tip 4: Use accountability tools
Making a SMARTER goal is one thing, but sticking with it takes regular reinforcement. Even with the best plan, once patients leave the office, there are many distractions from their goals. Accountability is the secret sauce to cultivating consistency. Fitness trackers are an affordable form of accountability. Studies show that wearing a fitness tracker can help people get up to 40 minutes of extra walking, compared with people who don’t wear trackers.
Additionally, clinicians can use different ways to offer exercise accountability. For example, more frequent check-ins, individually or in groups, can be helpful. The increase in telehealth has made interval visits easier. Reimbursement and time can limit clinician-level accountability, however. Other options are referring patients to online support groups or programs sponsored by the government or organizations. For years, I coled a Walk With a Doc chapter in Richmond, Va. There are chapters throughout the country.
Tip 5: Prepare and PLAN for setbacks
Breaking news: Most plans don’t go quite as envisioned. Accounting for the potential of setbacks early on helps patients set realistic expectations. As physicians and clinicians, we can help our patients anticipate a few likely obstacles. This may lessen the impact when a setback occurs. Also, it’s helpful to have the patient prepare for a setback with a PLAN for recovering quickly. PLAN stands for Ponder what happened; Learn from it; Adjust the original goal; Now get back on track. Getting back on track as soon as possible is important to keep patients motivated and prevent muscle deconditioning.
Exercise is medicine. Physical inactivity is a leading contributor to many preventable diseases. Although the physical activity statistics are disappointing, improvement is possible. Many systemic changes are needed to increase physical activity on a population level.
While waiting for more extensive changes, we have the power to equip patients with personalized, actionable tools for improving and maintaining physical activity.
We can transform one person at a time through our clinical encounters. Let’s use effective tools to help patients shift from “I Won’t Do It” to “I’m Doing It.”
Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness,” was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
“Just Do It” is a cute marketing slogan. But let’s face it: Clinically, it doesn’t work well. Most people just don’t exercise. according to recent data from the Centers for Disease Control and Prevention.
Furthermore, when surveyed about aerobic exercise and strength training, only 24.6% meet these weekly recommendations. These low rates of physical activity are alarming, given the immense benefits of exercise in improving mental and physical health and well-being.
Many people know that exercise is good for them but struggle to go workout consistently. I know firsthand how challenging this can be. In addition to being an integrative obesity specialist, I have gone from 0 minutes of physical activity in 2014 to becoming a fitness enthusiast who’s run more than 5,300 miles over 8 years. I know that as doctors and clinicians, we can profoundly influence our patients’ exercise journey.
Here are five tips to help motivate your patients make the change from “I Won’t Do It” to “I’m Doing It.”
Tip 1: ‘[Clinician], heal thyself’
Data don’t lie. Doctors who move more are more likely to counsel patients on exercise. I’ve been the doctor on both sides of the exercise spectrum. At my heaviest weight and lowest physical activity level, I felt hypocritical counseling patients on exercise.
If and when I counseled my patients on exercise, it was very directive and impersonal. When I started running consistently, I went to the opposite end of the spectrum. In my running zeal, it took a while for me to understand that not everyone wants to run dozens of miles a week. Shocking! Some people can’t handle intense workouts. The “I did it so you can too” perspective wasn’t helpful for long-term change in most patients.
What has been beneficial is recalling the obstacles and emotions I had (and still have) with staying consistent with physical activity. When physicians and clinicians move regularly, we’re more equipped to give our patients genuine counseling based on practicality rather than theory.
Now that self-reflection has been addressed, let’s get to patient counseling.
Tip 2: Motivate, don’t berate
Lectures on why patients should exercise are less helpful than asking, “Why aren›t you able to exercise more often?”
Asking open-ended questions is essential in motivational interviewing. Motivational interviewing promotes behavioral change through collaborative conversation.
Instead of telling the patient what to do, motivational interviewing seeks to establish a person’s why and create an effective plan based on their motivation. Asking open-ended questions is also helpful in determining any challenges to regular exercise, rather than calling these challenges “excuses,” which can be counterproductive.
I encourage patients to embrace challenges as opportunities for improvement. If they say: “I can’t find time to work out,” I suggest that they create time to work out by walking 10-15 minutes during lunch or after dinner. The information gleaned from open-ended questions helps set practical SMARTER goals, which we will discuss next.
Tip 3: Set SMARTER goals
After assessing the patient’s motivation and barriers, use this information to transform their desire to change into an actionable plan through a SMARTER goal. SMARTER stands for Specific, Measurable, Attainable, Relevant, Time-Sensitive, Enjoyable, and Rewarding. Practical goals have each of these components. That’s why “Just Do It” or even “Exercise 150 minutes a week” isn’t a clear path for actionable change. SMARTER goals go beyond what to do and help people personalize how to change.
For example, the SMARTER version of “exercise 150 minutes a week” for a busy person who works 50 hours a week may look like this: “My goal is to incorporate 150 minutes of physical activity through 60 minutes of aerobic exercise Monday through Friday (20-minute lunch walks) and 90 minutes of combination resistance training on the weekend (two 45-minute sessions) while listening to my favorite music. To meet my goal, I will reward myself by calling a friend to catch up or buy myself a new workout outfit.”
Exercise prescriptions are another helpful way to empower patients with a realistic exercise strategy. In my practice, I developed my own exercise prescription which focuses on overcoming time barriers to exercise and finding personally enjoyable exercises. To enhance self-directed physical activity, I›ve found it useful to have patients complete part of the “exercise prescription” on their own before or after their visit.
Tip 4: Use accountability tools
Making a SMARTER goal is one thing, but sticking with it takes regular reinforcement. Even with the best plan, once patients leave the office, there are many distractions from their goals. Accountability is the secret sauce to cultivating consistency. Fitness trackers are an affordable form of accountability. Studies show that wearing a fitness tracker can help people get up to 40 minutes of extra walking, compared with people who don’t wear trackers.
Additionally, clinicians can use different ways to offer exercise accountability. For example, more frequent check-ins, individually or in groups, can be helpful. The increase in telehealth has made interval visits easier. Reimbursement and time can limit clinician-level accountability, however. Other options are referring patients to online support groups or programs sponsored by the government or organizations. For years, I coled a Walk With a Doc chapter in Richmond, Va. There are chapters throughout the country.
Tip 5: Prepare and PLAN for setbacks
Breaking news: Most plans don’t go quite as envisioned. Accounting for the potential of setbacks early on helps patients set realistic expectations. As physicians and clinicians, we can help our patients anticipate a few likely obstacles. This may lessen the impact when a setback occurs. Also, it’s helpful to have the patient prepare for a setback with a PLAN for recovering quickly. PLAN stands for Ponder what happened; Learn from it; Adjust the original goal; Now get back on track. Getting back on track as soon as possible is important to keep patients motivated and prevent muscle deconditioning.
Exercise is medicine. Physical inactivity is a leading contributor to many preventable diseases. Although the physical activity statistics are disappointing, improvement is possible. Many systemic changes are needed to increase physical activity on a population level.
While waiting for more extensive changes, we have the power to equip patients with personalized, actionable tools for improving and maintaining physical activity.
We can transform one person at a time through our clinical encounters. Let’s use effective tools to help patients shift from “I Won’t Do It” to “I’m Doing It.”
Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness,” was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
“Just Do It” is a cute marketing slogan. But let’s face it: Clinically, it doesn’t work well. Most people just don’t exercise. according to recent data from the Centers for Disease Control and Prevention.
Furthermore, when surveyed about aerobic exercise and strength training, only 24.6% meet these weekly recommendations. These low rates of physical activity are alarming, given the immense benefits of exercise in improving mental and physical health and well-being.
Many people know that exercise is good for them but struggle to go workout consistently. I know firsthand how challenging this can be. In addition to being an integrative obesity specialist, I have gone from 0 minutes of physical activity in 2014 to becoming a fitness enthusiast who’s run more than 5,300 miles over 8 years. I know that as doctors and clinicians, we can profoundly influence our patients’ exercise journey.
Here are five tips to help motivate your patients make the change from “I Won’t Do It” to “I’m Doing It.”
Tip 1: ‘[Clinician], heal thyself’
Data don’t lie. Doctors who move more are more likely to counsel patients on exercise. I’ve been the doctor on both sides of the exercise spectrum. At my heaviest weight and lowest physical activity level, I felt hypocritical counseling patients on exercise.
If and when I counseled my patients on exercise, it was very directive and impersonal. When I started running consistently, I went to the opposite end of the spectrum. In my running zeal, it took a while for me to understand that not everyone wants to run dozens of miles a week. Shocking! Some people can’t handle intense workouts. The “I did it so you can too” perspective wasn’t helpful for long-term change in most patients.
What has been beneficial is recalling the obstacles and emotions I had (and still have) with staying consistent with physical activity. When physicians and clinicians move regularly, we’re more equipped to give our patients genuine counseling based on practicality rather than theory.
Now that self-reflection has been addressed, let’s get to patient counseling.
Tip 2: Motivate, don’t berate
Lectures on why patients should exercise are less helpful than asking, “Why aren›t you able to exercise more often?”
Asking open-ended questions is essential in motivational interviewing. Motivational interviewing promotes behavioral change through collaborative conversation.
Instead of telling the patient what to do, motivational interviewing seeks to establish a person’s why and create an effective plan based on their motivation. Asking open-ended questions is also helpful in determining any challenges to regular exercise, rather than calling these challenges “excuses,” which can be counterproductive.
I encourage patients to embrace challenges as opportunities for improvement. If they say: “I can’t find time to work out,” I suggest that they create time to work out by walking 10-15 minutes during lunch or after dinner. The information gleaned from open-ended questions helps set practical SMARTER goals, which we will discuss next.
Tip 3: Set SMARTER goals
After assessing the patient’s motivation and barriers, use this information to transform their desire to change into an actionable plan through a SMARTER goal. SMARTER stands for Specific, Measurable, Attainable, Relevant, Time-Sensitive, Enjoyable, and Rewarding. Practical goals have each of these components. That’s why “Just Do It” or even “Exercise 150 minutes a week” isn’t a clear path for actionable change. SMARTER goals go beyond what to do and help people personalize how to change.
For example, the SMARTER version of “exercise 150 minutes a week” for a busy person who works 50 hours a week may look like this: “My goal is to incorporate 150 minutes of physical activity through 60 minutes of aerobic exercise Monday through Friday (20-minute lunch walks) and 90 minutes of combination resistance training on the weekend (two 45-minute sessions) while listening to my favorite music. To meet my goal, I will reward myself by calling a friend to catch up or buy myself a new workout outfit.”
Exercise prescriptions are another helpful way to empower patients with a realistic exercise strategy. In my practice, I developed my own exercise prescription which focuses on overcoming time barriers to exercise and finding personally enjoyable exercises. To enhance self-directed physical activity, I›ve found it useful to have patients complete part of the “exercise prescription” on their own before or after their visit.
Tip 4: Use accountability tools
Making a SMARTER goal is one thing, but sticking with it takes regular reinforcement. Even with the best plan, once patients leave the office, there are many distractions from their goals. Accountability is the secret sauce to cultivating consistency. Fitness trackers are an affordable form of accountability. Studies show that wearing a fitness tracker can help people get up to 40 minutes of extra walking, compared with people who don’t wear trackers.
Additionally, clinicians can use different ways to offer exercise accountability. For example, more frequent check-ins, individually or in groups, can be helpful. The increase in telehealth has made interval visits easier. Reimbursement and time can limit clinician-level accountability, however. Other options are referring patients to online support groups or programs sponsored by the government or organizations. For years, I coled a Walk With a Doc chapter in Richmond, Va. There are chapters throughout the country.
Tip 5: Prepare and PLAN for setbacks
Breaking news: Most plans don’t go quite as envisioned. Accounting for the potential of setbacks early on helps patients set realistic expectations. As physicians and clinicians, we can help our patients anticipate a few likely obstacles. This may lessen the impact when a setback occurs. Also, it’s helpful to have the patient prepare for a setback with a PLAN for recovering quickly. PLAN stands for Ponder what happened; Learn from it; Adjust the original goal; Now get back on track. Getting back on track as soon as possible is important to keep patients motivated and prevent muscle deconditioning.
Exercise is medicine. Physical inactivity is a leading contributor to many preventable diseases. Although the physical activity statistics are disappointing, improvement is possible. Many systemic changes are needed to increase physical activity on a population level.
While waiting for more extensive changes, we have the power to equip patients with personalized, actionable tools for improving and maintaining physical activity.
We can transform one person at a time through our clinical encounters. Let’s use effective tools to help patients shift from “I Won’t Do It” to “I’m Doing It.”
Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness,” was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Mediterranean diet linked to 24% reduction in CVD risk in women
The Mediterranean diet appears to be associated with a lower incidence of cardiovascular disease (CVD) and mortality in women, new observational data suggest.
Those who had a higher adherence to a Mediterranean diet had a 24% lower risk for cardiovascular disease and 23% lower risk for death.
“A healthy diet is a huge factor in preventing heart disease. However, current guidelines on preventing heart disease lack sex-specific recommendations,” said senior author Sarah Zaman, MBBS, PhD, an associate professor of medicine and principal research fellow at the University of Sydney’s Westmead Applied Research Centre.
“Historically, research trials and studies have had predominantly male participants or lacked sex-specific analysis,” she said. “Our results will pave the way to bridge this gap and also highlight the need for more research to ensure health guidelines and policies include diverse perspectives.”
The study was published online in the journal Heart.
Analyzing cardiovascular outcomes
Dr. Zaman and colleagues conducted a systematic review and meta-analysis of 16 studies published between 2006 and 2021 that reported a Mediterranean diet score and included either all women or had stratified outcomes by sex. They excluded studies that referred to only certain components of the Mediterranean diet or combined it with other lifestyle-related factors.
The studies, which were mainly conducted in the United States and Europe, included 722,495 adult women without previous clinical or subclinical CVD, with a median follow-up of 12.5 years.
Higher Mediterranean diet adherence was defined as the highest category reporting the highest range of Mediterranean diet scores, and lower adherence was defined as the lowest category reporting lowest scores. Incident CVD included coronary heart disease, myocardial infarction, stroke, heart failure, cardiovascular death, major adverse cardiovascular events, major adverse cardiac cerebrovascular events, and patient-reported CVD.
Overall, higher adherence to a Mediterranean diet was associated with lower CVD incidence (hazard ratio, 0.76; 95% confidence interval, 0.72-0.81), total mortality (HR, 0.77; 95% CI, 0.74-0.80), and coronary heart disease (HR, 0.75; 95% CI, 0.65-0.87).
Stroke incidence was also lower among women who adhered to the Mediterranean diet, although it wasn’t considered statistically significant (HR, 0.87; 95% CI, 0.76-1.01).
Additional analyses found similar reductions in risk across women of different ethnicities. Higher Mediterranean diet adherence was associated with lower CVD incidence for both women of European descent (HR, 0.76; 95% CI, 0.59-0.98) and women of non-European descent – Asian, Native Hawaiian, and African American – (HR, 0.79; 95% CI, 0.72-0.87).
The results didn’t materially change in sensitivity analyses, the authors note. Excluding one study at a time, the pooled HRs for the highest versus the lowest Mediterranean diet adherence ranged from 0.76 (95% CI, 0.72-0.80) to 0.83 (95% CI, 0.70-0.98) for incident CVD and from 0.77 (95% CI, 0.75-0.80) to 0.77 (95% CI, 0.74-0.81) for total mortality among women.
At the same time, the authors pointed to several limitations, including the observational nature of all of the studies, the reliance on self-reported food frequency questionnaires, and heterogeneity in the adjustments for influential factors across the studies.
Additional considerations
Dr. Zaman and colleagues called for more sex-specific research in cardiology, including risk factors related to premature menopause, preeclampsia, gestational diabetes, and autoimmune diseases such as systemic lupus.
Future studies should also explore the underlying mechanisms that may explain the links between the Mediterranean diet, cardiovascular disease, and death, the authors write. For instance, the diet may reduce inflammation and cardiovascular risk factors through antioxidant and beneficial gut microbiome pathways. Other components of the diet – such as polyphenols, nitrates, omega-3 fatty acids, higher fiber intake, and reduced glycemic load – may also play a role.
“It was striking to see how strong the long-term cardioprotective properties of a Mediterranean-type dietary pattern were,” said Samia Mora, MD, MHS, a professor of medicine at Harvard Medical School and director of the Center for Lipid Metabolomics at Brigham and Women’s Hospital.
Dr. Mora, who wasn’t involved with this study, has researched potential mechanisms related to the Mediterranean diet, cardiovascular events, and diabetes in women. She and colleagues have found that women with high adherence to the diet are more likely to have lower inflammation, insulin resistance, body mass index, and blood pressure, as well as improved lipid and metabolic profiles.
“This could represent an opportunity to intervene earlier and more intensively on improving inflammation, insulin resistance, and cardiometabolic health through evidence-based dietary approaches such as the Mediterranean diet,” she said. “As health care providers, we should promote the healthy dietary attributes of the Mediterranean diet, especially as many of our patients in the U.S. are less familiar with the Mediterranean diet and how to incorporate its components into daily food intake.”
The study did not receive any funding. Dr. Zaman was supported by a Heart Foundation Future Leader Fellowship. The authors declared no conflicts of interest. Dr. Mora reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The Mediterranean diet appears to be associated with a lower incidence of cardiovascular disease (CVD) and mortality in women, new observational data suggest.
Those who had a higher adherence to a Mediterranean diet had a 24% lower risk for cardiovascular disease and 23% lower risk for death.
“A healthy diet is a huge factor in preventing heart disease. However, current guidelines on preventing heart disease lack sex-specific recommendations,” said senior author Sarah Zaman, MBBS, PhD, an associate professor of medicine and principal research fellow at the University of Sydney’s Westmead Applied Research Centre.
“Historically, research trials and studies have had predominantly male participants or lacked sex-specific analysis,” she said. “Our results will pave the way to bridge this gap and also highlight the need for more research to ensure health guidelines and policies include diverse perspectives.”
The study was published online in the journal Heart.
Analyzing cardiovascular outcomes
Dr. Zaman and colleagues conducted a systematic review and meta-analysis of 16 studies published between 2006 and 2021 that reported a Mediterranean diet score and included either all women or had stratified outcomes by sex. They excluded studies that referred to only certain components of the Mediterranean diet or combined it with other lifestyle-related factors.
The studies, which were mainly conducted in the United States and Europe, included 722,495 adult women without previous clinical or subclinical CVD, with a median follow-up of 12.5 years.
Higher Mediterranean diet adherence was defined as the highest category reporting the highest range of Mediterranean diet scores, and lower adherence was defined as the lowest category reporting lowest scores. Incident CVD included coronary heart disease, myocardial infarction, stroke, heart failure, cardiovascular death, major adverse cardiovascular events, major adverse cardiac cerebrovascular events, and patient-reported CVD.
Overall, higher adherence to a Mediterranean diet was associated with lower CVD incidence (hazard ratio, 0.76; 95% confidence interval, 0.72-0.81), total mortality (HR, 0.77; 95% CI, 0.74-0.80), and coronary heart disease (HR, 0.75; 95% CI, 0.65-0.87).
Stroke incidence was also lower among women who adhered to the Mediterranean diet, although it wasn’t considered statistically significant (HR, 0.87; 95% CI, 0.76-1.01).
Additional analyses found similar reductions in risk across women of different ethnicities. Higher Mediterranean diet adherence was associated with lower CVD incidence for both women of European descent (HR, 0.76; 95% CI, 0.59-0.98) and women of non-European descent – Asian, Native Hawaiian, and African American – (HR, 0.79; 95% CI, 0.72-0.87).
The results didn’t materially change in sensitivity analyses, the authors note. Excluding one study at a time, the pooled HRs for the highest versus the lowest Mediterranean diet adherence ranged from 0.76 (95% CI, 0.72-0.80) to 0.83 (95% CI, 0.70-0.98) for incident CVD and from 0.77 (95% CI, 0.75-0.80) to 0.77 (95% CI, 0.74-0.81) for total mortality among women.
At the same time, the authors pointed to several limitations, including the observational nature of all of the studies, the reliance on self-reported food frequency questionnaires, and heterogeneity in the adjustments for influential factors across the studies.
Additional considerations
Dr. Zaman and colleagues called for more sex-specific research in cardiology, including risk factors related to premature menopause, preeclampsia, gestational diabetes, and autoimmune diseases such as systemic lupus.
Future studies should also explore the underlying mechanisms that may explain the links between the Mediterranean diet, cardiovascular disease, and death, the authors write. For instance, the diet may reduce inflammation and cardiovascular risk factors through antioxidant and beneficial gut microbiome pathways. Other components of the diet – such as polyphenols, nitrates, omega-3 fatty acids, higher fiber intake, and reduced glycemic load – may also play a role.
“It was striking to see how strong the long-term cardioprotective properties of a Mediterranean-type dietary pattern were,” said Samia Mora, MD, MHS, a professor of medicine at Harvard Medical School and director of the Center for Lipid Metabolomics at Brigham and Women’s Hospital.
Dr. Mora, who wasn’t involved with this study, has researched potential mechanisms related to the Mediterranean diet, cardiovascular events, and diabetes in women. She and colleagues have found that women with high adherence to the diet are more likely to have lower inflammation, insulin resistance, body mass index, and blood pressure, as well as improved lipid and metabolic profiles.
“This could represent an opportunity to intervene earlier and more intensively on improving inflammation, insulin resistance, and cardiometabolic health through evidence-based dietary approaches such as the Mediterranean diet,” she said. “As health care providers, we should promote the healthy dietary attributes of the Mediterranean diet, especially as many of our patients in the U.S. are less familiar with the Mediterranean diet and how to incorporate its components into daily food intake.”
The study did not receive any funding. Dr. Zaman was supported by a Heart Foundation Future Leader Fellowship. The authors declared no conflicts of interest. Dr. Mora reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The Mediterranean diet appears to be associated with a lower incidence of cardiovascular disease (CVD) and mortality in women, new observational data suggest.
Those who had a higher adherence to a Mediterranean diet had a 24% lower risk for cardiovascular disease and 23% lower risk for death.
“A healthy diet is a huge factor in preventing heart disease. However, current guidelines on preventing heart disease lack sex-specific recommendations,” said senior author Sarah Zaman, MBBS, PhD, an associate professor of medicine and principal research fellow at the University of Sydney’s Westmead Applied Research Centre.
“Historically, research trials and studies have had predominantly male participants or lacked sex-specific analysis,” she said. “Our results will pave the way to bridge this gap and also highlight the need for more research to ensure health guidelines and policies include diverse perspectives.”
The study was published online in the journal Heart.
Analyzing cardiovascular outcomes
Dr. Zaman and colleagues conducted a systematic review and meta-analysis of 16 studies published between 2006 and 2021 that reported a Mediterranean diet score and included either all women or had stratified outcomes by sex. They excluded studies that referred to only certain components of the Mediterranean diet or combined it with other lifestyle-related factors.
The studies, which were mainly conducted in the United States and Europe, included 722,495 adult women without previous clinical or subclinical CVD, with a median follow-up of 12.5 years.
Higher Mediterranean diet adherence was defined as the highest category reporting the highest range of Mediterranean diet scores, and lower adherence was defined as the lowest category reporting lowest scores. Incident CVD included coronary heart disease, myocardial infarction, stroke, heart failure, cardiovascular death, major adverse cardiovascular events, major adverse cardiac cerebrovascular events, and patient-reported CVD.
Overall, higher adherence to a Mediterranean diet was associated with lower CVD incidence (hazard ratio, 0.76; 95% confidence interval, 0.72-0.81), total mortality (HR, 0.77; 95% CI, 0.74-0.80), and coronary heart disease (HR, 0.75; 95% CI, 0.65-0.87).
Stroke incidence was also lower among women who adhered to the Mediterranean diet, although it wasn’t considered statistically significant (HR, 0.87; 95% CI, 0.76-1.01).
Additional analyses found similar reductions in risk across women of different ethnicities. Higher Mediterranean diet adherence was associated with lower CVD incidence for both women of European descent (HR, 0.76; 95% CI, 0.59-0.98) and women of non-European descent – Asian, Native Hawaiian, and African American – (HR, 0.79; 95% CI, 0.72-0.87).
The results didn’t materially change in sensitivity analyses, the authors note. Excluding one study at a time, the pooled HRs for the highest versus the lowest Mediterranean diet adherence ranged from 0.76 (95% CI, 0.72-0.80) to 0.83 (95% CI, 0.70-0.98) for incident CVD and from 0.77 (95% CI, 0.75-0.80) to 0.77 (95% CI, 0.74-0.81) for total mortality among women.
At the same time, the authors pointed to several limitations, including the observational nature of all of the studies, the reliance on self-reported food frequency questionnaires, and heterogeneity in the adjustments for influential factors across the studies.
Additional considerations
Dr. Zaman and colleagues called for more sex-specific research in cardiology, including risk factors related to premature menopause, preeclampsia, gestational diabetes, and autoimmune diseases such as systemic lupus.
Future studies should also explore the underlying mechanisms that may explain the links between the Mediterranean diet, cardiovascular disease, and death, the authors write. For instance, the diet may reduce inflammation and cardiovascular risk factors through antioxidant and beneficial gut microbiome pathways. Other components of the diet – such as polyphenols, nitrates, omega-3 fatty acids, higher fiber intake, and reduced glycemic load – may also play a role.
“It was striking to see how strong the long-term cardioprotective properties of a Mediterranean-type dietary pattern were,” said Samia Mora, MD, MHS, a professor of medicine at Harvard Medical School and director of the Center for Lipid Metabolomics at Brigham and Women’s Hospital.
Dr. Mora, who wasn’t involved with this study, has researched potential mechanisms related to the Mediterranean diet, cardiovascular events, and diabetes in women. She and colleagues have found that women with high adherence to the diet are more likely to have lower inflammation, insulin resistance, body mass index, and blood pressure, as well as improved lipid and metabolic profiles.
“This could represent an opportunity to intervene earlier and more intensively on improving inflammation, insulin resistance, and cardiometabolic health through evidence-based dietary approaches such as the Mediterranean diet,” she said. “As health care providers, we should promote the healthy dietary attributes of the Mediterranean diet, especially as many of our patients in the U.S. are less familiar with the Mediterranean diet and how to incorporate its components into daily food intake.”
The study did not receive any funding. Dr. Zaman was supported by a Heart Foundation Future Leader Fellowship. The authors declared no conflicts of interest. Dr. Mora reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Ozempic: The latest weight loss craze and how over-prescribing is harming patients
Social media and mainstream media websites are full of stories on the new wonder weight loss drug: Ozempic. Even Hollywood stars are talking about it.
Recently, the zealous prescribing of this diabetes medication fueled a 6-month shortage making it difficult for anyone to get it. Part of the problem stems from digital access to these medications where a patient can get a prescription online or via a telemedicine platform. Additionally, certain weight loss programs contributed to promoting the weight loss benefits.
Ozempic is a glucagon-like peptide-1 (GLP-1) agonist, with the generic name semaglutide, that lowers hemoglobin A1c in patients with diabetes and lowers the risk of cardiovascular events. Semaglutide is also sold as Wegovy, which is indicated for weight loss. Both Ozempic and Wegovy are sold in multiple doses, but the target dose for Wegovy is higher.
Weight loss with Wegovy is, on average, higher than that seen with Ozempic. However, it is often more difficult to get Wegovy covered by health insurance companies.
As doctors, we must be stewards of the medications we are prescribing. Clearly, the Internet should not be driving our prescribing habits. Prescribing Ozempic for weight loss can make it more difficult for patients with diabetes to receive it, and we should consider other options until it is more available and/or receives FDA approval for treating obesity.
Most of us have seen our patients with diabetes having difficulty getting a prescription for Ozempic filled, either because it is on back-order or because of a lack of coverage. Insurance companies have no incentive to lower the cost when it is in such high demand at its current rate. For these patients, lowering their A1c can be life-saving and prevent complications of diabetes, such as kidney failure and heart disease. In our current environment, we should reserve prescribing Ozempic for our patients with diabetes who need it more. Wegovy is available and can be prescribed for patients wishing to lose weight.
Many patients are looking for a magic cure. Neither medication is that. Patients need to start with making lifestyle changes first. In primary care, advising on and helping patients implement those are often our most difficult tasks. However, no medication is going to work unless the patient makes adjustments to their diet and amount and type of movement they are doing. In patients who have a hard time changing their diet, lowering carbohydrate intake may be a good first step. Exercising, or being more active if a patient is unable to formally exercise, is an important therapy.
As we all know, metformin is the usual preferred method for the treatment of type 2 diabetes unless contraindicated in a given patient. There are many oral diabetes medications available, and which of these and how these are prescribed need to be tailored to the individual patient. Ozempic can be used when a patient is failing on metformin, or other oral meds, or if they would rather do a weekly injection rather than remembering to take daily pills, for example.
Obesity has reached epidemic proportions in the United States. According to the CDC, more than 40% of the U.S. population is obese. Additionally, millions of children between the ages of 2 and 19 are now considered obese, and the medical complications for these individuals ares yet to be seen. Plus, many of us are seeing higher frequencies of diabetes, hypertension, and other chronic medical conditions in adolescents in our daily practices.
Our war against obesity is a fight for future lives and having more tools available is definitely a help. Like with patients with diabetes, all treatment regimens should start off with lifestyle modifications. Fad diets rarely result in long-term weight loss.
There are several medications now available to help with weight loss, Wegovy being just one of them. Patients often come to us with their own personal preferences, and it is our job to guide them on the best course to take. Some people may prefer a weekly injection. There are oral medications available, such as Contrave and Phentermine, and the best one should be decided upon by the patient and doctor after a discussion of the risks.
Let’s stop prescribing Ozempic for weight loss because nonphysicians say we should. Leave it for our patients with diabetes, those whose lives may depend on taking it. If we didn’t have other medications available, it would be a very different story. But, we do, and we need to resist the pressure others place on us and do the right thing for all of our patients.
*This article was updated on 3/23/2023.
Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J. She has no conflicts related to this piece. You can contact her at [email protected].
Social media and mainstream media websites are full of stories on the new wonder weight loss drug: Ozempic. Even Hollywood stars are talking about it.
Recently, the zealous prescribing of this diabetes medication fueled a 6-month shortage making it difficult for anyone to get it. Part of the problem stems from digital access to these medications where a patient can get a prescription online or via a telemedicine platform. Additionally, certain weight loss programs contributed to promoting the weight loss benefits.
Ozempic is a glucagon-like peptide-1 (GLP-1) agonist, with the generic name semaglutide, that lowers hemoglobin A1c in patients with diabetes and lowers the risk of cardiovascular events. Semaglutide is also sold as Wegovy, which is indicated for weight loss. Both Ozempic and Wegovy are sold in multiple doses, but the target dose for Wegovy is higher.
Weight loss with Wegovy is, on average, higher than that seen with Ozempic. However, it is often more difficult to get Wegovy covered by health insurance companies.
As doctors, we must be stewards of the medications we are prescribing. Clearly, the Internet should not be driving our prescribing habits. Prescribing Ozempic for weight loss can make it more difficult for patients with diabetes to receive it, and we should consider other options until it is more available and/or receives FDA approval for treating obesity.
Most of us have seen our patients with diabetes having difficulty getting a prescription for Ozempic filled, either because it is on back-order or because of a lack of coverage. Insurance companies have no incentive to lower the cost when it is in such high demand at its current rate. For these patients, lowering their A1c can be life-saving and prevent complications of diabetes, such as kidney failure and heart disease. In our current environment, we should reserve prescribing Ozempic for our patients with diabetes who need it more. Wegovy is available and can be prescribed for patients wishing to lose weight.
Many patients are looking for a magic cure. Neither medication is that. Patients need to start with making lifestyle changes first. In primary care, advising on and helping patients implement those are often our most difficult tasks. However, no medication is going to work unless the patient makes adjustments to their diet and amount and type of movement they are doing. In patients who have a hard time changing their diet, lowering carbohydrate intake may be a good first step. Exercising, or being more active if a patient is unable to formally exercise, is an important therapy.
As we all know, metformin is the usual preferred method for the treatment of type 2 diabetes unless contraindicated in a given patient. There are many oral diabetes medications available, and which of these and how these are prescribed need to be tailored to the individual patient. Ozempic can be used when a patient is failing on metformin, or other oral meds, or if they would rather do a weekly injection rather than remembering to take daily pills, for example.
Obesity has reached epidemic proportions in the United States. According to the CDC, more than 40% of the U.S. population is obese. Additionally, millions of children between the ages of 2 and 19 are now considered obese, and the medical complications for these individuals ares yet to be seen. Plus, many of us are seeing higher frequencies of diabetes, hypertension, and other chronic medical conditions in adolescents in our daily practices.
Our war against obesity is a fight for future lives and having more tools available is definitely a help. Like with patients with diabetes, all treatment regimens should start off with lifestyle modifications. Fad diets rarely result in long-term weight loss.
There are several medications now available to help with weight loss, Wegovy being just one of them. Patients often come to us with their own personal preferences, and it is our job to guide them on the best course to take. Some people may prefer a weekly injection. There are oral medications available, such as Contrave and Phentermine, and the best one should be decided upon by the patient and doctor after a discussion of the risks.
Let’s stop prescribing Ozempic for weight loss because nonphysicians say we should. Leave it for our patients with diabetes, those whose lives may depend on taking it. If we didn’t have other medications available, it would be a very different story. But, we do, and we need to resist the pressure others place on us and do the right thing for all of our patients.
*This article was updated on 3/23/2023.
Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J. She has no conflicts related to this piece. You can contact her at [email protected].
Social media and mainstream media websites are full of stories on the new wonder weight loss drug: Ozempic. Even Hollywood stars are talking about it.
Recently, the zealous prescribing of this diabetes medication fueled a 6-month shortage making it difficult for anyone to get it. Part of the problem stems from digital access to these medications where a patient can get a prescription online or via a telemedicine platform. Additionally, certain weight loss programs contributed to promoting the weight loss benefits.
Ozempic is a glucagon-like peptide-1 (GLP-1) agonist, with the generic name semaglutide, that lowers hemoglobin A1c in patients with diabetes and lowers the risk of cardiovascular events. Semaglutide is also sold as Wegovy, which is indicated for weight loss. Both Ozempic and Wegovy are sold in multiple doses, but the target dose for Wegovy is higher.
Weight loss with Wegovy is, on average, higher than that seen with Ozempic. However, it is often more difficult to get Wegovy covered by health insurance companies.
As doctors, we must be stewards of the medications we are prescribing. Clearly, the Internet should not be driving our prescribing habits. Prescribing Ozempic for weight loss can make it more difficult for patients with diabetes to receive it, and we should consider other options until it is more available and/or receives FDA approval for treating obesity.
Most of us have seen our patients with diabetes having difficulty getting a prescription for Ozempic filled, either because it is on back-order or because of a lack of coverage. Insurance companies have no incentive to lower the cost when it is in such high demand at its current rate. For these patients, lowering their A1c can be life-saving and prevent complications of diabetes, such as kidney failure and heart disease. In our current environment, we should reserve prescribing Ozempic for our patients with diabetes who need it more. Wegovy is available and can be prescribed for patients wishing to lose weight.
Many patients are looking for a magic cure. Neither medication is that. Patients need to start with making lifestyle changes first. In primary care, advising on and helping patients implement those are often our most difficult tasks. However, no medication is going to work unless the patient makes adjustments to their diet and amount and type of movement they are doing. In patients who have a hard time changing their diet, lowering carbohydrate intake may be a good first step. Exercising, or being more active if a patient is unable to formally exercise, is an important therapy.
As we all know, metformin is the usual preferred method for the treatment of type 2 diabetes unless contraindicated in a given patient. There are many oral diabetes medications available, and which of these and how these are prescribed need to be tailored to the individual patient. Ozempic can be used when a patient is failing on metformin, or other oral meds, or if they would rather do a weekly injection rather than remembering to take daily pills, for example.
Obesity has reached epidemic proportions in the United States. According to the CDC, more than 40% of the U.S. population is obese. Additionally, millions of children between the ages of 2 and 19 are now considered obese, and the medical complications for these individuals ares yet to be seen. Plus, many of us are seeing higher frequencies of diabetes, hypertension, and other chronic medical conditions in adolescents in our daily practices.
Our war against obesity is a fight for future lives and having more tools available is definitely a help. Like with patients with diabetes, all treatment regimens should start off with lifestyle modifications. Fad diets rarely result in long-term weight loss.
There are several medications now available to help with weight loss, Wegovy being just one of them. Patients often come to us with their own personal preferences, and it is our job to guide them on the best course to take. Some people may prefer a weekly injection. There are oral medications available, such as Contrave and Phentermine, and the best one should be decided upon by the patient and doctor after a discussion of the risks.
Let’s stop prescribing Ozempic for weight loss because nonphysicians say we should. Leave it for our patients with diabetes, those whose lives may depend on taking it. If we didn’t have other medications available, it would be a very different story. But, we do, and we need to resist the pressure others place on us and do the right thing for all of our patients.
*This article was updated on 3/23/2023.
Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J. She has no conflicts related to this piece. You can contact her at [email protected].
TikTok’s fave weight loss drugs: Link to thyroid cancer?
With #Ozempic and #ozempicweightloss continuing to trend on social media, along with the mainstream media focusing on celebrities who rely on Ozempic (semaglutide) for weight loss, the daily requests for this new medication have been increasing.
Accompanying these requests are concerns and questions about potential risks, including this most recent message from one of my patients: “Dr. P – I saw the warnings. Is this medication going to make me get thyroid cancer? Please let me know!”
Let’s look at what we know to date, including recent studies, and how to advise our patients on this very hot topic.
Using GLP-1 receptor agonists for obesity
We have extensive prior experience with glucagon-like peptide 1 (GLP-1) receptor agonists, such as semaglutide, for treating type 2 diabetes and now recently as agents for weight loss.
Large clinical trials have documented the benefits of this medication class not only for weight reduction but also for cardiovascular and renal benefits in patients with diabetes. The subcutaneously injectable medications work by promoting insulin secretion, slowing gastric emptying, and suppressing glucagon secretion, with a low risk for hypoglycemia.
The Food and Drug Administration approved daily-injection GLP-1 agonist liraglutide for weight loss in 2014, and weekly-injection semaglutide for chronic weight management in 2021, in patients with a body mass index ≥ 27 with at least one weight-related condition or a BMI ≥ 30.
The brand name for semaglutide approved for weight loss is Wegovy, and the dose is slightly higher (maximum 2.4 mg/wk) than that of Ozempic (maximum 2.0 mg/wk), which is semaglutide approved for type 2 diabetes.
In trials for weight loss, data showed a mean change in body weight of almost 15% in the semaglutide group at week 68 compared with placebo, which is very impressive, particularly compared with other FDA-approved oral long-term weight loss medications.
The newest synthetic dual-acting agent is tirzepatide, which targets GLP-1 but is also a glucose-dependent insulinotropic polypeptide (GIP) agonist. The weekly subcutaneous injection was approved in May 2022 as Mounjaro for treating type 2 diabetes and produced even greater weight loss than semaglutide in clinical trials. Tirzepatide is now in trials for obesity and is under expedited review by the FDA for weight loss.
Why the concern about thyroid cancer?
Early on with the FDA approvals of GLP-1 agonists, a warning accompanied the products’ labels to not use this class of medications in patients with medullary thyroid cancer, a family history of medullary thyroid cancer, or multiple endocrine neoplasia syndrome type 2. This warning was based on data from animal studies.
Human pancreatic cells aren’t the only cells that express GLP-1 receptors. These receptors are also expressed by parafollicular cells (C cells) of the thyroid, which secrete calcitonin and are the cells involved in medullary thyroid cancer. A dose-related and duration-dependent increase in thyroid C-cell tumor incidence was noted in rodents. The same relationship was not demonstrated in monkeys. Humans have far fewer C cells than rats, and human C cells have very low expression of the GLP-1 receptor.
Over a decade ago, a study examining the FDA’s database of reported adverse events found an increased risk for thyroid cancer in patients treated with exenatide, another GLP-1 agonist. The reporting system wasn’t designed to distinguish thyroid cancer subtypes.
Numerous subsequent studies didn’t confirm this relationship. The LEADER trial looked at liraglutide in patients with type 2 diabetes and showed no effect of GLP-1 receptor activation on human serum calcitonin levels, C-cell proliferation, or C-cell malignancy. Similarly, a large meta-analysis in patients with type 2 diabetes didn’t find a statistically increased risk for thyroid cancer with liraglutide, and no thyroid malignancies were reported with exenatide.
Two U.S. administrative databases from commercial health plans (a retrospective cohort study and a nested case-control study) compared type 2 diabetes patients who were taking exenatide vs. other antidiabetic drugs and found that exenatide was not significantly associated with an increased risk for thyroid cancer.
And a recent meta-analysis of 45 trials showed no significant effects on the occurrence of thyroid cancer with GLP-1 receptor agonists. Of note, it did find an increased risk for overall thyroid disorders, although there was no clear statistically significant finding pointing to a specific thyroid disorder.
Differing from prior studies, a recent nationwide French health care system study provided newer data suggesting a moderate increased risk for thyroid cancer in a cohort of patients with type 2 diabetes who were taking GLP-1 agonists. The increase in relative risk was noted for all types of thyroid cancer in patients using GLP-1 receptor agonists for 1-3 years.
An accompanying commentary by Caroline A. Thompson, PhD, and Til Stürmer, MD, provides perspective on this study’s potential limitations. These include detection bias, as the study results focused only on the statistically significant data. Also discussed were limitations to the case-control design, issues with claims-based tumor type classification (unavailability of surgical pathology), and an inability to adjust for family history and obesity, which is a risk factor alone for thyroid cancer. There was also no adjustment for exposure to head/neck radiation.
While this study has important findings to consider, it deserves further investigation, with future studies linking data to tumor registry data before a change is made in clinical practice.
No clear relationship has been drawn between GLP-1 receptor agonists and thyroid cancer in humans. Numerous confounding factors limit the data. Studies generally don’t specify the type of thyroid cancer, and they lump medullary thyroid cancer, the rarest form, with papillary thyroid cancer.
Is a detection bias present where weight loss makes nodules more visible on the neck among those treated with GLP-1 agonists? And/or are patients treated with GLP-1 agonists being screened more stringently for thyroid nodules and/or cancer?
How to advise our patients and respond to the EMR messages
The TikTok videos may continue, the celebrity chatter may increase, and we, as physicians, will continue to look to real-world data with randomized controlled trials to tailor our decision-making and guide our patients.
Thyroid cancer remains a rare outcome, and GLP-1 receptor agonists remain a very important and beneficial treatment option for the right patient.
A version of this article first appeared on Medscape.com.
With #Ozempic and #ozempicweightloss continuing to trend on social media, along with the mainstream media focusing on celebrities who rely on Ozempic (semaglutide) for weight loss, the daily requests for this new medication have been increasing.
Accompanying these requests are concerns and questions about potential risks, including this most recent message from one of my patients: “Dr. P – I saw the warnings. Is this medication going to make me get thyroid cancer? Please let me know!”
Let’s look at what we know to date, including recent studies, and how to advise our patients on this very hot topic.
Using GLP-1 receptor agonists for obesity
We have extensive prior experience with glucagon-like peptide 1 (GLP-1) receptor agonists, such as semaglutide, for treating type 2 diabetes and now recently as agents for weight loss.
Large clinical trials have documented the benefits of this medication class not only for weight reduction but also for cardiovascular and renal benefits in patients with diabetes. The subcutaneously injectable medications work by promoting insulin secretion, slowing gastric emptying, and suppressing glucagon secretion, with a low risk for hypoglycemia.
The Food and Drug Administration approved daily-injection GLP-1 agonist liraglutide for weight loss in 2014, and weekly-injection semaglutide for chronic weight management in 2021, in patients with a body mass index ≥ 27 with at least one weight-related condition or a BMI ≥ 30.
The brand name for semaglutide approved for weight loss is Wegovy, and the dose is slightly higher (maximum 2.4 mg/wk) than that of Ozempic (maximum 2.0 mg/wk), which is semaglutide approved for type 2 diabetes.
In trials for weight loss, data showed a mean change in body weight of almost 15% in the semaglutide group at week 68 compared with placebo, which is very impressive, particularly compared with other FDA-approved oral long-term weight loss medications.
The newest synthetic dual-acting agent is tirzepatide, which targets GLP-1 but is also a glucose-dependent insulinotropic polypeptide (GIP) agonist. The weekly subcutaneous injection was approved in May 2022 as Mounjaro for treating type 2 diabetes and produced even greater weight loss than semaglutide in clinical trials. Tirzepatide is now in trials for obesity and is under expedited review by the FDA for weight loss.
Why the concern about thyroid cancer?
Early on with the FDA approvals of GLP-1 agonists, a warning accompanied the products’ labels to not use this class of medications in patients with medullary thyroid cancer, a family history of medullary thyroid cancer, or multiple endocrine neoplasia syndrome type 2. This warning was based on data from animal studies.
Human pancreatic cells aren’t the only cells that express GLP-1 receptors. These receptors are also expressed by parafollicular cells (C cells) of the thyroid, which secrete calcitonin and are the cells involved in medullary thyroid cancer. A dose-related and duration-dependent increase in thyroid C-cell tumor incidence was noted in rodents. The same relationship was not demonstrated in monkeys. Humans have far fewer C cells than rats, and human C cells have very low expression of the GLP-1 receptor.
Over a decade ago, a study examining the FDA’s database of reported adverse events found an increased risk for thyroid cancer in patients treated with exenatide, another GLP-1 agonist. The reporting system wasn’t designed to distinguish thyroid cancer subtypes.
Numerous subsequent studies didn’t confirm this relationship. The LEADER trial looked at liraglutide in patients with type 2 diabetes and showed no effect of GLP-1 receptor activation on human serum calcitonin levels, C-cell proliferation, or C-cell malignancy. Similarly, a large meta-analysis in patients with type 2 diabetes didn’t find a statistically increased risk for thyroid cancer with liraglutide, and no thyroid malignancies were reported with exenatide.
Two U.S. administrative databases from commercial health plans (a retrospective cohort study and a nested case-control study) compared type 2 diabetes patients who were taking exenatide vs. other antidiabetic drugs and found that exenatide was not significantly associated with an increased risk for thyroid cancer.
And a recent meta-analysis of 45 trials showed no significant effects on the occurrence of thyroid cancer with GLP-1 receptor agonists. Of note, it did find an increased risk for overall thyroid disorders, although there was no clear statistically significant finding pointing to a specific thyroid disorder.
Differing from prior studies, a recent nationwide French health care system study provided newer data suggesting a moderate increased risk for thyroid cancer in a cohort of patients with type 2 diabetes who were taking GLP-1 agonists. The increase in relative risk was noted for all types of thyroid cancer in patients using GLP-1 receptor agonists for 1-3 years.
An accompanying commentary by Caroline A. Thompson, PhD, and Til Stürmer, MD, provides perspective on this study’s potential limitations. These include detection bias, as the study results focused only on the statistically significant data. Also discussed were limitations to the case-control design, issues with claims-based tumor type classification (unavailability of surgical pathology), and an inability to adjust for family history and obesity, which is a risk factor alone for thyroid cancer. There was also no adjustment for exposure to head/neck radiation.
While this study has important findings to consider, it deserves further investigation, with future studies linking data to tumor registry data before a change is made in clinical practice.
No clear relationship has been drawn between GLP-1 receptor agonists and thyroid cancer in humans. Numerous confounding factors limit the data. Studies generally don’t specify the type of thyroid cancer, and they lump medullary thyroid cancer, the rarest form, with papillary thyroid cancer.
Is a detection bias present where weight loss makes nodules more visible on the neck among those treated with GLP-1 agonists? And/or are patients treated with GLP-1 agonists being screened more stringently for thyroid nodules and/or cancer?
How to advise our patients and respond to the EMR messages
The TikTok videos may continue, the celebrity chatter may increase, and we, as physicians, will continue to look to real-world data with randomized controlled trials to tailor our decision-making and guide our patients.
Thyroid cancer remains a rare outcome, and GLP-1 receptor agonists remain a very important and beneficial treatment option for the right patient.
A version of this article first appeared on Medscape.com.
With #Ozempic and #ozempicweightloss continuing to trend on social media, along with the mainstream media focusing on celebrities who rely on Ozempic (semaglutide) for weight loss, the daily requests for this new medication have been increasing.
Accompanying these requests are concerns and questions about potential risks, including this most recent message from one of my patients: “Dr. P – I saw the warnings. Is this medication going to make me get thyroid cancer? Please let me know!”
Let’s look at what we know to date, including recent studies, and how to advise our patients on this very hot topic.
Using GLP-1 receptor agonists for obesity
We have extensive prior experience with glucagon-like peptide 1 (GLP-1) receptor agonists, such as semaglutide, for treating type 2 diabetes and now recently as agents for weight loss.
Large clinical trials have documented the benefits of this medication class not only for weight reduction but also for cardiovascular and renal benefits in patients with diabetes. The subcutaneously injectable medications work by promoting insulin secretion, slowing gastric emptying, and suppressing glucagon secretion, with a low risk for hypoglycemia.
The Food and Drug Administration approved daily-injection GLP-1 agonist liraglutide for weight loss in 2014, and weekly-injection semaglutide for chronic weight management in 2021, in patients with a body mass index ≥ 27 with at least one weight-related condition or a BMI ≥ 30.
The brand name for semaglutide approved for weight loss is Wegovy, and the dose is slightly higher (maximum 2.4 mg/wk) than that of Ozempic (maximum 2.0 mg/wk), which is semaglutide approved for type 2 diabetes.
In trials for weight loss, data showed a mean change in body weight of almost 15% in the semaglutide group at week 68 compared with placebo, which is very impressive, particularly compared with other FDA-approved oral long-term weight loss medications.
The newest synthetic dual-acting agent is tirzepatide, which targets GLP-1 but is also a glucose-dependent insulinotropic polypeptide (GIP) agonist. The weekly subcutaneous injection was approved in May 2022 as Mounjaro for treating type 2 diabetes and produced even greater weight loss than semaglutide in clinical trials. Tirzepatide is now in trials for obesity and is under expedited review by the FDA for weight loss.
Why the concern about thyroid cancer?
Early on with the FDA approvals of GLP-1 agonists, a warning accompanied the products’ labels to not use this class of medications in patients with medullary thyroid cancer, a family history of medullary thyroid cancer, or multiple endocrine neoplasia syndrome type 2. This warning was based on data from animal studies.
Human pancreatic cells aren’t the only cells that express GLP-1 receptors. These receptors are also expressed by parafollicular cells (C cells) of the thyroid, which secrete calcitonin and are the cells involved in medullary thyroid cancer. A dose-related and duration-dependent increase in thyroid C-cell tumor incidence was noted in rodents. The same relationship was not demonstrated in monkeys. Humans have far fewer C cells than rats, and human C cells have very low expression of the GLP-1 receptor.
Over a decade ago, a study examining the FDA’s database of reported adverse events found an increased risk for thyroid cancer in patients treated with exenatide, another GLP-1 agonist. The reporting system wasn’t designed to distinguish thyroid cancer subtypes.
Numerous subsequent studies didn’t confirm this relationship. The LEADER trial looked at liraglutide in patients with type 2 diabetes and showed no effect of GLP-1 receptor activation on human serum calcitonin levels, C-cell proliferation, or C-cell malignancy. Similarly, a large meta-analysis in patients with type 2 diabetes didn’t find a statistically increased risk for thyroid cancer with liraglutide, and no thyroid malignancies were reported with exenatide.
Two U.S. administrative databases from commercial health plans (a retrospective cohort study and a nested case-control study) compared type 2 diabetes patients who were taking exenatide vs. other antidiabetic drugs and found that exenatide was not significantly associated with an increased risk for thyroid cancer.
And a recent meta-analysis of 45 trials showed no significant effects on the occurrence of thyroid cancer with GLP-1 receptor agonists. Of note, it did find an increased risk for overall thyroid disorders, although there was no clear statistically significant finding pointing to a specific thyroid disorder.
Differing from prior studies, a recent nationwide French health care system study provided newer data suggesting a moderate increased risk for thyroid cancer in a cohort of patients with type 2 diabetes who were taking GLP-1 agonists. The increase in relative risk was noted for all types of thyroid cancer in patients using GLP-1 receptor agonists for 1-3 years.
An accompanying commentary by Caroline A. Thompson, PhD, and Til Stürmer, MD, provides perspective on this study’s potential limitations. These include detection bias, as the study results focused only on the statistically significant data. Also discussed were limitations to the case-control design, issues with claims-based tumor type classification (unavailability of surgical pathology), and an inability to adjust for family history and obesity, which is a risk factor alone for thyroid cancer. There was also no adjustment for exposure to head/neck radiation.
While this study has important findings to consider, it deserves further investigation, with future studies linking data to tumor registry data before a change is made in clinical practice.
No clear relationship has been drawn between GLP-1 receptor agonists and thyroid cancer in humans. Numerous confounding factors limit the data. Studies generally don’t specify the type of thyroid cancer, and they lump medullary thyroid cancer, the rarest form, with papillary thyroid cancer.
Is a detection bias present where weight loss makes nodules more visible on the neck among those treated with GLP-1 agonists? And/or are patients treated with GLP-1 agonists being screened more stringently for thyroid nodules and/or cancer?
How to advise our patients and respond to the EMR messages
The TikTok videos may continue, the celebrity chatter may increase, and we, as physicians, will continue to look to real-world data with randomized controlled trials to tailor our decision-making and guide our patients.
Thyroid cancer remains a rare outcome, and GLP-1 receptor agonists remain a very important and beneficial treatment option for the right patient.
A version of this article first appeared on Medscape.com.
High caffeine levels may lower body fat, type 2 diabetes risks
the results of a new study suggest.
Explaining that caffeine has thermogenic effects, the researchers note that previous short-term studies have linked caffeine intake with reductions in weight and fat mass. And observational data have shown associations between coffee consumption and lower risks of type 2 diabetes and cardiovascular disease.
In an effort to isolate the effects of caffeine from those of other food and drink components, Susanna C. Larsson, PhD, of the Karolinska Institute, Stockholm, and colleagues used data from studies of mainly European populations to examine two specific genetic mutations that have been linked to a slower speed of caffeine metabolism.
The two gene variants resulted in “genetically predicted, lifelong, higher plasma caffeine concentrations,” the researchers note “and were associated with lower body mass index and fat mass, as well as a lower risk of type 2 diabetes.”
Approximately half of the effect of caffeine on type 2 diabetes was estimated to be mediated through body mass index (BMI) reduction.
The work was published online March 14 in BMJ Medicine.
“This publication supports existing studies suggesting a link between caffeine consumption and increased fat burn,” notes Stephen Lawrence, MBChB, Warwick (England) University. “The big leap of faith that the authors have made is to assume that the weight loss brought about by increased caffeine consumption is sufficient to reduce the risk of developing type 2 diabetes,” he told the UK Science Media Centre.
“It does not, however, prove cause and effect.”
The researchers agree, noting: “Further clinical study is warranted to investigate the translational potential of these findings towards reducing the burden of metabolic disease.”
Katarina Kos, MD, PhD, a senior lecturer in diabetes and obesity at the University of Exeter (England), emphasized that this genetic study “shows links and potential health benefits for people with certain genes attributed to a faster [caffeine] metabolism as a hereditary trait and potentially a better metabolism.”
“It does not study or recommend drinking more coffee, which was not the purpose of this research,” she told the UK Science Media Centre.
Using Mendelian randomization, Dr. Larsson and colleagues examined data that came from a genomewide association meta-analysis of 9,876 individuals of European ancestry from six population-based studies.
Genetically predicted higher plasma caffeine concentrations in those carrying the two gene variants were associated with a lower BMI, with one standard deviation increase in predicted plasma caffeine equaling about 4.8 kg/m2 in BMI (P < .001).
For whole-body fat mass, one standard deviation increase in plasma caffeine equaled a reduction of about 9.5 kg (P < .001). However, there was no significant association with fat-free body mass (P = .17).
Genetically predicted higher plasma caffeine concentrations were also associated with a lower risk for type 2 diabetes in the FinnGen study (odds ratio, 0.77 per standard deviation increase; P < .001) and the DIAMANTE consortia (0.84, P < .001).
Combined, the odds ratio of type 2 diabetes per standard deviation of plasma caffeine increase was 0.81 (P < .001).
Dr. Larsson and colleagues calculated that approximately 43% of the protective effect of plasma caffeine on type 2 diabetes was mediated through BMI.
They did not find any strong associations between genetically predicted plasma caffeine concentrations and risk of any of the studied cardiovascular disease outcomes (ischemic heart disease, atrial fibrillation, heart failure, and stroke).
The thermogenic response to caffeine has been previously quantified as an approximate 100 kcal increase in energy expenditure per 100 mg daily caffeine intake, an amount that could result in reduced obesity risk. Another possible mechanism is enhanced satiety and suppressed energy intake with higher caffeine levels, the researchers say.
“Long-term clinical studies investigating the effect of caffeine intake on fat mass and type 2 diabetes risk are warranted,” they note. “Randomized controlled trials are warranted to assess whether noncaloric caffeine-containing beverages might play a role in reducing the risk of obesity and type 2 diabetes.”
The study was supported by the Swedish Research Council for Health, Working Life and Welfare, Swedish Heart Lung Foundation, and Swedish Research Council. Dr. Larsson, Dr. Lawrence, and Dr. Kos have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
the results of a new study suggest.
Explaining that caffeine has thermogenic effects, the researchers note that previous short-term studies have linked caffeine intake with reductions in weight and fat mass. And observational data have shown associations between coffee consumption and lower risks of type 2 diabetes and cardiovascular disease.
In an effort to isolate the effects of caffeine from those of other food and drink components, Susanna C. Larsson, PhD, of the Karolinska Institute, Stockholm, and colleagues used data from studies of mainly European populations to examine two specific genetic mutations that have been linked to a slower speed of caffeine metabolism.
The two gene variants resulted in “genetically predicted, lifelong, higher plasma caffeine concentrations,” the researchers note “and were associated with lower body mass index and fat mass, as well as a lower risk of type 2 diabetes.”
Approximately half of the effect of caffeine on type 2 diabetes was estimated to be mediated through body mass index (BMI) reduction.
The work was published online March 14 in BMJ Medicine.
“This publication supports existing studies suggesting a link between caffeine consumption and increased fat burn,” notes Stephen Lawrence, MBChB, Warwick (England) University. “The big leap of faith that the authors have made is to assume that the weight loss brought about by increased caffeine consumption is sufficient to reduce the risk of developing type 2 diabetes,” he told the UK Science Media Centre.
“It does not, however, prove cause and effect.”
The researchers agree, noting: “Further clinical study is warranted to investigate the translational potential of these findings towards reducing the burden of metabolic disease.”
Katarina Kos, MD, PhD, a senior lecturer in diabetes and obesity at the University of Exeter (England), emphasized that this genetic study “shows links and potential health benefits for people with certain genes attributed to a faster [caffeine] metabolism as a hereditary trait and potentially a better metabolism.”
“It does not study or recommend drinking more coffee, which was not the purpose of this research,” she told the UK Science Media Centre.
Using Mendelian randomization, Dr. Larsson and colleagues examined data that came from a genomewide association meta-analysis of 9,876 individuals of European ancestry from six population-based studies.
Genetically predicted higher plasma caffeine concentrations in those carrying the two gene variants were associated with a lower BMI, with one standard deviation increase in predicted plasma caffeine equaling about 4.8 kg/m2 in BMI (P < .001).
For whole-body fat mass, one standard deviation increase in plasma caffeine equaled a reduction of about 9.5 kg (P < .001). However, there was no significant association with fat-free body mass (P = .17).
Genetically predicted higher plasma caffeine concentrations were also associated with a lower risk for type 2 diabetes in the FinnGen study (odds ratio, 0.77 per standard deviation increase; P < .001) and the DIAMANTE consortia (0.84, P < .001).
Combined, the odds ratio of type 2 diabetes per standard deviation of plasma caffeine increase was 0.81 (P < .001).
Dr. Larsson and colleagues calculated that approximately 43% of the protective effect of plasma caffeine on type 2 diabetes was mediated through BMI.
They did not find any strong associations between genetically predicted plasma caffeine concentrations and risk of any of the studied cardiovascular disease outcomes (ischemic heart disease, atrial fibrillation, heart failure, and stroke).
The thermogenic response to caffeine has been previously quantified as an approximate 100 kcal increase in energy expenditure per 100 mg daily caffeine intake, an amount that could result in reduced obesity risk. Another possible mechanism is enhanced satiety and suppressed energy intake with higher caffeine levels, the researchers say.
“Long-term clinical studies investigating the effect of caffeine intake on fat mass and type 2 diabetes risk are warranted,” they note. “Randomized controlled trials are warranted to assess whether noncaloric caffeine-containing beverages might play a role in reducing the risk of obesity and type 2 diabetes.”
The study was supported by the Swedish Research Council for Health, Working Life and Welfare, Swedish Heart Lung Foundation, and Swedish Research Council. Dr. Larsson, Dr. Lawrence, and Dr. Kos have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
the results of a new study suggest.
Explaining that caffeine has thermogenic effects, the researchers note that previous short-term studies have linked caffeine intake with reductions in weight and fat mass. And observational data have shown associations between coffee consumption and lower risks of type 2 diabetes and cardiovascular disease.
In an effort to isolate the effects of caffeine from those of other food and drink components, Susanna C. Larsson, PhD, of the Karolinska Institute, Stockholm, and colleagues used data from studies of mainly European populations to examine two specific genetic mutations that have been linked to a slower speed of caffeine metabolism.
The two gene variants resulted in “genetically predicted, lifelong, higher plasma caffeine concentrations,” the researchers note “and were associated with lower body mass index and fat mass, as well as a lower risk of type 2 diabetes.”
Approximately half of the effect of caffeine on type 2 diabetes was estimated to be mediated through body mass index (BMI) reduction.
The work was published online March 14 in BMJ Medicine.
“This publication supports existing studies suggesting a link between caffeine consumption and increased fat burn,” notes Stephen Lawrence, MBChB, Warwick (England) University. “The big leap of faith that the authors have made is to assume that the weight loss brought about by increased caffeine consumption is sufficient to reduce the risk of developing type 2 diabetes,” he told the UK Science Media Centre.
“It does not, however, prove cause and effect.”
The researchers agree, noting: “Further clinical study is warranted to investigate the translational potential of these findings towards reducing the burden of metabolic disease.”
Katarina Kos, MD, PhD, a senior lecturer in diabetes and obesity at the University of Exeter (England), emphasized that this genetic study “shows links and potential health benefits for people with certain genes attributed to a faster [caffeine] metabolism as a hereditary trait and potentially a better metabolism.”
“It does not study or recommend drinking more coffee, which was not the purpose of this research,” she told the UK Science Media Centre.
Using Mendelian randomization, Dr. Larsson and colleagues examined data that came from a genomewide association meta-analysis of 9,876 individuals of European ancestry from six population-based studies.
Genetically predicted higher plasma caffeine concentrations in those carrying the two gene variants were associated with a lower BMI, with one standard deviation increase in predicted plasma caffeine equaling about 4.8 kg/m2 in BMI (P < .001).
For whole-body fat mass, one standard deviation increase in plasma caffeine equaled a reduction of about 9.5 kg (P < .001). However, there was no significant association with fat-free body mass (P = .17).
Genetically predicted higher plasma caffeine concentrations were also associated with a lower risk for type 2 diabetes in the FinnGen study (odds ratio, 0.77 per standard deviation increase; P < .001) and the DIAMANTE consortia (0.84, P < .001).
Combined, the odds ratio of type 2 diabetes per standard deviation of plasma caffeine increase was 0.81 (P < .001).
Dr. Larsson and colleagues calculated that approximately 43% of the protective effect of plasma caffeine on type 2 diabetes was mediated through BMI.
They did not find any strong associations between genetically predicted plasma caffeine concentrations and risk of any of the studied cardiovascular disease outcomes (ischemic heart disease, atrial fibrillation, heart failure, and stroke).
The thermogenic response to caffeine has been previously quantified as an approximate 100 kcal increase in energy expenditure per 100 mg daily caffeine intake, an amount that could result in reduced obesity risk. Another possible mechanism is enhanced satiety and suppressed energy intake with higher caffeine levels, the researchers say.
“Long-term clinical studies investigating the effect of caffeine intake on fat mass and type 2 diabetes risk are warranted,” they note. “Randomized controlled trials are warranted to assess whether noncaloric caffeine-containing beverages might play a role in reducing the risk of obesity and type 2 diabetes.”
The study was supported by the Swedish Research Council for Health, Working Life and Welfare, Swedish Heart Lung Foundation, and Swedish Research Council. Dr. Larsson, Dr. Lawrence, and Dr. Kos have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM BMJ MEDICINE