Clinician Reviews

AMSTERDAM – Adults with heart failure with preserved ejection fraction (HFpEF) but without diabetes showed significant improvements in their heart failure-related symptoms and physical limitations, exercise function, and weight loss when treated with a weight-reducing dose of semaglutide for 52 weeks, compared with placebo, in the randomized STEP-HFpEF trial.

The results, which also showed the treatment’s safety in these patients, “indicate that treatment with semaglutide is a valuable therapeutic approach in the management of patients with HFpEF and obesity,” Mikhail Kosiborod, MD, said at the annual congress of the European Society of Cardiology.

Mitchel L. Zoler/MDedge News

The findings establish semaglutide, a glucagonlike peptide–1 (GLP-1) receptor agonist, as a second class of medication with proven efficacy and safety for people with HFpEF, joining two agents also proven beneficial for people with HFpEF, dapagliflozin (Farxiga) and empagliflozin (Jardiance), both from the class of sodium-glucose cotransporter 2 (SGLT2) inhibitors.

When administered at the approved dose for weight loss of 2.4 mg, injected subcutaneously weekly for 52 weeks, semaglutide (Wegovy) produced an average 7.8-point incremental improvement in patients’ scores on the Kansas City Cardiomyopathy Questionnaire (KCCQ), a validated measure of symptoms and functional limitations, compared with controls who received placebo injections, as well as an average incremental weight loss from baseline, compared with placebo, of 10.7%. Both were significant effects, compared with placebo, and clinically meaningful benefits for the study’s two primary endpoints.

Simultaneously with Kosiborod’s report the results also appeared in a report posted online in the New England Journal of Medicine.
 

A ‘paradigm shift’ for medical weight loss in cardiology

The findings from this study with 529 randomized patients immediately propelled the weight loss formulation of semaglutide into the ranks of agents used to treat and prevent cardiovascular disease events. This evolution in the indications for semaglutide will be driven not only by the STEP-HFpEF results but also by findings from the SELECT trial, which tested the same semaglutide weight-loss dose in people with obesity, established cardiovascular disease, and had positive top-line results for prevention of major cardiovascular adverse events, according to a press release from Novo Nordisk on Aug. 8.

The STEP-HFpEF and SELECT results will trigger “a paradigm shift” for cardiologists, who will now need to consider prescribing a weight-loss medication to many of their patients, agents that until now were not part of the usual pharmacologic toolbox for cardiologists, said Dr. Kosiborod, a cardiologist and codirector of the Haverty Cardiometabolic Center of Excellence at Saint Luke’s Mid America Heart Institute in Kansas City, Mo. This shift will require education to bring the clinical cardiology community on board, he added in an interview.

Given that semaglutide administered at this dose already has a Food and Drug Administration–approved indication for weight loss in people with obesity or overweight plus at least one comorbidity, clinicians could immediately start using the treatment in people with obesity and HFpEF, said Dr. Kosiborod and other cardiologists.

Weekly semaglutide injections “could be considered a treatment option right now” for people with obesity and HFpEF, Dr. Kosiborod said during a press briefing.

Other experts agreed, especially because the STEP-HFpEF results confirmed that weight loss treatment with semaglutide was safe in this population.
 

‘A terrific win for patients’

The new findings are “a terrific win and game changer for patients with HFpEF,” commented Gregg C. Fonarow, MD, professor and cochief of cardiology at the University of California, Los Angeles, who was not involved with the study.

“The magnitude of improvement in the patient-reported health status scores are large and impressive. These data support clinical use of this agent for individuals with HFpEF with a body mass index of 30 kg/m², patients who already fall within existing indications,” Dr. Fonarow said in an interview.

“Given the improvements in clinical outcomes in the STEP-HFpEF and SELECT trials, cardiologists should be prescribing these medications to eligible patients without conditions,” he added. “The perception of [semaglutide] needs to shift and be viewed as a component of the comprehensive medical therapies provided to individuals with established cardiovascular disease or HFpEF who also have elevated body mass index to improve their clinical outcomes.”

Mitchel L. Zoler/MDedge News

Historically, cardiologists have had a concern that weight loss was potentially harmful in people with heart failure and that obesity was protective, a phenomenon known as the “obesity paradox,” but the STEP-HFpEF data help disprove that notion, commented Nancy K. Sweitzer, MD, PhD, a heart failure specialist and vice chair of clinical research in the department of medicine at Washington University in St. Louis, who also was not involved in the study.
 

No signal of an obesity paradox

“There’s been a concern in the heart failure community to use weight-loss strategies in people with heart failure because of this, but this evidence provides a lot of confidence that it’s safe to use this weight loss treatment. The results show that patients feel better and lose weight with no signal of harm,” Dr. Sweitzer said in an interview.

The “encouraging findings” for semaglutide in patients with HFpEF “potentially add a much needed extra option for these patients and provide another upstream treatment for patients with signs of this condition plus a high body mass index,” commented Yigal M. Pinto, MD, PhD, in an editorial that accompanied the published report.

“How these findings translate to hard end points remains to be established and will be important in determining the role of GLP-1 agonism,” wrote Dr. Pinto, a professor and heart failure specialist at Amsterdam University Medical Center.

But Dr. Kosiborod said that the improvement seen in the KCCQ score was itself an important benefit for patients. “Heart failure is defined clinically based on symptoms,” he noted, and results in prior studies documented that patients value improvements in symptoms and physical limitations even more than they value “hard endpoints” such as survival.

The new findings, which indicate that two different and expensive classes of medications are now standard of care for many people with HFpEF and obesity – the SGLT2 inhibitors and the GLP-1 receptor agonist semaglutide – also raise concerns over patient access and affordability, as many U.S. insurers have a history of requiring prior authorization, high copays, or coverage denials for these two medical classes.

But Dr. Sweitzer and Dr. Kosiborod both said that the insurance-coverage climate seems, in just the past couple of years or so, to have dramatically improved, although it’s still not ideal.
 

Prior authorization hoops have decreased

“We still have prior-authorization hoops to jump through, but I expect these will continue to decrease over time as evidence for clinical benefits [from weight loss] continues to accumulate,” said Dr. Sweitzer.

And “the SELECT data mean that cardiologists will need to become comfortable prescribing GLP-1 receptor agonists,” she added.

“It’s not okay for insurers to say we are not going to cover weight loss medications because it’s a cosmetic indication,” said Dr. Kosiborod. “Obesity appears to be very important in the pathogenesis and progression of heart failure, and if patients derive substantial benefit, they should have access to this treatment.”

The improvements in KCCQ score, as well as in several secondary and exploratory endpoints including a significant reduction in C-reactive protein (an indication of a potent anti-inflammatory effect), an average 20 m increase in 6-minute walk distance, a significant average drop in N-terminal pro-brain natriuretic peptide, and a drop in heart failure hospitalizations or urgent heart failure visits (although the trial was not powered to show differences in clinical events), “were the largest benefits in these outcomes we’ve seen,” compared with any other medical intervention in people with HFpEF, he noted.

“About 80% of U.S. patients with HFpEF have obesity or overweight,” Dr. Kosiborod noted. Using semaglutide on these patients “is an issue of access and insurance coverage. My hope is that these and other data will favorably change this.”

A related trial with a similar design, STEP-HFpEF DM, is still in progress and testing the same semaglutide treatment in adults with HFpEF, obesity, and type 2 diabetes, noted Dr. Kosiborod, who is also lead investigator for that study. He said those results will likely become available before the end of 2023.

The study was funded by Novo Nordisk, the company that markets semaglutide (Wegovy). Dr. Kosiborod has been a consultant and adviser to and has received honoraria from Novo Nordisk. He has also been a consultant to numerous other companies, received research grants from AstraZeneca, Boehringer Ingelheim, and Pfizer, honoraria from AstraZeneca, and is a stockholder in Artera Health and Saghmos Therapeutics. Dr. Fonarow has been a consultant to Abbott, Amgen, AstraZeneca, CHF Solutions, Cytokinetics, Edwards, Janssen, Medtronic, Merck, Novartis, and Regeneron. Dr. Sweitzer reported no relevant financial relationships.

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

AMSTERDAM – Adults with heart failure with preserved ejection fraction (HFpEF) but without diabetes showed significant improvements in their heart failure-related symptoms and physical limitations, exercise function, and weight loss when treated with a weight-reducing dose of semaglutide for 52 weeks, compared with placebo, in the randomized STEP-HFpEF trial.

The results, which also showed the treatment’s safety in these patients, “indicate that treatment with semaglutide is a valuable therapeutic approach in the management of patients with HFpEF and obesity,” Mikhail Kosiborod, MD, said at the annual congress of the European Society of Cardiology.

Mitchel L. Zoler/MDedge News

The findings establish semaglutide, a glucagonlike peptide–1 (GLP-1) receptor agonist, as a second class of medication with proven efficacy and safety for people with HFpEF, joining two agents also proven beneficial for people with HFpEF, dapagliflozin (Farxiga) and empagliflozin (Jardiance), both from the class of sodium-glucose cotransporter 2 (SGLT2) inhibitors.

When administered at the approved dose for weight loss of 2.4 mg, injected subcutaneously weekly for 52 weeks, semaglutide (Wegovy) produced an average 7.8-point incremental improvement in patients’ scores on the Kansas City Cardiomyopathy Questionnaire (KCCQ), a validated measure of symptoms and functional limitations, compared with controls who received placebo injections, as well as an average incremental weight loss from baseline, compared with placebo, of 10.7%. Both were significant effects, compared with placebo, and clinically meaningful benefits for the study’s two primary endpoints.

Simultaneously with Kosiborod’s report the results also appeared in a report posted online in the New England Journal of Medicine.
 

A ‘paradigm shift’ for medical weight loss in cardiology

The findings from this study with 529 randomized patients immediately propelled the weight loss formulation of semaglutide into the ranks of agents used to treat and prevent cardiovascular disease events. This evolution in the indications for semaglutide will be driven not only by the STEP-HFpEF results but also by findings from the SELECT trial, which tested the same semaglutide weight-loss dose in people with obesity, established cardiovascular disease, and had positive top-line results for prevention of major cardiovascular adverse events, according to a press release from Novo Nordisk on Aug. 8.

The STEP-HFpEF and SELECT results will trigger “a paradigm shift” for cardiologists, who will now need to consider prescribing a weight-loss medication to many of their patients, agents that until now were not part of the usual pharmacologic toolbox for cardiologists, said Dr. Kosiborod, a cardiologist and codirector of the Haverty Cardiometabolic Center of Excellence at Saint Luke’s Mid America Heart Institute in Kansas City, Mo. This shift will require education to bring the clinical cardiology community on board, he added in an interview.

Given that semaglutide administered at this dose already has a Food and Drug Administration–approved indication for weight loss in people with obesity or overweight plus at least one comorbidity, clinicians could immediately start using the treatment in people with obesity and HFpEF, said Dr. Kosiborod and other cardiologists.

Weekly semaglutide injections “could be considered a treatment option right now” for people with obesity and HFpEF, Dr. Kosiborod said during a press briefing.

Other experts agreed, especially because the STEP-HFpEF results confirmed that weight loss treatment with semaglutide was safe in this population.
 

‘A terrific win for patients’

The new findings are “a terrific win and game changer for patients with HFpEF,” commented Gregg C. Fonarow, MD, professor and cochief of cardiology at the University of California, Los Angeles, who was not involved with the study.

“The magnitude of improvement in the patient-reported health status scores are large and impressive. These data support clinical use of this agent for individuals with HFpEF with a body mass index of 30 kg/m², patients who already fall within existing indications,” Dr. Fonarow said in an interview.

“Given the improvements in clinical outcomes in the STEP-HFpEF and SELECT trials, cardiologists should be prescribing these medications to eligible patients without conditions,” he added. “The perception of [semaglutide] needs to shift and be viewed as a component of the comprehensive medical therapies provided to individuals with established cardiovascular disease or HFpEF who also have elevated body mass index to improve their clinical outcomes.”

Mitchel L. Zoler/MDedge News

Historically, cardiologists have had a concern that weight loss was potentially harmful in people with heart failure and that obesity was protective, a phenomenon known as the “obesity paradox,” but the STEP-HFpEF data help disprove that notion, commented Nancy K. Sweitzer, MD, PhD, a heart failure specialist and vice chair of clinical research in the department of medicine at Washington University in St. Louis, who also was not involved in the study.
 

No signal of an obesity paradox

“There’s been a concern in the heart failure community to use weight-loss strategies in people with heart failure because of this, but this evidence provides a lot of confidence that it’s safe to use this weight loss treatment. The results show that patients feel better and lose weight with no signal of harm,” Dr. Sweitzer said in an interview.

The “encouraging findings” for semaglutide in patients with HFpEF “potentially add a much needed extra option for these patients and provide another upstream treatment for patients with signs of this condition plus a high body mass index,” commented Yigal M. Pinto, MD, PhD, in an editorial that accompanied the published report.

“How these findings translate to hard end points remains to be established and will be important in determining the role of GLP-1 agonism,” wrote Dr. Pinto, a professor and heart failure specialist at Amsterdam University Medical Center.

But Dr. Kosiborod said that the improvement seen in the KCCQ score was itself an important benefit for patients. “Heart failure is defined clinically based on symptoms,” he noted, and results in prior studies documented that patients value improvements in symptoms and physical limitations even more than they value “hard endpoints” such as survival.

The new findings, which indicate that two different and expensive classes of medications are now standard of care for many people with HFpEF and obesity – the SGLT2 inhibitors and the GLP-1 receptor agonist semaglutide – also raise concerns over patient access and affordability, as many U.S. insurers have a history of requiring prior authorization, high copays, or coverage denials for these two medical classes.

But Dr. Sweitzer and Dr. Kosiborod both said that the insurance-coverage climate seems, in just the past couple of years or so, to have dramatically improved, although it’s still not ideal.
 

Prior authorization hoops have decreased

“We still have prior-authorization hoops to jump through, but I expect these will continue to decrease over time as evidence for clinical benefits [from weight loss] continues to accumulate,” said Dr. Sweitzer.

And “the SELECT data mean that cardiologists will need to become comfortable prescribing GLP-1 receptor agonists,” she added.

“It’s not okay for insurers to say we are not going to cover weight loss medications because it’s a cosmetic indication,” said Dr. Kosiborod. “Obesity appears to be very important in the pathogenesis and progression of heart failure, and if patients derive substantial benefit, they should have access to this treatment.”

The improvements in KCCQ score, as well as in several secondary and exploratory endpoints including a significant reduction in C-reactive protein (an indication of a potent anti-inflammatory effect), an average 20 m increase in 6-minute walk distance, a significant average drop in N-terminal pro-brain natriuretic peptide, and a drop in heart failure hospitalizations or urgent heart failure visits (although the trial was not powered to show differences in clinical events), “were the largest benefits in these outcomes we’ve seen,” compared with any other medical intervention in people with HFpEF, he noted.

“About 80% of U.S. patients with HFpEF have obesity or overweight,” Dr. Kosiborod noted. Using semaglutide on these patients “is an issue of access and insurance coverage. My hope is that these and other data will favorably change this.”

A related trial with a similar design, STEP-HFpEF DM, is still in progress and testing the same semaglutide treatment in adults with HFpEF, obesity, and type 2 diabetes, noted Dr. Kosiborod, who is also lead investigator for that study. He said those results will likely become available before the end of 2023.

The study was funded by Novo Nordisk, the company that markets semaglutide (Wegovy). Dr. Kosiborod has been a consultant and adviser to and has received honoraria from Novo Nordisk. He has also been a consultant to numerous other companies, received research grants from AstraZeneca, Boehringer Ingelheim, and Pfizer, honoraria from AstraZeneca, and is a stockholder in Artera Health and Saghmos Therapeutics. Dr. Fonarow has been a consultant to Abbott, Amgen, AstraZeneca, CHF Solutions, Cytokinetics, Edwards, Janssen, Medtronic, Merck, Novartis, and Regeneron. Dr. Sweitzer reported no relevant financial relationships.

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

AMSTERDAM – Adults with heart failure with preserved ejection fraction (HFpEF) but without diabetes showed significant improvements in their heart failure-related symptoms and physical limitations, exercise function, and weight loss when treated with a weight-reducing dose of semaglutide for 52 weeks, compared with placebo, in the randomized STEP-HFpEF trial.

The results, which also showed the treatment’s safety in these patients, “indicate that treatment with semaglutide is a valuable therapeutic approach in the management of patients with HFpEF and obesity,” Mikhail Kosiborod, MD, said at the annual congress of the European Society of Cardiology.

Mitchel L. Zoler/MDedge News

The findings establish semaglutide, a glucagonlike peptide–1 (GLP-1) receptor agonist, as a second class of medication with proven efficacy and safety for people with HFpEF, joining two agents also proven beneficial for people with HFpEF, dapagliflozin (Farxiga) and empagliflozin (Jardiance), both from the class of sodium-glucose cotransporter 2 (SGLT2) inhibitors.

When administered at the approved dose for weight loss of 2.4 mg, injected subcutaneously weekly for 52 weeks, semaglutide (Wegovy) produced an average 7.8-point incremental improvement in patients’ scores on the Kansas City Cardiomyopathy Questionnaire (KCCQ), a validated measure of symptoms and functional limitations, compared with controls who received placebo injections, as well as an average incremental weight loss from baseline, compared with placebo, of 10.7%. Both were significant effects, compared with placebo, and clinically meaningful benefits for the study’s two primary endpoints.

Simultaneously with Kosiborod’s report the results also appeared in a report posted online in the New England Journal of Medicine.
 

A ‘paradigm shift’ for medical weight loss in cardiology

The findings from this study with 529 randomized patients immediately propelled the weight loss formulation of semaglutide into the ranks of agents used to treat and prevent cardiovascular disease events. This evolution in the indications for semaglutide will be driven not only by the STEP-HFpEF results but also by findings from the SELECT trial, which tested the same semaglutide weight-loss dose in people with obesity, established cardiovascular disease, and had positive top-line results for prevention of major cardiovascular adverse events, according to a press release from Novo Nordisk on Aug. 8.

The STEP-HFpEF and SELECT results will trigger “a paradigm shift” for cardiologists, who will now need to consider prescribing a weight-loss medication to many of their patients, agents that until now were not part of the usual pharmacologic toolbox for cardiologists, said Dr. Kosiborod, a cardiologist and codirector of the Haverty Cardiometabolic Center of Excellence at Saint Luke’s Mid America Heart Institute in Kansas City, Mo. This shift will require education to bring the clinical cardiology community on board, he added in an interview.

Given that semaglutide administered at this dose already has a Food and Drug Administration–approved indication for weight loss in people with obesity or overweight plus at least one comorbidity, clinicians could immediately start using the treatment in people with obesity and HFpEF, said Dr. Kosiborod and other cardiologists.

Weekly semaglutide injections “could be considered a treatment option right now” for people with obesity and HFpEF, Dr. Kosiborod said during a press briefing.

Other experts agreed, especially because the STEP-HFpEF results confirmed that weight loss treatment with semaglutide was safe in this population.
 

‘A terrific win for patients’

The new findings are “a terrific win and game changer for patients with HFpEF,” commented Gregg C. Fonarow, MD, professor and cochief of cardiology at the University of California, Los Angeles, who was not involved with the study.

“The magnitude of improvement in the patient-reported health status scores are large and impressive. These data support clinical use of this agent for individuals with HFpEF with a body mass index of 30 kg/m², patients who already fall within existing indications,” Dr. Fonarow said in an interview.

“Given the improvements in clinical outcomes in the STEP-HFpEF and SELECT trials, cardiologists should be prescribing these medications to eligible patients without conditions,” he added. “The perception of [semaglutide] needs to shift and be viewed as a component of the comprehensive medical therapies provided to individuals with established cardiovascular disease or HFpEF who also have elevated body mass index to improve their clinical outcomes.”

Mitchel L. Zoler/MDedge News

Historically, cardiologists have had a concern that weight loss was potentially harmful in people with heart failure and that obesity was protective, a phenomenon known as the “obesity paradox,” but the STEP-HFpEF data help disprove that notion, commented Nancy K. Sweitzer, MD, PhD, a heart failure specialist and vice chair of clinical research in the department of medicine at Washington University in St. Louis, who also was not involved in the study.
 

No signal of an obesity paradox

“There’s been a concern in the heart failure community to use weight-loss strategies in people with heart failure because of this, but this evidence provides a lot of confidence that it’s safe to use this weight loss treatment. The results show that patients feel better and lose weight with no signal of harm,” Dr. Sweitzer said in an interview.

The “encouraging findings” for semaglutide in patients with HFpEF “potentially add a much needed extra option for these patients and provide another upstream treatment for patients with signs of this condition plus a high body mass index,” commented Yigal M. Pinto, MD, PhD, in an editorial that accompanied the published report.

“How these findings translate to hard end points remains to be established and will be important in determining the role of GLP-1 agonism,” wrote Dr. Pinto, a professor and heart failure specialist at Amsterdam University Medical Center.

But Dr. Kosiborod said that the improvement seen in the KCCQ score was itself an important benefit for patients. “Heart failure is defined clinically based on symptoms,” he noted, and results in prior studies documented that patients value improvements in symptoms and physical limitations even more than they value “hard endpoints” such as survival.

The new findings, which indicate that two different and expensive classes of medications are now standard of care for many people with HFpEF and obesity – the SGLT2 inhibitors and the GLP-1 receptor agonist semaglutide – also raise concerns over patient access and affordability, as many U.S. insurers have a history of requiring prior authorization, high copays, or coverage denials for these two medical classes.

But Dr. Sweitzer and Dr. Kosiborod both said that the insurance-coverage climate seems, in just the past couple of years or so, to have dramatically improved, although it’s still not ideal.
 

Prior authorization hoops have decreased

“We still have prior-authorization hoops to jump through, but I expect these will continue to decrease over time as evidence for clinical benefits [from weight loss] continues to accumulate,” said Dr. Sweitzer.

And “the SELECT data mean that cardiologists will need to become comfortable prescribing GLP-1 receptor agonists,” she added.

“It’s not okay for insurers to say we are not going to cover weight loss medications because it’s a cosmetic indication,” said Dr. Kosiborod. “Obesity appears to be very important in the pathogenesis and progression of heart failure, and if patients derive substantial benefit, they should have access to this treatment.”

The improvements in KCCQ score, as well as in several secondary and exploratory endpoints including a significant reduction in C-reactive protein (an indication of a potent anti-inflammatory effect), an average 20 m increase in 6-minute walk distance, a significant average drop in N-terminal pro-brain natriuretic peptide, and a drop in heart failure hospitalizations or urgent heart failure visits (although the trial was not powered to show differences in clinical events), “were the largest benefits in these outcomes we’ve seen,” compared with any other medical intervention in people with HFpEF, he noted.

“About 80% of U.S. patients with HFpEF have obesity or overweight,” Dr. Kosiborod noted. Using semaglutide on these patients “is an issue of access and insurance coverage. My hope is that these and other data will favorably change this.”

A related trial with a similar design, STEP-HFpEF DM, is still in progress and testing the same semaglutide treatment in adults with HFpEF, obesity, and type 2 diabetes, noted Dr. Kosiborod, who is also lead investigator for that study. He said those results will likely become available before the end of 2023.

The study was funded by Novo Nordisk, the company that markets semaglutide (Wegovy). Dr. Kosiborod has been a consultant and adviser to and has received honoraria from Novo Nordisk. He has also been a consultant to numerous other companies, received research grants from AstraZeneca, Boehringer Ingelheim, and Pfizer, honoraria from AstraZeneca, and is a stockholder in Artera Health and Saghmos Therapeutics. Dr. Fonarow has been a consultant to Abbott, Amgen, AstraZeneca, CHF Solutions, Cytokinetics, Edwards, Janssen, Medtronic, Merck, Novartis, and Regeneron. Dr. Sweitzer reported no relevant financial relationships.

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

A stylish 40-something-year-old walks into my office looking mildly sheepish. She is a well-known actress who was recently panned by the paparazzi for having “too much cellulite” after they illegally photographed her playing with her child on a private beach.

Without a doubt, she will request semaglutide (Ozempic) before long, but first we will need to wade through the morass of social condemnation out there about Ozempic to assure her that she is being neither immoral nor reckless for considering it.

After nearly 20 years of practicing medicine with a focus on weight loss and preventive care, here is how I see the situation:

Ozempic is nothing new, people! Endocrinologists have been using this class of medication since Byetta hit the market in 2005. We have had 18 years to make informed risk-benefit analyses.

People are obsessed with the risk for pancreatitis. Any type of weight loss can cause gallstones, and this is what can trigger pancreatitis. Unless you’re the type of person who worries that your balanced Weight Watchers diet is going to cause pancreatitis, you should probably remove this risk from your calculations.

Glucagonlike peptide–1 (GLP-1) receptor agonists are naturally occurring gut hormones that reduce inflammatory cascades and clotting risk. We are not giving a dangerous treatment (e.g., fen-phen) that increases cardiovascular risk – quite the contrary, in fact.

Just because influencers are promoting a product doesn’t mean the product is inherently worthless. One of my patients accused me of prescribing a medication that is the “laughingstock of America.” Try telling that to the scores of cardiologists who send patients to my colleagues and me to start Ozempic to help lower their patients’ risk for stroke and heart attack. Or tell this to my patient who survived an episode of rapid atrial fibrillation and was told by his cardiologist that he definitely would have died if he had not lost 30 pounds from Ozempic in the preceding year.

Sometimes it seems like society has become more judgmental about Ozempic than about plastic surgery for weight loss. If we have to choose between liposuction (which doesn’t reduce visceral fat – the dangerous type of fat) or Ozempic, the latter clearly wins because of its real health benefits.

How does it make any sense to say that this medication should be reserved for patients who already have obesity and type 2 diabetes? Why should we penalize patients who have not yet reached those thresholds by denying access to preventive care? Don’t we constantly hear about how our health care system would be much more efficient if we focused on preventive care and not just treatment?

Some people claim that we have to limit access to this medication because of drug shortages. Thankfully, the United States responds to supply and demand economics and will quickly adjust. 

I’ve had more patients than I can possibly number with severe binge eating disorders (resistant to years of therapy and medication) who finally developed healthy relationships with food while taking these types of medications. Mounjaro, I’m talking about you…

I always hear the argument that it is immoral to give these medications to patients with a history of restrictive eating patterns. Although every patient needs to be carefully evaluated, often these medications remove food as both the enemy and primary focus of every waking thought. They allow patients to refocus on other aspects of their lives – such as family, friends, hobbies, work – and regain a sense of purpose. If anyone wants to run a trial on this little hypothesis of mine, please reach out to me. 

Okay, I agree you might get a little constipated (most often described by patients as the “rabbit pellet phenomenon”), but it’s a small price to pay, no? I’ll throw in a few prunes with the prescription.

Suffice it to say, I did give my 40-something-year-old patient the medication she desired, and she has a new lease on life (as well as better blood pressure and cholesterol).

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

A stylish 40-something-year-old walks into my office looking mildly sheepish. She is a well-known actress who was recently panned by the paparazzi for having “too much cellulite” after they illegally photographed her playing with her child on a private beach.

Without a doubt, she will request semaglutide (Ozempic) before long, but first we will need to wade through the morass of social condemnation out there about Ozempic to assure her that she is being neither immoral nor reckless for considering it.

After nearly 20 years of practicing medicine with a focus on weight loss and preventive care, here is how I see the situation:

Ozempic is nothing new, people! Endocrinologists have been using this class of medication since Byetta hit the market in 2005. We have had 18 years to make informed risk-benefit analyses.

People are obsessed with the risk for pancreatitis. Any type of weight loss can cause gallstones, and this is what can trigger pancreatitis. Unless you’re the type of person who worries that your balanced Weight Watchers diet is going to cause pancreatitis, you should probably remove this risk from your calculations.

Glucagonlike peptide–1 (GLP-1) receptor agonists are naturally occurring gut hormones that reduce inflammatory cascades and clotting risk. We are not giving a dangerous treatment (e.g., fen-phen) that increases cardiovascular risk – quite the contrary, in fact.

Just because influencers are promoting a product doesn’t mean the product is inherently worthless. One of my patients accused me of prescribing a medication that is the “laughingstock of America.” Try telling that to the scores of cardiologists who send patients to my colleagues and me to start Ozempic to help lower their patients’ risk for stroke and heart attack. Or tell this to my patient who survived an episode of rapid atrial fibrillation and was told by his cardiologist that he definitely would have died if he had not lost 30 pounds from Ozempic in the preceding year.

Sometimes it seems like society has become more judgmental about Ozempic than about plastic surgery for weight loss. If we have to choose between liposuction (which doesn’t reduce visceral fat – the dangerous type of fat) or Ozempic, the latter clearly wins because of its real health benefits.

How does it make any sense to say that this medication should be reserved for patients who already have obesity and type 2 diabetes? Why should we penalize patients who have not yet reached those thresholds by denying access to preventive care? Don’t we constantly hear about how our health care system would be much more efficient if we focused on preventive care and not just treatment?

Some people claim that we have to limit access to this medication because of drug shortages. Thankfully, the United States responds to supply and demand economics and will quickly adjust. 

I’ve had more patients than I can possibly number with severe binge eating disorders (resistant to years of therapy and medication) who finally developed healthy relationships with food while taking these types of medications. Mounjaro, I’m talking about you…

I always hear the argument that it is immoral to give these medications to patients with a history of restrictive eating patterns. Although every patient needs to be carefully evaluated, often these medications remove food as both the enemy and primary focus of every waking thought. They allow patients to refocus on other aspects of their lives – such as family, friends, hobbies, work – and regain a sense of purpose. If anyone wants to run a trial on this little hypothesis of mine, please reach out to me. 

Okay, I agree you might get a little constipated (most often described by patients as the “rabbit pellet phenomenon”), but it’s a small price to pay, no? I’ll throw in a few prunes with the prescription.

Suffice it to say, I did give my 40-something-year-old patient the medication she desired, and she has a new lease on life (as well as better blood pressure and cholesterol).

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

A stylish 40-something-year-old walks into my office looking mildly sheepish. She is a well-known actress who was recently panned by the paparazzi for having “too much cellulite” after they illegally photographed her playing with her child on a private beach.

Without a doubt, she will request semaglutide (Ozempic) before long, but first we will need to wade through the morass of social condemnation out there about Ozempic to assure her that she is being neither immoral nor reckless for considering it.

After nearly 20 years of practicing medicine with a focus on weight loss and preventive care, here is how I see the situation:

Ozempic is nothing new, people! Endocrinologists have been using this class of medication since Byetta hit the market in 2005. We have had 18 years to make informed risk-benefit analyses.

People are obsessed with the risk for pancreatitis. Any type of weight loss can cause gallstones, and this is what can trigger pancreatitis. Unless you’re the type of person who worries that your balanced Weight Watchers diet is going to cause pancreatitis, you should probably remove this risk from your calculations.

Glucagonlike peptide–1 (GLP-1) receptor agonists are naturally occurring gut hormones that reduce inflammatory cascades and clotting risk. We are not giving a dangerous treatment (e.g., fen-phen) that increases cardiovascular risk – quite the contrary, in fact.

Just because influencers are promoting a product doesn’t mean the product is inherently worthless. One of my patients accused me of prescribing a medication that is the “laughingstock of America.” Try telling that to the scores of cardiologists who send patients to my colleagues and me to start Ozempic to help lower their patients’ risk for stroke and heart attack. Or tell this to my patient who survived an episode of rapid atrial fibrillation and was told by his cardiologist that he definitely would have died if he had not lost 30 pounds from Ozempic in the preceding year.

Sometimes it seems like society has become more judgmental about Ozempic than about plastic surgery for weight loss. If we have to choose between liposuction (which doesn’t reduce visceral fat – the dangerous type of fat) or Ozempic, the latter clearly wins because of its real health benefits.

How does it make any sense to say that this medication should be reserved for patients who already have obesity and type 2 diabetes? Why should we penalize patients who have not yet reached those thresholds by denying access to preventive care? Don’t we constantly hear about how our health care system would be much more efficient if we focused on preventive care and not just treatment?

Some people claim that we have to limit access to this medication because of drug shortages. Thankfully, the United States responds to supply and demand economics and will quickly adjust. 

I’ve had more patients than I can possibly number with severe binge eating disorders (resistant to years of therapy and medication) who finally developed healthy relationships with food while taking these types of medications. Mounjaro, I’m talking about you…

I always hear the argument that it is immoral to give these medications to patients with a history of restrictive eating patterns. Although every patient needs to be carefully evaluated, often these medications remove food as both the enemy and primary focus of every waking thought. They allow patients to refocus on other aspects of their lives – such as family, friends, hobbies, work – and regain a sense of purpose. If anyone wants to run a trial on this little hypothesis of mine, please reach out to me. 

Okay, I agree you might get a little constipated (most often described by patients as the “rabbit pellet phenomenon”), but it’s a small price to pay, no? I’ll throw in a few prunes with the prescription.

Suffice it to say, I did give my 40-something-year-old patient the medication she desired, and she has a new lease on life (as well as better blood pressure and cholesterol).

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

A new strain of COVID-19 that was identified only a week ago in the United States has prompted the Centers for Disease Control and Prevention to take the rare step of issuing a formal message that it could evade vaccines or the protection of natural immunity. 

The strain is called BA.2.86 and is of particular concern because of its more than 30 mutations, which means it may behave very differently than previous versions of the virus. That number of mutations is on par with the difference between variants so serious that they were formally named, such as between Delta and Omicron, the CDC explained in the risk assessment issued Aug. 23.

Worldwide, health agencies are issuing a flurry of updates on BA.2.86. The strain only recently landed on the World Health Organization’s radar when it was named a “variant under monitoring” on Aug. 17. The CDC announced the same day that it had been detected in the United States.

Among the characteristics the CDC monitors for are how contagious a strain is, how well it responds to treatment, and how severely it affects people.

“BA.2.86 may be more capable of causing infection in people who have previously had COVID-19 or who have received COVID-19 vaccines,” the CDC risk assessment stated.

The agency is evaluating how well the forthcoming updated vaccine, due out in September, performs against BA.2.86.

A new forecast also released this week by the CDC predicts hospitalizations due to the virus will continue their upward trend through at least mid-September. Currently, about 1,800 people are hospitalized daily with COVID-19. The new prediction shows that number has a small potential to drop as low as 1,100 daily, but it could also increase by as many as 7,500 per day. The most likely scenario lands somewhere in the middle of that range, with daily hospital admissions of between 2,000 and 4,000 people by Sept. 18.

The CDC said there is “no evidence” that BA.2.86 is causing more severe illness but said that could change as more information becomes available. Health experts typically gauge severity by the rate of COVID hospitalizations.

The journal Nature reported that many scientists see similarities between the emergence of BA.2.86 and that of Omicron, which rapidly spread around the world in late 2021.

“There’s a little bit of déjà vu all over again,” University of Michigan virologist Adam Lauring, MD, PhD, whose lab detected one of the first U.S. cases of BA.2.86, told Nature.

Dr. Lauring, as well as the CDC and the WHO, all caution that more data is needed to truly understand the threat posed by BA.2.86.

“There’s good reason to think it won’t be like the Omicron wave, but it’s early days,” Dr. Lauring said.

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

A new strain of COVID-19 that was identified only a week ago in the United States has prompted the Centers for Disease Control and Prevention to take the rare step of issuing a formal message that it could evade vaccines or the protection of natural immunity. 

The strain is called BA.2.86 and is of particular concern because of its more than 30 mutations, which means it may behave very differently than previous versions of the virus. That number of mutations is on par with the difference between variants so serious that they were formally named, such as between Delta and Omicron, the CDC explained in the risk assessment issued Aug. 23.

Worldwide, health agencies are issuing a flurry of updates on BA.2.86. The strain only recently landed on the World Health Organization’s radar when it was named a “variant under monitoring” on Aug. 17. The CDC announced the same day that it had been detected in the United States.

Among the characteristics the CDC monitors for are how contagious a strain is, how well it responds to treatment, and how severely it affects people.

“BA.2.86 may be more capable of causing infection in people who have previously had COVID-19 or who have received COVID-19 vaccines,” the CDC risk assessment stated.

The agency is evaluating how well the forthcoming updated vaccine, due out in September, performs against BA.2.86.

A new forecast also released this week by the CDC predicts hospitalizations due to the virus will continue their upward trend through at least mid-September. Currently, about 1,800 people are hospitalized daily with COVID-19. The new prediction shows that number has a small potential to drop as low as 1,100 daily, but it could also increase by as many as 7,500 per day. The most likely scenario lands somewhere in the middle of that range, with daily hospital admissions of between 2,000 and 4,000 people by Sept. 18.

The CDC said there is “no evidence” that BA.2.86 is causing more severe illness but said that could change as more information becomes available. Health experts typically gauge severity by the rate of COVID hospitalizations.

The journal Nature reported that many scientists see similarities between the emergence of BA.2.86 and that of Omicron, which rapidly spread around the world in late 2021.

“There’s a little bit of déjà vu all over again,” University of Michigan virologist Adam Lauring, MD, PhD, whose lab detected one of the first U.S. cases of BA.2.86, told Nature.

Dr. Lauring, as well as the CDC and the WHO, all caution that more data is needed to truly understand the threat posed by BA.2.86.

“There’s good reason to think it won’t be like the Omicron wave, but it’s early days,” Dr. Lauring said.

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

A new strain of COVID-19 that was identified only a week ago in the United States has prompted the Centers for Disease Control and Prevention to take the rare step of issuing a formal message that it could evade vaccines or the protection of natural immunity. 

The strain is called BA.2.86 and is of particular concern because of its more than 30 mutations, which means it may behave very differently than previous versions of the virus. That number of mutations is on par with the difference between variants so serious that they were formally named, such as between Delta and Omicron, the CDC explained in the risk assessment issued Aug. 23.

Worldwide, health agencies are issuing a flurry of updates on BA.2.86. The strain only recently landed on the World Health Organization’s radar when it was named a “variant under monitoring” on Aug. 17. The CDC announced the same day that it had been detected in the United States.

Among the characteristics the CDC monitors for are how contagious a strain is, how well it responds to treatment, and how severely it affects people.

“BA.2.86 may be more capable of causing infection in people who have previously had COVID-19 or who have received COVID-19 vaccines,” the CDC risk assessment stated.

The agency is evaluating how well the forthcoming updated vaccine, due out in September, performs against BA.2.86.

A new forecast also released this week by the CDC predicts hospitalizations due to the virus will continue their upward trend through at least mid-September. Currently, about 1,800 people are hospitalized daily with COVID-19. The new prediction shows that number has a small potential to drop as low as 1,100 daily, but it could also increase by as many as 7,500 per day. The most likely scenario lands somewhere in the middle of that range, with daily hospital admissions of between 2,000 and 4,000 people by Sept. 18.

The CDC said there is “no evidence” that BA.2.86 is causing more severe illness but said that could change as more information becomes available. Health experts typically gauge severity by the rate of COVID hospitalizations.

The journal Nature reported that many scientists see similarities between the emergence of BA.2.86 and that of Omicron, which rapidly spread around the world in late 2021.

“There’s a little bit of déjà vu all over again,” University of Michigan virologist Adam Lauring, MD, PhD, whose lab detected one of the first U.S. cases of BA.2.86, told Nature.

Dr. Lauring, as well as the CDC and the WHO, all caution that more data is needed to truly understand the threat posed by BA.2.86.

“There’s good reason to think it won’t be like the Omicron wave, but it’s early days,” Dr. Lauring said.

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

Doctor, if you are caring for patients with diabetes, I sure hope you know more about it than I do. The longer I live, it seems, the less I understand.

In a free society, people can do what they want, and that’s great except when it isn’t. That’s why societies develop ethics and even public laws if ethics are not strong enough to protect us from ourselves and others.
 

Sugar, sugar

When I was growing up in small-town Alabama during the Depression and World War II, we called it sugar diabetes. Eat too much sugar, you got fat; your blood sugar went up, and you spilled sugar into your urine. Diabetes was fairly rare, and so was obesity. Doctors treated it by limiting the intake of sugar (and various sweet foods), along with attempting weight loss. If that didn’t do the trick, insulin injections.

From then until now, note these trends.

• 1920: 0.2% of the population
• 1930: 0.3% of the population
• 1940: 0.4% of the population

In 2020, although 11.3% of the population was diagnosed with type 2 diabetes, the unknown undiagnosed proportion could be much higher.

Notice a correlation between sugar consumption and prevalence of diabetes? Of course, correlation is not causation, but at the same time, it sure as hell is not negation. Such concordance can be considered hypothesis generating. It may not be true causation, but it’s a good bet when 89% of people with diabetes have overweight or obesity.

What did the entire medical, public health, government, agriculture, nursing, food manufacturing, marketing, advertising, restaurant, and education constituencies do about this as it was happening? They observed, documented, gave lip service, and wrung their hands in public a bit. I do not believe that this is an organized active conspiracy; it would take too many players cooperating over too long a period of time. But it certainly may be a passive conspiracy, and primary care physicians and their patients are trapped.

The proper daily practice of medicine consists of one patient, one physician, one moment, and one decision. Let it be a shared decision, informed by the best evidence and taking cost into consideration. That encounter represents an opportunity, a responsibility, and a conundrum.

Individual health is subsumed under the collective health of the public. As such, a patient’s health is out of the control of both physician and patient; instead, patients are the beneficiaries or victims of the “marketplace.” Humans are frail and easily taken advantage of by the brilliant and highly motivated strategic planning and execution of Big Agriculture, Big Food, Big Pharma, Big Marketing, and Big Money-Driven Medicine and generally failed by Big Government, Big Public Health, Big Education, Big Psychology, and Big Religion.
 

Rethinking diabetes

Consider diabetes as one of many examples. What a terrific deal for capitalism. First, the system spends decades fattening us up; then, it makes massive amounts of money off of the myriad complications of the fattened populace; then it discovers (invents) long-term, very expensive, compelling treatments to slim us down, with no end in sight, and still without ever understanding the true nature of diabetes.

Gary Taubes’s great new book, “Rethinking Diabetes: What Science Reveals About Diet, Insulin, and Successful Treatments,” is being published by Alfred A. Knopf in early 2024.

It is 404 pages of (dense) text, with 401 numbered references and footnotes, a bibliography of 790 references, alphabetically arranged for easy cross-checking, and a 25-page index.

Remember Mr. Taubes’s earlier definitive historical treatises: “Good Calories, Bad Calories” (2007), “Why We Get Fat” (2010), “The Case Against Sugar” (2016), and “The Case for Keto” (2020)?

This new book is more like “Good Calories, Bad Calories”: long, dense, detailed, definitive, and of great historical reference value, including original research information from other countries in other languages. The author told me that the many early research reference sources were available only in German and that his use of generative artificial intelligence as an assistant researcher was of great value.

Nonphysician author Mr. Taubes uses his deep understanding of science and history to inform his long-honed talents of impartial investigative journalism as he attempts to understand and then explain why after all these years, the medical scientific community still does not have a sound consensus about the essence of diabetes, diet, insulin, and proper prevention and treatment at a level that is actually effective – amazing and so sad.

To signal these evolved and evolving conflicts, the book includes the following chapters:

• “Rise of the Carbohydrate-Rich and Very-Low-Carbohydrate Diets”
• “The Fear of Fat and High-Fat Diets”
• “Insulin and The End of Carbohydrate Restriction and Low Blood Sugar”

Yes, it is difficult. Imagine the bookend segments: “The Nature of Medical Knowledge” and “The Conflicts of Evidence-Based Medicine.” There is also a detailed discussion of good versus bad science spanning three long chapters.

If all that reads like a greatly confused mess to you then you’re beginning to understand. If you are a fan of an unbiased explication of the evolution of understanding the ins and outs of scientific history in richly documented detail, this is a book for you. It’s not a quick nor easy read. And don’t expect to discover whether the newest wonder drugs for weight loss and control of diabetes will be the long-term solution for people with obesity and diabetes worldwide.

Obesity and overweight are major risk factors for type 2 diabetes. About 90% of patients with diabetes have either overweight or obesity. Thus, the complications of these two conditions, which largely overlap, include atherosclerotic cardiovascular disease; myocardial infarction; stroke; hypertension; metabolic syndrome; lower-extremity gangrene; chronic kidney disease; retinopathy; glaucoma; cataracts; disabling osteoarthritis; breast, endometrial, colon, and other cancers; fatty liver; sleep apnea; and peripheral neuropathy. These diseases create a major lucrative business for a wide swathe of medical and surgical specialties, plus hospital, clinic, device, pharmaceutical, and food industries.

In summary, we’ve just been through 40 years of failure to recognize the sugar-elephant in the room and intervene with serious preventive efforts. Forty years of fleshing out both the populace and the American medical-industrial complex (AMIC). Talk about a sweet spot. The only successful long-term treatment of obesity (and with it, diabetes) is prevention. Don’t emphasize losing weight. Focus on preventing excessive weight gain, right now, for the population, beginning with yourselves. Otherwise, we continue openly to perpetuate a terrific deal for the AMIC, a travesty for everyone else. Time for some industrial grade penance and a course correction.

Meanwhile, here we are living out Big Pharma’s dream of a big populace, produced by the agriculture and food industries, enjoyed by capitalism after failures of education, medicine, and public health: a seemingly endless supply of people living with big complications who are ready for big (expensive, new) medications to fix the world’s big health problems.

Dr. Lundberg is editor in chief, Cancer Commons. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Doctor, if you are caring for patients with diabetes, I sure hope you know more about it than I do. The longer I live, it seems, the less I understand.

In a free society, people can do what they want, and that’s great except when it isn’t. That’s why societies develop ethics and even public laws if ethics are not strong enough to protect us from ourselves and others.
 

Sugar, sugar

When I was growing up in small-town Alabama during the Depression and World War II, we called it sugar diabetes. Eat too much sugar, you got fat; your blood sugar went up, and you spilled sugar into your urine. Diabetes was fairly rare, and so was obesity. Doctors treated it by limiting the intake of sugar (and various sweet foods), along with attempting weight loss. If that didn’t do the trick, insulin injections.

From then until now, note these trends.

• 1920: 0.2% of the population
• 1930: 0.3% of the population
• 1940: 0.4% of the population

In 2020, although 11.3% of the population was diagnosed with type 2 diabetes, the unknown undiagnosed proportion could be much higher.

Notice a correlation between sugar consumption and prevalence of diabetes? Of course, correlation is not causation, but at the same time, it sure as hell is not negation. Such concordance can be considered hypothesis generating. It may not be true causation, but it’s a good bet when 89% of people with diabetes have overweight or obesity.

What did the entire medical, public health, government, agriculture, nursing, food manufacturing, marketing, advertising, restaurant, and education constituencies do about this as it was happening? They observed, documented, gave lip service, and wrung their hands in public a bit. I do not believe that this is an organized active conspiracy; it would take too many players cooperating over too long a period of time. But it certainly may be a passive conspiracy, and primary care physicians and their patients are trapped.

The proper daily practice of medicine consists of one patient, one physician, one moment, and one decision. Let it be a shared decision, informed by the best evidence and taking cost into consideration. That encounter represents an opportunity, a responsibility, and a conundrum.

Individual health is subsumed under the collective health of the public. As such, a patient’s health is out of the control of both physician and patient; instead, patients are the beneficiaries or victims of the “marketplace.” Humans are frail and easily taken advantage of by the brilliant and highly motivated strategic planning and execution of Big Agriculture, Big Food, Big Pharma, Big Marketing, and Big Money-Driven Medicine and generally failed by Big Government, Big Public Health, Big Education, Big Psychology, and Big Religion.
 

Rethinking diabetes

Consider diabetes as one of many examples. What a terrific deal for capitalism. First, the system spends decades fattening us up; then, it makes massive amounts of money off of the myriad complications of the fattened populace; then it discovers (invents) long-term, very expensive, compelling treatments to slim us down, with no end in sight, and still without ever understanding the true nature of diabetes.

Gary Taubes’s great new book, “Rethinking Diabetes: What Science Reveals About Diet, Insulin, and Successful Treatments,” is being published by Alfred A. Knopf in early 2024.

It is 404 pages of (dense) text, with 401 numbered references and footnotes, a bibliography of 790 references, alphabetically arranged for easy cross-checking, and a 25-page index.

Remember Mr. Taubes’s earlier definitive historical treatises: “Good Calories, Bad Calories” (2007), “Why We Get Fat” (2010), “The Case Against Sugar” (2016), and “The Case for Keto” (2020)?

This new book is more like “Good Calories, Bad Calories”: long, dense, detailed, definitive, and of great historical reference value, including original research information from other countries in other languages. The author told me that the many early research reference sources were available only in German and that his use of generative artificial intelligence as an assistant researcher was of great value.

Nonphysician author Mr. Taubes uses his deep understanding of science and history to inform his long-honed talents of impartial investigative journalism as he attempts to understand and then explain why after all these years, the medical scientific community still does not have a sound consensus about the essence of diabetes, diet, insulin, and proper prevention and treatment at a level that is actually effective – amazing and so sad.

To signal these evolved and evolving conflicts, the book includes the following chapters:

• “Rise of the Carbohydrate-Rich and Very-Low-Carbohydrate Diets”
• “The Fear of Fat and High-Fat Diets”
• “Insulin and The End of Carbohydrate Restriction and Low Blood Sugar”

Yes, it is difficult. Imagine the bookend segments: “The Nature of Medical Knowledge” and “The Conflicts of Evidence-Based Medicine.” There is also a detailed discussion of good versus bad science spanning three long chapters.

If all that reads like a greatly confused mess to you then you’re beginning to understand. If you are a fan of an unbiased explication of the evolution of understanding the ins and outs of scientific history in richly documented detail, this is a book for you. It’s not a quick nor easy read. And don’t expect to discover whether the newest wonder drugs for weight loss and control of diabetes will be the long-term solution for people with obesity and diabetes worldwide.

Obesity and overweight are major risk factors for type 2 diabetes. About 90% of patients with diabetes have either overweight or obesity. Thus, the complications of these two conditions, which largely overlap, include atherosclerotic cardiovascular disease; myocardial infarction; stroke; hypertension; metabolic syndrome; lower-extremity gangrene; chronic kidney disease; retinopathy; glaucoma; cataracts; disabling osteoarthritis; breast, endometrial, colon, and other cancers; fatty liver; sleep apnea; and peripheral neuropathy. These diseases create a major lucrative business for a wide swathe of medical and surgical specialties, plus hospital, clinic, device, pharmaceutical, and food industries.

In summary, we’ve just been through 40 years of failure to recognize the sugar-elephant in the room and intervene with serious preventive efforts. Forty years of fleshing out both the populace and the American medical-industrial complex (AMIC). Talk about a sweet spot. The only successful long-term treatment of obesity (and with it, diabetes) is prevention. Don’t emphasize losing weight. Focus on preventing excessive weight gain, right now, for the population, beginning with yourselves. Otherwise, we continue openly to perpetuate a terrific deal for the AMIC, a travesty for everyone else. Time for some industrial grade penance and a course correction.

Meanwhile, here we are living out Big Pharma’s dream of a big populace, produced by the agriculture and food industries, enjoyed by capitalism after failures of education, medicine, and public health: a seemingly endless supply of people living with big complications who are ready for big (expensive, new) medications to fix the world’s big health problems.

Dr. Lundberg is editor in chief, Cancer Commons. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Doctor, if you are caring for patients with diabetes, I sure hope you know more about it than I do. The longer I live, it seems, the less I understand.

In a free society, people can do what they want, and that’s great except when it isn’t. That’s why societies develop ethics and even public laws if ethics are not strong enough to protect us from ourselves and others.
 

Sugar, sugar

When I was growing up in small-town Alabama during the Depression and World War II, we called it sugar diabetes. Eat too much sugar, you got fat; your blood sugar went up, and you spilled sugar into your urine. Diabetes was fairly rare, and so was obesity. Doctors treated it by limiting the intake of sugar (and various sweet foods), along with attempting weight loss. If that didn’t do the trick, insulin injections.

From then until now, note these trends.

• 1920: 0.2% of the population
• 1930: 0.3% of the population
• 1940: 0.4% of the population

In 2020, although 11.3% of the population was diagnosed with type 2 diabetes, the unknown undiagnosed proportion could be much higher.

Notice a correlation between sugar consumption and prevalence of diabetes? Of course, correlation is not causation, but at the same time, it sure as hell is not negation. Such concordance can be considered hypothesis generating. It may not be true causation, but it’s a good bet when 89% of people with diabetes have overweight or obesity.

What did the entire medical, public health, government, agriculture, nursing, food manufacturing, marketing, advertising, restaurant, and education constituencies do about this as it was happening? They observed, documented, gave lip service, and wrung their hands in public a bit. I do not believe that this is an organized active conspiracy; it would take too many players cooperating over too long a period of time. But it certainly may be a passive conspiracy, and primary care physicians and their patients are trapped.

The proper daily practice of medicine consists of one patient, one physician, one moment, and one decision. Let it be a shared decision, informed by the best evidence and taking cost into consideration. That encounter represents an opportunity, a responsibility, and a conundrum.

Individual health is subsumed under the collective health of the public. As such, a patient’s health is out of the control of both physician and patient; instead, patients are the beneficiaries or victims of the “marketplace.” Humans are frail and easily taken advantage of by the brilliant and highly motivated strategic planning and execution of Big Agriculture, Big Food, Big Pharma, Big Marketing, and Big Money-Driven Medicine and generally failed by Big Government, Big Public Health, Big Education, Big Psychology, and Big Religion.
 

Rethinking diabetes

Consider diabetes as one of many examples. What a terrific deal for capitalism. First, the system spends decades fattening us up; then, it makes massive amounts of money off of the myriad complications of the fattened populace; then it discovers (invents) long-term, very expensive, compelling treatments to slim us down, with no end in sight, and still without ever understanding the true nature of diabetes.

Gary Taubes’s great new book, “Rethinking Diabetes: What Science Reveals About Diet, Insulin, and Successful Treatments,” is being published by Alfred A. Knopf in early 2024.

It is 404 pages of (dense) text, with 401 numbered references and footnotes, a bibliography of 790 references, alphabetically arranged for easy cross-checking, and a 25-page index.

Remember Mr. Taubes’s earlier definitive historical treatises: “Good Calories, Bad Calories” (2007), “Why We Get Fat” (2010), “The Case Against Sugar” (2016), and “The Case for Keto” (2020)?

This new book is more like “Good Calories, Bad Calories”: long, dense, detailed, definitive, and of great historical reference value, including original research information from other countries in other languages. The author told me that the many early research reference sources were available only in German and that his use of generative artificial intelligence as an assistant researcher was of great value.

Nonphysician author Mr. Taubes uses his deep understanding of science and history to inform his long-honed talents of impartial investigative journalism as he attempts to understand and then explain why after all these years, the medical scientific community still does not have a sound consensus about the essence of diabetes, diet, insulin, and proper prevention and treatment at a level that is actually effective – amazing and so sad.

To signal these evolved and evolving conflicts, the book includes the following chapters:

• “Rise of the Carbohydrate-Rich and Very-Low-Carbohydrate Diets”
• “The Fear of Fat and High-Fat Diets”
• “Insulin and The End of Carbohydrate Restriction and Low Blood Sugar”

Yes, it is difficult. Imagine the bookend segments: “The Nature of Medical Knowledge” and “The Conflicts of Evidence-Based Medicine.” There is also a detailed discussion of good versus bad science spanning three long chapters.

If all that reads like a greatly confused mess to you then you’re beginning to understand. If you are a fan of an unbiased explication of the evolution of understanding the ins and outs of scientific history in richly documented detail, this is a book for you. It’s not a quick nor easy read. And don’t expect to discover whether the newest wonder drugs for weight loss and control of diabetes will be the long-term solution for people with obesity and diabetes worldwide.

Obesity and overweight are major risk factors for type 2 diabetes. About 90% of patients with diabetes have either overweight or obesity. Thus, the complications of these two conditions, which largely overlap, include atherosclerotic cardiovascular disease; myocardial infarction; stroke; hypertension; metabolic syndrome; lower-extremity gangrene; chronic kidney disease; retinopathy; glaucoma; cataracts; disabling osteoarthritis; breast, endometrial, colon, and other cancers; fatty liver; sleep apnea; and peripheral neuropathy. These diseases create a major lucrative business for a wide swathe of medical and surgical specialties, plus hospital, clinic, device, pharmaceutical, and food industries.

In summary, we’ve just been through 40 years of failure to recognize the sugar-elephant in the room and intervene with serious preventive efforts. Forty years of fleshing out both the populace and the American medical-industrial complex (AMIC). Talk about a sweet spot. The only successful long-term treatment of obesity (and with it, diabetes) is prevention. Don’t emphasize losing weight. Focus on preventing excessive weight gain, right now, for the population, beginning with yourselves. Otherwise, we continue openly to perpetuate a terrific deal for the AMIC, a travesty for everyone else. Time for some industrial grade penance and a course correction.

Meanwhile, here we are living out Big Pharma’s dream of a big populace, produced by the agriculture and food industries, enjoyed by capitalism after failures of education, medicine, and public health: a seemingly endless supply of people living with big complications who are ready for big (expensive, new) medications to fix the world’s big health problems.

Dr. Lundberg is editor in chief, Cancer Commons. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Significant reductions in hemoglobin A1c have occurred over time among adults with type 1 diabetes as their use of diabetes technology has increased, yet there is still room for improvement, new data suggest.

The new findings are from a study involving patients at the Barbara Davis Center for Diabetes Adult Clinic between Jan. 1, 2014, and Dec. 31, 2021. They show that as technology use has increased, A1c levels have dropped in parallel. Moreover, progression from use of stand-alone continuous glucose monitors (CGMs) to automated insulin delivery systems (AIDs), which comprise insulin pumps and connected CGMs, furthered that progress.

The findings “are in agreement with American Diabetes Association standards of care, and recent international consensus recommending CGM and AID for most people with type 1 diabetes, and early initiation of diabetes technology from the onset of type 1 diabetes,” write Kagan E. Karakus, MD, of the University of Colorado’s Barbara Davis Center, Aurora, and colleagues in the article, which was published online in Diabetes Care.

“It’s very rewarding to us. We can see clearly that the uptake is going up and the A1c is dropping,” lead author Viral N. Shah, MD, of the Barbara Davis Center, told this news organization.

On the flip side, A1c levels rose significantly over the study period among nonusers of technology. “We cannot rule out provider bias for not prescribing diabetes technology among those with higher A1c or from disadvantaged socioeconomic backgrounds,” Dr. Karakus and colleagues write.

Also of note, even with use of the most advanced AID systems available during the study period, just under half of patients were still not achieving A1c levels below 7%. “The technology helps, but it’s not perfect,” Dr. Shah observed.

This study is the first to examine the relationship of A1c with technology use over time, in contrast to prior cross-sectional studies. “The intention here was to look at the landscape over a decade,” Dr. Shah said.
 

As overall use of technology use rose, A1c levels fell

The analysis included data for 4,174 unique patients (mean number of patients, 1,988/yr); 15,903 clinic visits were included over the 8-year study period. Technology use was defined as CGM use without an AID system or with an AID system.

Over the study period, diabetes technology use increased from 26.9% to 82.7% of the clinic population (P < .001). At the same time, the overall proportion patients who achieved the A1c goal of less than 7% increased from 32.3% to 41.7%, while the mean A1c level dropped from 7.7% to 7.5% (P < .001).

But among the technology nonusers, A1c rose from 7.85% in 2014 to 8.4% in 2021 (P < .001).

Regardless of diabetes technology use, White patients (about 80% of the total study population) had significantly lower A1c than non-White patients (7.5% vs. 7.7% for technology users [P = .02]; 8.0% vs. 8.3% for nontechnology users [P < .001]).

The non-White group was too small to enable the researchers to break down the data by technology type. Nonetheless, Dr. Shah said, “As a clinician, I can say that the penetration of diabetes technology in non-White populations remains low. These are also the people more vulnerable for socioeconomic and psychosocial reasons.”

The A1c increase among technology nonusers may be a result of a statistical artifact, as the number of those individuals was much lower in 2021 than in 2014. It’s possible that those remaining individuals have exceedingly high A1c levels, bringing the average up. “It’s still not good, though,” Dr. Shah said.
 

The more technology, the lower the A1c

Over the study period, the proportion of stand-alone CGM users rose from 26.9% to 44.1%, while use of AIDs rose from 0% in 2014 and 2015 to 38.6% in 2021. The latter group included patients who used first-generation Medtronic 670G and 770G devices and second-generation Tandem t:slim X2 with Control-IQ devices.

Between 2017 and 2021, AIDs users had significantly lower A1c levels than nontechnology users: 7.4% vs. 8.1% in 2017, and 7.3% vs. 8.4% in 2021 (P < .001 for every year). CGM users also had significantly lower A1c levels than nonusers at all time points (P < .001 per year).

The proportions achieving an A1c less than 7% differed significantly across users of CGMs, AIDs, and no technology (P < .01 for all years). In 2021, the percentage of people who achieved an A1c less than 7% were 50.9% with AIDs and 44.1% for CGMs vs, just 15.2% with no technology.
 

Work to be done: Why aren’t more achieving < 7% with AIDs?

Asked why only slightly more than half of patients who used AIDs achieved A1c levels below 7%, Dr. Shah listed three possibilities:

First, the 7% goal doesn’t apply to everyone with type 1 diabetes, including those with multiple comorbidities or with short life expectancy, for whom the recommended goal is 7.5%-8.0% to prevent hypoglycemia. “We didn’t separate out patients by A1c goals. If we add that, the number might go up,” Dr. Shah said.

Second, AID technology is continually improving, but it’s not perfect. Users still must enter carbohydrate counts and signal the devices for exercise, which can lead to errors. “It’s a wonderful technology for overnight control, but still, during the daytime, there are so many factors with the user interface and how much a person is engaged with the technology,” Dr. Shah explained.

Third, he said, “Unfortunately, obesity is increasing in type 1 diabetes, and insulin doses are increasing. Higher BMI [body mass index] and more insulin resistance can mean higher A1c. I really think for many patients, we probably will need an adjunct therapy, such as an SGLT2 [sodium-glucose cotransporter-2] inhibitor or a GLP-1 [glucagonlike peptide-1] agonist, even though they’re not approved in type 1 diabetes, for both glycemic and metabolic control including weight. I think that’s another missing piece.”

He also pointed out, “If someone has an A1c of 7.5%, I don’t expect a huge change. But if they’re at 10%, a drop to 8% is a huge change.”

Overall, Dr. Shah said, the news from the study is good. “In the past, only 30% were achieving an A1c less than 7%. Now we’re 20% above that. ... It’s a glass half full.”

Dr. Karakus has disclosed no relevant financial relationships. Dr. Shah has received, through the University of Colorado, research support from Novo Nordisk, Insulet, Tandem Diabetes, and Dexcom, and honoraria from Medscape, Lifescan, Novo Nordisk, and DKSH Singapore for advisory board attendance and from Insulet and Dexcom for speaking engagements.

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

Significant reductions in hemoglobin A1c have occurred over time among adults with type 1 diabetes as their use of diabetes technology has increased, yet there is still room for improvement, new data suggest.

The new findings are from a study involving patients at the Barbara Davis Center for Diabetes Adult Clinic between Jan. 1, 2014, and Dec. 31, 2021. They show that as technology use has increased, A1c levels have dropped in parallel. Moreover, progression from use of stand-alone continuous glucose monitors (CGMs) to automated insulin delivery systems (AIDs), which comprise insulin pumps and connected CGMs, furthered that progress.

The findings “are in agreement with American Diabetes Association standards of care, and recent international consensus recommending CGM and AID for most people with type 1 diabetes, and early initiation of diabetes technology from the onset of type 1 diabetes,” write Kagan E. Karakus, MD, of the University of Colorado’s Barbara Davis Center, Aurora, and colleagues in the article, which was published online in Diabetes Care.

“It’s very rewarding to us. We can see clearly that the uptake is going up and the A1c is dropping,” lead author Viral N. Shah, MD, of the Barbara Davis Center, told this news organization.

On the flip side, A1c levels rose significantly over the study period among nonusers of technology. “We cannot rule out provider bias for not prescribing diabetes technology among those with higher A1c or from disadvantaged socioeconomic backgrounds,” Dr. Karakus and colleagues write.

Also of note, even with use of the most advanced AID systems available during the study period, just under half of patients were still not achieving A1c levels below 7%. “The technology helps, but it’s not perfect,” Dr. Shah observed.

This study is the first to examine the relationship of A1c with technology use over time, in contrast to prior cross-sectional studies. “The intention here was to look at the landscape over a decade,” Dr. Shah said.
 

As overall use of technology use rose, A1c levels fell

The analysis included data for 4,174 unique patients (mean number of patients, 1,988/yr); 15,903 clinic visits were included over the 8-year study period. Technology use was defined as CGM use without an AID system or with an AID system.

Over the study period, diabetes technology use increased from 26.9% to 82.7% of the clinic population (P < .001). At the same time, the overall proportion patients who achieved the A1c goal of less than 7% increased from 32.3% to 41.7%, while the mean A1c level dropped from 7.7% to 7.5% (P < .001).

But among the technology nonusers, A1c rose from 7.85% in 2014 to 8.4% in 2021 (P < .001).

Regardless of diabetes technology use, White patients (about 80% of the total study population) had significantly lower A1c than non-White patients (7.5% vs. 7.7% for technology users [P = .02]; 8.0% vs. 8.3% for nontechnology users [P < .001]).

The non-White group was too small to enable the researchers to break down the data by technology type. Nonetheless, Dr. Shah said, “As a clinician, I can say that the penetration of diabetes technology in non-White populations remains low. These are also the people more vulnerable for socioeconomic and psychosocial reasons.”

The A1c increase among technology nonusers may be a result of a statistical artifact, as the number of those individuals was much lower in 2021 than in 2014. It’s possible that those remaining individuals have exceedingly high A1c levels, bringing the average up. “It’s still not good, though,” Dr. Shah said.
 

The more technology, the lower the A1c

Over the study period, the proportion of stand-alone CGM users rose from 26.9% to 44.1%, while use of AIDs rose from 0% in 2014 and 2015 to 38.6% in 2021. The latter group included patients who used first-generation Medtronic 670G and 770G devices and second-generation Tandem t:slim X2 with Control-IQ devices.

Between 2017 and 2021, AIDs users had significantly lower A1c levels than nontechnology users: 7.4% vs. 8.1% in 2017, and 7.3% vs. 8.4% in 2021 (P < .001 for every year). CGM users also had significantly lower A1c levels than nonusers at all time points (P < .001 per year).

The proportions achieving an A1c less than 7% differed significantly across users of CGMs, AIDs, and no technology (P < .01 for all years). In 2021, the percentage of people who achieved an A1c less than 7% were 50.9% with AIDs and 44.1% for CGMs vs, just 15.2% with no technology.
 

Work to be done: Why aren’t more achieving < 7% with AIDs?

Asked why only slightly more than half of patients who used AIDs achieved A1c levels below 7%, Dr. Shah listed three possibilities:

First, the 7% goal doesn’t apply to everyone with type 1 diabetes, including those with multiple comorbidities or with short life expectancy, for whom the recommended goal is 7.5%-8.0% to prevent hypoglycemia. “We didn’t separate out patients by A1c goals. If we add that, the number might go up,” Dr. Shah said.

Second, AID technology is continually improving, but it’s not perfect. Users still must enter carbohydrate counts and signal the devices for exercise, which can lead to errors. “It’s a wonderful technology for overnight control, but still, during the daytime, there are so many factors with the user interface and how much a person is engaged with the technology,” Dr. Shah explained.

Third, he said, “Unfortunately, obesity is increasing in type 1 diabetes, and insulin doses are increasing. Higher BMI [body mass index] and more insulin resistance can mean higher A1c. I really think for many patients, we probably will need an adjunct therapy, such as an SGLT2 [sodium-glucose cotransporter-2] inhibitor or a GLP-1 [glucagonlike peptide-1] agonist, even though they’re not approved in type 1 diabetes, for both glycemic and metabolic control including weight. I think that’s another missing piece.”

He also pointed out, “If someone has an A1c of 7.5%, I don’t expect a huge change. But if they’re at 10%, a drop to 8% is a huge change.”

Overall, Dr. Shah said, the news from the study is good. “In the past, only 30% were achieving an A1c less than 7%. Now we’re 20% above that. ... It’s a glass half full.”

Dr. Karakus has disclosed no relevant financial relationships. Dr. Shah has received, through the University of Colorado, research support from Novo Nordisk, Insulet, Tandem Diabetes, and Dexcom, and honoraria from Medscape, Lifescan, Novo Nordisk, and DKSH Singapore for advisory board attendance and from Insulet and Dexcom for speaking engagements.

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

Significant reductions in hemoglobin A1c have occurred over time among adults with type 1 diabetes as their use of diabetes technology has increased, yet there is still room for improvement, new data suggest.

The new findings are from a study involving patients at the Barbara Davis Center for Diabetes Adult Clinic between Jan. 1, 2014, and Dec. 31, 2021. They show that as technology use has increased, A1c levels have dropped in parallel. Moreover, progression from use of stand-alone continuous glucose monitors (CGMs) to automated insulin delivery systems (AIDs), which comprise insulin pumps and connected CGMs, furthered that progress.

The findings “are in agreement with American Diabetes Association standards of care, and recent international consensus recommending CGM and AID for most people with type 1 diabetes, and early initiation of diabetes technology from the onset of type 1 diabetes,” write Kagan E. Karakus, MD, of the University of Colorado’s Barbara Davis Center, Aurora, and colleagues in the article, which was published online in Diabetes Care.

“It’s very rewarding to us. We can see clearly that the uptake is going up and the A1c is dropping,” lead author Viral N. Shah, MD, of the Barbara Davis Center, told this news organization.

On the flip side, A1c levels rose significantly over the study period among nonusers of technology. “We cannot rule out provider bias for not prescribing diabetes technology among those with higher A1c or from disadvantaged socioeconomic backgrounds,” Dr. Karakus and colleagues write.

Also of note, even with use of the most advanced AID systems available during the study period, just under half of patients were still not achieving A1c levels below 7%. “The technology helps, but it’s not perfect,” Dr. Shah observed.

This study is the first to examine the relationship of A1c with technology use over time, in contrast to prior cross-sectional studies. “The intention here was to look at the landscape over a decade,” Dr. Shah said.
 

As overall use of technology use rose, A1c levels fell

The analysis included data for 4,174 unique patients (mean number of patients, 1,988/yr); 15,903 clinic visits were included over the 8-year study period. Technology use was defined as CGM use without an AID system or with an AID system.

Over the study period, diabetes technology use increased from 26.9% to 82.7% of the clinic population (P < .001). At the same time, the overall proportion patients who achieved the A1c goal of less than 7% increased from 32.3% to 41.7%, while the mean A1c level dropped from 7.7% to 7.5% (P < .001).

But among the technology nonusers, A1c rose from 7.85% in 2014 to 8.4% in 2021 (P < .001).

Regardless of diabetes technology use, White patients (about 80% of the total study population) had significantly lower A1c than non-White patients (7.5% vs. 7.7% for technology users [P = .02]; 8.0% vs. 8.3% for nontechnology users [P < .001]).

The non-White group was too small to enable the researchers to break down the data by technology type. Nonetheless, Dr. Shah said, “As a clinician, I can say that the penetration of diabetes technology in non-White populations remains low. These are also the people more vulnerable for socioeconomic and psychosocial reasons.”

The A1c increase among technology nonusers may be a result of a statistical artifact, as the number of those individuals was much lower in 2021 than in 2014. It’s possible that those remaining individuals have exceedingly high A1c levels, bringing the average up. “It’s still not good, though,” Dr. Shah said.
 

The more technology, the lower the A1c

Over the study period, the proportion of stand-alone CGM users rose from 26.9% to 44.1%, while use of AIDs rose from 0% in 2014 and 2015 to 38.6% in 2021. The latter group included patients who used first-generation Medtronic 670G and 770G devices and second-generation Tandem t:slim X2 with Control-IQ devices.

Between 2017 and 2021, AIDs users had significantly lower A1c levels than nontechnology users: 7.4% vs. 8.1% in 2017, and 7.3% vs. 8.4% in 2021 (P < .001 for every year). CGM users also had significantly lower A1c levels than nonusers at all time points (P < .001 per year).

The proportions achieving an A1c less than 7% differed significantly across users of CGMs, AIDs, and no technology (P < .01 for all years). In 2021, the percentage of people who achieved an A1c less than 7% were 50.9% with AIDs and 44.1% for CGMs vs, just 15.2% with no technology.
 

Work to be done: Why aren’t more achieving < 7% with AIDs?

Asked why only slightly more than half of patients who used AIDs achieved A1c levels below 7%, Dr. Shah listed three possibilities:

First, the 7% goal doesn’t apply to everyone with type 1 diabetes, including those with multiple comorbidities or with short life expectancy, for whom the recommended goal is 7.5%-8.0% to prevent hypoglycemia. “We didn’t separate out patients by A1c goals. If we add that, the number might go up,” Dr. Shah said.

Second, AID technology is continually improving, but it’s not perfect. Users still must enter carbohydrate counts and signal the devices for exercise, which can lead to errors. “It’s a wonderful technology for overnight control, but still, during the daytime, there are so many factors with the user interface and how much a person is engaged with the technology,” Dr. Shah explained.

Third, he said, “Unfortunately, obesity is increasing in type 1 diabetes, and insulin doses are increasing. Higher BMI [body mass index] and more insulin resistance can mean higher A1c. I really think for many patients, we probably will need an adjunct therapy, such as an SGLT2 [sodium-glucose cotransporter-2] inhibitor or a GLP-1 [glucagonlike peptide-1] agonist, even though they’re not approved in type 1 diabetes, for both glycemic and metabolic control including weight. I think that’s another missing piece.”

He also pointed out, “If someone has an A1c of 7.5%, I don’t expect a huge change. But if they’re at 10%, a drop to 8% is a huge change.”

Overall, Dr. Shah said, the news from the study is good. “In the past, only 30% were achieving an A1c less than 7%. Now we’re 20% above that. ... It’s a glass half full.”

Dr. Karakus has disclosed no relevant financial relationships. Dr. Shah has received, through the University of Colorado, research support from Novo Nordisk, Insulet, Tandem Diabetes, and Dexcom, and honoraria from Medscape, Lifescan, Novo Nordisk, and DKSH Singapore for advisory board attendance and from Insulet and Dexcom for speaking engagements.

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

Clinicians are using dupilumab off label to treat a wider range of allergic conditions in adults and children.

The drug, marketed as Dupixent, is currently approved in the United States to treat atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis in adults. Dupilumab is also approved to treat eosinophilic esophagitis in patients aged 12 years and older and atopic dermatitis and asthma in some patients as young as age 6 months.

As the roster of approved and off-label indications grows, skin specialists said, pediatricians and other primary care providers should become familiar with the drug – given the increasing likelihood that their patients may be taking the medication.

The U.S. Food and Drug Administration first approved dupilumab in 2017 for eczema and has continued to add new treatment indications, the most recent being for prurigo nodularis, in 2022. Sanofi, which markets the drug with Regeneron, announced in April 2022 that some 430,000 patients worldwide were taking the drug – a figure it hoped to raise by 1.5 million by 2025.
 

A well-tolerated – if expensive – drug

Dupilumab, an interleukin-4 (IL-4) receptor alpha-antagonist biologic, blocks both IL-4 and IL-13 signaling, Marlys Fassett, MD, PhD, associate professor of dermatology at the University of California, San Francisco, told this news organization.

Dr. Fassett said she prescribes the drug off label for chronic idiopathic urticaria, including in older patients, and finds that the side effects in older patients are similar to those in younger people. The medication costs $36,000 per year, although some patients can get it more cheaply.

“Dupixent is a super-safe drug because it doesn’t immunosuppress any other part of the immune system, so you still have good antibacterial, antiviral, and antifungal immunity,” she added. “That makes perfect sense as a biological mechanism, and it’s been found safe in clinical trials.”

Case reports of potential adverse reactions to dupilumab have included ocular surface disease, lichen planus, and rash on the face and neck.

“We’re still learning about complications and are watching patients carefully,” said Marissa J. Perman, MD, section chief of dermatology at Children’s Hospital of Philadelphia.

Many people with atopic dermatitis also have other allergic conditions, such as contact dermatitis, asthma, prurigo nodularis, allergic rhinitis, and seasonal allergies. Each of these conditions has a pathway that depends on IL-4 receptors, Dr. Fassett said.

“It’s amazing how many conditions Dupixent improves. Sometimes we prescribe on-label Dupixent for atopic dermatitis, and inadvertently, the drug also improves that patient’s other, off-label conditions,” Dr. Fassett said. “I think that’s the best evidence that Dupixent works in these off-label cases.”

Lindsay C. Strowd, MD, associate professor of dermatology at Wake Forest University, Winston-Salem, N.C., said she uses off-label dupilumab to treat bullous pemphigoid and intense pruritus of unknown etiology.

“And several times I have treated drug reaction with eosinophilia and systemic symptoms, a rare adverse drug reaction that causes a rash and eosinophilia,” Dr. Strowd added.

Tissa Hata, MD, professor of medicine and clinical service chief at the University of California, San Diego, mainly treats elderly patients. She uses dupilumab to treat bullous pemphigoid and chronic pruritus. “There have been reports of using Dupixent to treat adult alopecia areata, chronic urticaria, localized scleroderma, and even keloids,” she told this news organization.

As a pediatric dermatologist, Dr. Perman treats children with atopic dermatitis as young as 3 months of age. She also uses dupilumab for alopecia areata, graft vs. host disease, and pruritus not otherwise specified.

Conjunctivitis and facial redness are two side effects Dr. Fassett sometimes sees with dupilumab. They occur similarly with all conditions and in all age groups. “We don’t know why they occur, and we don’t always know how to alleviate them,” she said. “So a small number of patients stop using Dupixent because they can’t tolerate those two side effects.

“We’re not worried about infection risk,” Dr. Fassett said. “Your patients may have heard of dupilumab as an immunosuppressant, but its immunosuppression is very focused. You can reassure them that they’re not at increased risk for viral or bacterial infections when they’re on this drug.”

“I don’t think there are any different safety signals to watch for with on-label vs. off-label Dupixent use,” Dr. Strowd added. “In general, the medicine is very safe.”

Dr. Hata said she is impressed with dupilumab’s safety in her elderly patients. All her patients older than 85 years who have taken the drug for bullous pemphigoid have tolerated it well, she said.

“Dupixent seems to be a safe alternative for elderly patients with pruritus because they often cannot tolerate sedating antihistamines due to the risk of falling,” Dr. Hata said. “And UV therapy may be difficult for elderly patients due to problems with transport.”

Although some of Dr. Hata’s elderly patients with atopic dermatitis have discontinued use of the drug after developing conjunctivitis, none taking the drug off label have discontinued it because of side effects, she noted.

“Dupixent manages the condition, but it is not a cure,” Dr. Fassett noted. “Based on the current data, we think it’s safe and effective to take long term, potentially for life.”

Making injections less bothersome

Dupilumab is injected subcutaneously from a single-dose prefilled syringe or a prefilled pen (syringe hidden in an opaque sheath), typically in the thigh, arm, abdomen, or buttocks. According to Sanofi and Regeneron, patients receive dupilumab injections every 2 to 4 weeks in doses based on their age and weight.

“The medication is somewhat viscous, so taking the syringe or pen out of the refrigerator ahead of time to warm it up can make the experience less painful,” Dr. Strowd advised. “For pediatric patients, I sometimes prescribe topical lidocaine applied 30 minutes before injection.”

Dr. Hata suggested icing the skin prior to injecting or distracting the patient by tapping a different area of the skin.

For her pediatric patients, Dr. Perman said she uses “lots of distraction, EMLA cream, and having one person hold the child while a second person injects.”

Clinic and pharmacy staff may show patients how to inject properly, Dr. Fassett added; and the product website provides injection tutorials.
 

Off-label dupixent can be expensive, difficult to obtain

The list price per injection, regardless of dose, is around $1,800. But according to the company’s website, most patients have health insurance or qualify for other assistance, so “very few patients pay the list price.”

Even so, “due to cost and insurance coverage hurdles, obtaining Dupixent for off-label use can be difficult,” Dr. Strowd said.

“In academic medicine, we can obtain drugs for our patients that community doctors may not get approval for,” Dr. Fassett added. “Community doctors can use information in the medical literature and in news articles to press insurance companies to spend money to provide their patients with Dupixent.”

The experts who commented have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Clinicians are using dupilumab off label to treat a wider range of allergic conditions in adults and children.

The drug, marketed as Dupixent, is currently approved in the United States to treat atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis in adults. Dupilumab is also approved to treat eosinophilic esophagitis in patients aged 12 years and older and atopic dermatitis and asthma in some patients as young as age 6 months.

As the roster of approved and off-label indications grows, skin specialists said, pediatricians and other primary care providers should become familiar with the drug – given the increasing likelihood that their patients may be taking the medication.

The U.S. Food and Drug Administration first approved dupilumab in 2017 for eczema and has continued to add new treatment indications, the most recent being for prurigo nodularis, in 2022. Sanofi, which markets the drug with Regeneron, announced in April 2022 that some 430,000 patients worldwide were taking the drug – a figure it hoped to raise by 1.5 million by 2025.
 

A well-tolerated – if expensive – drug

Dupilumab, an interleukin-4 (IL-4) receptor alpha-antagonist biologic, blocks both IL-4 and IL-13 signaling, Marlys Fassett, MD, PhD, associate professor of dermatology at the University of California, San Francisco, told this news organization.

Dr. Fassett said she prescribes the drug off label for chronic idiopathic urticaria, including in older patients, and finds that the side effects in older patients are similar to those in younger people. The medication costs $36,000 per year, although some patients can get it more cheaply.

“Dupixent is a super-safe drug because it doesn’t immunosuppress any other part of the immune system, so you still have good antibacterial, antiviral, and antifungal immunity,” she added. “That makes perfect sense as a biological mechanism, and it’s been found safe in clinical trials.”

Case reports of potential adverse reactions to dupilumab have included ocular surface disease, lichen planus, and rash on the face and neck.

“We’re still learning about complications and are watching patients carefully,” said Marissa J. Perman, MD, section chief of dermatology at Children’s Hospital of Philadelphia.

Many people with atopic dermatitis also have other allergic conditions, such as contact dermatitis, asthma, prurigo nodularis, allergic rhinitis, and seasonal allergies. Each of these conditions has a pathway that depends on IL-4 receptors, Dr. Fassett said.

“It’s amazing how many conditions Dupixent improves. Sometimes we prescribe on-label Dupixent for atopic dermatitis, and inadvertently, the drug also improves that patient’s other, off-label conditions,” Dr. Fassett said. “I think that’s the best evidence that Dupixent works in these off-label cases.”

Lindsay C. Strowd, MD, associate professor of dermatology at Wake Forest University, Winston-Salem, N.C., said she uses off-label dupilumab to treat bullous pemphigoid and intense pruritus of unknown etiology.

“And several times I have treated drug reaction with eosinophilia and systemic symptoms, a rare adverse drug reaction that causes a rash and eosinophilia,” Dr. Strowd added.

Tissa Hata, MD, professor of medicine and clinical service chief at the University of California, San Diego, mainly treats elderly patients. She uses dupilumab to treat bullous pemphigoid and chronic pruritus. “There have been reports of using Dupixent to treat adult alopecia areata, chronic urticaria, localized scleroderma, and even keloids,” she told this news organization.

As a pediatric dermatologist, Dr. Perman treats children with atopic dermatitis as young as 3 months of age. She also uses dupilumab for alopecia areata, graft vs. host disease, and pruritus not otherwise specified.

Conjunctivitis and facial redness are two side effects Dr. Fassett sometimes sees with dupilumab. They occur similarly with all conditions and in all age groups. “We don’t know why they occur, and we don’t always know how to alleviate them,” she said. “So a small number of patients stop using Dupixent because they can’t tolerate those two side effects.

“We’re not worried about infection risk,” Dr. Fassett said. “Your patients may have heard of dupilumab as an immunosuppressant, but its immunosuppression is very focused. You can reassure them that they’re not at increased risk for viral or bacterial infections when they’re on this drug.”

“I don’t think there are any different safety signals to watch for with on-label vs. off-label Dupixent use,” Dr. Strowd added. “In general, the medicine is very safe.”

Dr. Hata said she is impressed with dupilumab’s safety in her elderly patients. All her patients older than 85 years who have taken the drug for bullous pemphigoid have tolerated it well, she said.

“Dupixent seems to be a safe alternative for elderly patients with pruritus because they often cannot tolerate sedating antihistamines due to the risk of falling,” Dr. Hata said. “And UV therapy may be difficult for elderly patients due to problems with transport.”

Although some of Dr. Hata’s elderly patients with atopic dermatitis have discontinued use of the drug after developing conjunctivitis, none taking the drug off label have discontinued it because of side effects, she noted.

“Dupixent manages the condition, but it is not a cure,” Dr. Fassett noted. “Based on the current data, we think it’s safe and effective to take long term, potentially for life.”

Making injections less bothersome

Dupilumab is injected subcutaneously from a single-dose prefilled syringe or a prefilled pen (syringe hidden in an opaque sheath), typically in the thigh, arm, abdomen, or buttocks. According to Sanofi and Regeneron, patients receive dupilumab injections every 2 to 4 weeks in doses based on their age and weight.

“The medication is somewhat viscous, so taking the syringe or pen out of the refrigerator ahead of time to warm it up can make the experience less painful,” Dr. Strowd advised. “For pediatric patients, I sometimes prescribe topical lidocaine applied 30 minutes before injection.”

Dr. Hata suggested icing the skin prior to injecting or distracting the patient by tapping a different area of the skin.

For her pediatric patients, Dr. Perman said she uses “lots of distraction, EMLA cream, and having one person hold the child while a second person injects.”

Clinic and pharmacy staff may show patients how to inject properly, Dr. Fassett added; and the product website provides injection tutorials.
 

Off-label dupixent can be expensive, difficult to obtain

The list price per injection, regardless of dose, is around $1,800. But according to the company’s website, most patients have health insurance or qualify for other assistance, so “very few patients pay the list price.”

Even so, “due to cost and insurance coverage hurdles, obtaining Dupixent for off-label use can be difficult,” Dr. Strowd said.

“In academic medicine, we can obtain drugs for our patients that community doctors may not get approval for,” Dr. Fassett added. “Community doctors can use information in the medical literature and in news articles to press insurance companies to spend money to provide their patients with Dupixent.”

The experts who commented have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Clinicians are using dupilumab off label to treat a wider range of allergic conditions in adults and children.

The drug, marketed as Dupixent, is currently approved in the United States to treat atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis in adults. Dupilumab is also approved to treat eosinophilic esophagitis in patients aged 12 years and older and atopic dermatitis and asthma in some patients as young as age 6 months.

As the roster of approved and off-label indications grows, skin specialists said, pediatricians and other primary care providers should become familiar with the drug – given the increasing likelihood that their patients may be taking the medication.

The U.S. Food and Drug Administration first approved dupilumab in 2017 for eczema and has continued to add new treatment indications, the most recent being for prurigo nodularis, in 2022. Sanofi, which markets the drug with Regeneron, announced in April 2022 that some 430,000 patients worldwide were taking the drug – a figure it hoped to raise by 1.5 million by 2025.
 

A well-tolerated – if expensive – drug

Dupilumab, an interleukin-4 (IL-4) receptor alpha-antagonist biologic, blocks both IL-4 and IL-13 signaling, Marlys Fassett, MD, PhD, associate professor of dermatology at the University of California, San Francisco, told this news organization.

Dr. Fassett said she prescribes the drug off label for chronic idiopathic urticaria, including in older patients, and finds that the side effects in older patients are similar to those in younger people. The medication costs $36,000 per year, although some patients can get it more cheaply.

“Dupixent is a super-safe drug because it doesn’t immunosuppress any other part of the immune system, so you still have good antibacterial, antiviral, and antifungal immunity,” she added. “That makes perfect sense as a biological mechanism, and it’s been found safe in clinical trials.”

Case reports of potential adverse reactions to dupilumab have included ocular surface disease, lichen planus, and rash on the face and neck.

“We’re still learning about complications and are watching patients carefully,” said Marissa J. Perman, MD, section chief of dermatology at Children’s Hospital of Philadelphia.

Many people with atopic dermatitis also have other allergic conditions, such as contact dermatitis, asthma, prurigo nodularis, allergic rhinitis, and seasonal allergies. Each of these conditions has a pathway that depends on IL-4 receptors, Dr. Fassett said.

“It’s amazing how many conditions Dupixent improves. Sometimes we prescribe on-label Dupixent for atopic dermatitis, and inadvertently, the drug also improves that patient’s other, off-label conditions,” Dr. Fassett said. “I think that’s the best evidence that Dupixent works in these off-label cases.”

Lindsay C. Strowd, MD, associate professor of dermatology at Wake Forest University, Winston-Salem, N.C., said she uses off-label dupilumab to treat bullous pemphigoid and intense pruritus of unknown etiology.

“And several times I have treated drug reaction with eosinophilia and systemic symptoms, a rare adverse drug reaction that causes a rash and eosinophilia,” Dr. Strowd added.

Tissa Hata, MD, professor of medicine and clinical service chief at the University of California, San Diego, mainly treats elderly patients. She uses dupilumab to treat bullous pemphigoid and chronic pruritus. “There have been reports of using Dupixent to treat adult alopecia areata, chronic urticaria, localized scleroderma, and even keloids,” she told this news organization.

As a pediatric dermatologist, Dr. Perman treats children with atopic dermatitis as young as 3 months of age. She also uses dupilumab for alopecia areata, graft vs. host disease, and pruritus not otherwise specified.

Conjunctivitis and facial redness are two side effects Dr. Fassett sometimes sees with dupilumab. They occur similarly with all conditions and in all age groups. “We don’t know why they occur, and we don’t always know how to alleviate them,” she said. “So a small number of patients stop using Dupixent because they can’t tolerate those two side effects.

“We’re not worried about infection risk,” Dr. Fassett said. “Your patients may have heard of dupilumab as an immunosuppressant, but its immunosuppression is very focused. You can reassure them that they’re not at increased risk for viral or bacterial infections when they’re on this drug.”

“I don’t think there are any different safety signals to watch for with on-label vs. off-label Dupixent use,” Dr. Strowd added. “In general, the medicine is very safe.”

Dr. Hata said she is impressed with dupilumab’s safety in her elderly patients. All her patients older than 85 years who have taken the drug for bullous pemphigoid have tolerated it well, she said.

“Dupixent seems to be a safe alternative for elderly patients with pruritus because they often cannot tolerate sedating antihistamines due to the risk of falling,” Dr. Hata said. “And UV therapy may be difficult for elderly patients due to problems with transport.”

Although some of Dr. Hata’s elderly patients with atopic dermatitis have discontinued use of the drug after developing conjunctivitis, none taking the drug off label have discontinued it because of side effects, she noted.

“Dupixent manages the condition, but it is not a cure,” Dr. Fassett noted. “Based on the current data, we think it’s safe and effective to take long term, potentially for life.”

Making injections less bothersome

Dupilumab is injected subcutaneously from a single-dose prefilled syringe or a prefilled pen (syringe hidden in an opaque sheath), typically in the thigh, arm, abdomen, or buttocks. According to Sanofi and Regeneron, patients receive dupilumab injections every 2 to 4 weeks in doses based on their age and weight.

“The medication is somewhat viscous, so taking the syringe or pen out of the refrigerator ahead of time to warm it up can make the experience less painful,” Dr. Strowd advised. “For pediatric patients, I sometimes prescribe topical lidocaine applied 30 minutes before injection.”

Dr. Hata suggested icing the skin prior to injecting or distracting the patient by tapping a different area of the skin.

For her pediatric patients, Dr. Perman said she uses “lots of distraction, EMLA cream, and having one person hold the child while a second person injects.”

Clinic and pharmacy staff may show patients how to inject properly, Dr. Fassett added; and the product website provides injection tutorials.
 

Off-label dupixent can be expensive, difficult to obtain

The list price per injection, regardless of dose, is around $1,800. But according to the company’s website, most patients have health insurance or qualify for other assistance, so “very few patients pay the list price.”

Even so, “due to cost and insurance coverage hurdles, obtaining Dupixent for off-label use can be difficult,” Dr. Strowd said.

“In academic medicine, we can obtain drugs for our patients that community doctors may not get approval for,” Dr. Fassett added. “Community doctors can use information in the medical literature and in news articles to press insurance companies to spend money to provide their patients with Dupixent.”

The experts who commented have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

People may get more protection against COVID-19 if they get their vaccinations and boosters in the same arm, a new study says.

Scientists in Germany looked at health data for 303 people who got the mRNA vaccine and then a booster shot. Their antibody levels were measured two weeks after the second shot. None of the people had had COVID before the vaccinations.

Scientists found that the number of protective “killer T cells” was higher in the 147 study participants who got both shots in the same arm, said the study published in EBioMedicine.

The killer cells were found in 67% of cases in which both shots went into the same arm, compared with 43% of cases with different arms.

“That may suggest that that ipsilateral vaccination (in the same arm) is more likely to provide better protection should the vaccinated person become infected with the SARS-CoV-2 virus,” Laura Ziegler, a doctoral student at Saarland University, Germany, said in a news release.

William Schaffner, MD, a professor in the Division of Infectious Diseases at Vanderbilt University Medical Center, Nashville, Tenn., told CBS News that same-arm vaccinations may work better because the cells that provide the immune response are in local lymph nodes.

There’s greater immunological response if the immune cells in the lymph nodes are restimulated in the same place, said Dr. Schaffner, who was not involved in the German study.

The scientists from Saarland University said more research is needed before they can be certain that having vaccinations in the same arm is actually more effective for COVID shots and sequential vaccinations against diseases such as the flu.

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

People may get more protection against COVID-19 if they get their vaccinations and boosters in the same arm, a new study says.

Scientists in Germany looked at health data for 303 people who got the mRNA vaccine and then a booster shot. Their antibody levels were measured two weeks after the second shot. None of the people had had COVID before the vaccinations.

Scientists found that the number of protective “killer T cells” was higher in the 147 study participants who got both shots in the same arm, said the study published in EBioMedicine.

The killer cells were found in 67% of cases in which both shots went into the same arm, compared with 43% of cases with different arms.

“That may suggest that that ipsilateral vaccination (in the same arm) is more likely to provide better protection should the vaccinated person become infected with the SARS-CoV-2 virus,” Laura Ziegler, a doctoral student at Saarland University, Germany, said in a news release.

William Schaffner, MD, a professor in the Division of Infectious Diseases at Vanderbilt University Medical Center, Nashville, Tenn., told CBS News that same-arm vaccinations may work better because the cells that provide the immune response are in local lymph nodes.

There’s greater immunological response if the immune cells in the lymph nodes are restimulated in the same place, said Dr. Schaffner, who was not involved in the German study.

The scientists from Saarland University said more research is needed before they can be certain that having vaccinations in the same arm is actually more effective for COVID shots and sequential vaccinations against diseases such as the flu.

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

People may get more protection against COVID-19 if they get their vaccinations and boosters in the same arm, a new study says.

Scientists in Germany looked at health data for 303 people who got the mRNA vaccine and then a booster shot. Their antibody levels were measured two weeks after the second shot. None of the people had had COVID before the vaccinations.

Scientists found that the number of protective “killer T cells” was higher in the 147 study participants who got both shots in the same arm, said the study published in EBioMedicine.

The killer cells were found in 67% of cases in which both shots went into the same arm, compared with 43% of cases with different arms.

“That may suggest that that ipsilateral vaccination (in the same arm) is more likely to provide better protection should the vaccinated person become infected with the SARS-CoV-2 virus,” Laura Ziegler, a doctoral student at Saarland University, Germany, said in a news release.

William Schaffner, MD, a professor in the Division of Infectious Diseases at Vanderbilt University Medical Center, Nashville, Tenn., told CBS News that same-arm vaccinations may work better because the cells that provide the immune response are in local lymph nodes.

There’s greater immunological response if the immune cells in the lymph nodes are restimulated in the same place, said Dr. Schaffner, who was not involved in the German study.

The scientists from Saarland University said more research is needed before they can be certain that having vaccinations in the same arm is actually more effective for COVID shots and sequential vaccinations against diseases such as the flu.

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

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

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

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

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

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

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

The European Medicines Agency has validated the marketing authorization application for delgocitinib cream, for the treatment of adults with chronic moderate to severe hand eczema, which marks the beginning of the review process for the treatment by the EMA’s Committee for Medicinal Products for Human Use.

Delgocitinib is an investigational topical pan–Janus kinase inhibitor that inhibits activation of the JAK-STAT pathway.

The development follows results reported from two phase 3 clinical trials known as DELTA 1 and DELTA 2, which evaluated the safety and efficacy of delgocitinib cream applications twice per day compared with a vehicle cream in adults with mild to severe chronic hand eczema. Results of DELTA 1 were presented at the 2023 annual meeting of the American Academy of Dermatology. A multisite, open-label extension trial known as DELTA 3 is still in progress.

According to a press release from LEO Pharma, which is developing the product, the efficacy and safety of delgocitinib cream have not been evaluated by any regulatory authority. In 2020, the drug was granted fast-track designation by the Food and Drug Administration for the potential treatment of adults with moderate to severe chronic hand eczema. There are currently no treatment options available in the United States specifically approved for treating the condition.



 

The European Medicines Agency has validated the marketing authorization application for delgocitinib cream, for the treatment of adults with chronic moderate to severe hand eczema, which marks the beginning of the review process for the treatment by the EMA’s Committee for Medicinal Products for Human Use.

Delgocitinib is an investigational topical pan–Janus kinase inhibitor that inhibits activation of the JAK-STAT pathway.

The development follows results reported from two phase 3 clinical trials known as DELTA 1 and DELTA 2, which evaluated the safety and efficacy of delgocitinib cream applications twice per day compared with a vehicle cream in adults with mild to severe chronic hand eczema. Results of DELTA 1 were presented at the 2023 annual meeting of the American Academy of Dermatology. A multisite, open-label extension trial known as DELTA 3 is still in progress.

According to a press release from LEO Pharma, which is developing the product, the efficacy and safety of delgocitinib cream have not been evaluated by any regulatory authority. In 2020, the drug was granted fast-track designation by the Food and Drug Administration for the potential treatment of adults with moderate to severe chronic hand eczema. There are currently no treatment options available in the United States specifically approved for treating the condition.



 

The European Medicines Agency has validated the marketing authorization application for delgocitinib cream, for the treatment of adults with chronic moderate to severe hand eczema, which marks the beginning of the review process for the treatment by the EMA’s Committee for Medicinal Products for Human Use.

Delgocitinib is an investigational topical pan–Janus kinase inhibitor that inhibits activation of the JAK-STAT pathway.

The development follows results reported from two phase 3 clinical trials known as DELTA 1 and DELTA 2, which evaluated the safety and efficacy of delgocitinib cream applications twice per day compared with a vehicle cream in adults with mild to severe chronic hand eczema. Results of DELTA 1 were presented at the 2023 annual meeting of the American Academy of Dermatology. A multisite, open-label extension trial known as DELTA 3 is still in progress.

According to a press release from LEO Pharma, which is developing the product, the efficacy and safety of delgocitinib cream have not been evaluated by any regulatory authority. In 2020, the drug was granted fast-track designation by the Food and Drug Administration for the potential treatment of adults with moderate to severe chronic hand eczema. There are currently no treatment options available in the United States specifically approved for treating the condition.