Diabetes Hub

This transcript has been edited for clarity. 

Akshay B. Jain, MD: I’m Dr. Akshay Jain, an endocrinologist from Vancouver, and I’m joined by Dr. James Kim, a primary care physician from Calgary, Canada. 

Both Dr. Kim and I attended ADA 2024. We went over all our learnings and decided that there was a whole heap of clinical pearls that we learned from the conference. We thought it would be awesome if we could share our learnings with all of you, both from a primary care lens and from an endocrinology perspective.

One study Dr. Kim and I learned about, and we think has some definite nuances in management of people living with diabetes, regards inhaled insulin. When we have patients in our clinic who have perhaps failed multiple oral agents or have very high blood sugars, we obviously want to consider starting them on insulin for type 2 diabetes.

Sometimes there is a significant barrier, which is related to the needles. There’s an actual term for this: trypanophobia — a fear of needles. For the longest time, people have not wanted to take insulin or injectables because there’s only one way of administering it, which is subcutaneous.

Enter now inhaled insulin. We saw studies at the ADA 2024 conference that looked at a new inhaled insulin called Afrezza. Afrezza essentially is a short-acting insulin, so it’s kind of like a prandial insulin derivative, where it can be inhaled by an individual and it will work for mealtime control of blood sugars.

Dr. Kim, in your practice, how often do you see people not wanting to take shots, and has this been a big barrier for you in starting insulin? 

James W. Kim, MBBCh, PgDip, MScCH: Thank you for having me. To answer your question, absolutely I encounter this on a weekly basis — and I’m not even an endocrinologist. I just have an interest in diabetes. There are a number of patients that I think will benefit massively with insulin but they’re needle-phobic. You taught me that word, but I can never pronounce it, so my apologies for not remembering that phobia. I’m just going to call it needle phobia because I’m a simple-minded person.

The needle phobia is massive. I think there’s a definite fear of the needle, but there’s also a fear of failure. As soon as an injection is mentioned, many patients feel they failed miserably. There’s an emotional roller coaster that happens.

I’m sure, Dr. Jain, you have seen many patients, especially from Asia, who would say: “Oh, my auntie got on insulin and 3 months later, she got a kidney transplant.” “My uncle started on insulin and he unfortunately passed away a couple of months later.” Unfortunately, they’re blaming many of those things on insulin.

I also have a number of patients who said they were on insulin before many years ago, and they experienced some severe hypoglycemic events, and they don’t want to get on the insulin ever again. This is unfortunate because you know that if those patients, those aunties and uncles, were on insulin long before, maybe we could have saved their legs and kidneys, and potentially death.

Now we have advanced so much with insulin that hypoglycemia does occur, but much less than before. We still have many barriers when it comes to insulin initiations. Therefore, having this idea of inhaled insulin is fantastic, and I think we can get many more patients on insulin — the medication they actually need.

Dr. Jain: Absolutely. From the studies on inhaled insulin at ADA 2024, the key thing I found very interesting, regarding the pharmacokinetics of the insulin, was that it’s working very quickly. It starts working within minutes of administering it.

Additionally, it lasts in the body only for a shorter duration of time, compared with other injectable short-acting insulins, so it lasts in the body. The active insulin time is roughly about 2 hours or so, based on the studies, which in my mind opens up a whole world of possibilities because it means that people can take another correctional insulin if the blood sugars are still high after taking their first inhaled dose. You can take another dose subsequently without worrying about stacking of insulin. 

Many of us are familiar with this term, which is if you take two shots of short-acting insulin too close to each other, the insulin doses might add up and there can be a big drop in the blood sugars; it’s called stacking of insulin. This can be potentially avoided. 

Similarly, if you take your dinnertime inhaled insulin and the sugars are still high around bedtime, you could take a smaller dose of the inhaled insulin and not worry about middle-of-the-night hypoglycemia because the effect of the insulin would be only for a little while.

That’s one key learning that I found very helpful. The other important thing that I found was that this is not for everyone, so there are some restrictions. Essentially, the contraindication is that people who have asthma or COPD cannot be prescribed an inhaled insulin.

What are your thoughts, Dr. Kim, based on this for your practice in primary care? 

Dr. Kim: It is very fascinating, for sure. I cannot wait to get hold of this insulin. I can already think of some patients who may benefit. You’ve mentioned the asthma and COPD patients, and that makes more sense because there is an actual airway problem.

I also wonder what will happen to patients who have restrictive airway disease, where asthma and COPD fall under obstructive airway disease. What if they have obesity, where it’s really pressing into the diaphragm, and where they may not be able to take the deep breath in? How will they react?

What about someone who’s got a cold, someone who has postnasal drip, or someone who tends to cough frequently? What about egg allergies? There are many question marks around this insulin before initiating these medications. There is excitement, but there are also many questions at the same time.

Dr. Jain: I think these are very important, practical considerations that we’ll uncover as we start using more of this in clinical practice. The other important thing to note is that the presenters told us it’s important to monitor pulmonary function tests. It’s important to get a baseline pulmonary function test, and then we have to do another one in 6 months, followed by annually thereafter.

If, at any point of time, the FEV1 drops by 20% or more, then that would be an indication for discontinuation of the inhaled insulin. The pulmonary function test does not need to be one of those fancier ones. The study group would just do office spirometries. I’m wondering, Dr. Kim, in primary care, do you think this could potentially be a rate-limiting factor?

Dr. Kim: In Alberta, where I reside, no. Spirometry is very easily accessible in the province. For example, in Calgary alone, we have a population of about 1.3 million people. We have over 13 or 15 companies that can do this spirometry. We can get these things done literally within a week or 2.

However, I am aware that, in other provinces in Canada, it can definitely be a huge rate-limiting factor. Not everyone has the office-based spirometry, and definitely not within the primary care office. It has to be referred out to these private companies, most likely, and some of the rural areas will have to rely on the provincial hospitals, where the access can be even more challenging. 

On the day of the actual spirometry, if the person has a cough or is not feeling well, it’s going to be a problem because you don’t want the spirometry to be infected with a whole bunch of viruses. You’ll have to cancel that and it can be a bit of an issue.

Dr. Jain: Many of our viewers are from the United States and other parts of the world, and spirometry is quite easily accessible in most places. As an endocrinologist, I must confess that it’s been a long time since I’ve even ordered a spirometry or any clinical form of pulmonary function test. Once I start using the inhaled insulin, I’ll need to start brushing up on my pulmonary function test knowledge. 

I think these are exciting times. At least we’ve got something to offer to people who would have otherwise not taken any insulin at all. There’s certainly that hope that now there’s a different way to administer this, and hopefully it can only get better from here on.
 

Dr. Jain is a clinical instructor, Department of Endocrinology, University of British Columbia, Vancouver. Dr. Kim is a clinical assistant professor, Department of Family Medicine, University of Calgary in Alberta. Both disclosed conflicts of interest with numerous pharmaceutical companies.

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

This transcript has been edited for clarity. 

Akshay B. Jain, MD: I’m Dr. Akshay Jain, an endocrinologist from Vancouver, and I’m joined by Dr. James Kim, a primary care physician from Calgary, Canada. 

Both Dr. Kim and I attended ADA 2024. We went over all our learnings and decided that there was a whole heap of clinical pearls that we learned from the conference. We thought it would be awesome if we could share our learnings with all of you, both from a primary care lens and from an endocrinology perspective.

One study Dr. Kim and I learned about, and we think has some definite nuances in management of people living with diabetes, regards inhaled insulin. When we have patients in our clinic who have perhaps failed multiple oral agents or have very high blood sugars, we obviously want to consider starting them on insulin for type 2 diabetes.

Sometimes there is a significant barrier, which is related to the needles. There’s an actual term for this: trypanophobia — a fear of needles. For the longest time, people have not wanted to take insulin or injectables because there’s only one way of administering it, which is subcutaneous.

Enter now inhaled insulin. We saw studies at the ADA 2024 conference that looked at a new inhaled insulin called Afrezza. Afrezza essentially is a short-acting insulin, so it’s kind of like a prandial insulin derivative, where it can be inhaled by an individual and it will work for mealtime control of blood sugars.

Dr. Kim, in your practice, how often do you see people not wanting to take shots, and has this been a big barrier for you in starting insulin? 

James W. Kim, MBBCh, PgDip, MScCH: Thank you for having me. To answer your question, absolutely I encounter this on a weekly basis — and I’m not even an endocrinologist. I just have an interest in diabetes. There are a number of patients that I think will benefit massively with insulin but they’re needle-phobic. You taught me that word, but I can never pronounce it, so my apologies for not remembering that phobia. I’m just going to call it needle phobia because I’m a simple-minded person.

The needle phobia is massive. I think there’s a definite fear of the needle, but there’s also a fear of failure. As soon as an injection is mentioned, many patients feel they failed miserably. There’s an emotional roller coaster that happens.

I’m sure, Dr. Jain, you have seen many patients, especially from Asia, who would say: “Oh, my auntie got on insulin and 3 months later, she got a kidney transplant.” “My uncle started on insulin and he unfortunately passed away a couple of months later.” Unfortunately, they’re blaming many of those things on insulin.

I also have a number of patients who said they were on insulin before many years ago, and they experienced some severe hypoglycemic events, and they don’t want to get on the insulin ever again. This is unfortunate because you know that if those patients, those aunties and uncles, were on insulin long before, maybe we could have saved their legs and kidneys, and potentially death.

Now we have advanced so much with insulin that hypoglycemia does occur, but much less than before. We still have many barriers when it comes to insulin initiations. Therefore, having this idea of inhaled insulin is fantastic, and I think we can get many more patients on insulin — the medication they actually need.

Dr. Jain: Absolutely. From the studies on inhaled insulin at ADA 2024, the key thing I found very interesting, regarding the pharmacokinetics of the insulin, was that it’s working very quickly. It starts working within minutes of administering it.

Additionally, it lasts in the body only for a shorter duration of time, compared with other injectable short-acting insulins, so it lasts in the body. The active insulin time is roughly about 2 hours or so, based on the studies, which in my mind opens up a whole world of possibilities because it means that people can take another correctional insulin if the blood sugars are still high after taking their first inhaled dose. You can take another dose subsequently without worrying about stacking of insulin. 

Many of us are familiar with this term, which is if you take two shots of short-acting insulin too close to each other, the insulin doses might add up and there can be a big drop in the blood sugars; it’s called stacking of insulin. This can be potentially avoided. 

Similarly, if you take your dinnertime inhaled insulin and the sugars are still high around bedtime, you could take a smaller dose of the inhaled insulin and not worry about middle-of-the-night hypoglycemia because the effect of the insulin would be only for a little while.

That’s one key learning that I found very helpful. The other important thing that I found was that this is not for everyone, so there are some restrictions. Essentially, the contraindication is that people who have asthma or COPD cannot be prescribed an inhaled insulin.

What are your thoughts, Dr. Kim, based on this for your practice in primary care? 

Dr. Kim: It is very fascinating, for sure. I cannot wait to get hold of this insulin. I can already think of some patients who may benefit. You’ve mentioned the asthma and COPD patients, and that makes more sense because there is an actual airway problem.

I also wonder what will happen to patients who have restrictive airway disease, where asthma and COPD fall under obstructive airway disease. What if they have obesity, where it’s really pressing into the diaphragm, and where they may not be able to take the deep breath in? How will they react?

What about someone who’s got a cold, someone who has postnasal drip, or someone who tends to cough frequently? What about egg allergies? There are many question marks around this insulin before initiating these medications. There is excitement, but there are also many questions at the same time.

Dr. Jain: I think these are very important, practical considerations that we’ll uncover as we start using more of this in clinical practice. The other important thing to note is that the presenters told us it’s important to monitor pulmonary function tests. It’s important to get a baseline pulmonary function test, and then we have to do another one in 6 months, followed by annually thereafter.

If, at any point of time, the FEV1 drops by 20% or more, then that would be an indication for discontinuation of the inhaled insulin. The pulmonary function test does not need to be one of those fancier ones. The study group would just do office spirometries. I’m wondering, Dr. Kim, in primary care, do you think this could potentially be a rate-limiting factor?

Dr. Kim: In Alberta, where I reside, no. Spirometry is very easily accessible in the province. For example, in Calgary alone, we have a population of about 1.3 million people. We have over 13 or 15 companies that can do this spirometry. We can get these things done literally within a week or 2.

However, I am aware that, in other provinces in Canada, it can definitely be a huge rate-limiting factor. Not everyone has the office-based spirometry, and definitely not within the primary care office. It has to be referred out to these private companies, most likely, and some of the rural areas will have to rely on the provincial hospitals, where the access can be even more challenging. 

On the day of the actual spirometry, if the person has a cough or is not feeling well, it’s going to be a problem because you don’t want the spirometry to be infected with a whole bunch of viruses. You’ll have to cancel that and it can be a bit of an issue.

Dr. Jain: Many of our viewers are from the United States and other parts of the world, and spirometry is quite easily accessible in most places. As an endocrinologist, I must confess that it’s been a long time since I’ve even ordered a spirometry or any clinical form of pulmonary function test. Once I start using the inhaled insulin, I’ll need to start brushing up on my pulmonary function test knowledge. 

I think these are exciting times. At least we’ve got something to offer to people who would have otherwise not taken any insulin at all. There’s certainly that hope that now there’s a different way to administer this, and hopefully it can only get better from here on.
 

Dr. Jain is a clinical instructor, Department of Endocrinology, University of British Columbia, Vancouver. Dr. Kim is a clinical assistant professor, Department of Family Medicine, University of Calgary in Alberta. Both disclosed conflicts of interest with numerous pharmaceutical companies.

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

This transcript has been edited for clarity. 

Akshay B. Jain, MD: I’m Dr. Akshay Jain, an endocrinologist from Vancouver, and I’m joined by Dr. James Kim, a primary care physician from Calgary, Canada. 

Both Dr. Kim and I attended ADA 2024. We went over all our learnings and decided that there was a whole heap of clinical pearls that we learned from the conference. We thought it would be awesome if we could share our learnings with all of you, both from a primary care lens and from an endocrinology perspective.

One study Dr. Kim and I learned about, and we think has some definite nuances in management of people living with diabetes, regards inhaled insulin. When we have patients in our clinic who have perhaps failed multiple oral agents or have very high blood sugars, we obviously want to consider starting them on insulin for type 2 diabetes.

Sometimes there is a significant barrier, which is related to the needles. There’s an actual term for this: trypanophobia — a fear of needles. For the longest time, people have not wanted to take insulin or injectables because there’s only one way of administering it, which is subcutaneous.

Enter now inhaled insulin. We saw studies at the ADA 2024 conference that looked at a new inhaled insulin called Afrezza. Afrezza essentially is a short-acting insulin, so it’s kind of like a prandial insulin derivative, where it can be inhaled by an individual and it will work for mealtime control of blood sugars.

Dr. Kim, in your practice, how often do you see people not wanting to take shots, and has this been a big barrier for you in starting insulin? 

James W. Kim, MBBCh, PgDip, MScCH: Thank you for having me. To answer your question, absolutely I encounter this on a weekly basis — and I’m not even an endocrinologist. I just have an interest in diabetes. There are a number of patients that I think will benefit massively with insulin but they’re needle-phobic. You taught me that word, but I can never pronounce it, so my apologies for not remembering that phobia. I’m just going to call it needle phobia because I’m a simple-minded person.

The needle phobia is massive. I think there’s a definite fear of the needle, but there’s also a fear of failure. As soon as an injection is mentioned, many patients feel they failed miserably. There’s an emotional roller coaster that happens.

I’m sure, Dr. Jain, you have seen many patients, especially from Asia, who would say: “Oh, my auntie got on insulin and 3 months later, she got a kidney transplant.” “My uncle started on insulin and he unfortunately passed away a couple of months later.” Unfortunately, they’re blaming many of those things on insulin.

I also have a number of patients who said they were on insulin before many years ago, and they experienced some severe hypoglycemic events, and they don’t want to get on the insulin ever again. This is unfortunate because you know that if those patients, those aunties and uncles, were on insulin long before, maybe we could have saved their legs and kidneys, and potentially death.

Now we have advanced so much with insulin that hypoglycemia does occur, but much less than before. We still have many barriers when it comes to insulin initiations. Therefore, having this idea of inhaled insulin is fantastic, and I think we can get many more patients on insulin — the medication they actually need.

Dr. Jain: Absolutely. From the studies on inhaled insulin at ADA 2024, the key thing I found very interesting, regarding the pharmacokinetics of the insulin, was that it’s working very quickly. It starts working within minutes of administering it.

Additionally, it lasts in the body only for a shorter duration of time, compared with other injectable short-acting insulins, so it lasts in the body. The active insulin time is roughly about 2 hours or so, based on the studies, which in my mind opens up a whole world of possibilities because it means that people can take another correctional insulin if the blood sugars are still high after taking their first inhaled dose. You can take another dose subsequently without worrying about stacking of insulin. 

Many of us are familiar with this term, which is if you take two shots of short-acting insulin too close to each other, the insulin doses might add up and there can be a big drop in the blood sugars; it’s called stacking of insulin. This can be potentially avoided. 

Similarly, if you take your dinnertime inhaled insulin and the sugars are still high around bedtime, you could take a smaller dose of the inhaled insulin and not worry about middle-of-the-night hypoglycemia because the effect of the insulin would be only for a little while.

That’s one key learning that I found very helpful. The other important thing that I found was that this is not for everyone, so there are some restrictions. Essentially, the contraindication is that people who have asthma or COPD cannot be prescribed an inhaled insulin.

What are your thoughts, Dr. Kim, based on this for your practice in primary care? 

Dr. Kim: It is very fascinating, for sure. I cannot wait to get hold of this insulin. I can already think of some patients who may benefit. You’ve mentioned the asthma and COPD patients, and that makes more sense because there is an actual airway problem.

I also wonder what will happen to patients who have restrictive airway disease, where asthma and COPD fall under obstructive airway disease. What if they have obesity, where it’s really pressing into the diaphragm, and where they may not be able to take the deep breath in? How will they react?

What about someone who’s got a cold, someone who has postnasal drip, or someone who tends to cough frequently? What about egg allergies? There are many question marks around this insulin before initiating these medications. There is excitement, but there are also many questions at the same time.

Dr. Jain: I think these are very important, practical considerations that we’ll uncover as we start using more of this in clinical practice. The other important thing to note is that the presenters told us it’s important to monitor pulmonary function tests. It’s important to get a baseline pulmonary function test, and then we have to do another one in 6 months, followed by annually thereafter.

If, at any point of time, the FEV1 drops by 20% or more, then that would be an indication for discontinuation of the inhaled insulin. The pulmonary function test does not need to be one of those fancier ones. The study group would just do office spirometries. I’m wondering, Dr. Kim, in primary care, do you think this could potentially be a rate-limiting factor?

Dr. Kim: In Alberta, where I reside, no. Spirometry is very easily accessible in the province. For example, in Calgary alone, we have a population of about 1.3 million people. We have over 13 or 15 companies that can do this spirometry. We can get these things done literally within a week or 2.

However, I am aware that, in other provinces in Canada, it can definitely be a huge rate-limiting factor. Not everyone has the office-based spirometry, and definitely not within the primary care office. It has to be referred out to these private companies, most likely, and some of the rural areas will have to rely on the provincial hospitals, where the access can be even more challenging. 

On the day of the actual spirometry, if the person has a cough or is not feeling well, it’s going to be a problem because you don’t want the spirometry to be infected with a whole bunch of viruses. You’ll have to cancel that and it can be a bit of an issue.

Dr. Jain: Many of our viewers are from the United States and other parts of the world, and spirometry is quite easily accessible in most places. As an endocrinologist, I must confess that it’s been a long time since I’ve even ordered a spirometry or any clinical form of pulmonary function test. Once I start using the inhaled insulin, I’ll need to start brushing up on my pulmonary function test knowledge. 

I think these are exciting times. At least we’ve got something to offer to people who would have otherwise not taken any insulin at all. There’s certainly that hope that now there’s a different way to administer this, and hopefully it can only get better from here on.
 

Dr. Jain is a clinical instructor, Department of Endocrinology, University of British Columbia, Vancouver. Dr. Kim is a clinical assistant professor, Department of Family Medicine, University of Calgary in Alberta. Both disclosed conflicts of interest with numerous pharmaceutical companies.

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

A recent report by this news organization of a vitamin D clinical practice guideline released by the Endocrine Society in June triggered an outpouring of objections in the comments section from doctors and other readers.

A society press release listed the key new recommendations on the use of vitamin D supplementation and screening to reduce disease risks in individuals without established indications for such treatment or testing:

• For healthy adults younger than 75, no supplementation at doses above the recommended dietary intakes.
• Populations that may benefit from higher doses include: children and adolescents 18 and younger to prevent rickets and to reduce risk for respiratory infection, individuals 75 and older to possibly lower mortality risk, “pregnant people” to potentially reduce various risks, and people with prediabetes to potentially reduce risk of progression.
• No routine testing for 25-hydroxyvitamin D levels because outcome-specific benefits based on those levels have not been identified (including screening in people with dark complexion or obesity).
• Based on insufficient evidence, the panel could not determine specific blood-level thresholds for 25-hydroxyvitamin D for adequacy or for target levels for disease prevention.

This news organization covered the guideline release and simultaneous presentation at the Endocrine Society annual meeting. In response to the coverage, more than 200 doctors and other readers expressed concerns about the guideline, and some said outright that they would not follow it (readers quoted below are identified by the usernames they registered with on the website).

One reader who posted as Dr. Joseph Destefano went so far as to call the guideline “dangerous” and “almost ... evil.” Ironically, some readers attacked this news organization, thinking that the coverage implied an endorsement, rather than a news report.
 

Ignores Potential Benefits

Although the guideline is said to be for people who are “otherwise healthy” (other than the exceptions noted above), many readers were concerned that the recommendations ignore the potential benefits of supplementation for other health conditions relevant to patients and other populations.

“They address issues dealing only with endocrinology and bone health for the most part,” Dr. Emilio Gonzalez wrote. “However, vitamin D insufficiency and deficiency are not rare, and they impact the treatment of autoimmune disorders, chronic pain control, immunosuppression, cancer prevention, cardiovascular health, etc. There is plenty of literature in this regard.”

“They make these claims as if quality studies contradicting their guidelines have not been out there for years,” Dr. Brian Batcheldor said. “What about the huge demographic with diseases that impact intestinal absorption, eg, Crohn’s and celiac disease, cystic fibrosis, and ulcerative colitis? What about the one in nine that now have autoimmune diseases still awaiting diagnosis? What about night workers or anyone with more restricted access to sun exposure? How about those whose cultural or religious dress code limit skin exposure?”

The latter group was also mentioned in a post from Dr. Eve Finkelstein who said, “They don’t take into account women who are totally covered for religious reasons. They have no skin other than part of their face exposed. It does not make sense not to supplement them. Ignoring women’s health needs seems to be the norm.”

“I don’t think they considered the oral health effects of vitamin D deficiency,” pointed out commenter Corie Lewis. “Excess dental calculus (tartar) from excess calcium/phosphate in saliva significantly increases an individual’s periodontal disease risks (gum disease), and low saliva calcium/phosphate increases dental caries (cavities) risks, which generally indicates an imbalance of the oral microbiome. Vitamin D can help create balance and reduce those oral health risks.”

Noted Kimberley Morris-Windisch, “Having worked in rheumatology and pain for most of my career, I have seen too many people benefit from correcting deficiency of vitamin D. To ignore this is to miss opportunities to improve patient health.” Furthermore, “I find it unlikely that it would only improve mortality after age 75. That makes no sense.”

“Also,” she added, “what is the number [needed] to harm? In my 25 years, I have seen vitamin D toxicity once and an excessively high level without symptoms one other time.”

“WHY? Just WHY?” lamented Anne Kinchen. “Low levels in pregnant women have long-term effects on the developing fetus — higher and earlier rates of osteopenia in female children, weaker immune systems overall. There are just SO many reasons to test. These guidelines for no testing are absurd!”
 

No Screening, No Need for Decision-Making?

Several readers questioned the society’s rationale for not screening, as expressed by session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine.

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it,” Dr. Rosen said. “That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen. ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life. ... Screening is probably not worthwhile in any age group.”

Among the reader comments in this regard:

“So misguided. Don’t look because we don’t know what do to with data. That’s the message this article exposes. The recommendation is do nothing. But, doing nothing IS an action — not a default.” (Lisa Tracy)

“So now, you will not screen for vitamin D because you do not know what to do next? See a naturopathic doctor — we know what to do next!” (Dr. Joyce Roberson)

“Gee, how do we treat it? ... What to do? Sounds incompetent at minimum. I suspect it’s vital, easy, and inexpensive ... so hide it.” (Holly Kohley)

“Just because we do not know is not a rationale for not testing. The opposite should be done.” (Dr. JJ Gold)
 

Caters to Industry?

Many commentators intimated that pharma and/or insurance company considerations played a role in the recommendations. Their comments included the following:

“I have been under the impression people do routine checkups to verify there are no hidden problems. If only some testing is done, the probability of not finding a problem is huge. ... Preventive healthcare should be looking for something to prevent instead of waiting until they can cure it. Of course, it might come back to ‘follow the money.’ It is much more profitable to diagnose and treat than it is to prevent.” (Grace Kyser)

“The current irrational ‘recommendation’ gives insurance companies an excuse to deny ALL tests of vitamin D — even if the proper code is supplied. The result is — people suffer. This recommendation does harm!” (Dr JJ Gold)

“Essentially, they are saying let’s not screen ‘healthy’ individuals and ignore it altogether. Better to wait till they’re old, pregnant, or already sick and diagnosed with a disease. This is the problem with the healthcare in this country.” (Brittney Lesher)

“Until allopathic medicine stops waiting for severe symptoms to develop before even screening for potential health problems, the most expensive healthcare (aka, sick care) system in the world will continue to be content to focus on medical emergencies and ignore prevention. ...” (Dean Raffelock)

“Don’t test? Are you kidding me? Especially when people are supplementing? That is akin to taking a blood pressure medication without measuring blood pressures! ... Don’t test? Don’t supplement? ... I have only one explanation for such nonsense: Pharma lives off sick people, not healthy ones.” (Georg Schlomka)

On a somewhat conciliatory and pointed note, Dr Francesca Luna-Rudin commented, “I would like to remind all of my fellow physicians that recommendations should be regarded as just that, a ‘recommendation.’ As doctors, we can use guidelines and recommendations in our practice, but if a new one is presented that does not make sense or would lead to harm based on our education and training, then we are not bound to follow it!”

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

A recent report by this news organization of a vitamin D clinical practice guideline released by the Endocrine Society in June triggered an outpouring of objections in the comments section from doctors and other readers.

A society press release listed the key new recommendations on the use of vitamin D supplementation and screening to reduce disease risks in individuals without established indications for such treatment or testing:

• For healthy adults younger than 75, no supplementation at doses above the recommended dietary intakes.
• Populations that may benefit from higher doses include: children and adolescents 18 and younger to prevent rickets and to reduce risk for respiratory infection, individuals 75 and older to possibly lower mortality risk, “pregnant people” to potentially reduce various risks, and people with prediabetes to potentially reduce risk of progression.
• No routine testing for 25-hydroxyvitamin D levels because outcome-specific benefits based on those levels have not been identified (including screening in people with dark complexion or obesity).
• Based on insufficient evidence, the panel could not determine specific blood-level thresholds for 25-hydroxyvitamin D for adequacy or for target levels for disease prevention.

This news organization covered the guideline release and simultaneous presentation at the Endocrine Society annual meeting. In response to the coverage, more than 200 doctors and other readers expressed concerns about the guideline, and some said outright that they would not follow it (readers quoted below are identified by the usernames they registered with on the website).

One reader who posted as Dr. Joseph Destefano went so far as to call the guideline “dangerous” and “almost ... evil.” Ironically, some readers attacked this news organization, thinking that the coverage implied an endorsement, rather than a news report.
 

Ignores Potential Benefits

Although the guideline is said to be for people who are “otherwise healthy” (other than the exceptions noted above), many readers were concerned that the recommendations ignore the potential benefits of supplementation for other health conditions relevant to patients and other populations.

“They address issues dealing only with endocrinology and bone health for the most part,” Dr. Emilio Gonzalez wrote. “However, vitamin D insufficiency and deficiency are not rare, and they impact the treatment of autoimmune disorders, chronic pain control, immunosuppression, cancer prevention, cardiovascular health, etc. There is plenty of literature in this regard.”

“They make these claims as if quality studies contradicting their guidelines have not been out there for years,” Dr. Brian Batcheldor said. “What about the huge demographic with diseases that impact intestinal absorption, eg, Crohn’s and celiac disease, cystic fibrosis, and ulcerative colitis? What about the one in nine that now have autoimmune diseases still awaiting diagnosis? What about night workers or anyone with more restricted access to sun exposure? How about those whose cultural or religious dress code limit skin exposure?”

The latter group was also mentioned in a post from Dr. Eve Finkelstein who said, “They don’t take into account women who are totally covered for religious reasons. They have no skin other than part of their face exposed. It does not make sense not to supplement them. Ignoring women’s health needs seems to be the norm.”

“I don’t think they considered the oral health effects of vitamin D deficiency,” pointed out commenter Corie Lewis. “Excess dental calculus (tartar) from excess calcium/phosphate in saliva significantly increases an individual’s periodontal disease risks (gum disease), and low saliva calcium/phosphate increases dental caries (cavities) risks, which generally indicates an imbalance of the oral microbiome. Vitamin D can help create balance and reduce those oral health risks.”

Noted Kimberley Morris-Windisch, “Having worked in rheumatology and pain for most of my career, I have seen too many people benefit from correcting deficiency of vitamin D. To ignore this is to miss opportunities to improve patient health.” Furthermore, “I find it unlikely that it would only improve mortality after age 75. That makes no sense.”

“Also,” she added, “what is the number [needed] to harm? In my 25 years, I have seen vitamin D toxicity once and an excessively high level without symptoms one other time.”

“WHY? Just WHY?” lamented Anne Kinchen. “Low levels in pregnant women have long-term effects on the developing fetus — higher and earlier rates of osteopenia in female children, weaker immune systems overall. There are just SO many reasons to test. These guidelines for no testing are absurd!”
 

No Screening, No Need for Decision-Making?

Several readers questioned the society’s rationale for not screening, as expressed by session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine.

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it,” Dr. Rosen said. “That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen. ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life. ... Screening is probably not worthwhile in any age group.”

Among the reader comments in this regard:

“So misguided. Don’t look because we don’t know what do to with data. That’s the message this article exposes. The recommendation is do nothing. But, doing nothing IS an action — not a default.” (Lisa Tracy)

“So now, you will not screen for vitamin D because you do not know what to do next? See a naturopathic doctor — we know what to do next!” (Dr. Joyce Roberson)

“Gee, how do we treat it? ... What to do? Sounds incompetent at minimum. I suspect it’s vital, easy, and inexpensive ... so hide it.” (Holly Kohley)

“Just because we do not know is not a rationale for not testing. The opposite should be done.” (Dr. JJ Gold)
 

Caters to Industry?

Many commentators intimated that pharma and/or insurance company considerations played a role in the recommendations. Their comments included the following:

“I have been under the impression people do routine checkups to verify there are no hidden problems. If only some testing is done, the probability of not finding a problem is huge. ... Preventive healthcare should be looking for something to prevent instead of waiting until they can cure it. Of course, it might come back to ‘follow the money.’ It is much more profitable to diagnose and treat than it is to prevent.” (Grace Kyser)

“The current irrational ‘recommendation’ gives insurance companies an excuse to deny ALL tests of vitamin D — even if the proper code is supplied. The result is — people suffer. This recommendation does harm!” (Dr JJ Gold)

“Essentially, they are saying let’s not screen ‘healthy’ individuals and ignore it altogether. Better to wait till they’re old, pregnant, or already sick and diagnosed with a disease. This is the problem with the healthcare in this country.” (Brittney Lesher)

“Until allopathic medicine stops waiting for severe symptoms to develop before even screening for potential health problems, the most expensive healthcare (aka, sick care) system in the world will continue to be content to focus on medical emergencies and ignore prevention. ...” (Dean Raffelock)

“Don’t test? Are you kidding me? Especially when people are supplementing? That is akin to taking a blood pressure medication without measuring blood pressures! ... Don’t test? Don’t supplement? ... I have only one explanation for such nonsense: Pharma lives off sick people, not healthy ones.” (Georg Schlomka)

On a somewhat conciliatory and pointed note, Dr Francesca Luna-Rudin commented, “I would like to remind all of my fellow physicians that recommendations should be regarded as just that, a ‘recommendation.’ As doctors, we can use guidelines and recommendations in our practice, but if a new one is presented that does not make sense or would lead to harm based on our education and training, then we are not bound to follow it!”

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

A recent report by this news organization of a vitamin D clinical practice guideline released by the Endocrine Society in June triggered an outpouring of objections in the comments section from doctors and other readers.

A society press release listed the key new recommendations on the use of vitamin D supplementation and screening to reduce disease risks in individuals without established indications for such treatment or testing:

• For healthy adults younger than 75, no supplementation at doses above the recommended dietary intakes.
• Populations that may benefit from higher doses include: children and adolescents 18 and younger to prevent rickets and to reduce risk for respiratory infection, individuals 75 and older to possibly lower mortality risk, “pregnant people” to potentially reduce various risks, and people with prediabetes to potentially reduce risk of progression.
• No routine testing for 25-hydroxyvitamin D levels because outcome-specific benefits based on those levels have not been identified (including screening in people with dark complexion or obesity).
• Based on insufficient evidence, the panel could not determine specific blood-level thresholds for 25-hydroxyvitamin D for adequacy or for target levels for disease prevention.

This news organization covered the guideline release and simultaneous presentation at the Endocrine Society annual meeting. In response to the coverage, more than 200 doctors and other readers expressed concerns about the guideline, and some said outright that they would not follow it (readers quoted below are identified by the usernames they registered with on the website).

One reader who posted as Dr. Joseph Destefano went so far as to call the guideline “dangerous” and “almost ... evil.” Ironically, some readers attacked this news organization, thinking that the coverage implied an endorsement, rather than a news report.
 

Ignores Potential Benefits

Although the guideline is said to be for people who are “otherwise healthy” (other than the exceptions noted above), many readers were concerned that the recommendations ignore the potential benefits of supplementation for other health conditions relevant to patients and other populations.

“They address issues dealing only with endocrinology and bone health for the most part,” Dr. Emilio Gonzalez wrote. “However, vitamin D insufficiency and deficiency are not rare, and they impact the treatment of autoimmune disorders, chronic pain control, immunosuppression, cancer prevention, cardiovascular health, etc. There is plenty of literature in this regard.”

“They make these claims as if quality studies contradicting their guidelines have not been out there for years,” Dr. Brian Batcheldor said. “What about the huge demographic with diseases that impact intestinal absorption, eg, Crohn’s and celiac disease, cystic fibrosis, and ulcerative colitis? What about the one in nine that now have autoimmune diseases still awaiting diagnosis? What about night workers or anyone with more restricted access to sun exposure? How about those whose cultural or religious dress code limit skin exposure?”

The latter group was also mentioned in a post from Dr. Eve Finkelstein who said, “They don’t take into account women who are totally covered for religious reasons. They have no skin other than part of their face exposed. It does not make sense not to supplement them. Ignoring women’s health needs seems to be the norm.”

“I don’t think they considered the oral health effects of vitamin D deficiency,” pointed out commenter Corie Lewis. “Excess dental calculus (tartar) from excess calcium/phosphate in saliva significantly increases an individual’s periodontal disease risks (gum disease), and low saliva calcium/phosphate increases dental caries (cavities) risks, which generally indicates an imbalance of the oral microbiome. Vitamin D can help create balance and reduce those oral health risks.”

Noted Kimberley Morris-Windisch, “Having worked in rheumatology and pain for most of my career, I have seen too many people benefit from correcting deficiency of vitamin D. To ignore this is to miss opportunities to improve patient health.” Furthermore, “I find it unlikely that it would only improve mortality after age 75. That makes no sense.”

“Also,” she added, “what is the number [needed] to harm? In my 25 years, I have seen vitamin D toxicity once and an excessively high level without symptoms one other time.”

“WHY? Just WHY?” lamented Anne Kinchen. “Low levels in pregnant women have long-term effects on the developing fetus — higher and earlier rates of osteopenia in female children, weaker immune systems overall. There are just SO many reasons to test. These guidelines for no testing are absurd!”
 

No Screening, No Need for Decision-Making?

Several readers questioned the society’s rationale for not screening, as expressed by session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine.

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it,” Dr. Rosen said. “That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen. ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life. ... Screening is probably not worthwhile in any age group.”

Among the reader comments in this regard:

“So misguided. Don’t look because we don’t know what do to with data. That’s the message this article exposes. The recommendation is do nothing. But, doing nothing IS an action — not a default.” (Lisa Tracy)

“So now, you will not screen for vitamin D because you do not know what to do next? See a naturopathic doctor — we know what to do next!” (Dr. Joyce Roberson)

“Gee, how do we treat it? ... What to do? Sounds incompetent at minimum. I suspect it’s vital, easy, and inexpensive ... so hide it.” (Holly Kohley)

“Just because we do not know is not a rationale for not testing. The opposite should be done.” (Dr. JJ Gold)
 

Caters to Industry?

Many commentators intimated that pharma and/or insurance company considerations played a role in the recommendations. Their comments included the following:

“I have been under the impression people do routine checkups to verify there are no hidden problems. If only some testing is done, the probability of not finding a problem is huge. ... Preventive healthcare should be looking for something to prevent instead of waiting until they can cure it. Of course, it might come back to ‘follow the money.’ It is much more profitable to diagnose and treat than it is to prevent.” (Grace Kyser)

“The current irrational ‘recommendation’ gives insurance companies an excuse to deny ALL tests of vitamin D — even if the proper code is supplied. The result is — people suffer. This recommendation does harm!” (Dr JJ Gold)

“Essentially, they are saying let’s not screen ‘healthy’ individuals and ignore it altogether. Better to wait till they’re old, pregnant, or already sick and diagnosed with a disease. This is the problem with the healthcare in this country.” (Brittney Lesher)

“Until allopathic medicine stops waiting for severe symptoms to develop before even screening for potential health problems, the most expensive healthcare (aka, sick care) system in the world will continue to be content to focus on medical emergencies and ignore prevention. ...” (Dean Raffelock)

“Don’t test? Are you kidding me? Especially when people are supplementing? That is akin to taking a blood pressure medication without measuring blood pressures! ... Don’t test? Don’t supplement? ... I have only one explanation for such nonsense: Pharma lives off sick people, not healthy ones.” (Georg Schlomka)

On a somewhat conciliatory and pointed note, Dr Francesca Luna-Rudin commented, “I would like to remind all of my fellow physicians that recommendations should be regarded as just that, a ‘recommendation.’ As doctors, we can use guidelines and recommendations in our practice, but if a new one is presented that does not make sense or would lead to harm based on our education and training, then we are not bound to follow it!”

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

Concerned about your patient’s type 2 diabetes risk? Along with the usual preventive strategies — like diet and exercise and, when appropriate, glucagon-like peptide 1 (GLP-1) agonists — there’s another simple, no-risk strategy that just might help: Turning off the light at night.

A study in The Lancet found that people who were exposed to the most light between 12:30 a.m. and 6 a.m. were 1.5 times more likely to develop diabetes than those who remained in darkness during that time frame.

The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.

“Those previous studies likely underestimated the effect,” said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, “since they did not capture indoor light environments.”

Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.

“This is really a phenomenal study,” said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham’s Diabetes Research Center, who was not involved in the study. “This is the first large-scale study we have looking at people’s light exposure patterns and linking it to their long-term health.”
 

What the Study Showed

The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.

“About half of the people that we looked at had very dim levels of light at night, so less than 1 lux — that basically means less than candlelight,” said Dr. Phillips. “They were the people who were protected against type 2 diabetes.”

Those exposed to more light at night — defined in the study as 12:30 a.m.–6 a.m. — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.

Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That’s about the risk increase you’d get from having a family history of type 2 diabetes, the researchers said.

Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, “we still found there was this very strong relationship between light exposure and risk of type 2 diabetes,” said Dr. Phillips.
 

How Light at Night May Increase Diabetes Risk

The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.

Light at night can disrupt the circadian rhythm, or your body’s internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.

One’s internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.

Dr. Phillips speculated that the sleep hormone melatonin also plays a role.

“Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses,” Dr. Phillips said. “So if you’re chronically getting light exposure at night, that’s reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes.”

Previous studies have explored melatonin supplementation to help manage diabetes. “However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far,” Dr. Miedlich said.
 

Takeaways

Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.

That said, “there’s no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes,” said Dr. Phillips.

Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and GLP-1 agonists.

“Probably a GLP-1 agonist is going to be more effective,” Dr. Peterson said. “But this is still a fairly large effect without having to go through the expense of buying a GLP-1 or losing a lot of weight or making a big lifestyle change.”

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

Concerned about your patient’s type 2 diabetes risk? Along with the usual preventive strategies — like diet and exercise and, when appropriate, glucagon-like peptide 1 (GLP-1) agonists — there’s another simple, no-risk strategy that just might help: Turning off the light at night.

A study in The Lancet found that people who were exposed to the most light between 12:30 a.m. and 6 a.m. were 1.5 times more likely to develop diabetes than those who remained in darkness during that time frame.

The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.

“Those previous studies likely underestimated the effect,” said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, “since they did not capture indoor light environments.”

Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.

“This is really a phenomenal study,” said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham’s Diabetes Research Center, who was not involved in the study. “This is the first large-scale study we have looking at people’s light exposure patterns and linking it to their long-term health.”
 

What the Study Showed

The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.

“About half of the people that we looked at had very dim levels of light at night, so less than 1 lux — that basically means less than candlelight,” said Dr. Phillips. “They were the people who were protected against type 2 diabetes.”

Those exposed to more light at night — defined in the study as 12:30 a.m.–6 a.m. — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.

Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That’s about the risk increase you’d get from having a family history of type 2 diabetes, the researchers said.

Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, “we still found there was this very strong relationship between light exposure and risk of type 2 diabetes,” said Dr. Phillips.
 

How Light at Night May Increase Diabetes Risk

The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.

Light at night can disrupt the circadian rhythm, or your body’s internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.

One’s internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.

Dr. Phillips speculated that the sleep hormone melatonin also plays a role.

“Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses,” Dr. Phillips said. “So if you’re chronically getting light exposure at night, that’s reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes.”

Previous studies have explored melatonin supplementation to help manage diabetes. “However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far,” Dr. Miedlich said.
 

Takeaways

Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.

That said, “there’s no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes,” said Dr. Phillips.

Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and GLP-1 agonists.

“Probably a GLP-1 agonist is going to be more effective,” Dr. Peterson said. “But this is still a fairly large effect without having to go through the expense of buying a GLP-1 or losing a lot of weight or making a big lifestyle change.”

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

Concerned about your patient’s type 2 diabetes risk? Along with the usual preventive strategies — like diet and exercise and, when appropriate, glucagon-like peptide 1 (GLP-1) agonists — there’s another simple, no-risk strategy that just might help: Turning off the light at night.

A study in The Lancet found that people who were exposed to the most light between 12:30 a.m. and 6 a.m. were 1.5 times more likely to develop diabetes than those who remained in darkness during that time frame.

The study builds on growing evidence linking nighttime light exposure to type 2 diabetes risk. But unlike previous large studies that relied on satellite data of outdoor light levels (an indirect measure of light exposure), the recent study looked at personal light exposure — that is, light measured directly on individuals — as recorded by a wrist-worn sensor.

“Those previous studies likely underestimated the effect,” said study author Andrew Phillips, PhD, professor of sleep health at Flinders University in Adelaide, Australia, “since they did not capture indoor light environments.”

Using data from 85,000 participants from the UK Biobank, the recent study is the largest to date linking diabetes risk to personal light exposure at night.

“This is really a phenomenal study,” said Courtney Peterson, PhD, a scientist at the University of Alabama at Birmingham’s Diabetes Research Center, who was not involved in the study. “This is the first large-scale study we have looking at people’s light exposure patterns and linking it to their long-term health.”
 

What the Study Showed

The participants wore the light sensors for a week, recording day and night light from all sources — whether from sunlight, lamps, streetlights, or digital screens. The researchers then tracked participants for 8 years.

“About half of the people that we looked at had very dim levels of light at night, so less than 1 lux — that basically means less than candlelight,” said Dr. Phillips. “They were the people who were protected against type 2 diabetes.”

Those exposed to more light at night — defined in the study as 12:30 a.m.–6 a.m. — had a higher risk for type 2 diabetes. The risk went up as a dose response, Phillips said: The brighter the light exposure, the higher the diabetes risk.

Participants in the top 10% of light exposure — who were exposed to about 48 lux , or the equivalent of relatively dim overhead lighting — were 1.5 times more likely to develop diabetes than those in the dark. That’s about the risk increase you’d get from having a family history of type 2 diabetes, the researchers said.

Even when they controlled for factors like socioeconomic status, smoking, diet, exercise, and shift work, “we still found there was this very strong relationship between light exposure and risk of type 2 diabetes,” said Dr. Phillips.
 

How Light at Night May Increase Diabetes Risk

The results are not entirely surprising, said endocrinologist Susanne Miedlich, MD, a professor at the University of Rochester Medical Center, Rochester, New York, who was not involved in the study.

Light at night can disrupt the circadian rhythm, or your body’s internal 24-hour cycle. And scientists have long known that circadian rhythm is important for all kinds of biologic processes, including how the body manages blood sugar.

One’s internal clock regulates food intake, sugar absorption, and the release of insulin. Dysregulation in the circadian rhythm is associated with insulin resistance, a precursor to type 2 diabetes.

Dr. Phillips speculated that the sleep hormone melatonin also plays a role.

“Melatonin does a lot of things, but one of the things that it does is it manages our glucose and our insulin responses,” Dr. Phillips said. “So if you’re chronically getting light exposure at night, that’s reducing a level of melatonin that, in the long term, could lead to poor metabolic outcomes.”

Previous studies have explored melatonin supplementation to help manage diabetes. “However, while melatonin clearly regulates circadian rhythms, its utility as a drug to prevent diabetes has not really panned out thus far,” Dr. Miedlich said.
 

Takeaways

Interventional studies are needed to confirm whether strategies like powering down screens, turning off lights, or using blackout curtains could reduce diabetes risk.

That said, “there’s no reason not to tell people to get healthy light exposure patterns and sleep, especially in the context of diabetes,” said Dr. Phillips.

Other known strategies for reducing diabetes risk include intensive lifestyle programs, which reduce risk by up to 58%, and GLP-1 agonists.

“Probably a GLP-1 agonist is going to be more effective,” Dr. Peterson said. “But this is still a fairly large effect without having to go through the expense of buying a GLP-1 or losing a lot of weight or making a big lifestyle change.”

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

ORLANDO, FLORIDA — Cannabis users may have a “healthier inflammatory cytokine profile, better insulin sensitivity, and higher levels of physical activity than nonusers,” all of which can be linked to a potentially lower risk for diabetes, ongoing research suggests.

In the findings from the SONIC trial, Angela Bryan, PhD, professor and codirector of CUChange at the University of Colorado, Boulder, and colleagues hypothesized that “those inflammatory profiles would improve over the course of 4 weeks, particularly for those using a CBD [cannabidiol] as opposed to a THC [tetrahydrocannabinol] product.”

She presented the findings at the American Diabetes Association (ADA) 84th Scientific Sessions.

Other recent work by Dr. Bryan and her colleagues focused on the public health implications of cannabis legalization. One study examined the acute effects of legal-market cannabis on regular users’ subjective responses while running and found that cannabis use prior to exercise may lead to more enjoyment and runner’s high symptoms, although it also led to feelings of greater exertion. The positive effects could make exercise more appealing to individuals — including those with or at risk for diabetes — who might not otherwise engage in it, Bryan suggested.

Another study found that CBD-dominant forms of cannabis were associated with acute tension reduction, which might lead to longer-term reductions in anxiety. Bryan said the findings could be relevant in the context of diabetes distress.
 

‘Complicated’ Connection to Diabetes

In the SONIC study, participants who were regular cannabis users had an average age of 30 years and had body mass index (BMI) in the healthy range; 86% were White individuals, and 59% were men. They were matched with a similar group of individuals who had not used cannabis for at least a year. At baseline, participants’ NSDR Healthy Eating Index score overall was 51.24, showing a “need for improvement/poor diet.” 

“Folks were maybe not killing it in the dietary domain,” Dr. Bryan acknowledged. “However, they were absolutely killing it in the physical activity domain.”

The researchers did oral glucose tolerance tests to calculate participants’ Matsuda index of insulin sensitivity and measured inflammatory markers, including tumor necrosis factor alpha, interleukin 6 (IL6), IL1 beta, IL12, interferon gamma, IL4, and monocyte chemoattractant protein 1 (MCP-1). In a “randomized encouragement” design, users were assigned to purchase and use a flower product for 4 weeks, however much they wanted. They completed daily assessments of their cannabis use, alcohol use, diet, and physical activity.

Between-group eating patterns were similar over the 4 weeks, with cannabis users reporting “marginally” more servings of salty snacks and food relative to nonusers. None of the daily associations were moderated by which cannabis product was used.

At 4 weeks, the team repeated the tests and, surprisingly, found no change in participants’ inflammatory markers. But what “popped out,” she said, was the “stark difference” between users and nonusers, with users having significantly lower levels of inflammatory biomarkers, circulating cytokines than the nonusers.

An exception were levels of MCP-1, which increased over time in the users but didn’t change in nonusers. Bryan said the finding is “perplexing” and asked the audience for thoughts, especially given that MCP-1 levels are positively associated with diabetes.

After controlling for BMI and inflammation, “we saw absolutely no effects of group or group by time interaction on the Matsuda index of insulin sensitivity,” she said. “Seemingly, there are no chronic effects of cannabis use on insulin sensitivity.”

Regarding limitations, Dr. Bryan acknowledged that the study is being conducted with “a very healthy sample of individuals who exercise a lot, and that might be factoring into our results, especially on insulin sensitivity.” The team could not use “gold standard” randomization because of the schedule-1 status of CannaVan cannabis, and the MCP-1 findings are difficult to interpret.

Furthermore, she noted, “our day-to-day level data show only slight differences in behavior between those who use cannabis and those who don’t and also very slight differences between users’ behavior on days that they use vs days that they don’t.

“I think all of this put together shows us that the relationship between cannabis use and potential implications for diabetes is a lot more complicated than just couch to couchlock [very deep relaxation/sedation] or runner’s high,” she said.
 

Bring On the CannaVan

The team’s next step, currently underway, is to get an acute response to cannabis with an oral glucose tolerance test that’s done immediately after the participant uses a product. Since cannabis is a schedule-1 drug, it can’t be taken into the laboratory. Therefore, the researchers are using a CannaVan — a mobile lab. “We drive it to their homes, they come out, we draw blood, and we send them back into their homes to use as much of their product as they want,” Bryan explained. “They come back out to the van. They do all the follow-up assessments. We take blood again to verify their exposure. And that’s how we collect those data.”

“Invite me back next year, and I will tell you what we found,” she quipped.

Dr. Bryan had no disclosures to report. 

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

ORLANDO, FLORIDA — Cannabis users may have a “healthier inflammatory cytokine profile, better insulin sensitivity, and higher levels of physical activity than nonusers,” all of which can be linked to a potentially lower risk for diabetes, ongoing research suggests.

In the findings from the SONIC trial, Angela Bryan, PhD, professor and codirector of CUChange at the University of Colorado, Boulder, and colleagues hypothesized that “those inflammatory profiles would improve over the course of 4 weeks, particularly for those using a CBD [cannabidiol] as opposed to a THC [tetrahydrocannabinol] product.”

She presented the findings at the American Diabetes Association (ADA) 84th Scientific Sessions.

Other recent work by Dr. Bryan and her colleagues focused on the public health implications of cannabis legalization. One study examined the acute effects of legal-market cannabis on regular users’ subjective responses while running and found that cannabis use prior to exercise may lead to more enjoyment and runner’s high symptoms, although it also led to feelings of greater exertion. The positive effects could make exercise more appealing to individuals — including those with or at risk for diabetes — who might not otherwise engage in it, Bryan suggested.

Another study found that CBD-dominant forms of cannabis were associated with acute tension reduction, which might lead to longer-term reductions in anxiety. Bryan said the findings could be relevant in the context of diabetes distress.
 

‘Complicated’ Connection to Diabetes

In the SONIC study, participants who were regular cannabis users had an average age of 30 years and had body mass index (BMI) in the healthy range; 86% were White individuals, and 59% were men. They were matched with a similar group of individuals who had not used cannabis for at least a year. At baseline, participants’ NSDR Healthy Eating Index score overall was 51.24, showing a “need for improvement/poor diet.” 

“Folks were maybe not killing it in the dietary domain,” Dr. Bryan acknowledged. “However, they were absolutely killing it in the physical activity domain.”

The researchers did oral glucose tolerance tests to calculate participants’ Matsuda index of insulin sensitivity and measured inflammatory markers, including tumor necrosis factor alpha, interleukin 6 (IL6), IL1 beta, IL12, interferon gamma, IL4, and monocyte chemoattractant protein 1 (MCP-1). In a “randomized encouragement” design, users were assigned to purchase and use a flower product for 4 weeks, however much they wanted. They completed daily assessments of their cannabis use, alcohol use, diet, and physical activity.

Between-group eating patterns were similar over the 4 weeks, with cannabis users reporting “marginally” more servings of salty snacks and food relative to nonusers. None of the daily associations were moderated by which cannabis product was used.

At 4 weeks, the team repeated the tests and, surprisingly, found no change in participants’ inflammatory markers. But what “popped out,” she said, was the “stark difference” between users and nonusers, with users having significantly lower levels of inflammatory biomarkers, circulating cytokines than the nonusers.

An exception were levels of MCP-1, which increased over time in the users but didn’t change in nonusers. Bryan said the finding is “perplexing” and asked the audience for thoughts, especially given that MCP-1 levels are positively associated with diabetes.

After controlling for BMI and inflammation, “we saw absolutely no effects of group or group by time interaction on the Matsuda index of insulin sensitivity,” she said. “Seemingly, there are no chronic effects of cannabis use on insulin sensitivity.”

Regarding limitations, Dr. Bryan acknowledged that the study is being conducted with “a very healthy sample of individuals who exercise a lot, and that might be factoring into our results, especially on insulin sensitivity.” The team could not use “gold standard” randomization because of the schedule-1 status of CannaVan cannabis, and the MCP-1 findings are difficult to interpret.

Furthermore, she noted, “our day-to-day level data show only slight differences in behavior between those who use cannabis and those who don’t and also very slight differences between users’ behavior on days that they use vs days that they don’t.

“I think all of this put together shows us that the relationship between cannabis use and potential implications for diabetes is a lot more complicated than just couch to couchlock [very deep relaxation/sedation] or runner’s high,” she said.
 

Bring On the CannaVan

The team’s next step, currently underway, is to get an acute response to cannabis with an oral glucose tolerance test that’s done immediately after the participant uses a product. Since cannabis is a schedule-1 drug, it can’t be taken into the laboratory. Therefore, the researchers are using a CannaVan — a mobile lab. “We drive it to their homes, they come out, we draw blood, and we send them back into their homes to use as much of their product as they want,” Bryan explained. “They come back out to the van. They do all the follow-up assessments. We take blood again to verify their exposure. And that’s how we collect those data.”

“Invite me back next year, and I will tell you what we found,” she quipped.

Dr. Bryan had no disclosures to report. 

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

ORLANDO, FLORIDA — Cannabis users may have a “healthier inflammatory cytokine profile, better insulin sensitivity, and higher levels of physical activity than nonusers,” all of which can be linked to a potentially lower risk for diabetes, ongoing research suggests.

In the findings from the SONIC trial, Angela Bryan, PhD, professor and codirector of CUChange at the University of Colorado, Boulder, and colleagues hypothesized that “those inflammatory profiles would improve over the course of 4 weeks, particularly for those using a CBD [cannabidiol] as opposed to a THC [tetrahydrocannabinol] product.”

She presented the findings at the American Diabetes Association (ADA) 84th Scientific Sessions.

Other recent work by Dr. Bryan and her colleagues focused on the public health implications of cannabis legalization. One study examined the acute effects of legal-market cannabis on regular users’ subjective responses while running and found that cannabis use prior to exercise may lead to more enjoyment and runner’s high symptoms, although it also led to feelings of greater exertion. The positive effects could make exercise more appealing to individuals — including those with or at risk for diabetes — who might not otherwise engage in it, Bryan suggested.

Another study found that CBD-dominant forms of cannabis were associated with acute tension reduction, which might lead to longer-term reductions in anxiety. Bryan said the findings could be relevant in the context of diabetes distress.
 

‘Complicated’ Connection to Diabetes

In the SONIC study, participants who were regular cannabis users had an average age of 30 years and had body mass index (BMI) in the healthy range; 86% were White individuals, and 59% were men. They were matched with a similar group of individuals who had not used cannabis for at least a year. At baseline, participants’ NSDR Healthy Eating Index score overall was 51.24, showing a “need for improvement/poor diet.” 

“Folks were maybe not killing it in the dietary domain,” Dr. Bryan acknowledged. “However, they were absolutely killing it in the physical activity domain.”

The researchers did oral glucose tolerance tests to calculate participants’ Matsuda index of insulin sensitivity and measured inflammatory markers, including tumor necrosis factor alpha, interleukin 6 (IL6), IL1 beta, IL12, interferon gamma, IL4, and monocyte chemoattractant protein 1 (MCP-1). In a “randomized encouragement” design, users were assigned to purchase and use a flower product for 4 weeks, however much they wanted. They completed daily assessments of their cannabis use, alcohol use, diet, and physical activity.

Between-group eating patterns were similar over the 4 weeks, with cannabis users reporting “marginally” more servings of salty snacks and food relative to nonusers. None of the daily associations were moderated by which cannabis product was used.

At 4 weeks, the team repeated the tests and, surprisingly, found no change in participants’ inflammatory markers. But what “popped out,” she said, was the “stark difference” between users and nonusers, with users having significantly lower levels of inflammatory biomarkers, circulating cytokines than the nonusers.

An exception were levels of MCP-1, which increased over time in the users but didn’t change in nonusers. Bryan said the finding is “perplexing” and asked the audience for thoughts, especially given that MCP-1 levels are positively associated with diabetes.

After controlling for BMI and inflammation, “we saw absolutely no effects of group or group by time interaction on the Matsuda index of insulin sensitivity,” she said. “Seemingly, there are no chronic effects of cannabis use on insulin sensitivity.”

Regarding limitations, Dr. Bryan acknowledged that the study is being conducted with “a very healthy sample of individuals who exercise a lot, and that might be factoring into our results, especially on insulin sensitivity.” The team could not use “gold standard” randomization because of the schedule-1 status of CannaVan cannabis, and the MCP-1 findings are difficult to interpret.

Furthermore, she noted, “our day-to-day level data show only slight differences in behavior between those who use cannabis and those who don’t and also very slight differences between users’ behavior on days that they use vs days that they don’t.

“I think all of this put together shows us that the relationship between cannabis use and potential implications for diabetes is a lot more complicated than just couch to couchlock [very deep relaxation/sedation] or runner’s high,” she said.
 

Bring On the CannaVan

The team’s next step, currently underway, is to get an acute response to cannabis with an oral glucose tolerance test that’s done immediately after the participant uses a product. Since cannabis is a schedule-1 drug, it can’t be taken into the laboratory. Therefore, the researchers are using a CannaVan — a mobile lab. “We drive it to their homes, they come out, we draw blood, and we send them back into their homes to use as much of their product as they want,” Bryan explained. “They come back out to the van. They do all the follow-up assessments. We take blood again to verify their exposure. And that’s how we collect those data.”

“Invite me back next year, and I will tell you what we found,” she quipped.

Dr. Bryan had no disclosures to report. 

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

ORLANDO, FLORIDA — An analysis of data from 137 patients suggested testing whether people have a trait known as abnormal postprandial satiety (APS), or hungry gut, can predict how well they may respond to the obesity drug semaglutide, although it failed to establish this link for the somewhat similar tirzepatide.

At the American Diabetes Association (ADA) Scientific Sessions, Maria Daniela Hurtado Andrade, MD, PhD, of the Mayo Clinic, Jacksonville, Florida, presented results of a study using the MyPhenome Hungry Gut test, which was developed through machine learning, a form of artificial intelligence. 

The test is part of the MyPhenome obesity phenotyping portfolio from Phenomix Sciences, a company founded by Mayo Clinic physicians, scientists, and researchers Andres Acosta, MD, PhD, and Michael Camilleri, MD, DSc. 

At the ADA meeting, Dr. Hurtado Andrade discussed a test of 137 adults: 91 were considered to have a positive biomarker for abnormal postprandial satiety (APS+), and 46 who did not have it were classified as APS−. These were patients of the Mayo Clinic who were already taking obesity drugs and agreed to phenotyping. Of this group, 113 were on semaglutide and 24 on tirzepatide.

At 12 months, among those taking semaglutide, patients classified as APS+ achieved a mean 18% body weight loss compared with 10% in those classified as APS−. But the test didn’t find these kinds of differences for the tirzepatide group, with a mean 19.4% body weight loss in the APS+ group and a mean loss of 22.1% in the APS− group.

Further studies are warranted to assess the clinical utility of these biomarkers, Dr. Hurtado Andrade said. But these findings do support “the use of precision medicine for obesity based on an individual’s genetic background,” she said.

Dr. Hurtado Andrade’s presentation impressed fellow researchers who noted it as an early step toward the long-sought goal of more personalized medicine.

Daniel S. Hsia, MD, of Emory University, Atlanta, who led the ADA session at which Dr. Hurtado Andrade presented, said it was good to see new information being presented about using genetic risk scoring in obesity.

“The numbers were very small for the tirzepatide group as compared to the semaglutide group, so it’s a little hard to really come to any significant conclusions,” Dr. Hsia said in an interview.

At the ADA meeting, Ajay D. Rao, MD, MMSc, of Temple University, Philadelphia, said clinicians are excited about the idea of having biomarkers to aid in decisions about approaches to obesity.

In a follow-up interview with this news organization, Dr. Rao said he too is looking to see more testing of this approach to care, while describing Hurtado Andrade’s work as a “very well-done study.”

“We still need to see more large-scale studies of responsiveness to certain interventions,” he said. 

Dr. Hurtado Andrade noted that researchers at academic centers such as Mayo can try to hone in the combination of genetic and other factors that led to obesity, such as emotional eating patterns and abnormal postprandial satiety. 

But this approach is not widely scalable, as it demands resources of time and staffing that not all clinicians and patients enjoy.

“To overcome this challenge, our team has been working on developing biomarkers” such as the machine-learning gene risk score used to predict abnormal postprandial satiety, she said.

Findings for a related project were presented in May at Digestive Disease Week, as this news organization reported earlier. In that study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the glucagon-like peptide 1 receptor agonist semaglutide.

This news organization separately asked Phenomix about the sales of MyPhenome Test kits. These cost $499, and about 500 tests have been sold since commercialization started last year, a spokesperson said.

The study was funded by Phenomix Sciences. Separately, Dr. Hurtado Andrade has worked as a consultant for Novo Nordisk and received research support from the National Institutes of Health. 

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

ORLANDO, FLORIDA — An analysis of data from 137 patients suggested testing whether people have a trait known as abnormal postprandial satiety (APS), or hungry gut, can predict how well they may respond to the obesity drug semaglutide, although it failed to establish this link for the somewhat similar tirzepatide.

At the American Diabetes Association (ADA) Scientific Sessions, Maria Daniela Hurtado Andrade, MD, PhD, of the Mayo Clinic, Jacksonville, Florida, presented results of a study using the MyPhenome Hungry Gut test, which was developed through machine learning, a form of artificial intelligence. 

The test is part of the MyPhenome obesity phenotyping portfolio from Phenomix Sciences, a company founded by Mayo Clinic physicians, scientists, and researchers Andres Acosta, MD, PhD, and Michael Camilleri, MD, DSc. 

At the ADA meeting, Dr. Hurtado Andrade discussed a test of 137 adults: 91 were considered to have a positive biomarker for abnormal postprandial satiety (APS+), and 46 who did not have it were classified as APS−. These were patients of the Mayo Clinic who were already taking obesity drugs and agreed to phenotyping. Of this group, 113 were on semaglutide and 24 on tirzepatide.

At 12 months, among those taking semaglutide, patients classified as APS+ achieved a mean 18% body weight loss compared with 10% in those classified as APS−. But the test didn’t find these kinds of differences for the tirzepatide group, with a mean 19.4% body weight loss in the APS+ group and a mean loss of 22.1% in the APS− group.

Further studies are warranted to assess the clinical utility of these biomarkers, Dr. Hurtado Andrade said. But these findings do support “the use of precision medicine for obesity based on an individual’s genetic background,” she said.

Dr. Hurtado Andrade’s presentation impressed fellow researchers who noted it as an early step toward the long-sought goal of more personalized medicine.

Daniel S. Hsia, MD, of Emory University, Atlanta, who led the ADA session at which Dr. Hurtado Andrade presented, said it was good to see new information being presented about using genetic risk scoring in obesity.

“The numbers were very small for the tirzepatide group as compared to the semaglutide group, so it’s a little hard to really come to any significant conclusions,” Dr. Hsia said in an interview.

At the ADA meeting, Ajay D. Rao, MD, MMSc, of Temple University, Philadelphia, said clinicians are excited about the idea of having biomarkers to aid in decisions about approaches to obesity.

In a follow-up interview with this news organization, Dr. Rao said he too is looking to see more testing of this approach to care, while describing Hurtado Andrade’s work as a “very well-done study.”

“We still need to see more large-scale studies of responsiveness to certain interventions,” he said. 

Dr. Hurtado Andrade noted that researchers at academic centers such as Mayo can try to hone in the combination of genetic and other factors that led to obesity, such as emotional eating patterns and abnormal postprandial satiety. 

But this approach is not widely scalable, as it demands resources of time and staffing that not all clinicians and patients enjoy.

“To overcome this challenge, our team has been working on developing biomarkers” such as the machine-learning gene risk score used to predict abnormal postprandial satiety, she said.

Findings for a related project were presented in May at Digestive Disease Week, as this news organization reported earlier. In that study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the glucagon-like peptide 1 receptor agonist semaglutide.

This news organization separately asked Phenomix about the sales of MyPhenome Test kits. These cost $499, and about 500 tests have been sold since commercialization started last year, a spokesperson said.

The study was funded by Phenomix Sciences. Separately, Dr. Hurtado Andrade has worked as a consultant for Novo Nordisk and received research support from the National Institutes of Health. 

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

ORLANDO, FLORIDA — An analysis of data from 137 patients suggested testing whether people have a trait known as abnormal postprandial satiety (APS), or hungry gut, can predict how well they may respond to the obesity drug semaglutide, although it failed to establish this link for the somewhat similar tirzepatide.

At the American Diabetes Association (ADA) Scientific Sessions, Maria Daniela Hurtado Andrade, MD, PhD, of the Mayo Clinic, Jacksonville, Florida, presented results of a study using the MyPhenome Hungry Gut test, which was developed through machine learning, a form of artificial intelligence. 

The test is part of the MyPhenome obesity phenotyping portfolio from Phenomix Sciences, a company founded by Mayo Clinic physicians, scientists, and researchers Andres Acosta, MD, PhD, and Michael Camilleri, MD, DSc. 

At the ADA meeting, Dr. Hurtado Andrade discussed a test of 137 adults: 91 were considered to have a positive biomarker for abnormal postprandial satiety (APS+), and 46 who did not have it were classified as APS−. These were patients of the Mayo Clinic who were already taking obesity drugs and agreed to phenotyping. Of this group, 113 were on semaglutide and 24 on tirzepatide.

At 12 months, among those taking semaglutide, patients classified as APS+ achieved a mean 18% body weight loss compared with 10% in those classified as APS−. But the test didn’t find these kinds of differences for the tirzepatide group, with a mean 19.4% body weight loss in the APS+ group and a mean loss of 22.1% in the APS− group.

Further studies are warranted to assess the clinical utility of these biomarkers, Dr. Hurtado Andrade said. But these findings do support “the use of precision medicine for obesity based on an individual’s genetic background,” she said.

Dr. Hurtado Andrade’s presentation impressed fellow researchers who noted it as an early step toward the long-sought goal of more personalized medicine.

Daniel S. Hsia, MD, of Emory University, Atlanta, who led the ADA session at which Dr. Hurtado Andrade presented, said it was good to see new information being presented about using genetic risk scoring in obesity.

“The numbers were very small for the tirzepatide group as compared to the semaglutide group, so it’s a little hard to really come to any significant conclusions,” Dr. Hsia said in an interview.

At the ADA meeting, Ajay D. Rao, MD, MMSc, of Temple University, Philadelphia, said clinicians are excited about the idea of having biomarkers to aid in decisions about approaches to obesity.

In a follow-up interview with this news organization, Dr. Rao said he too is looking to see more testing of this approach to care, while describing Hurtado Andrade’s work as a “very well-done study.”

“We still need to see more large-scale studies of responsiveness to certain interventions,” he said. 

Dr. Hurtado Andrade noted that researchers at academic centers such as Mayo can try to hone in the combination of genetic and other factors that led to obesity, such as emotional eating patterns and abnormal postprandial satiety. 

But this approach is not widely scalable, as it demands resources of time and staffing that not all clinicians and patients enjoy.

“To overcome this challenge, our team has been working on developing biomarkers” such as the machine-learning gene risk score used to predict abnormal postprandial satiety, she said.

Findings for a related project were presented in May at Digestive Disease Week, as this news organization reported earlier. In that study, researchers calculated the genetic risk score for 84 adults undergoing weight loss interventions at Mayo Clinic who were prescribed the glucagon-like peptide 1 receptor agonist semaglutide.

This news organization separately asked Phenomix about the sales of MyPhenome Test kits. These cost $499, and about 500 tests have been sold since commercialization started last year, a spokesperson said.

The study was funded by Phenomix Sciences. Separately, Dr. Hurtado Andrade has worked as a consultant for Novo Nordisk and received research support from the National Institutes of Health. 

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

TOPLINE:

A triple combination therapy (TCT) of metformin, dapagliflozin, and saxagliptin is an effective and safe treatment option for drug-naive patients with type 2 diabetes (T2D) compared with stepwise add-on therapy.

METHODOLOGY:

• Current guidelines recommend early combination therapy to extend the time to treatment failure, reduce the risk for diabetic complications, and prevent clinical inertia in patients with T2D.
• This randomized controlled open-label trial conducted at nine sites in South Korea included 105 drug-naive patients with T2D (mean age, 49.5 years; 32.4% women) who either received triple therapy (metformin, dapagliflozin, and saxagliptin) or stepwise add-on therapy (initiated with metformin, followed by glimepiride and sitagliptin for those with baseline hemoglobin A1c levels < 9.0% or with initial dual metformin and glimepiride in those with A1c levels ≥ 9.0% followed by sitagliptin).
• The primary outcome was the proportion of patients who achieved A1c levels < 6.5% without hypoglycemia, weight gain ≥ 5%, or discontinuation of drugs because of adverse events at week 104.
• The secondary outcomes were the proportion of patients whose A1c levels dropped to < 7.0% at weeks 56 and 104 and dropped to < 6.5% at week 56, all without hypoglycemia, weight gain, nor discontinuation due to adverse events.

TAKEAWAY:

• At week 104, a higher proportion of patients in the triple therapy group achieved the primary outcome than those in the stepwise add-on therapy group (39.0% vs 17.1%; P = .027).
• In both groups, a similar proportion of patients (46.3%) achieved A1c levels < 6.5% at week 104, but the proportion of patients without hypoglycemia, weight gain, or discontinuation because of adverse events was higher in the triple therapy group than those in the stepwise add-on therapy group (83.3% vs 38.0%; P < .001).

IN PRACTICE:

The authors wrote: “Although the glycemic efficacy of each drug in the TCT was modest, the combination of these drugs resulted in a 2-year durable glycemic efficacy, with greater than a 2.5% reduction in A1c levels from baseline. The overall results of this study suggest a novel strategy for initial combination therapy in newly diagnosed T2D patients.”

SOURCE:

The study was led by Nam Hoon Kim, MD, of the Department of Internal Medicine, Korea University College of Medicine, Seoul. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study had a relatively small sample size as compared with previous clinical trials. More people in the standard therapy group had A1c levels ≥ 9.0%, which resulted in more than double the number of people receiving dual combination therapy over monotherapy in that group. The trial duration was insufficient to evaluate the cardiovascular outcomes.

DISCLOSURES:

The study was funded by AstraZeneca. Some authors reported financial ties with AstraZeneca and other pharmaceutical and medical device companies as members of advisory boards or recipients of grants, consulting fees, honoraria, or lecture fees.

A version of this article appeared on Medscape.com.

TOPLINE:

A triple combination therapy (TCT) of metformin, dapagliflozin, and saxagliptin is an effective and safe treatment option for drug-naive patients with type 2 diabetes (T2D) compared with stepwise add-on therapy.

METHODOLOGY:

• Current guidelines recommend early combination therapy to extend the time to treatment failure, reduce the risk for diabetic complications, and prevent clinical inertia in patients with T2D.
• This randomized controlled open-label trial conducted at nine sites in South Korea included 105 drug-naive patients with T2D (mean age, 49.5 years; 32.4% women) who either received triple therapy (metformin, dapagliflozin, and saxagliptin) or stepwise add-on therapy (initiated with metformin, followed by glimepiride and sitagliptin for those with baseline hemoglobin A1c levels < 9.0% or with initial dual metformin and glimepiride in those with A1c levels ≥ 9.0% followed by sitagliptin).
• The primary outcome was the proportion of patients who achieved A1c levels < 6.5% without hypoglycemia, weight gain ≥ 5%, or discontinuation of drugs because of adverse events at week 104.
• The secondary outcomes were the proportion of patients whose A1c levels dropped to < 7.0% at weeks 56 and 104 and dropped to < 6.5% at week 56, all without hypoglycemia, weight gain, nor discontinuation due to adverse events.

TAKEAWAY:

• At week 104, a higher proportion of patients in the triple therapy group achieved the primary outcome than those in the stepwise add-on therapy group (39.0% vs 17.1%; P = .027).
• In both groups, a similar proportion of patients (46.3%) achieved A1c levels < 6.5% at week 104, but the proportion of patients without hypoglycemia, weight gain, or discontinuation because of adverse events was higher in the triple therapy group than those in the stepwise add-on therapy group (83.3% vs 38.0%; P < .001).

IN PRACTICE:

The authors wrote: “Although the glycemic efficacy of each drug in the TCT was modest, the combination of these drugs resulted in a 2-year durable glycemic efficacy, with greater than a 2.5% reduction in A1c levels from baseline. The overall results of this study suggest a novel strategy for initial combination therapy in newly diagnosed T2D patients.”

SOURCE:

The study was led by Nam Hoon Kim, MD, of the Department of Internal Medicine, Korea University College of Medicine, Seoul. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study had a relatively small sample size as compared with previous clinical trials. More people in the standard therapy group had A1c levels ≥ 9.0%, which resulted in more than double the number of people receiving dual combination therapy over monotherapy in that group. The trial duration was insufficient to evaluate the cardiovascular outcomes.

DISCLOSURES:

The study was funded by AstraZeneca. Some authors reported financial ties with AstraZeneca and other pharmaceutical and medical device companies as members of advisory boards or recipients of grants, consulting fees, honoraria, or lecture fees.

A version of this article appeared on Medscape.com.

TOPLINE:

A triple combination therapy (TCT) of metformin, dapagliflozin, and saxagliptin is an effective and safe treatment option for drug-naive patients with type 2 diabetes (T2D) compared with stepwise add-on therapy.

METHODOLOGY:

• Current guidelines recommend early combination therapy to extend the time to treatment failure, reduce the risk for diabetic complications, and prevent clinical inertia in patients with T2D.
• This randomized controlled open-label trial conducted at nine sites in South Korea included 105 drug-naive patients with T2D (mean age, 49.5 years; 32.4% women) who either received triple therapy (metformin, dapagliflozin, and saxagliptin) or stepwise add-on therapy (initiated with metformin, followed by glimepiride and sitagliptin for those with baseline hemoglobin A1c levels < 9.0% or with initial dual metformin and glimepiride in those with A1c levels ≥ 9.0% followed by sitagliptin).
• The primary outcome was the proportion of patients who achieved A1c levels < 6.5% without hypoglycemia, weight gain ≥ 5%, or discontinuation of drugs because of adverse events at week 104.
• The secondary outcomes were the proportion of patients whose A1c levels dropped to < 7.0% at weeks 56 and 104 and dropped to < 6.5% at week 56, all without hypoglycemia, weight gain, nor discontinuation due to adverse events.

TAKEAWAY:

• At week 104, a higher proportion of patients in the triple therapy group achieved the primary outcome than those in the stepwise add-on therapy group (39.0% vs 17.1%; P = .027).
• In both groups, a similar proportion of patients (46.3%) achieved A1c levels < 6.5% at week 104, but the proportion of patients without hypoglycemia, weight gain, or discontinuation because of adverse events was higher in the triple therapy group than those in the stepwise add-on therapy group (83.3% vs 38.0%; P < .001).

IN PRACTICE:

The authors wrote: “Although the glycemic efficacy of each drug in the TCT was modest, the combination of these drugs resulted in a 2-year durable glycemic efficacy, with greater than a 2.5% reduction in A1c levels from baseline. The overall results of this study suggest a novel strategy for initial combination therapy in newly diagnosed T2D patients.”

SOURCE:

The study was led by Nam Hoon Kim, MD, of the Department of Internal Medicine, Korea University College of Medicine, Seoul. It was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study had a relatively small sample size as compared with previous clinical trials. More people in the standard therapy group had A1c levels ≥ 9.0%, which resulted in more than double the number of people receiving dual combination therapy over monotherapy in that group. The trial duration was insufficient to evaluate the cardiovascular outcomes.

DISCLOSURES:

The study was funded by AstraZeneca. Some authors reported financial ties with AstraZeneca and other pharmaceutical and medical device companies as members of advisory boards or recipients of grants, consulting fees, honoraria, or lecture fees.

A version of this article appeared on Medscape.com.

It seems intuitive that, because people with type 2 diabetes (T2D) generally need to avoid sugar, clinicians should recommend eating foods and using recipes containing artificial sweeteners such as sucralose instead.

Splenda, which produces sucralose and other non-sugar sweeteners (NSS), is a sponsor of the American Diabetes Association (ADA) Diabetes Food Hub. Earlier in 2024, the ADA settled a lawsuit regarding its former director of nutrition’s refusal to approve recipes containing sucralose (Splenda), which she believed “flew in the face of the ADA’s mission.” 

Experts agree that, while artificial sweeteners may help in certain scenarios, they can also be harmful.

“There’s not a lot of evidence that sweeteners like sucralose provide significant benefits, especially over the long term,” said Susan Swithers, PhD, professor, department of psychological sciences and associate dean for faculty affairs at Purdue University, West Lafayette, Indiana.

Dr. Swithers authored an article several years ago cautioning that consuming nonnutritive sweeteners in beverages not only fails to prevent disease but also is associated with an increase in risks for the same health outcomes associated with sugar-sweetened beverages, including T2D, cardiovascular disease, hypertension, and stroke.

“At this point, we have pretty good evidence that these chemicals that were once touted as being completely inert are, in fact, not inert,” she said. “We know that they’re unlikely to be toxic in the short term, but they are not benign, and they have consequences. Right now, we have little understanding of the outcomes of consumption of these products chronically.”
 

What the Science Says

In 2023, the World Health Organization (WHO) released a guideline on NSS that recommended against their use for weight control or to reduce the risk for noncommunicable diseases.

The systematic review and meta-analysis upon which the guideline is based found that high intakes of NSS were associated with increases in body mass index and, as Dr. Swithers found, risks of developing T2D, cardiovascular events, and any type of stroke, as well as hypertension, bladder cancer, and all-cause mortality.

In a press release announcing the guideline, Francesco Branca, WHO director for Nutrition and Food Safety, said, “NSS are not essential dietary factors and have no nutritional value. People should reduce the sweetness of the diet altogether, starting early in life, to improve their health.” 

The “common” NSS named by WHO included sucralose, as well as acesulfame K, aspartame, advantame, cyclamates, neotame, saccharin, stevia, and stevia derivatives.

If NSS consumption can increase T2D risk, what about people who already have T2D? 

Some research suggests that NSS may affect people with and without T2D differently, said Dr. Swithers. For example, one small study showed that sucralose enhanced glucagon-like peptide 1 release and lowered blood glucose in healthy patients but not in patients with newly diagnosed T2D.

Similarly, Jotham Suez, PhD, an assistant professor in the department of molecular microbiology and immunology at Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, said in an interview that his group “showed for the first time in 2014 that disruption of the microbiome by artificial sweeteners is causally linked to disrupted glycemic control.” 

Recently, the team studied the impact of sucralose, aspartame, saccharin, and stevia in healthy adults and “were surprised to discover that all four sweeteners altered gut bacteria and the molecules they secrete,” he said. However, subsequent glucose tolerance tests in healthy humans showed varying results, “suggesting that human microbiome responses to the nonnutritive sweeteners we assessed are highly personalized and may lead to glycemic alterations in some, but not all, consumers depending on their microbes and the sweeteners they consume.” 

Nevertheless, a recent review led by researchers in Mexico concluded that sucralose consumption “is associated with various adverse health effects. Despite being considered safe following previous studies, recent research suggests possible links to systemic inflammation, metabolic diseases, disruptions in gut microbiota, liver damage, and toxic effects at the cellular level.” 

In addition, they wrote, “it is crucial to highlight the persistence of sucralose in the body, its ability to cross the placenta, and its presence in breast milk, raising concerns about prenatal and neonatal exposure.” 

Sabyasachi Sen, MD, a professor of biochemistry and molecular medicine at George Washington School of Medicine & Health Sciences, Washington, DC, has led and coauthored preclinical and clinical studies demonstrating the potential ill effects of sucralose and other artificial sweeteners. One showed that sucralose and acesulfame potassium–containing diet soda altered microbial taxa in two pilot studies in healthy young adults; another showed a connection between artificial sweeteners and inflammation.

But Dr. Sen’s current work is directed at his team’s finding that sucralose promotes the accumulation of reactive oxygen species and adipogenesis in human stem cells, he said in an interview. “It is essentially an additive that is clearly harmful to cells. Our concern is that stem cells are going to remain in the system for a long period of time. If it is causing inflammation in these cells, then that may lead to adverse outcomes.”

Ruchi Mathur, MD, director of the Diabetes Outpatient Treatment & Education Center at Cedars-Sinai in Los Angeles, California, is the principal investigator of a recent study suggesting that non-aspartame NSS and aspartame alone may alter the structure and function of the stool and duodenal microbiomes. Levels of circulating inflammatory markers were also altered in participants who consumed artificial sweeteners, compared with control participants who did not.

In addition to these potential adverse effects, “we have to think about the fact that patients with diabetes often have other comorbidities like obesity and are at higher risk for cardiovascular disease and other conditions,” she said in an interview. “If you’re taking a patient who’s already at risk for those things and you don’t have a detailed discussion with them about pros and cons, you’re doing them a disservice.” 
 

Industry Interests

Addressing the largely negative but varying findings, Dr. Swithers said, “one of the difficulties with getting clear answers about the science is that the food and beverage industry has an interest in confusing the picture. If people are selling or using a product, the best thing is for them not have a clear reason to change their behavior. All that needs to happen is for them to be able say, ‘well, it’s not clear, and we don’t really know what’s going on, so I’m just going to keep doing what I’m doing.’ Then the producers and sellers of that product have won.” 

“As Upton Sinclair said,” she added, “‘It is difficult to get a man to understand something when his salary depends on his not understanding it.’ When organizations like ADA appear to be promoting a product like sucralose, and they’re not always being clear about disclosing the funding, I think that’s problematic.”

In fact, some recipes in the ADA’s hub that contain Splenda are marked sponsored, such as the four-ingredient peanut butter cookies; others, such as gluten-free brownies, are not — even though the latter contains “1/4 cup plus 1 tbsp” of Splenda Sugar Blend (Splenda produces several nonnutritive sweeteners, not all of which contain sucralose). Splenda is a sponsor of the ADA’s hub.
 

Consume in Moderation?

Regarding the use of Splenda products, Robert Gabbay, MD, PhD, the ADA’s chief scientific and medical officer, said in an interview that “some people with diabetes are accustomed to regularly consuming sugar-sweetened products, which can make management of their diabetes more challenging. As highlighted in the ADA’s Standards of Care, nonnutritive sweeteners (containing few or no calories) may be an acceptable substitute for sweeteners that contain sugar and calories when consumed in moderation. By providing a diabetes-friendly way to prepare foods people are used to eating, we can meet people where they are in offering support to effectively manage their diabetes.”

Of course, “moderation” means different things to different people. “With sucralose in particular, you can bake with it, you can cook with it, and beverages and packaged foods contain it, so it’s easy to end up overconsuming foods that may be fine if they’re occasional treats but aren’t healthy choices to have every single day,” Dr. Swithers said. “If you’re having a cookie containing sucralose once a week, it’s not a big deal, but if you’re having a cookie or a brownie every day, that’s something different.”

“I think ‘everything in moderation’ is a very reasonable approach here,” Dr. Mathur said. “Anything too much is probably not good, and that includes sweeteners like sucralose and others.”

Dr. Suez, whose team is currently exploring the mechanisms through which gut bacteria interact with nonnutritive sweeteners in the pathogenesis of cardiometabolic diseases, was more circumspect.

“We believe that additional, long-term, and non–industry-sponsored studies in humans are needed before we can make a recommendation in favor or against the use of nonnutritive sweeteners,” he said.

“However, our results demonstrating that nonnutritive sweeteners are not inert, when taken together with a growing body of evidence on potential harms of these sweeteners, merit caution until additional studies are completed,” he added. “Our findings do not imply in any way that sugar consumption, shown to be harmful to human health in many studies, is superior to nonnutritive sweeteners. Sugar consumption should be minimized, especially in individuals with obesity or diabetes. Of all the options, unsweetened beverages, specifically water, seem to be the safest and best options.”

Dr. Sen, who also “tries to convince patients to have sparkling or cold bottled water,” instead of artificially sweetened soda, agreed. “If a diabetes patient is trying to choose between sugar and sucralose, I’m not sure which one is worse.”

Dr. Swithers, Dr. Mathur, Dr. Sen, and Dr. Suez declared no competing interests.

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

It seems intuitive that, because people with type 2 diabetes (T2D) generally need to avoid sugar, clinicians should recommend eating foods and using recipes containing artificial sweeteners such as sucralose instead.

Splenda, which produces sucralose and other non-sugar sweeteners (NSS), is a sponsor of the American Diabetes Association (ADA) Diabetes Food Hub. Earlier in 2024, the ADA settled a lawsuit regarding its former director of nutrition’s refusal to approve recipes containing sucralose (Splenda), which she believed “flew in the face of the ADA’s mission.” 

Experts agree that, while artificial sweeteners may help in certain scenarios, they can also be harmful.

“There’s not a lot of evidence that sweeteners like sucralose provide significant benefits, especially over the long term,” said Susan Swithers, PhD, professor, department of psychological sciences and associate dean for faculty affairs at Purdue University, West Lafayette, Indiana.

Dr. Swithers authored an article several years ago cautioning that consuming nonnutritive sweeteners in beverages not only fails to prevent disease but also is associated with an increase in risks for the same health outcomes associated with sugar-sweetened beverages, including T2D, cardiovascular disease, hypertension, and stroke.

“At this point, we have pretty good evidence that these chemicals that were once touted as being completely inert are, in fact, not inert,” she said. “We know that they’re unlikely to be toxic in the short term, but they are not benign, and they have consequences. Right now, we have little understanding of the outcomes of consumption of these products chronically.”
 

What the Science Says

In 2023, the World Health Organization (WHO) released a guideline on NSS that recommended against their use for weight control or to reduce the risk for noncommunicable diseases.

The systematic review and meta-analysis upon which the guideline is based found that high intakes of NSS were associated with increases in body mass index and, as Dr. Swithers found, risks of developing T2D, cardiovascular events, and any type of stroke, as well as hypertension, bladder cancer, and all-cause mortality.

In a press release announcing the guideline, Francesco Branca, WHO director for Nutrition and Food Safety, said, “NSS are not essential dietary factors and have no nutritional value. People should reduce the sweetness of the diet altogether, starting early in life, to improve their health.” 

The “common” NSS named by WHO included sucralose, as well as acesulfame K, aspartame, advantame, cyclamates, neotame, saccharin, stevia, and stevia derivatives.

If NSS consumption can increase T2D risk, what about people who already have T2D? 

Some research suggests that NSS may affect people with and without T2D differently, said Dr. Swithers. For example, one small study showed that sucralose enhanced glucagon-like peptide 1 release and lowered blood glucose in healthy patients but not in patients with newly diagnosed T2D.

Similarly, Jotham Suez, PhD, an assistant professor in the department of molecular microbiology and immunology at Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, said in an interview that his group “showed for the first time in 2014 that disruption of the microbiome by artificial sweeteners is causally linked to disrupted glycemic control.” 

Recently, the team studied the impact of sucralose, aspartame, saccharin, and stevia in healthy adults and “were surprised to discover that all four sweeteners altered gut bacteria and the molecules they secrete,” he said. However, subsequent glucose tolerance tests in healthy humans showed varying results, “suggesting that human microbiome responses to the nonnutritive sweeteners we assessed are highly personalized and may lead to glycemic alterations in some, but not all, consumers depending on their microbes and the sweeteners they consume.” 

Nevertheless, a recent review led by researchers in Mexico concluded that sucralose consumption “is associated with various adverse health effects. Despite being considered safe following previous studies, recent research suggests possible links to systemic inflammation, metabolic diseases, disruptions in gut microbiota, liver damage, and toxic effects at the cellular level.” 

In addition, they wrote, “it is crucial to highlight the persistence of sucralose in the body, its ability to cross the placenta, and its presence in breast milk, raising concerns about prenatal and neonatal exposure.” 

Sabyasachi Sen, MD, a professor of biochemistry and molecular medicine at George Washington School of Medicine & Health Sciences, Washington, DC, has led and coauthored preclinical and clinical studies demonstrating the potential ill effects of sucralose and other artificial sweeteners. One showed that sucralose and acesulfame potassium–containing diet soda altered microbial taxa in two pilot studies in healthy young adults; another showed a connection between artificial sweeteners and inflammation.

But Dr. Sen’s current work is directed at his team’s finding that sucralose promotes the accumulation of reactive oxygen species and adipogenesis in human stem cells, he said in an interview. “It is essentially an additive that is clearly harmful to cells. Our concern is that stem cells are going to remain in the system for a long period of time. If it is causing inflammation in these cells, then that may lead to adverse outcomes.”

Ruchi Mathur, MD, director of the Diabetes Outpatient Treatment & Education Center at Cedars-Sinai in Los Angeles, California, is the principal investigator of a recent study suggesting that non-aspartame NSS and aspartame alone may alter the structure and function of the stool and duodenal microbiomes. Levels of circulating inflammatory markers were also altered in participants who consumed artificial sweeteners, compared with control participants who did not.

In addition to these potential adverse effects, “we have to think about the fact that patients with diabetes often have other comorbidities like obesity and are at higher risk for cardiovascular disease and other conditions,” she said in an interview. “If you’re taking a patient who’s already at risk for those things and you don’t have a detailed discussion with them about pros and cons, you’re doing them a disservice.” 
 

Industry Interests

Addressing the largely negative but varying findings, Dr. Swithers said, “one of the difficulties with getting clear answers about the science is that the food and beverage industry has an interest in confusing the picture. If people are selling or using a product, the best thing is for them not have a clear reason to change their behavior. All that needs to happen is for them to be able say, ‘well, it’s not clear, and we don’t really know what’s going on, so I’m just going to keep doing what I’m doing.’ Then the producers and sellers of that product have won.” 

“As Upton Sinclair said,” she added, “‘It is difficult to get a man to understand something when his salary depends on his not understanding it.’ When organizations like ADA appear to be promoting a product like sucralose, and they’re not always being clear about disclosing the funding, I think that’s problematic.”

In fact, some recipes in the ADA’s hub that contain Splenda are marked sponsored, such as the four-ingredient peanut butter cookies; others, such as gluten-free brownies, are not — even though the latter contains “1/4 cup plus 1 tbsp” of Splenda Sugar Blend (Splenda produces several nonnutritive sweeteners, not all of which contain sucralose). Splenda is a sponsor of the ADA’s hub.
 

Consume in Moderation?

Regarding the use of Splenda products, Robert Gabbay, MD, PhD, the ADA’s chief scientific and medical officer, said in an interview that “some people with diabetes are accustomed to regularly consuming sugar-sweetened products, which can make management of their diabetes more challenging. As highlighted in the ADA’s Standards of Care, nonnutritive sweeteners (containing few or no calories) may be an acceptable substitute for sweeteners that contain sugar and calories when consumed in moderation. By providing a diabetes-friendly way to prepare foods people are used to eating, we can meet people where they are in offering support to effectively manage their diabetes.”

Of course, “moderation” means different things to different people. “With sucralose in particular, you can bake with it, you can cook with it, and beverages and packaged foods contain it, so it’s easy to end up overconsuming foods that may be fine if they’re occasional treats but aren’t healthy choices to have every single day,” Dr. Swithers said. “If you’re having a cookie containing sucralose once a week, it’s not a big deal, but if you’re having a cookie or a brownie every day, that’s something different.”

“I think ‘everything in moderation’ is a very reasonable approach here,” Dr. Mathur said. “Anything too much is probably not good, and that includes sweeteners like sucralose and others.”

Dr. Suez, whose team is currently exploring the mechanisms through which gut bacteria interact with nonnutritive sweeteners in the pathogenesis of cardiometabolic diseases, was more circumspect.

“We believe that additional, long-term, and non–industry-sponsored studies in humans are needed before we can make a recommendation in favor or against the use of nonnutritive sweeteners,” he said.

“However, our results demonstrating that nonnutritive sweeteners are not inert, when taken together with a growing body of evidence on potential harms of these sweeteners, merit caution until additional studies are completed,” he added. “Our findings do not imply in any way that sugar consumption, shown to be harmful to human health in many studies, is superior to nonnutritive sweeteners. Sugar consumption should be minimized, especially in individuals with obesity or diabetes. Of all the options, unsweetened beverages, specifically water, seem to be the safest and best options.”

Dr. Sen, who also “tries to convince patients to have sparkling or cold bottled water,” instead of artificially sweetened soda, agreed. “If a diabetes patient is trying to choose between sugar and sucralose, I’m not sure which one is worse.”

Dr. Swithers, Dr. Mathur, Dr. Sen, and Dr. Suez declared no competing interests.

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

It seems intuitive that, because people with type 2 diabetes (T2D) generally need to avoid sugar, clinicians should recommend eating foods and using recipes containing artificial sweeteners such as sucralose instead.

Splenda, which produces sucralose and other non-sugar sweeteners (NSS), is a sponsor of the American Diabetes Association (ADA) Diabetes Food Hub. Earlier in 2024, the ADA settled a lawsuit regarding its former director of nutrition’s refusal to approve recipes containing sucralose (Splenda), which she believed “flew in the face of the ADA’s mission.” 

Experts agree that, while artificial sweeteners may help in certain scenarios, they can also be harmful.

“There’s not a lot of evidence that sweeteners like sucralose provide significant benefits, especially over the long term,” said Susan Swithers, PhD, professor, department of psychological sciences and associate dean for faculty affairs at Purdue University, West Lafayette, Indiana.

Dr. Swithers authored an article several years ago cautioning that consuming nonnutritive sweeteners in beverages not only fails to prevent disease but also is associated with an increase in risks for the same health outcomes associated with sugar-sweetened beverages, including T2D, cardiovascular disease, hypertension, and stroke.

“At this point, we have pretty good evidence that these chemicals that were once touted as being completely inert are, in fact, not inert,” she said. “We know that they’re unlikely to be toxic in the short term, but they are not benign, and they have consequences. Right now, we have little understanding of the outcomes of consumption of these products chronically.”
 

What the Science Says

In 2023, the World Health Organization (WHO) released a guideline on NSS that recommended against their use for weight control or to reduce the risk for noncommunicable diseases.

The systematic review and meta-analysis upon which the guideline is based found that high intakes of NSS were associated with increases in body mass index and, as Dr. Swithers found, risks of developing T2D, cardiovascular events, and any type of stroke, as well as hypertension, bladder cancer, and all-cause mortality.

In a press release announcing the guideline, Francesco Branca, WHO director for Nutrition and Food Safety, said, “NSS are not essential dietary factors and have no nutritional value. People should reduce the sweetness of the diet altogether, starting early in life, to improve their health.” 

The “common” NSS named by WHO included sucralose, as well as acesulfame K, aspartame, advantame, cyclamates, neotame, saccharin, stevia, and stevia derivatives.

If NSS consumption can increase T2D risk, what about people who already have T2D? 

Some research suggests that NSS may affect people with and without T2D differently, said Dr. Swithers. For example, one small study showed that sucralose enhanced glucagon-like peptide 1 release and lowered blood glucose in healthy patients but not in patients with newly diagnosed T2D.

Similarly, Jotham Suez, PhD, an assistant professor in the department of molecular microbiology and immunology at Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, said in an interview that his group “showed for the first time in 2014 that disruption of the microbiome by artificial sweeteners is causally linked to disrupted glycemic control.” 

Recently, the team studied the impact of sucralose, aspartame, saccharin, and stevia in healthy adults and “were surprised to discover that all four sweeteners altered gut bacteria and the molecules they secrete,” he said. However, subsequent glucose tolerance tests in healthy humans showed varying results, “suggesting that human microbiome responses to the nonnutritive sweeteners we assessed are highly personalized and may lead to glycemic alterations in some, but not all, consumers depending on their microbes and the sweeteners they consume.” 

Nevertheless, a recent review led by researchers in Mexico concluded that sucralose consumption “is associated with various adverse health effects. Despite being considered safe following previous studies, recent research suggests possible links to systemic inflammation, metabolic diseases, disruptions in gut microbiota, liver damage, and toxic effects at the cellular level.” 

In addition, they wrote, “it is crucial to highlight the persistence of sucralose in the body, its ability to cross the placenta, and its presence in breast milk, raising concerns about prenatal and neonatal exposure.” 

Sabyasachi Sen, MD, a professor of biochemistry and molecular medicine at George Washington School of Medicine & Health Sciences, Washington, DC, has led and coauthored preclinical and clinical studies demonstrating the potential ill effects of sucralose and other artificial sweeteners. One showed that sucralose and acesulfame potassium–containing diet soda altered microbial taxa in two pilot studies in healthy young adults; another showed a connection between artificial sweeteners and inflammation.

But Dr. Sen’s current work is directed at his team’s finding that sucralose promotes the accumulation of reactive oxygen species and adipogenesis in human stem cells, he said in an interview. “It is essentially an additive that is clearly harmful to cells. Our concern is that stem cells are going to remain in the system for a long period of time. If it is causing inflammation in these cells, then that may lead to adverse outcomes.”

Ruchi Mathur, MD, director of the Diabetes Outpatient Treatment & Education Center at Cedars-Sinai in Los Angeles, California, is the principal investigator of a recent study suggesting that non-aspartame NSS and aspartame alone may alter the structure and function of the stool and duodenal microbiomes. Levels of circulating inflammatory markers were also altered in participants who consumed artificial sweeteners, compared with control participants who did not.

In addition to these potential adverse effects, “we have to think about the fact that patients with diabetes often have other comorbidities like obesity and are at higher risk for cardiovascular disease and other conditions,” she said in an interview. “If you’re taking a patient who’s already at risk for those things and you don’t have a detailed discussion with them about pros and cons, you’re doing them a disservice.” 
 

Industry Interests

Addressing the largely negative but varying findings, Dr. Swithers said, “one of the difficulties with getting clear answers about the science is that the food and beverage industry has an interest in confusing the picture. If people are selling or using a product, the best thing is for them not have a clear reason to change their behavior. All that needs to happen is for them to be able say, ‘well, it’s not clear, and we don’t really know what’s going on, so I’m just going to keep doing what I’m doing.’ Then the producers and sellers of that product have won.” 

“As Upton Sinclair said,” she added, “‘It is difficult to get a man to understand something when his salary depends on his not understanding it.’ When organizations like ADA appear to be promoting a product like sucralose, and they’re not always being clear about disclosing the funding, I think that’s problematic.”

In fact, some recipes in the ADA’s hub that contain Splenda are marked sponsored, such as the four-ingredient peanut butter cookies; others, such as gluten-free brownies, are not — even though the latter contains “1/4 cup plus 1 tbsp” of Splenda Sugar Blend (Splenda produces several nonnutritive sweeteners, not all of which contain sucralose). Splenda is a sponsor of the ADA’s hub.
 

Consume in Moderation?

Regarding the use of Splenda products, Robert Gabbay, MD, PhD, the ADA’s chief scientific and medical officer, said in an interview that “some people with diabetes are accustomed to regularly consuming sugar-sweetened products, which can make management of their diabetes more challenging. As highlighted in the ADA’s Standards of Care, nonnutritive sweeteners (containing few or no calories) may be an acceptable substitute for sweeteners that contain sugar and calories when consumed in moderation. By providing a diabetes-friendly way to prepare foods people are used to eating, we can meet people where they are in offering support to effectively manage their diabetes.”

Of course, “moderation” means different things to different people. “With sucralose in particular, you can bake with it, you can cook with it, and beverages and packaged foods contain it, so it’s easy to end up overconsuming foods that may be fine if they’re occasional treats but aren’t healthy choices to have every single day,” Dr. Swithers said. “If you’re having a cookie containing sucralose once a week, it’s not a big deal, but if you’re having a cookie or a brownie every day, that’s something different.”

“I think ‘everything in moderation’ is a very reasonable approach here,” Dr. Mathur said. “Anything too much is probably not good, and that includes sweeteners like sucralose and others.”

Dr. Suez, whose team is currently exploring the mechanisms through which gut bacteria interact with nonnutritive sweeteners in the pathogenesis of cardiometabolic diseases, was more circumspect.

“We believe that additional, long-term, and non–industry-sponsored studies in humans are needed before we can make a recommendation in favor or against the use of nonnutritive sweeteners,” he said.

“However, our results demonstrating that nonnutritive sweeteners are not inert, when taken together with a growing body of evidence on potential harms of these sweeteners, merit caution until additional studies are completed,” he added. “Our findings do not imply in any way that sugar consumption, shown to be harmful to human health in many studies, is superior to nonnutritive sweeteners. Sugar consumption should be minimized, especially in individuals with obesity or diabetes. Of all the options, unsweetened beverages, specifically water, seem to be the safest and best options.”

Dr. Sen, who also “tries to convince patients to have sparkling or cold bottled water,” instead of artificially sweetened soda, agreed. “If a diabetes patient is trying to choose between sugar and sucralose, I’m not sure which one is worse.”

Dr. Swithers, Dr. Mathur, Dr. Sen, and Dr. Suez declared no competing interests.

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

TOPLINE:

Less than 7 hours of sleep per night is common in individuals with type 1 diabetes (T1D) but is tied to poor cardiometabolic health, particularly in adolescents.

METHODOLOGY:

• Sleep is recognized as an important factor in diabetes assessment and treatment by the 2023 American Diabetes Association’s Standards of Medical Care in Diabetes, but it is unclear whether sleep may improve health outcomes across the lifespan in patients with T1D.
• This secondary analysis of the BCQR-T1D crossover trial investigated the link between sleep and cardiometabolic health in 42 adults (age, 19-60 years) and 42 adolescents (age, 12-18 years) with T1D.
• Participants had T1D duration greater than 9 months and received bromocriptine quick-release (BCQR) therapy or placebo for 4 weeks and then switched between the treatments in a separate 4-week period.
• They underwent laboratory testing and anthropometric measurements. Also, continuous glucose monitoring data were collected for a week during each treatment phase along with an accompanying insulin dosing diary.
• Participants were required to wear an actigraphy monitor on the wrist of their nondominant hand for 7 days during each treatment phase to estimate sleep duration.

TAKEAWAY:

• Most adolescents (62%) and adults (74%) with T1D reported less than 7 hours of sleep at baseline.
• Participants with insufficient sleep versus those without insufficient sleep (< 7 vs > 7 hours) had a larger waist circumference and higher mean body mass index, systolic blood pressure, and pulse pressure, as well as lower estimated insulin sensitivity and brachial artery distensibility (P < .05 for all).
• When stratified by age, only adolescents with T1D with insufficient sleep had significant differences in most health outcomes by sleep duration status, except that adults with less than 7 hours of sleep had higher pulse pressure than those with more than 7 hours of sleep.
• Compared with placebo, BCQR slightly improved sleeping parameters in adolescents by delaying their time of waking up and prolonging their time in bed.

IN PRACTICE:

“Sleep may be an important and novel target for improving health in individuals with T1D, particularly when initiated in adolescence or early in diabetes,” the authors wrote.

SOURCE:

Stacey L. Simon, PhD, and Janet K. Snell-Bergeon, PhD, University of Colorado Anschutz Medical Campus, Aurora, led this study, which was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study lacked polysomnography or melatonin assessment to quantify circadian rhythms and subjective sleep quality ratings. It also had no objective measurement of the timing of the daily pills of BCQR, which, when taken in the morning, are hypothesized to reset the circadian rhythm for hypothalamic dopamine and serotonin. The recommended sleep duration of 8 hours for adolescents was not used as the cutoff value due to too few participants who qualified. Also, this study›s findings may be affected by the fact that participants were recruited throughout the year, while adolescents show different sleeping patterns during the academic year compared with school breaks.

DISCLOSURES:

This work was supported by a JDRF grant. Two authors declared receiving equipment, honoraria for lectures, and support for conference travel, which were all unrelated to this study.

A version of this article appeared on Medscape.com.

TOPLINE:

Less than 7 hours of sleep per night is common in individuals with type 1 diabetes (T1D) but is tied to poor cardiometabolic health, particularly in adolescents.

METHODOLOGY:

• Sleep is recognized as an important factor in diabetes assessment and treatment by the 2023 American Diabetes Association’s Standards of Medical Care in Diabetes, but it is unclear whether sleep may improve health outcomes across the lifespan in patients with T1D.
• This secondary analysis of the BCQR-T1D crossover trial investigated the link between sleep and cardiometabolic health in 42 adults (age, 19-60 years) and 42 adolescents (age, 12-18 years) with T1D.
• Participants had T1D duration greater than 9 months and received bromocriptine quick-release (BCQR) therapy or placebo for 4 weeks and then switched between the treatments in a separate 4-week period.
• They underwent laboratory testing and anthropometric measurements. Also, continuous glucose monitoring data were collected for a week during each treatment phase along with an accompanying insulin dosing diary.
• Participants were required to wear an actigraphy monitor on the wrist of their nondominant hand for 7 days during each treatment phase to estimate sleep duration.

TAKEAWAY:

• Most adolescents (62%) and adults (74%) with T1D reported less than 7 hours of sleep at baseline.
• Participants with insufficient sleep versus those without insufficient sleep (< 7 vs > 7 hours) had a larger waist circumference and higher mean body mass index, systolic blood pressure, and pulse pressure, as well as lower estimated insulin sensitivity and brachial artery distensibility (P < .05 for all).
• When stratified by age, only adolescents with T1D with insufficient sleep had significant differences in most health outcomes by sleep duration status, except that adults with less than 7 hours of sleep had higher pulse pressure than those with more than 7 hours of sleep.
• Compared with placebo, BCQR slightly improved sleeping parameters in adolescents by delaying their time of waking up and prolonging their time in bed.

IN PRACTICE:

“Sleep may be an important and novel target for improving health in individuals with T1D, particularly when initiated in adolescence or early in diabetes,” the authors wrote.

SOURCE:

Stacey L. Simon, PhD, and Janet K. Snell-Bergeon, PhD, University of Colorado Anschutz Medical Campus, Aurora, led this study, which was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study lacked polysomnography or melatonin assessment to quantify circadian rhythms and subjective sleep quality ratings. It also had no objective measurement of the timing of the daily pills of BCQR, which, when taken in the morning, are hypothesized to reset the circadian rhythm for hypothalamic dopamine and serotonin. The recommended sleep duration of 8 hours for adolescents was not used as the cutoff value due to too few participants who qualified. Also, this study›s findings may be affected by the fact that participants were recruited throughout the year, while adolescents show different sleeping patterns during the academic year compared with school breaks.

DISCLOSURES:

This work was supported by a JDRF grant. Two authors declared receiving equipment, honoraria for lectures, and support for conference travel, which were all unrelated to this study.

A version of this article appeared on Medscape.com.

TOPLINE:

Less than 7 hours of sleep per night is common in individuals with type 1 diabetes (T1D) but is tied to poor cardiometabolic health, particularly in adolescents.

METHODOLOGY:

• Sleep is recognized as an important factor in diabetes assessment and treatment by the 2023 American Diabetes Association’s Standards of Medical Care in Diabetes, but it is unclear whether sleep may improve health outcomes across the lifespan in patients with T1D.
• This secondary analysis of the BCQR-T1D crossover trial investigated the link between sleep and cardiometabolic health in 42 adults (age, 19-60 years) and 42 adolescents (age, 12-18 years) with T1D.
• Participants had T1D duration greater than 9 months and received bromocriptine quick-release (BCQR) therapy or placebo for 4 weeks and then switched between the treatments in a separate 4-week period.
• They underwent laboratory testing and anthropometric measurements. Also, continuous glucose monitoring data were collected for a week during each treatment phase along with an accompanying insulin dosing diary.
• Participants were required to wear an actigraphy monitor on the wrist of their nondominant hand for 7 days during each treatment phase to estimate sleep duration.

TAKEAWAY:

• Most adolescents (62%) and adults (74%) with T1D reported less than 7 hours of sleep at baseline.
• Participants with insufficient sleep versus those without insufficient sleep (< 7 vs > 7 hours) had a larger waist circumference and higher mean body mass index, systolic blood pressure, and pulse pressure, as well as lower estimated insulin sensitivity and brachial artery distensibility (P < .05 for all).
• When stratified by age, only adolescents with T1D with insufficient sleep had significant differences in most health outcomes by sleep duration status, except that adults with less than 7 hours of sleep had higher pulse pressure than those with more than 7 hours of sleep.
• Compared with placebo, BCQR slightly improved sleeping parameters in adolescents by delaying their time of waking up and prolonging their time in bed.

IN PRACTICE:

“Sleep may be an important and novel target for improving health in individuals with T1D, particularly when initiated in adolescence or early in diabetes,” the authors wrote.

SOURCE:

Stacey L. Simon, PhD, and Janet K. Snell-Bergeon, PhD, University of Colorado Anschutz Medical Campus, Aurora, led this study, which was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study lacked polysomnography or melatonin assessment to quantify circadian rhythms and subjective sleep quality ratings. It also had no objective measurement of the timing of the daily pills of BCQR, which, when taken in the morning, are hypothesized to reset the circadian rhythm for hypothalamic dopamine and serotonin. The recommended sleep duration of 8 hours for adolescents was not used as the cutoff value due to too few participants who qualified. Also, this study›s findings may be affected by the fact that participants were recruited throughout the year, while adolescents show different sleeping patterns during the academic year compared with school breaks.

DISCLOSURES:

This work was supported by a JDRF grant. Two authors declared receiving equipment, honoraria for lectures, and support for conference travel, which were all unrelated to this study.

A version of this article appeared on Medscape.com.

You are what you eat, as the adage goes. But a growing body of evidence indicates that it’s not just what and how much you eat that influence your health. How fast and when you eat also play a role.

Research now indicates that these two factors may affect the risk for gastrointestinal problems, obesity, and type 2 diabetes (T2D). Because meal timing and speed of consumption are modifiable, they present new opportunities to change patient behavior to help prevent and perhaps address these conditions.

Not So Fast

Most people are well acquainted with the short-term gastrointestinal effects of eating too quickly, which include indigestion, gas, bloating, and nausea. But regularly eating too fast can cause long-term consequences.

Obtaining a sense of fullness is key to staving off overeating and excess caloric intake. However, it takes approximately 20 minutes for the stomach to alert the brain to feelings of fullness. Eat too quickly and the fullness signaling might not set in until you’ve consumed more calories than intended. Research links this habit to excess body weight.

The practice also can lead to gastrointestinal diseases over the long term because overeating causes food to remain in the stomach longer, thus prolonging the time that the gastric mucosa is exposed to gastric acids.

A study of 10,893 adults in Korea reported that those with the fastest eating speed (< 5 min/meal) had a 1.7 times greater likelihood of endoscopic erosive gastritis than those with the slowest times (≥ 15 min/meal). Faster eating also was linked to increased risk for functional dyspepsia in a study involving 89 young-adult female military cadets in Korea with relatively controlled eating patterns.

On the extreme end of the spectrum, researchers who performed an assessment of a competitive speed eater speculated that the observed physiological accommodation required for the role (expanding the stomach to form a large flaccid sac) makes speed eaters vulnerable to morbid obesity, gastroparesis, intractable nausea and vomiting, and the need for gastrectomy.

The risk for metabolic changes and eventual development of T2D also appear to be linked to how quickly food is consumed.

Two clinical studies conducted in Japan — a cohort study of 2050 male factory workers and a nationwide study with 197,825 participants — identified a significant association between faster eating and T2D and insulin resistance. A case-control study involving 234 patients with new onset T2D and 468 controls from Lithuania linked faster eating to a greater than twofold risk for T2D. And a Chinese cross-sectional study of 7972 adults indicated that faster eating significantly increased the risk for metabolic syndrome, elevated blood pressure, and central obesity in adults.

Various hypotheses have been proposed to explain why fast eating may upset metabolic processes, including a delayed sense of fullness contributing to spiking postprandial glucose levels, lack of time for mastication causing higher glucose concentrations, and the triggering of specific cytokines (eg, interleukin-1 beta and interleukin-6) that lead to insulin resistance. It is also possible that the association is the result of people who eat quickly having relatively higher body weights, which translates to a higher risk for T2D.

However, there’s an opportunity in the association of rapid meal consumption with gastrointestinal and metabolic diseases, as people can slow the speed at which they eat so they feel full before they overeat.

A 2019 study in which 21 participants were instructed to eat a 600-kcal meal at a “normal” or “slow” pace (6 minutes or 24 minutes) found that the latter group reported feeling fuller while consuming fewer calories.

This approach may not work for all patients, however. There’s evidence to suggest that tactics to slow down eating may not limit the energy intake of those who are already overweight or obese.

Patients with obesity may physiologically differ in their processing of food, according to Michael Camilleri, MD, consultant in the Division of Gastroenterology and Hepatology at Mayo Clinic in Rochester, Minnesota.

“We have demonstrated that about 20%-25% of people with obesity actually have rapid gastric emptying,” he told this news organization. “As a result, they don’t feel full after they eat a meal and that might impact the total volume of food that they eat before they really feel full.”

The Ideal Time to Eat

It’s not only the speed at which individuals eat that may influence outcomes but when they take their meals. Research indicates that eating earlier in the day to align meals with the body’s circadian rhythms in metabolism offers health benefits.

“The focus would be to eat a meal that syncs during those daytime hours,” Collin Popp, PhD, MS, RD, a research scientist at the NYU Grossman School of Medicine in New York, told this news organization. “I typically suggest patients have their largest meal in the morning, whether that’s a large or medium-sized breakfast, or a big lunch.”

A recent cross-sectional study of 2050 participants found that having the largest meal at lunch protected against obesity (odds ratio [OR], 0.71), whereas having it at dinner increased the risk for obesity (OR, 1.67) and led to higher body mass index.

Consuming the majority of calories in meals earlier in the day may have metabolic health benefits, as well.

A 2015 randomized controlled trial involving 18 adults with obesity and T2D found that eating a high-energy breakfast and a low-energy dinner leads to reduced hyperglycemia throughout the day compared with eating a low-energy breakfast and a high-energy dinner.

Time-restricted eating (TRE), a form of intermittent fasting, also can improve metabolic health depending on the time of day.

A 2023 meta-analysis found that TRE was more effective at reducing fasting glucose levels in participants who were overweight and obese if done earlier rather than later in the day. Similarly, a 2022 study involving 82 healthy patients without diabetes or obesity found that early TRE was more effective than mid-day TRE at improving insulin sensitivity and that it improved fasting glucose and reduced total body mass and adiposity, while mid-day TRE did not.

A study that analyzed the effects of TRE in eight adult men with overweight and prediabetes found “better insulin resistance when the window of food consumption was earlier in the day,» noted endocrinologist Beverly Tchang, MD, an assistant professor of clinical medicine at Weill Cornell Medicine with a focus on obesity medication.

Patients May Benefit From Behavioral Interventions

Patients potentially negatively affected by eating too quickly or at late hours may benefit from adopting behavioral interventions to address these tendencies. To determine if a patient is a candidate for such interventions, Dr. Popp recommends starting with a simple conversation.

“When I first meet patients, I always ask them to describe to me a typical day for how they eat — when they’re eating, what they’re eating, the food quality, who are they with — to see if there’s social aspects to it. Then try and make the recommendations based on that,” said Dr. Popp, whose work focuses on biobehavioral interventions for the treatment and prevention of obesity, T2D, and other cardiometabolic outcomes.

Dr. Tchang said she encourages her patients to be mindful of hunger and fullness cues.

“Eat if you’re hungry; don’t force yourself to eat if you’re not hungry,” she said. “If you’re not sure whether you’re hungry or not, speak to a doctor because this points to an abnormality in your appetite-regulation system, which can be helped with GLP-1 [glucagon-like peptide 1] receptor agonists.”

Adjusting what patients eat can help them improve their meal timing.

“For example, we know that a high-fiber diet or a diet that has a large amount of fat in it tends to empty from the stomach slower,” Dr. Camilleri said. “That might give a sensation of fullness that lasts longer and that might prevent, for instance, the ingestion of the next meal.”

Those trying to eat more slowly are advised to seek out foods that are hard in texture and minimally processed.

A study involving 50 patients with healthy weights found that hard foods are consumed more slowly than soft foods and that energy intake is lowest with hard, minimally processed foods. Combining hard-textured foods with explicit instructions to reduce eating speed has also been shown to be an effective strategy. For those inclined to seek out technology-based solution, evidence suggests that a self-monitoring wearable device can slow the eating rate.

Although the evidence is mounting that the timing and duration of meals have an impact on certain chronic diseases, clinicians should remember that these two factors are far from the most important contributors, Dr. Popp said.

“We also have to consider total caloric intake, food quality, sleep, alcohol use, smoking, and physical activity,” he said. “Meal timing should be considered as under the umbrella of health that is important for a lot of folks.”

A version of this article appeared on Medscape.com.

You are what you eat, as the adage goes. But a growing body of evidence indicates that it’s not just what and how much you eat that influence your health. How fast and when you eat also play a role.

Research now indicates that these two factors may affect the risk for gastrointestinal problems, obesity, and type 2 diabetes (T2D). Because meal timing and speed of consumption are modifiable, they present new opportunities to change patient behavior to help prevent and perhaps address these conditions.

Not So Fast

Most people are well acquainted with the short-term gastrointestinal effects of eating too quickly, which include indigestion, gas, bloating, and nausea. But regularly eating too fast can cause long-term consequences.

Obtaining a sense of fullness is key to staving off overeating and excess caloric intake. However, it takes approximately 20 minutes for the stomach to alert the brain to feelings of fullness. Eat too quickly and the fullness signaling might not set in until you’ve consumed more calories than intended. Research links this habit to excess body weight.

The practice also can lead to gastrointestinal diseases over the long term because overeating causes food to remain in the stomach longer, thus prolonging the time that the gastric mucosa is exposed to gastric acids.

A study of 10,893 adults in Korea reported that those with the fastest eating speed (< 5 min/meal) had a 1.7 times greater likelihood of endoscopic erosive gastritis than those with the slowest times (≥ 15 min/meal). Faster eating also was linked to increased risk for functional dyspepsia in a study involving 89 young-adult female military cadets in Korea with relatively controlled eating patterns.

On the extreme end of the spectrum, researchers who performed an assessment of a competitive speed eater speculated that the observed physiological accommodation required for the role (expanding the stomach to form a large flaccid sac) makes speed eaters vulnerable to morbid obesity, gastroparesis, intractable nausea and vomiting, and the need for gastrectomy.

The risk for metabolic changes and eventual development of T2D also appear to be linked to how quickly food is consumed.

Two clinical studies conducted in Japan — a cohort study of 2050 male factory workers and a nationwide study with 197,825 participants — identified a significant association between faster eating and T2D and insulin resistance. A case-control study involving 234 patients with new onset T2D and 468 controls from Lithuania linked faster eating to a greater than twofold risk for T2D. And a Chinese cross-sectional study of 7972 adults indicated that faster eating significantly increased the risk for metabolic syndrome, elevated blood pressure, and central obesity in adults.

Various hypotheses have been proposed to explain why fast eating may upset metabolic processes, including a delayed sense of fullness contributing to spiking postprandial glucose levels, lack of time for mastication causing higher glucose concentrations, and the triggering of specific cytokines (eg, interleukin-1 beta and interleukin-6) that lead to insulin resistance. It is also possible that the association is the result of people who eat quickly having relatively higher body weights, which translates to a higher risk for T2D.

However, there’s an opportunity in the association of rapid meal consumption with gastrointestinal and metabolic diseases, as people can slow the speed at which they eat so they feel full before they overeat.

A 2019 study in which 21 participants were instructed to eat a 600-kcal meal at a “normal” or “slow” pace (6 minutes or 24 minutes) found that the latter group reported feeling fuller while consuming fewer calories.

This approach may not work for all patients, however. There’s evidence to suggest that tactics to slow down eating may not limit the energy intake of those who are already overweight or obese.

Patients with obesity may physiologically differ in their processing of food, according to Michael Camilleri, MD, consultant in the Division of Gastroenterology and Hepatology at Mayo Clinic in Rochester, Minnesota.

“We have demonstrated that about 20%-25% of people with obesity actually have rapid gastric emptying,” he told this news organization. “As a result, they don’t feel full after they eat a meal and that might impact the total volume of food that they eat before they really feel full.”

The Ideal Time to Eat

It’s not only the speed at which individuals eat that may influence outcomes but when they take their meals. Research indicates that eating earlier in the day to align meals with the body’s circadian rhythms in metabolism offers health benefits.

“The focus would be to eat a meal that syncs during those daytime hours,” Collin Popp, PhD, MS, RD, a research scientist at the NYU Grossman School of Medicine in New York, told this news organization. “I typically suggest patients have their largest meal in the morning, whether that’s a large or medium-sized breakfast, or a big lunch.”

A recent cross-sectional study of 2050 participants found that having the largest meal at lunch protected against obesity (odds ratio [OR], 0.71), whereas having it at dinner increased the risk for obesity (OR, 1.67) and led to higher body mass index.

Consuming the majority of calories in meals earlier in the day may have metabolic health benefits, as well.

A 2015 randomized controlled trial involving 18 adults with obesity and T2D found that eating a high-energy breakfast and a low-energy dinner leads to reduced hyperglycemia throughout the day compared with eating a low-energy breakfast and a high-energy dinner.

Time-restricted eating (TRE), a form of intermittent fasting, also can improve metabolic health depending on the time of day.

A 2023 meta-analysis found that TRE was more effective at reducing fasting glucose levels in participants who were overweight and obese if done earlier rather than later in the day. Similarly, a 2022 study involving 82 healthy patients without diabetes or obesity found that early TRE was more effective than mid-day TRE at improving insulin sensitivity and that it improved fasting glucose and reduced total body mass and adiposity, while mid-day TRE did not.

A study that analyzed the effects of TRE in eight adult men with overweight and prediabetes found “better insulin resistance when the window of food consumption was earlier in the day,» noted endocrinologist Beverly Tchang, MD, an assistant professor of clinical medicine at Weill Cornell Medicine with a focus on obesity medication.

Patients May Benefit From Behavioral Interventions

Patients potentially negatively affected by eating too quickly or at late hours may benefit from adopting behavioral interventions to address these tendencies. To determine if a patient is a candidate for such interventions, Dr. Popp recommends starting with a simple conversation.

“When I first meet patients, I always ask them to describe to me a typical day for how they eat — when they’re eating, what they’re eating, the food quality, who are they with — to see if there’s social aspects to it. Then try and make the recommendations based on that,” said Dr. Popp, whose work focuses on biobehavioral interventions for the treatment and prevention of obesity, T2D, and other cardiometabolic outcomes.

Dr. Tchang said she encourages her patients to be mindful of hunger and fullness cues.

“Eat if you’re hungry; don’t force yourself to eat if you’re not hungry,” she said. “If you’re not sure whether you’re hungry or not, speak to a doctor because this points to an abnormality in your appetite-regulation system, which can be helped with GLP-1 [glucagon-like peptide 1] receptor agonists.”

Adjusting what patients eat can help them improve their meal timing.

“For example, we know that a high-fiber diet or a diet that has a large amount of fat in it tends to empty from the stomach slower,” Dr. Camilleri said. “That might give a sensation of fullness that lasts longer and that might prevent, for instance, the ingestion of the next meal.”

Those trying to eat more slowly are advised to seek out foods that are hard in texture and minimally processed.

A study involving 50 patients with healthy weights found that hard foods are consumed more slowly than soft foods and that energy intake is lowest with hard, minimally processed foods. Combining hard-textured foods with explicit instructions to reduce eating speed has also been shown to be an effective strategy. For those inclined to seek out technology-based solution, evidence suggests that a self-monitoring wearable device can slow the eating rate.

Although the evidence is mounting that the timing and duration of meals have an impact on certain chronic diseases, clinicians should remember that these two factors are far from the most important contributors, Dr. Popp said.

“We also have to consider total caloric intake, food quality, sleep, alcohol use, smoking, and physical activity,” he said. “Meal timing should be considered as under the umbrella of health that is important for a lot of folks.”

A version of this article appeared on Medscape.com.

You are what you eat, as the adage goes. But a growing body of evidence indicates that it’s not just what and how much you eat that influence your health. How fast and when you eat also play a role.

Research now indicates that these two factors may affect the risk for gastrointestinal problems, obesity, and type 2 diabetes (T2D). Because meal timing and speed of consumption are modifiable, they present new opportunities to change patient behavior to help prevent and perhaps address these conditions.

Not So Fast

Most people are well acquainted with the short-term gastrointestinal effects of eating too quickly, which include indigestion, gas, bloating, and nausea. But regularly eating too fast can cause long-term consequences.

Obtaining a sense of fullness is key to staving off overeating and excess caloric intake. However, it takes approximately 20 minutes for the stomach to alert the brain to feelings of fullness. Eat too quickly and the fullness signaling might not set in until you’ve consumed more calories than intended. Research links this habit to excess body weight.

The practice also can lead to gastrointestinal diseases over the long term because overeating causes food to remain in the stomach longer, thus prolonging the time that the gastric mucosa is exposed to gastric acids.

A study of 10,893 adults in Korea reported that those with the fastest eating speed (< 5 min/meal) had a 1.7 times greater likelihood of endoscopic erosive gastritis than those with the slowest times (≥ 15 min/meal). Faster eating also was linked to increased risk for functional dyspepsia in a study involving 89 young-adult female military cadets in Korea with relatively controlled eating patterns.

On the extreme end of the spectrum, researchers who performed an assessment of a competitive speed eater speculated that the observed physiological accommodation required for the role (expanding the stomach to form a large flaccid sac) makes speed eaters vulnerable to morbid obesity, gastroparesis, intractable nausea and vomiting, and the need for gastrectomy.

The risk for metabolic changes and eventual development of T2D also appear to be linked to how quickly food is consumed.

Two clinical studies conducted in Japan — a cohort study of 2050 male factory workers and a nationwide study with 197,825 participants — identified a significant association between faster eating and T2D and insulin resistance. A case-control study involving 234 patients with new onset T2D and 468 controls from Lithuania linked faster eating to a greater than twofold risk for T2D. And a Chinese cross-sectional study of 7972 adults indicated that faster eating significantly increased the risk for metabolic syndrome, elevated blood pressure, and central obesity in adults.

Various hypotheses have been proposed to explain why fast eating may upset metabolic processes, including a delayed sense of fullness contributing to spiking postprandial glucose levels, lack of time for mastication causing higher glucose concentrations, and the triggering of specific cytokines (eg, interleukin-1 beta and interleukin-6) that lead to insulin resistance. It is also possible that the association is the result of people who eat quickly having relatively higher body weights, which translates to a higher risk for T2D.

However, there’s an opportunity in the association of rapid meal consumption with gastrointestinal and metabolic diseases, as people can slow the speed at which they eat so they feel full before they overeat.

A 2019 study in which 21 participants were instructed to eat a 600-kcal meal at a “normal” or “slow” pace (6 minutes or 24 minutes) found that the latter group reported feeling fuller while consuming fewer calories.

This approach may not work for all patients, however. There’s evidence to suggest that tactics to slow down eating may not limit the energy intake of those who are already overweight or obese.

Patients with obesity may physiologically differ in their processing of food, according to Michael Camilleri, MD, consultant in the Division of Gastroenterology and Hepatology at Mayo Clinic in Rochester, Minnesota.

“We have demonstrated that about 20%-25% of people with obesity actually have rapid gastric emptying,” he told this news organization. “As a result, they don’t feel full after they eat a meal and that might impact the total volume of food that they eat before they really feel full.”

The Ideal Time to Eat

It’s not only the speed at which individuals eat that may influence outcomes but when they take their meals. Research indicates that eating earlier in the day to align meals with the body’s circadian rhythms in metabolism offers health benefits.

“The focus would be to eat a meal that syncs during those daytime hours,” Collin Popp, PhD, MS, RD, a research scientist at the NYU Grossman School of Medicine in New York, told this news organization. “I typically suggest patients have their largest meal in the morning, whether that’s a large or medium-sized breakfast, or a big lunch.”

A recent cross-sectional study of 2050 participants found that having the largest meal at lunch protected against obesity (odds ratio [OR], 0.71), whereas having it at dinner increased the risk for obesity (OR, 1.67) and led to higher body mass index.

Consuming the majority of calories in meals earlier in the day may have metabolic health benefits, as well.

A 2015 randomized controlled trial involving 18 adults with obesity and T2D found that eating a high-energy breakfast and a low-energy dinner leads to reduced hyperglycemia throughout the day compared with eating a low-energy breakfast and a high-energy dinner.

Time-restricted eating (TRE), a form of intermittent fasting, also can improve metabolic health depending on the time of day.

A 2023 meta-analysis found that TRE was more effective at reducing fasting glucose levels in participants who were overweight and obese if done earlier rather than later in the day. Similarly, a 2022 study involving 82 healthy patients without diabetes or obesity found that early TRE was more effective than mid-day TRE at improving insulin sensitivity and that it improved fasting glucose and reduced total body mass and adiposity, while mid-day TRE did not.

A study that analyzed the effects of TRE in eight adult men with overweight and prediabetes found “better insulin resistance when the window of food consumption was earlier in the day,» noted endocrinologist Beverly Tchang, MD, an assistant professor of clinical medicine at Weill Cornell Medicine with a focus on obesity medication.

Patients May Benefit From Behavioral Interventions

Patients potentially negatively affected by eating too quickly or at late hours may benefit from adopting behavioral interventions to address these tendencies. To determine if a patient is a candidate for such interventions, Dr. Popp recommends starting with a simple conversation.

“When I first meet patients, I always ask them to describe to me a typical day for how they eat — when they’re eating, what they’re eating, the food quality, who are they with — to see if there’s social aspects to it. Then try and make the recommendations based on that,” said Dr. Popp, whose work focuses on biobehavioral interventions for the treatment and prevention of obesity, T2D, and other cardiometabolic outcomes.

Dr. Tchang said she encourages her patients to be mindful of hunger and fullness cues.

“Eat if you’re hungry; don’t force yourself to eat if you’re not hungry,” she said. “If you’re not sure whether you’re hungry or not, speak to a doctor because this points to an abnormality in your appetite-regulation system, which can be helped with GLP-1 [glucagon-like peptide 1] receptor agonists.”

Adjusting what patients eat can help them improve their meal timing.

“For example, we know that a high-fiber diet or a diet that has a large amount of fat in it tends to empty from the stomach slower,” Dr. Camilleri said. “That might give a sensation of fullness that lasts longer and that might prevent, for instance, the ingestion of the next meal.”

Those trying to eat more slowly are advised to seek out foods that are hard in texture and minimally processed.

A study involving 50 patients with healthy weights found that hard foods are consumed more slowly than soft foods and that energy intake is lowest with hard, minimally processed foods. Combining hard-textured foods with explicit instructions to reduce eating speed has also been shown to be an effective strategy. For those inclined to seek out technology-based solution, evidence suggests that a self-monitoring wearable device can slow the eating rate.

Although the evidence is mounting that the timing and duration of meals have an impact on certain chronic diseases, clinicians should remember that these two factors are far from the most important contributors, Dr. Popp said.

“We also have to consider total caloric intake, food quality, sleep, alcohol use, smoking, and physical activity,” he said. “Meal timing should be considered as under the umbrella of health that is important for a lot of folks.”

A version of this article appeared on Medscape.com.

TOPLINE:

Tirzepatide vs basal insulins led to greater improvements in A1c and postprandial glucose (PPG) levels in patients with type 2 diabetes (T2D), regardless of different baseline PPG or fasting serum glucose (FSG) levels.

METHODOLOGY:

• Tirzepatide led to better glycemic control than insulin degludec and insulin glargine in the SURPASS-3 and SURPASS-4 trials, respectively, but the effect on FSG and PPG levels was not evaluated.
• In this post hoc analysis, the researchers assessed changes in various glycemic parameters in 3314 patients with T2D who were randomly assigned to receive tirzepatide (5, 10, or 15 mg), insulin degludec, or insulin glargine.
• Based on the median baseline glucose values, the patients were stratified into four subgroups: Low FSG/low PPG, low FSG/high PPG, high FSG/low PPG, and high FSG/high PPG.
• The outcomes of interest were changes in FSG, PPG, A1c, and body weight from baseline to week 52.

TAKEAWAY:

• Tirzepatide and basal insulins effectively lowered A1c, PPG levels, and FSG levels at 52 weeks across all patient subgroups (all P < .05).
• All three doses of tirzepatide resulted in greater reductions in both A1c and PPG levels than in basal insulins (all P < .05).
• In the high FSG/high PPG subgroup, a greater reduction in FSG levels was observed with tirzepatide 10- and 15-mg doses vs insulin glargine (both P < .05) and insulin degludec vs tirzepatide 5 mg (P < .001).
• Furthermore, at week 52, tirzepatide led to body weight reduction (P < .05), but insulin treatment led to an increase in body weight (P < .05) in all subgroups.

IN PRACTICE:

“Treatment with tirzepatide was consistently associated with more reduced PPG levels compared with insulin treatment across subgroups, including in participants with lower baseline PPG levels, in turn leading to greater A1c reductions,” the authors wrote.

SOURCE:

This study was led by Francesco Giorgino, MD, PhD, of the Section of Internal Medicine, Endocrinology, Andrology, and Metabolic Diseases, University of Bari Aldo Moro, Bari, Italy, and was published online in Diabetes Care.

LIMITATIONS:

The limitations include post hoc nature of the study and the short treatment duration. The trials included only patients with diabetes and overweight or obesity, and therefore, the study findings may not be generalizable to other populations.

DISCLOSURES:

This study and the SURPASS trials were funded by Eli Lilly and Company. Four authors declared being employees and shareholders of Eli Lilly and Company. The other authors declared having several ties with various sources, including Eli Lilly and Company.

A version of this article appeared on Medscape.com.

TOPLINE:

Tirzepatide vs basal insulins led to greater improvements in A1c and postprandial glucose (PPG) levels in patients with type 2 diabetes (T2D), regardless of different baseline PPG or fasting serum glucose (FSG) levels.

METHODOLOGY:

• Tirzepatide led to better glycemic control than insulin degludec and insulin glargine in the SURPASS-3 and SURPASS-4 trials, respectively, but the effect on FSG and PPG levels was not evaluated.
• In this post hoc analysis, the researchers assessed changes in various glycemic parameters in 3314 patients with T2D who were randomly assigned to receive tirzepatide (5, 10, or 15 mg), insulin degludec, or insulin glargine.
• Based on the median baseline glucose values, the patients were stratified into four subgroups: Low FSG/low PPG, low FSG/high PPG, high FSG/low PPG, and high FSG/high PPG.
• The outcomes of interest were changes in FSG, PPG, A1c, and body weight from baseline to week 52.

TAKEAWAY:

• Tirzepatide and basal insulins effectively lowered A1c, PPG levels, and FSG levels at 52 weeks across all patient subgroups (all P < .05).
• All three doses of tirzepatide resulted in greater reductions in both A1c and PPG levels than in basal insulins (all P < .05).
• In the high FSG/high PPG subgroup, a greater reduction in FSG levels was observed with tirzepatide 10- and 15-mg doses vs insulin glargine (both P < .05) and insulin degludec vs tirzepatide 5 mg (P < .001).
• Furthermore, at week 52, tirzepatide led to body weight reduction (P < .05), but insulin treatment led to an increase in body weight (P < .05) in all subgroups.

IN PRACTICE:

“Treatment with tirzepatide was consistently associated with more reduced PPG levels compared with insulin treatment across subgroups, including in participants with lower baseline PPG levels, in turn leading to greater A1c reductions,” the authors wrote.

SOURCE:

This study was led by Francesco Giorgino, MD, PhD, of the Section of Internal Medicine, Endocrinology, Andrology, and Metabolic Diseases, University of Bari Aldo Moro, Bari, Italy, and was published online in Diabetes Care.

LIMITATIONS:

The limitations include post hoc nature of the study and the short treatment duration. The trials included only patients with diabetes and overweight or obesity, and therefore, the study findings may not be generalizable to other populations.

DISCLOSURES:

This study and the SURPASS trials were funded by Eli Lilly and Company. Four authors declared being employees and shareholders of Eli Lilly and Company. The other authors declared having several ties with various sources, including Eli Lilly and Company.

A version of this article appeared on Medscape.com.

TOPLINE:

Tirzepatide vs basal insulins led to greater improvements in A1c and postprandial glucose (PPG) levels in patients with type 2 diabetes (T2D), regardless of different baseline PPG or fasting serum glucose (FSG) levels.

METHODOLOGY:

• Tirzepatide led to better glycemic control than insulin degludec and insulin glargine in the SURPASS-3 and SURPASS-4 trials, respectively, but the effect on FSG and PPG levels was not evaluated.
• In this post hoc analysis, the researchers assessed changes in various glycemic parameters in 3314 patients with T2D who were randomly assigned to receive tirzepatide (5, 10, or 15 mg), insulin degludec, or insulin glargine.
• Based on the median baseline glucose values, the patients were stratified into four subgroups: Low FSG/low PPG, low FSG/high PPG, high FSG/low PPG, and high FSG/high PPG.
• The outcomes of interest were changes in FSG, PPG, A1c, and body weight from baseline to week 52.

TAKEAWAY:

• Tirzepatide and basal insulins effectively lowered A1c, PPG levels, and FSG levels at 52 weeks across all patient subgroups (all P < .05).
• All three doses of tirzepatide resulted in greater reductions in both A1c and PPG levels than in basal insulins (all P < .05).
• In the high FSG/high PPG subgroup, a greater reduction in FSG levels was observed with tirzepatide 10- and 15-mg doses vs insulin glargine (both P < .05) and insulin degludec vs tirzepatide 5 mg (P < .001).
• Furthermore, at week 52, tirzepatide led to body weight reduction (P < .05), but insulin treatment led to an increase in body weight (P < .05) in all subgroups.

IN PRACTICE:

“Treatment with tirzepatide was consistently associated with more reduced PPG levels compared with insulin treatment across subgroups, including in participants with lower baseline PPG levels, in turn leading to greater A1c reductions,” the authors wrote.

SOURCE:

This study was led by Francesco Giorgino, MD, PhD, of the Section of Internal Medicine, Endocrinology, Andrology, and Metabolic Diseases, University of Bari Aldo Moro, Bari, Italy, and was published online in Diabetes Care.

LIMITATIONS:

The limitations include post hoc nature of the study and the short treatment duration. The trials included only patients with diabetes and overweight or obesity, and therefore, the study findings may not be generalizable to other populations.

DISCLOSURES:

This study and the SURPASS trials were funded by Eli Lilly and Company. Four authors declared being employees and shareholders of Eli Lilly and Company. The other authors declared having several ties with various sources, including Eli Lilly and Company.

A version of this article appeared on Medscape.com.