Commentary

I have written before about the COSMOS study and its finding that multivitamins (and chocolate) did not improve brain or cardiovascular health. So I was surprised to read that a “new” study found that vitamins can forestall dementia and age-related cognitive decline.

Upon closer look, the new data are neither new nor convincing, at least to me.

©Graça Victoria/iStockphoto.com

Chocolate and multivitamins for CVD and cancer prevention

The large randomized COSMOS trial was supposed to be the definitive study on chocolate that would establish its heart-health benefits without a doubt. Or, rather, the benefits of a cocoa bean extract in pill form given to healthy, older volunteers. The COSMOS study was negative. Chocolate, or the cocoa bean extract they used, did not reduce cardiovascular events.

And yet for all the prepublication importance attached to COSMOS, it is scarcely mentioned. Had it been positive, rest assured that Mars, the candy bar company that cofunded the research, and other interested parties would have been shouting it from the rooftops. As it is, they’re already spinning it.

Which brings us to the multivitamin component. COSMOS actually had a 2 × 2 design. In other words, there were four groups in this study: chocolate plus multivitamin, chocolate plus placebo, placebo plus multivitamin, and placebo plus placebo. This type of study design allows you to study two different interventions simultaneously, provided that they are independent and do not interact with each other. In addition to the primary cardiovascular endpoint, they also studied a cancer endpoint.

The multivitamin supplement didn’t reduce cardiovascular events either. Nor did it affect cancer outcomes. The main COSMOS study was negative and reinforced what countless other studies have proven: Taking a daily multivitamin does not reduce your risk of having a heart attack or developing cancer.
 

But wait, there’s more: COSMOS-Mind

But no researcher worth his salt studies just one or two endpoints in a study. The participants also underwent neurologic and memory testing. These results were reported separately in the COSMOS-Mind study.

COSMOS-Mind is often described as a separate (or “new”) study. In reality, it included the same participants from the original COSMOS trial and measured yet another primary outcome of cognitive performance on a series of tests administered by telephone. Although there is nothing inherently wrong with studying multiple outcomes in your patient population (after all, that salami isn’t going to slice itself), they cannot all be primary outcomes. Some, by necessity, must be secondary hypothesis–generating outcomes. If you test enough endpoints, multiple hypothesis testing dictates that eventually you will get a positive result simply by chance.

There was a time when the neurocognitive outcomes of COSMOS would have been reported in the same paper as the cardiovascular outcomes, but that time seems to have passed us by. Researchers live or die by the number of their publications, and there is an inherent advantage to squeezing as many publications as possible from the same dataset. Though, to be fair, the journal would probably have asked them to split up the paper as well.

In brief, the cocoa extract again fell short in COSMOS-Mind, but the multivitamin arm did better on the composite cognitive outcome. It was a fairly small difference – a 0.07-point improvement on the z-score at the 3-year mark (the z-score is the mean divided by the standard deviation). Much was also made of the fact that the improvement seemed to vary by prior history of cardiovascular disease (CVD). Those with a history of CVD had a 0.11-point improvement, whereas those without had a 0.06-point improvement. The authors couldn’t offer a definitive explanation for these findings. Any argument that multivitamins improve cardiovascular health and therefore prevent vascular dementia has to contend with the fact that the main COSMOS study didn’t show a cardiovascular benefit for vitamins. Speculation that you are treating nutritional deficiencies is exactly that: speculation.

A more salient question is: What does a 0.07-point improvement on the z-score mean clinically? This study didn’t assess whether a multivitamin supplement prevented dementia or allowed people to live independently for longer. In fairness, that would have been exceptionally difficult to do and would have required a much longer study.

Their one attempt to quantify the cognitive benefit clinically was a calculation about normal age-related decline. Test scores were 0.045 points lower for every 1-year increase in age among participants (their mean age was 73 years). So the authors contend that a 0.07-point increase, or the 0.083-point increase that they found at year 3, corresponds to 1.8 years of age-related decline forestalled. Whether this is an appropriate assumption, I leave for the reader to decide.
 

COSMOS-Web and replication

The results of COSMOS-Mind were seemingly bolstered by the recent publication of COSMOS-Web. Although I’ve seen this study described as having replicated the results of COSMOS-Mind, that description is a bit misleading. This was yet another ancillary COSMOS study; more than half of the 2,262 participants in COSMOS-Mind were also included in COSMOS-Web. Replicating results in the same people isn’t true replication.

The main difference between COSMOS-Mind and COSMOS-Web is that the former used a telephone interview to administer the cognitive tests and the latter used the Internet. They also had different endpoints, with COSMOS-Web looking at immediate recall rather than a global test composite.

COSMOS-Web was a positive study in that patients getting the multivitamin supplement did better on the test for immediate memory recall (remembering a list of 20 words), though they didn’t improve on tests of memory retention, executive function, or novel object recognition (basically a test where subjects have to identify matching geometric patterns and then recall them later). They were able to remember an additional 0.71 word on average, compared with 0.44 word in the placebo group. (For the record, it found no benefit for the cocoa extract).

Everybody does better on memory tests the second time around because practice makes perfect, hence the improvement in the placebo group. This benefit at 1 year did not survive to the end of follow-up at 3 years, in contrast to COSMOS-Mind, where the benefit was not apparent at 1 year and seen only at year 3. A history of cardiovascular disease didn’t seem to affect the results in COSMOS-Web as it did in COSMOS-Mind. As far as replications go, COSMOS-Web has some very non-negligible differences, compared with COSMOS-Mind. This incongruity, especially given the overlap in the patient populations is hard to reconcile. If COSMOS-Web was supposed to assuage any doubts that persisted after COSMOS-Mind, it hasn’t for me.
 

One of these studies is not like the others

Finally, although the COSMOS trial and all its ancillary study analyses suggest a neurocognitive benefit to multivitamin supplementation, it’s not the first study to test the matter. The Age-Related Eye Disease Study looked at vitamin C, vitamin E, beta-carotene, zinc, and copper. There was no benefit on any of the six cognitive tests administered to patients. The Women’s Health Study, the Women’s Antioxidant Cardiovascular Study and PREADViSE have all failed to show any benefit to the various vitamins and minerals they studied. A meta-analysis of 11 trials found no benefit to B vitamins in slowing cognitive aging.

The claim that COSMOS is the “first” study to test the hypothesis hinges on some careful wordplay. Prior studies tested specific vitamins, not a multivitamin. In the discussion of the paper, these other studies are critiqued for being short term. But the Physicians’ Health Study II did in fact study a multivitamin and assessed cognitive performance on average 2.5 years after randomization. It found no benefit. The authors of COSMOS-Web critiqued the 2.5-year wait to perform cognitive testing, saying it would have missed any short-term benefits. Although, given that they simultaneously praised their 3 years of follow-up, the criticism is hard to fully accept or even understand.

Whether follow-up is short or long, uses individual vitamins or a multivitamin, the results excluding COSMOS are uniformly negative. I for one am skeptical that a multivitamin or any individual vitamin can prevent dementia. Same goes for chocolate.

Do enough tests in the same population, and something will rise above the noise just by chance. When you get a positive result in your research, it’s always exciting. But when a slew of studies that came before you are negative, you aren’t groundbreaking. You’re an outlier.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

I have written before about the COSMOS study and its finding that multivitamins (and chocolate) did not improve brain or cardiovascular health. So I was surprised to read that a “new” study found that vitamins can forestall dementia and age-related cognitive decline.

Upon closer look, the new data are neither new nor convincing, at least to me.

©Graça Victoria/iStockphoto.com

Chocolate and multivitamins for CVD and cancer prevention

The large randomized COSMOS trial was supposed to be the definitive study on chocolate that would establish its heart-health benefits without a doubt. Or, rather, the benefits of a cocoa bean extract in pill form given to healthy, older volunteers. The COSMOS study was negative. Chocolate, or the cocoa bean extract they used, did not reduce cardiovascular events.

And yet for all the prepublication importance attached to COSMOS, it is scarcely mentioned. Had it been positive, rest assured that Mars, the candy bar company that cofunded the research, and other interested parties would have been shouting it from the rooftops. As it is, they’re already spinning it.

Which brings us to the multivitamin component. COSMOS actually had a 2 × 2 design. In other words, there were four groups in this study: chocolate plus multivitamin, chocolate plus placebo, placebo plus multivitamin, and placebo plus placebo. This type of study design allows you to study two different interventions simultaneously, provided that they are independent and do not interact with each other. In addition to the primary cardiovascular endpoint, they also studied a cancer endpoint.

The multivitamin supplement didn’t reduce cardiovascular events either. Nor did it affect cancer outcomes. The main COSMOS study was negative and reinforced what countless other studies have proven: Taking a daily multivitamin does not reduce your risk of having a heart attack or developing cancer.
 

But wait, there’s more: COSMOS-Mind

But no researcher worth his salt studies just one or two endpoints in a study. The participants also underwent neurologic and memory testing. These results were reported separately in the COSMOS-Mind study.

COSMOS-Mind is often described as a separate (or “new”) study. In reality, it included the same participants from the original COSMOS trial and measured yet another primary outcome of cognitive performance on a series of tests administered by telephone. Although there is nothing inherently wrong with studying multiple outcomes in your patient population (after all, that salami isn’t going to slice itself), they cannot all be primary outcomes. Some, by necessity, must be secondary hypothesis–generating outcomes. If you test enough endpoints, multiple hypothesis testing dictates that eventually you will get a positive result simply by chance.

There was a time when the neurocognitive outcomes of COSMOS would have been reported in the same paper as the cardiovascular outcomes, but that time seems to have passed us by. Researchers live or die by the number of their publications, and there is an inherent advantage to squeezing as many publications as possible from the same dataset. Though, to be fair, the journal would probably have asked them to split up the paper as well.

In brief, the cocoa extract again fell short in COSMOS-Mind, but the multivitamin arm did better on the composite cognitive outcome. It was a fairly small difference – a 0.07-point improvement on the z-score at the 3-year mark (the z-score is the mean divided by the standard deviation). Much was also made of the fact that the improvement seemed to vary by prior history of cardiovascular disease (CVD). Those with a history of CVD had a 0.11-point improvement, whereas those without had a 0.06-point improvement. The authors couldn’t offer a definitive explanation for these findings. Any argument that multivitamins improve cardiovascular health and therefore prevent vascular dementia has to contend with the fact that the main COSMOS study didn’t show a cardiovascular benefit for vitamins. Speculation that you are treating nutritional deficiencies is exactly that: speculation.

A more salient question is: What does a 0.07-point improvement on the z-score mean clinically? This study didn’t assess whether a multivitamin supplement prevented dementia or allowed people to live independently for longer. In fairness, that would have been exceptionally difficult to do and would have required a much longer study.

Their one attempt to quantify the cognitive benefit clinically was a calculation about normal age-related decline. Test scores were 0.045 points lower for every 1-year increase in age among participants (their mean age was 73 years). So the authors contend that a 0.07-point increase, or the 0.083-point increase that they found at year 3, corresponds to 1.8 years of age-related decline forestalled. Whether this is an appropriate assumption, I leave for the reader to decide.
 

COSMOS-Web and replication

The results of COSMOS-Mind were seemingly bolstered by the recent publication of COSMOS-Web. Although I’ve seen this study described as having replicated the results of COSMOS-Mind, that description is a bit misleading. This was yet another ancillary COSMOS study; more than half of the 2,262 participants in COSMOS-Mind were also included in COSMOS-Web. Replicating results in the same people isn’t true replication.

The main difference between COSMOS-Mind and COSMOS-Web is that the former used a telephone interview to administer the cognitive tests and the latter used the Internet. They also had different endpoints, with COSMOS-Web looking at immediate recall rather than a global test composite.

COSMOS-Web was a positive study in that patients getting the multivitamin supplement did better on the test for immediate memory recall (remembering a list of 20 words), though they didn’t improve on tests of memory retention, executive function, or novel object recognition (basically a test where subjects have to identify matching geometric patterns and then recall them later). They were able to remember an additional 0.71 word on average, compared with 0.44 word in the placebo group. (For the record, it found no benefit for the cocoa extract).

Everybody does better on memory tests the second time around because practice makes perfect, hence the improvement in the placebo group. This benefit at 1 year did not survive to the end of follow-up at 3 years, in contrast to COSMOS-Mind, where the benefit was not apparent at 1 year and seen only at year 3. A history of cardiovascular disease didn’t seem to affect the results in COSMOS-Web as it did in COSMOS-Mind. As far as replications go, COSMOS-Web has some very non-negligible differences, compared with COSMOS-Mind. This incongruity, especially given the overlap in the patient populations is hard to reconcile. If COSMOS-Web was supposed to assuage any doubts that persisted after COSMOS-Mind, it hasn’t for me.
 

One of these studies is not like the others

Finally, although the COSMOS trial and all its ancillary study analyses suggest a neurocognitive benefit to multivitamin supplementation, it’s not the first study to test the matter. The Age-Related Eye Disease Study looked at vitamin C, vitamin E, beta-carotene, zinc, and copper. There was no benefit on any of the six cognitive tests administered to patients. The Women’s Health Study, the Women’s Antioxidant Cardiovascular Study and PREADViSE have all failed to show any benefit to the various vitamins and minerals they studied. A meta-analysis of 11 trials found no benefit to B vitamins in slowing cognitive aging.

The claim that COSMOS is the “first” study to test the hypothesis hinges on some careful wordplay. Prior studies tested specific vitamins, not a multivitamin. In the discussion of the paper, these other studies are critiqued for being short term. But the Physicians’ Health Study II did in fact study a multivitamin and assessed cognitive performance on average 2.5 years after randomization. It found no benefit. The authors of COSMOS-Web critiqued the 2.5-year wait to perform cognitive testing, saying it would have missed any short-term benefits. Although, given that they simultaneously praised their 3 years of follow-up, the criticism is hard to fully accept or even understand.

Whether follow-up is short or long, uses individual vitamins or a multivitamin, the results excluding COSMOS are uniformly negative. I for one am skeptical that a multivitamin or any individual vitamin can prevent dementia. Same goes for chocolate.

Do enough tests in the same population, and something will rise above the noise just by chance. When you get a positive result in your research, it’s always exciting. But when a slew of studies that came before you are negative, you aren’t groundbreaking. You’re an outlier.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

I have written before about the COSMOS study and its finding that multivitamins (and chocolate) did not improve brain or cardiovascular health. So I was surprised to read that a “new” study found that vitamins can forestall dementia and age-related cognitive decline.

Upon closer look, the new data are neither new nor convincing, at least to me.

©Graça Victoria/iStockphoto.com

Chocolate and multivitamins for CVD and cancer prevention

The large randomized COSMOS trial was supposed to be the definitive study on chocolate that would establish its heart-health benefits without a doubt. Or, rather, the benefits of a cocoa bean extract in pill form given to healthy, older volunteers. The COSMOS study was negative. Chocolate, or the cocoa bean extract they used, did not reduce cardiovascular events.

And yet for all the prepublication importance attached to COSMOS, it is scarcely mentioned. Had it been positive, rest assured that Mars, the candy bar company that cofunded the research, and other interested parties would have been shouting it from the rooftops. As it is, they’re already spinning it.

Which brings us to the multivitamin component. COSMOS actually had a 2 × 2 design. In other words, there were four groups in this study: chocolate plus multivitamin, chocolate plus placebo, placebo plus multivitamin, and placebo plus placebo. This type of study design allows you to study two different interventions simultaneously, provided that they are independent and do not interact with each other. In addition to the primary cardiovascular endpoint, they also studied a cancer endpoint.

The multivitamin supplement didn’t reduce cardiovascular events either. Nor did it affect cancer outcomes. The main COSMOS study was negative and reinforced what countless other studies have proven: Taking a daily multivitamin does not reduce your risk of having a heart attack or developing cancer.
 

But wait, there’s more: COSMOS-Mind

But no researcher worth his salt studies just one or two endpoints in a study. The participants also underwent neurologic and memory testing. These results were reported separately in the COSMOS-Mind study.

COSMOS-Mind is often described as a separate (or “new”) study. In reality, it included the same participants from the original COSMOS trial and measured yet another primary outcome of cognitive performance on a series of tests administered by telephone. Although there is nothing inherently wrong with studying multiple outcomes in your patient population (after all, that salami isn’t going to slice itself), they cannot all be primary outcomes. Some, by necessity, must be secondary hypothesis–generating outcomes. If you test enough endpoints, multiple hypothesis testing dictates that eventually you will get a positive result simply by chance.

There was a time when the neurocognitive outcomes of COSMOS would have been reported in the same paper as the cardiovascular outcomes, but that time seems to have passed us by. Researchers live or die by the number of their publications, and there is an inherent advantage to squeezing as many publications as possible from the same dataset. Though, to be fair, the journal would probably have asked them to split up the paper as well.

In brief, the cocoa extract again fell short in COSMOS-Mind, but the multivitamin arm did better on the composite cognitive outcome. It was a fairly small difference – a 0.07-point improvement on the z-score at the 3-year mark (the z-score is the mean divided by the standard deviation). Much was also made of the fact that the improvement seemed to vary by prior history of cardiovascular disease (CVD). Those with a history of CVD had a 0.11-point improvement, whereas those without had a 0.06-point improvement. The authors couldn’t offer a definitive explanation for these findings. Any argument that multivitamins improve cardiovascular health and therefore prevent vascular dementia has to contend with the fact that the main COSMOS study didn’t show a cardiovascular benefit for vitamins. Speculation that you are treating nutritional deficiencies is exactly that: speculation.

A more salient question is: What does a 0.07-point improvement on the z-score mean clinically? This study didn’t assess whether a multivitamin supplement prevented dementia or allowed people to live independently for longer. In fairness, that would have been exceptionally difficult to do and would have required a much longer study.

Their one attempt to quantify the cognitive benefit clinically was a calculation about normal age-related decline. Test scores were 0.045 points lower for every 1-year increase in age among participants (their mean age was 73 years). So the authors contend that a 0.07-point increase, or the 0.083-point increase that they found at year 3, corresponds to 1.8 years of age-related decline forestalled. Whether this is an appropriate assumption, I leave for the reader to decide.
 

COSMOS-Web and replication

The results of COSMOS-Mind were seemingly bolstered by the recent publication of COSMOS-Web. Although I’ve seen this study described as having replicated the results of COSMOS-Mind, that description is a bit misleading. This was yet another ancillary COSMOS study; more than half of the 2,262 participants in COSMOS-Mind were also included in COSMOS-Web. Replicating results in the same people isn’t true replication.

The main difference between COSMOS-Mind and COSMOS-Web is that the former used a telephone interview to administer the cognitive tests and the latter used the Internet. They also had different endpoints, with COSMOS-Web looking at immediate recall rather than a global test composite.

COSMOS-Web was a positive study in that patients getting the multivitamin supplement did better on the test for immediate memory recall (remembering a list of 20 words), though they didn’t improve on tests of memory retention, executive function, or novel object recognition (basically a test where subjects have to identify matching geometric patterns and then recall them later). They were able to remember an additional 0.71 word on average, compared with 0.44 word in the placebo group. (For the record, it found no benefit for the cocoa extract).

Everybody does better on memory tests the second time around because practice makes perfect, hence the improvement in the placebo group. This benefit at 1 year did not survive to the end of follow-up at 3 years, in contrast to COSMOS-Mind, where the benefit was not apparent at 1 year and seen only at year 3. A history of cardiovascular disease didn’t seem to affect the results in COSMOS-Web as it did in COSMOS-Mind. As far as replications go, COSMOS-Web has some very non-negligible differences, compared with COSMOS-Mind. This incongruity, especially given the overlap in the patient populations is hard to reconcile. If COSMOS-Web was supposed to assuage any doubts that persisted after COSMOS-Mind, it hasn’t for me.
 

One of these studies is not like the others

Finally, although the COSMOS trial and all its ancillary study analyses suggest a neurocognitive benefit to multivitamin supplementation, it’s not the first study to test the matter. The Age-Related Eye Disease Study looked at vitamin C, vitamin E, beta-carotene, zinc, and copper. There was no benefit on any of the six cognitive tests administered to patients. The Women’s Health Study, the Women’s Antioxidant Cardiovascular Study and PREADViSE have all failed to show any benefit to the various vitamins and minerals they studied. A meta-analysis of 11 trials found no benefit to B vitamins in slowing cognitive aging.

The claim that COSMOS is the “first” study to test the hypothesis hinges on some careful wordplay. Prior studies tested specific vitamins, not a multivitamin. In the discussion of the paper, these other studies are critiqued for being short term. But the Physicians’ Health Study II did in fact study a multivitamin and assessed cognitive performance on average 2.5 years after randomization. It found no benefit. The authors of COSMOS-Web critiqued the 2.5-year wait to perform cognitive testing, saying it would have missed any short-term benefits. Although, given that they simultaneously praised their 3 years of follow-up, the criticism is hard to fully accept or even understand.

Whether follow-up is short or long, uses individual vitamins or a multivitamin, the results excluding COSMOS are uniformly negative. I for one am skeptical that a multivitamin or any individual vitamin can prevent dementia. Same goes for chocolate.

Do enough tests in the same population, and something will rise above the noise just by chance. When you get a positive result in your research, it’s always exciting. But when a slew of studies that came before you are negative, you aren’t groundbreaking. You’re an outlier.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The short-form video hosting service TikTok has become a mainstream platform for individuals to share their ideas and educate the public regarding dermatologic diseases such as atopic dermatitis, alopecia, and acne. Users can create and post videos, leave comments, and indicate their interest in or approval of certain content by “liking” videos. In 2022, according to a Pew Research Center survey, approximately 67% of American teenagers aged 13 to 17 years reported using TikTok at least once.¹ This population, along with the rest of its users, are increasing their use of TikTok to share information on dermatologic topics such as acne and isotretinoin.^2,3 Spironolactone is an effective medication for acne but is not as widely known to the public as other acne medications such as retinoids, salicylic acid, and benzoyl peroxide. Being aware of youth exposure to media related to acne and spironolactone can help dermatologists understand gaps in education and refine their interactions with this patient population.

To gain insight into youth exposure to spironolactone, we conducted a search of TikTok on July 26, 2022, using the term #spironolactone to retrieve the top 50 videos identified by TikTok under the “Top” tab on spironolactone. Search results and the top 10 comments for each video were reviewed. The total number of views and likes for the top 50 videos were 6,735,992 and 851,856, respectively.

Videos were subdivided into educational information related to spironolactone and/or skin care (32% [16/50]), discussion of side effects of spironolactone (26% [13/50]), those with noticeable improvement of acne following treatment with spironolactone (20% [10/50]), recommendations to see a physician or dermatologist to treat acne (10% [5/50]), and other (12% [6/50]). Other takeaways from the top 50 videos included the following:

• Common side effects: irregular periods (10% [5/50]), frequent urination (8% [4/50]), dizziness/lightheadedness (8% [4/50]), and breast tenderness (6% [3/50])
• Longest reported use of spironolactone: 4 years, with complete acne resolution
• Average treatment length prior to noticeable results: 4 to 6 months, with the shortest being 1 month
• Reported dosages of spironolactone: ranged from 50 to 200 mg/d. The most common dosage was 100 mg/d (10% [5/50]). The lowest reported dosage was 50 mg/d (4% [2/50]), while the highest reported dosage was 200 mg/d (2% [1/50])
• Self-reported concurrent use of spironolactone with a combined oral contraceptive: drospirenoneTimes New Roman–ethinyl estradiol (4% [2/50]), norethindrone acetateTimes New Roman–ethinyl estradiol/ferrous fumarate (2% [1/50]), and norgestimateTimes New Roman–ethinyl estradiol (2% [1/50])
• Negative experiences with side effects and lack of acne improvement that led to treatment cessation: 8% (4/50).

Even though spironolactone is not as well-known as other treatments for acne, we found many TikTok users posting about, commenting on, and highlighting the relevance of this therapeutic option. There was no suggestion in any of the videos that spironolactone could be obtained without physician care and/or prescription. A prior report discussing youth sentiment of isotretinoin use on TikTok found that popular videos and videos with the most likes focused on the drug’s positive impact on acne improvement, while comments displayed heightened desires to learn more about isotretinoin and its side effects.³ Our analysis showed a similar response to spironolactone. In all videos showcasing the skin before and after treatment, there were noticeable improvements in the poster’s acne. Most of the video comments displayed a desire to learn more about spironolactone and its side effects. There also were many questions about time to noticeable results. In contrast to the study on isotretinoin,³ the most-liked spironolactone videos contained educational information about spironolactone and/or skin care rather than focusing solely on the impact of the drug on acne. Additionally, the study on isotretinoin found no videos mentioning the importance of seeing a dermatologist or other health care professional,³ while our search found multiple videos (10% [5/50]) on spironolactone that advised seeking physician help. In fact, several popular videos (8% [4/50]) were created by board-certified dermatologists who mainly focused on providing educational information. This difference in educational content may be attributed to spironolactone’s lesser-known function in treating acne. Furthermore, the comments suggested a growing interest in learning more about spironolactone as a treatment option for acne, specifically its mechanism of action and side effects.

With nearly 2 billion monthly active users globally and 94.1 million monthly active users in the United States (as of March 2023),⁴ TikTok is a popular social media platform that allows dermatologists to better understand youth sentiment on acne treatments such as spironolactone and isotretinoin and also provides an opportunity for medical education to reach a larger audience. This increased youth insight from TikTok can be utilized by dermatologists to make more informed decisions in developing patient-centered care that appeals to the adolescent population.

The short-form video hosting service TikTok has become a mainstream platform for individuals to share their ideas and educate the public regarding dermatologic diseases such as atopic dermatitis, alopecia, and acne. Users can create and post videos, leave comments, and indicate their interest in or approval of certain content by “liking” videos. In 2022, according to a Pew Research Center survey, approximately 67% of American teenagers aged 13 to 17 years reported using TikTok at least once.¹ This population, along with the rest of its users, are increasing their use of TikTok to share information on dermatologic topics such as acne and isotretinoin.^2,3 Spironolactone is an effective medication for acne but is not as widely known to the public as other acne medications such as retinoids, salicylic acid, and benzoyl peroxide. Being aware of youth exposure to media related to acne and spironolactone can help dermatologists understand gaps in education and refine their interactions with this patient population.

To gain insight into youth exposure to spironolactone, we conducted a search of TikTok on July 26, 2022, using the term #spironolactone to retrieve the top 50 videos identified by TikTok under the “Top” tab on spironolactone. Search results and the top 10 comments for each video were reviewed. The total number of views and likes for the top 50 videos were 6,735,992 and 851,856, respectively.

Videos were subdivided into educational information related to spironolactone and/or skin care (32% [16/50]), discussion of side effects of spironolactone (26% [13/50]), those with noticeable improvement of acne following treatment with spironolactone (20% [10/50]), recommendations to see a physician or dermatologist to treat acne (10% [5/50]), and other (12% [6/50]). Other takeaways from the top 50 videos included the following:

• Common side effects: irregular periods (10% [5/50]), frequent urination (8% [4/50]), dizziness/lightheadedness (8% [4/50]), and breast tenderness (6% [3/50])
• Longest reported use of spironolactone: 4 years, with complete acne resolution
• Average treatment length prior to noticeable results: 4 to 6 months, with the shortest being 1 month
• Reported dosages of spironolactone: ranged from 50 to 200 mg/d. The most common dosage was 100 mg/d (10% [5/50]). The lowest reported dosage was 50 mg/d (4% [2/50]), while the highest reported dosage was 200 mg/d (2% [1/50])
• Self-reported concurrent use of spironolactone with a combined oral contraceptive: drospirenoneTimes New Roman–ethinyl estradiol (4% [2/50]), norethindrone acetateTimes New Roman–ethinyl estradiol/ferrous fumarate (2% [1/50]), and norgestimateTimes New Roman–ethinyl estradiol (2% [1/50])
• Negative experiences with side effects and lack of acne improvement that led to treatment cessation: 8% (4/50).

Even though spironolactone is not as well-known as other treatments for acne, we found many TikTok users posting about, commenting on, and highlighting the relevance of this therapeutic option. There was no suggestion in any of the videos that spironolactone could be obtained without physician care and/or prescription. A prior report discussing youth sentiment of isotretinoin use on TikTok found that popular videos and videos with the most likes focused on the drug’s positive impact on acne improvement, while comments displayed heightened desires to learn more about isotretinoin and its side effects.³ Our analysis showed a similar response to spironolactone. In all videos showcasing the skin before and after treatment, there were noticeable improvements in the poster’s acne. Most of the video comments displayed a desire to learn more about spironolactone and its side effects. There also were many questions about time to noticeable results. In contrast to the study on isotretinoin,³ the most-liked spironolactone videos contained educational information about spironolactone and/or skin care rather than focusing solely on the impact of the drug on acne. Additionally, the study on isotretinoin found no videos mentioning the importance of seeing a dermatologist or other health care professional,³ while our search found multiple videos (10% [5/50]) on spironolactone that advised seeking physician help. In fact, several popular videos (8% [4/50]) were created by board-certified dermatologists who mainly focused on providing educational information. This difference in educational content may be attributed to spironolactone’s lesser-known function in treating acne. Furthermore, the comments suggested a growing interest in learning more about spironolactone as a treatment option for acne, specifically its mechanism of action and side effects.

With nearly 2 billion monthly active users globally and 94.1 million monthly active users in the United States (as of March 2023),⁴ TikTok is a popular social media platform that allows dermatologists to better understand youth sentiment on acne treatments such as spironolactone and isotretinoin and also provides an opportunity for medical education to reach a larger audience. This increased youth insight from TikTok can be utilized by dermatologists to make more informed decisions in developing patient-centered care that appeals to the adolescent population.

The short-form video hosting service TikTok has become a mainstream platform for individuals to share their ideas and educate the public regarding dermatologic diseases such as atopic dermatitis, alopecia, and acne. Users can create and post videos, leave comments, and indicate their interest in or approval of certain content by “liking” videos. In 2022, according to a Pew Research Center survey, approximately 67% of American teenagers aged 13 to 17 years reported using TikTok at least once.¹ This population, along with the rest of its users, are increasing their use of TikTok to share information on dermatologic topics such as acne and isotretinoin.^2,3 Spironolactone is an effective medication for acne but is not as widely known to the public as other acne medications such as retinoids, salicylic acid, and benzoyl peroxide. Being aware of youth exposure to media related to acne and spironolactone can help dermatologists understand gaps in education and refine their interactions with this patient population.

To gain insight into youth exposure to spironolactone, we conducted a search of TikTok on July 26, 2022, using the term #spironolactone to retrieve the top 50 videos identified by TikTok under the “Top” tab on spironolactone. Search results and the top 10 comments for each video were reviewed. The total number of views and likes for the top 50 videos were 6,735,992 and 851,856, respectively.

Videos were subdivided into educational information related to spironolactone and/or skin care (32% [16/50]), discussion of side effects of spironolactone (26% [13/50]), those with noticeable improvement of acne following treatment with spironolactone (20% [10/50]), recommendations to see a physician or dermatologist to treat acne (10% [5/50]), and other (12% [6/50]). Other takeaways from the top 50 videos included the following:

• Common side effects: irregular periods (10% [5/50]), frequent urination (8% [4/50]), dizziness/lightheadedness (8% [4/50]), and breast tenderness (6% [3/50])
• Longest reported use of spironolactone: 4 years, with complete acne resolution
• Average treatment length prior to noticeable results: 4 to 6 months, with the shortest being 1 month
• Reported dosages of spironolactone: ranged from 50 to 200 mg/d. The most common dosage was 100 mg/d (10% [5/50]). The lowest reported dosage was 50 mg/d (4% [2/50]), while the highest reported dosage was 200 mg/d (2% [1/50])
• Self-reported concurrent use of spironolactone with a combined oral contraceptive: drospirenoneTimes New Roman–ethinyl estradiol (4% [2/50]), norethindrone acetateTimes New Roman–ethinyl estradiol/ferrous fumarate (2% [1/50]), and norgestimateTimes New Roman–ethinyl estradiol (2% [1/50])
• Negative experiences with side effects and lack of acne improvement that led to treatment cessation: 8% (4/50).

Even though spironolactone is not as well-known as other treatments for acne, we found many TikTok users posting about, commenting on, and highlighting the relevance of this therapeutic option. There was no suggestion in any of the videos that spironolactone could be obtained without physician care and/or prescription. A prior report discussing youth sentiment of isotretinoin use on TikTok found that popular videos and videos with the most likes focused on the drug’s positive impact on acne improvement, while comments displayed heightened desires to learn more about isotretinoin and its side effects.³ Our analysis showed a similar response to spironolactone. In all videos showcasing the skin before and after treatment, there were noticeable improvements in the poster’s acne. Most of the video comments displayed a desire to learn more about spironolactone and its side effects. There also were many questions about time to noticeable results. In contrast to the study on isotretinoin,³ the most-liked spironolactone videos contained educational information about spironolactone and/or skin care rather than focusing solely on the impact of the drug on acne. Additionally, the study on isotretinoin found no videos mentioning the importance of seeing a dermatologist or other health care professional,³ while our search found multiple videos (10% [5/50]) on spironolactone that advised seeking physician help. In fact, several popular videos (8% [4/50]) were created by board-certified dermatologists who mainly focused on providing educational information. This difference in educational content may be attributed to spironolactone’s lesser-known function in treating acne. Furthermore, the comments suggested a growing interest in learning more about spironolactone as a treatment option for acne, specifically its mechanism of action and side effects.

With nearly 2 billion monthly active users globally and 94.1 million monthly active users in the United States (as of March 2023),⁴ TikTok is a popular social media platform that allows dermatologists to better understand youth sentiment on acne treatments such as spironolactone and isotretinoin and also provides an opportunity for medical education to reach a larger audience. This increased youth insight from TikTok can be utilized by dermatologists to make more informed decisions in developing patient-centered care that appeals to the adolescent population.

In a striking convergence of veterinary biology and medical science, researchers from the University of Sheffield (England) have unveiled findings that could potentially advance the treatment of diabetic foot ulcers, a condition affecting an estimated 18.6 million people worldwide. The unexpected ingredient in this potentially transformative therapy? Feces from endangered species, sourced from Yorkshire Wildlife Park, Doncaster, England.

The scourge of antibiotic resistance

Diabetic foot ulcers are a significant challenge in health care, not only because of their prevalence but also because of the alarming rise of antibiotic-resistant bacterial infections. Current antibiotic treatments frequently fail, leading to life-altering consequences like amputations and significant health care costs – estimated at one-third of the total direct costs of diabetes care. The critical need for alternative therapies has propelled scientists into a pressing search for novel antimicrobial agents.

A pioneering approach: zoo poo as bioactive goldmine

Led by Professor Graham Stafford, chair of molecular microbiology at the University of Sheffield, the research team began to explore a rather unorthodox resource: the fecal matter of endangered animals like Guinea baboons, lemurs, and Visayan pigs. While such a source might seem surprising at first glance, the rationale becomes clear when considering the nature of bacteriophages.

What are bacteriophages?

Bacteriophages, commonly known as phages, are viruses that selectively target and kill bacteria. Despite being the most prevalent biological entities on Earth, their therapeutic potential has remained largely untapped. What makes bacteriophages particularly interesting is their ability to kill antibiotic-resistant bacteria – a feature making them prime candidates for treating otherwise unmanageable diabetic foot ulcers. (Armstrong DG, et al; Fish R, et al).

Findings and future directions

Professor Stafford and his team discovered that the feces of several endangered animals harbored bacteriophages capable of killing bacterial strains resistant to antibiotics. The findings not only hold promise for a groundbreaking treatment but also provide another compelling reason to conserve endangered species: Their inherent biodiversity might contain cures for a range of infectious diseases.

While research is ongoing and clinical trials have not yet begun, the preliminary results are overwhelmingly promising. Phages isolated from the feces could potentially be incorporated into dressings for ulcers, creating a novel treatment modality that is both effective and cost-saving.

We often look to complex technologies and synthetic materials for medical science breakthroughs, yet sometimes the most innovative solutions can be found in the most overlooked places. In this case, the feces of endangered species could turn out to be a vital asset in battling antibiotic resistance, thus affecting diabetic foot care in ways we never imagined possible.

The research conducted at the University of Sheffield also serves as a powerful argument for a One Health approach – a multidisciplinary field focusing on the interconnectedness of human, animal, and environmental health.

This intriguing work reaffirms the need for an interdisciplinary approach in tackling the world’s pressing health care challenges. The collaborative efforts between the University of Sheffield and Yorkshire Wildlife Park exemplify how academic research and conservation can come together to yield solutions for some of the most devastating and costly health conditions, while also underscoring the invaluable role that biodiversity plays in our collective well-being. Here’s to teaming up to act against amputation worldwide.

Dr. Armstrong is professor of surgery and director of limb preservation at University of Southern California, Los Angeles. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

In a striking convergence of veterinary biology and medical science, researchers from the University of Sheffield (England) have unveiled findings that could potentially advance the treatment of diabetic foot ulcers, a condition affecting an estimated 18.6 million people worldwide. The unexpected ingredient in this potentially transformative therapy? Feces from endangered species, sourced from Yorkshire Wildlife Park, Doncaster, England.

The scourge of antibiotic resistance

Diabetic foot ulcers are a significant challenge in health care, not only because of their prevalence but also because of the alarming rise of antibiotic-resistant bacterial infections. Current antibiotic treatments frequently fail, leading to life-altering consequences like amputations and significant health care costs – estimated at one-third of the total direct costs of diabetes care. The critical need for alternative therapies has propelled scientists into a pressing search for novel antimicrobial agents.

A pioneering approach: zoo poo as bioactive goldmine

Led by Professor Graham Stafford, chair of molecular microbiology at the University of Sheffield, the research team began to explore a rather unorthodox resource: the fecal matter of endangered animals like Guinea baboons, lemurs, and Visayan pigs. While such a source might seem surprising at first glance, the rationale becomes clear when considering the nature of bacteriophages.

What are bacteriophages?

Bacteriophages, commonly known as phages, are viruses that selectively target and kill bacteria. Despite being the most prevalent biological entities on Earth, their therapeutic potential has remained largely untapped. What makes bacteriophages particularly interesting is their ability to kill antibiotic-resistant bacteria – a feature making them prime candidates for treating otherwise unmanageable diabetic foot ulcers. (Armstrong DG, et al; Fish R, et al).

Findings and future directions

Professor Stafford and his team discovered that the feces of several endangered animals harbored bacteriophages capable of killing bacterial strains resistant to antibiotics. The findings not only hold promise for a groundbreaking treatment but also provide another compelling reason to conserve endangered species: Their inherent biodiversity might contain cures for a range of infectious diseases.

While research is ongoing and clinical trials have not yet begun, the preliminary results are overwhelmingly promising. Phages isolated from the feces could potentially be incorporated into dressings for ulcers, creating a novel treatment modality that is both effective and cost-saving.

We often look to complex technologies and synthetic materials for medical science breakthroughs, yet sometimes the most innovative solutions can be found in the most overlooked places. In this case, the feces of endangered species could turn out to be a vital asset in battling antibiotic resistance, thus affecting diabetic foot care in ways we never imagined possible.

The research conducted at the University of Sheffield also serves as a powerful argument for a One Health approach – a multidisciplinary field focusing on the interconnectedness of human, animal, and environmental health.

This intriguing work reaffirms the need for an interdisciplinary approach in tackling the world’s pressing health care challenges. The collaborative efforts between the University of Sheffield and Yorkshire Wildlife Park exemplify how academic research and conservation can come together to yield solutions for some of the most devastating and costly health conditions, while also underscoring the invaluable role that biodiversity plays in our collective well-being. Here’s to teaming up to act against amputation worldwide.

Dr. Armstrong is professor of surgery and director of limb preservation at University of Southern California, Los Angeles. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

In a striking convergence of veterinary biology and medical science, researchers from the University of Sheffield (England) have unveiled findings that could potentially advance the treatment of diabetic foot ulcers, a condition affecting an estimated 18.6 million people worldwide. The unexpected ingredient in this potentially transformative therapy? Feces from endangered species, sourced from Yorkshire Wildlife Park, Doncaster, England.

The scourge of antibiotic resistance

Diabetic foot ulcers are a significant challenge in health care, not only because of their prevalence but also because of the alarming rise of antibiotic-resistant bacterial infections. Current antibiotic treatments frequently fail, leading to life-altering consequences like amputations and significant health care costs – estimated at one-third of the total direct costs of diabetes care. The critical need for alternative therapies has propelled scientists into a pressing search for novel antimicrobial agents.

A pioneering approach: zoo poo as bioactive goldmine

Led by Professor Graham Stafford, chair of molecular microbiology at the University of Sheffield, the research team began to explore a rather unorthodox resource: the fecal matter of endangered animals like Guinea baboons, lemurs, and Visayan pigs. While such a source might seem surprising at first glance, the rationale becomes clear when considering the nature of bacteriophages.

What are bacteriophages?

Bacteriophages, commonly known as phages, are viruses that selectively target and kill bacteria. Despite being the most prevalent biological entities on Earth, their therapeutic potential has remained largely untapped. What makes bacteriophages particularly interesting is their ability to kill antibiotic-resistant bacteria – a feature making them prime candidates for treating otherwise unmanageable diabetic foot ulcers. (Armstrong DG, et al; Fish R, et al).

Findings and future directions

Professor Stafford and his team discovered that the feces of several endangered animals harbored bacteriophages capable of killing bacterial strains resistant to antibiotics. The findings not only hold promise for a groundbreaking treatment but also provide another compelling reason to conserve endangered species: Their inherent biodiversity might contain cures for a range of infectious diseases.

While research is ongoing and clinical trials have not yet begun, the preliminary results are overwhelmingly promising. Phages isolated from the feces could potentially be incorporated into dressings for ulcers, creating a novel treatment modality that is both effective and cost-saving.

We often look to complex technologies and synthetic materials for medical science breakthroughs, yet sometimes the most innovative solutions can be found in the most overlooked places. In this case, the feces of endangered species could turn out to be a vital asset in battling antibiotic resistance, thus affecting diabetic foot care in ways we never imagined possible.

The research conducted at the University of Sheffield also serves as a powerful argument for a One Health approach – a multidisciplinary field focusing on the interconnectedness of human, animal, and environmental health.

This intriguing work reaffirms the need for an interdisciplinary approach in tackling the world’s pressing health care challenges. The collaborative efforts between the University of Sheffield and Yorkshire Wildlife Park exemplify how academic research and conservation can come together to yield solutions for some of the most devastating and costly health conditions, while also underscoring the invaluable role that biodiversity plays in our collective well-being. Here’s to teaming up to act against amputation worldwide.

Dr. Armstrong is professor of surgery and director of limb preservation at University of Southern California, Los Angeles. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

A 36-year-old woman presents to your office for assistance with weight loss. She usually weighs around 150 lb, but she had two pregnancies in the past 4 years and has gained 70 lb. Her current weight is 220 lb with a body mass index (BMI) of 36.6 kg/m2, and she has been unable to lose any weight despite diet and exercise. She reports back pain and generalized fatigue but is primarily worried about developing type 2 diabetes, which runs in her family. Her insurance covers weight loss medications, but she is asking if she can take “Ozempic off-label” or “compounded semaglutide” instead because Wegovy isn’t available at her local pharmacy.

More and more people are turning to “medical weight management” to drop pounds and improve their health. This is a strategy that adds pharmacotherapy to lifestyle modifications to treat the chronic disease of obesity, and it is analogous to the treatment of high blood pressure or high cholesterol with medications.

This patient meets the criteria set forth by the American Heart Association, American College of Cardiology, and The Obesity Society for the management of obesity with antiobesity medications:

• BMI ≥ 30 or BMI ≥ 27 with weight-related comorbidities and
• Has been unable to achieve ≥ 5% weight loss with lifestyle changes alone.

Several U.S. Food and Drug Administration–approved antiobesity medications have been proven to cause clinically significant weight loss:

• orlistat (Alli or Xenical).
• phentermine/topiramate (Qsymia).
• naltrexone/bupropion (Contrave).
• liraglutide 3.0 mg subcutaneously daily (Saxenda).
• semaglutide 2.4 mg subcutaneously weekly (Wegovy).

When considering an antiobesity medication for a patient, it’s important to discuss efficacy, side-effect profile, contraindications, cost and coverage, and long-term use.

In this commentary, we’ll specifically focus on semaglutide (Wegovy) as it is currently the most effective FDA-approved medication for weight loss.
 

Efficacy

In a phase 3 clinical trial, patients on semaglutide 2.4 mg weekly lost an average of 15% of their body weight at 68 weeks, or approximately 33 lb. It is important to note that there is variability in treatment response to semaglutide 2.4 mg, just like with any other medication. About 1 in 3 individuals lost ≥ 20% of their weight, but about 1 in every 10 patients did not lose any weight.

In this patient, who has a family history of type 2 diabetes, weight loss with semaglutide 2.4 mg will probably reduce her risk of developing diabetes. With just 5%-10% weight loss, she will see improvements in her blood glucose, blood pressure, and cholesterol. Even greater weight loss (≥ 10%) has been associated with resolution of fatty liver and sleep apnea.
 

Side effects

Before starting semaglutide, patients should be counseled about potential gastrointestinal side effects, including nausea, upset stomach, diarrhea, constipation, and reflux.

Side effects can be managed with dietary modifications, over-the-counter treatments, and slow dose escalation. Some common tips include:

• Eat slowly.
• Eat a bland diet.
• Avoid fatty or fried foods.
• Avoid lying down immediately after eating.
• Prioritize water and fiber intake to mitigate constipation.
• Use over-the-counter treatments as needed (for example, laxative for constipation).

Most of these side effects are present only during dose escalation and resolve once the patient is on a stable dose.

Patients should be counseled about the less than 1% risk for gallbladder issues or pancreatitis. They should be instructed to go to an urgent care or emergency room if they develop severe abdominal pain, recurrent vomiting, or the inability to eat or drink.
 

Contraindications

We don’t prescribe GLP-1 receptor agonists, including semaglutide 2.4 mg, in patients with a personal or family history of medullary thyroid cancer. GLP-1 agonists are contraindicated in patients with a history of pancreatitis or gastroparesis. All FDA-approved antiobesity medications are contraindicated in women who are breastfeeding or trying for pregnancy. If this patient would like to pursue pregnancy again, semaglutide 2.4 mg should be stopped 2 months prior to conception.

Access

In this case, the patient’s insurance covered semaglutide 2.4 mg with a copay of $25 per month. Without insurance, semaglutide 2.4 mg (Wegovy) costs about $1,400 per month, and semaglutide 2.0 mg (Ozempic), the formulation approved for type 2 diabetes, costs up to $1,000 per month. These price ranges are often cost-prohibitive and unsustainable, especially because these medications are intended for long-term use.

Currently, Medicare does not cover antiobesity medications nor do most state Medicaid plans. Therefore, these medications are usually not considered by patients who have Medicare or Medicaid insurance.

Because insurance coverage varies and out-of-pocket costs can be prohibitive, many individuals seek other ways of acquiring semaglutide. The off-label use of semaglutide 2.0 mg (Ozempic) for obesity is scientifically supported and safe, whereas the use of compounded semaglutide is risky due to lack of regulation.

Compounded semaglutide should be avoided, given that these products are not controlled by the FDA, and adverse events have been reported in connection with compounded semaglutide.

In our clinical practice, patients have reported advertisements for “generic semaglutide” compounded with vitamins like vitamin B12 or B6. This is a significant area of concern because some vitamins (for instance, vitamin B6) are toxic at high doses.

We discussed the dangers of compounded semaglutide with our patient and told her that this isn’t something we recommend prescribing. If the patient didn’t want to wait for semaglutide 2.4 mg to be available at her pharmacy, we discussed alternative medications used for the management of obesity, such as other FDA-approved GLP-1 agonists (that is, liraglutide 3.0 mg) and off-label medications. In this case, the patient opted to wait for semaglutide 2.4 mg because she preferred a weekly injectable medication, given her busy lifestyle as a new mom.

Dr. Schmitz, of Weill Cornell Medicine, New York, disclosed no relevant financial relationships. Dr. Tchang, of Weill Cornell Medicine and the Iris Cantor Women's Health Center, both in New York, serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for Gelesis and Novo Nordisk, and has received income from Gelesis.

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

A 36-year-old woman presents to your office for assistance with weight loss. She usually weighs around 150 lb, but she had two pregnancies in the past 4 years and has gained 70 lb. Her current weight is 220 lb with a body mass index (BMI) of 36.6 kg/m2, and she has been unable to lose any weight despite diet and exercise. She reports back pain and generalized fatigue but is primarily worried about developing type 2 diabetes, which runs in her family. Her insurance covers weight loss medications, but she is asking if she can take “Ozempic off-label” or “compounded semaglutide” instead because Wegovy isn’t available at her local pharmacy.

More and more people are turning to “medical weight management” to drop pounds and improve their health. This is a strategy that adds pharmacotherapy to lifestyle modifications to treat the chronic disease of obesity, and it is analogous to the treatment of high blood pressure or high cholesterol with medications.

This patient meets the criteria set forth by the American Heart Association, American College of Cardiology, and The Obesity Society for the management of obesity with antiobesity medications:

• BMI ≥ 30 or BMI ≥ 27 with weight-related comorbidities and
• Has been unable to achieve ≥ 5% weight loss with lifestyle changes alone.

Several U.S. Food and Drug Administration–approved antiobesity medications have been proven to cause clinically significant weight loss:

• orlistat (Alli or Xenical).
• phentermine/topiramate (Qsymia).
• naltrexone/bupropion (Contrave).
• liraglutide 3.0 mg subcutaneously daily (Saxenda).
• semaglutide 2.4 mg subcutaneously weekly (Wegovy).

When considering an antiobesity medication for a patient, it’s important to discuss efficacy, side-effect profile, contraindications, cost and coverage, and long-term use.

In this commentary, we’ll specifically focus on semaglutide (Wegovy) as it is currently the most effective FDA-approved medication for weight loss.
 

Efficacy

In a phase 3 clinical trial, patients on semaglutide 2.4 mg weekly lost an average of 15% of their body weight at 68 weeks, or approximately 33 lb. It is important to note that there is variability in treatment response to semaglutide 2.4 mg, just like with any other medication. About 1 in 3 individuals lost ≥ 20% of their weight, but about 1 in every 10 patients did not lose any weight.

In this patient, who has a family history of type 2 diabetes, weight loss with semaglutide 2.4 mg will probably reduce her risk of developing diabetes. With just 5%-10% weight loss, she will see improvements in her blood glucose, blood pressure, and cholesterol. Even greater weight loss (≥ 10%) has been associated with resolution of fatty liver and sleep apnea.
 

Side effects

Before starting semaglutide, patients should be counseled about potential gastrointestinal side effects, including nausea, upset stomach, diarrhea, constipation, and reflux.

Side effects can be managed with dietary modifications, over-the-counter treatments, and slow dose escalation. Some common tips include:

• Eat slowly.
• Eat a bland diet.
• Avoid fatty or fried foods.
• Avoid lying down immediately after eating.
• Prioritize water and fiber intake to mitigate constipation.
• Use over-the-counter treatments as needed (for example, laxative for constipation).

Most of these side effects are present only during dose escalation and resolve once the patient is on a stable dose.

Patients should be counseled about the less than 1% risk for gallbladder issues or pancreatitis. They should be instructed to go to an urgent care or emergency room if they develop severe abdominal pain, recurrent vomiting, or the inability to eat or drink.
 

Contraindications

We don’t prescribe GLP-1 receptor agonists, including semaglutide 2.4 mg, in patients with a personal or family history of medullary thyroid cancer. GLP-1 agonists are contraindicated in patients with a history of pancreatitis or gastroparesis. All FDA-approved antiobesity medications are contraindicated in women who are breastfeeding or trying for pregnancy. If this patient would like to pursue pregnancy again, semaglutide 2.4 mg should be stopped 2 months prior to conception.

Access

In this case, the patient’s insurance covered semaglutide 2.4 mg with a copay of $25 per month. Without insurance, semaglutide 2.4 mg (Wegovy) costs about $1,400 per month, and semaglutide 2.0 mg (Ozempic), the formulation approved for type 2 diabetes, costs up to $1,000 per month. These price ranges are often cost-prohibitive and unsustainable, especially because these medications are intended for long-term use.

Currently, Medicare does not cover antiobesity medications nor do most state Medicaid plans. Therefore, these medications are usually not considered by patients who have Medicare or Medicaid insurance.

Because insurance coverage varies and out-of-pocket costs can be prohibitive, many individuals seek other ways of acquiring semaglutide. The off-label use of semaglutide 2.0 mg (Ozempic) for obesity is scientifically supported and safe, whereas the use of compounded semaglutide is risky due to lack of regulation.

Compounded semaglutide should be avoided, given that these products are not controlled by the FDA, and adverse events have been reported in connection with compounded semaglutide.

In our clinical practice, patients have reported advertisements for “generic semaglutide” compounded with vitamins like vitamin B12 or B6. This is a significant area of concern because some vitamins (for instance, vitamin B6) are toxic at high doses.

We discussed the dangers of compounded semaglutide with our patient and told her that this isn’t something we recommend prescribing. If the patient didn’t want to wait for semaglutide 2.4 mg to be available at her pharmacy, we discussed alternative medications used for the management of obesity, such as other FDA-approved GLP-1 agonists (that is, liraglutide 3.0 mg) and off-label medications. In this case, the patient opted to wait for semaglutide 2.4 mg because she preferred a weekly injectable medication, given her busy lifestyle as a new mom.

Dr. Schmitz, of Weill Cornell Medicine, New York, disclosed no relevant financial relationships. Dr. Tchang, of Weill Cornell Medicine and the Iris Cantor Women's Health Center, both in New York, serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for Gelesis and Novo Nordisk, and has received income from Gelesis.

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

A 36-year-old woman presents to your office for assistance with weight loss. She usually weighs around 150 lb, but she had two pregnancies in the past 4 years and has gained 70 lb. Her current weight is 220 lb with a body mass index (BMI) of 36.6 kg/m2, and she has been unable to lose any weight despite diet and exercise. She reports back pain and generalized fatigue but is primarily worried about developing type 2 diabetes, which runs in her family. Her insurance covers weight loss medications, but she is asking if she can take “Ozempic off-label” or “compounded semaglutide” instead because Wegovy isn’t available at her local pharmacy.

More and more people are turning to “medical weight management” to drop pounds and improve their health. This is a strategy that adds pharmacotherapy to lifestyle modifications to treat the chronic disease of obesity, and it is analogous to the treatment of high blood pressure or high cholesterol with medications.

This patient meets the criteria set forth by the American Heart Association, American College of Cardiology, and The Obesity Society for the management of obesity with antiobesity medications:

• BMI ≥ 30 or BMI ≥ 27 with weight-related comorbidities and
• Has been unable to achieve ≥ 5% weight loss with lifestyle changes alone.

Several U.S. Food and Drug Administration–approved antiobesity medications have been proven to cause clinically significant weight loss:

• orlistat (Alli or Xenical).
• phentermine/topiramate (Qsymia).
• naltrexone/bupropion (Contrave).
• liraglutide 3.0 mg subcutaneously daily (Saxenda).
• semaglutide 2.4 mg subcutaneously weekly (Wegovy).

When considering an antiobesity medication for a patient, it’s important to discuss efficacy, side-effect profile, contraindications, cost and coverage, and long-term use.

In this commentary, we’ll specifically focus on semaglutide (Wegovy) as it is currently the most effective FDA-approved medication for weight loss.
 

Efficacy

In a phase 3 clinical trial, patients on semaglutide 2.4 mg weekly lost an average of 15% of their body weight at 68 weeks, or approximately 33 lb. It is important to note that there is variability in treatment response to semaglutide 2.4 mg, just like with any other medication. About 1 in 3 individuals lost ≥ 20% of their weight, but about 1 in every 10 patients did not lose any weight.

In this patient, who has a family history of type 2 diabetes, weight loss with semaglutide 2.4 mg will probably reduce her risk of developing diabetes. With just 5%-10% weight loss, she will see improvements in her blood glucose, blood pressure, and cholesterol. Even greater weight loss (≥ 10%) has been associated with resolution of fatty liver and sleep apnea.
 

Side effects

Before starting semaglutide, patients should be counseled about potential gastrointestinal side effects, including nausea, upset stomach, diarrhea, constipation, and reflux.

Side effects can be managed with dietary modifications, over-the-counter treatments, and slow dose escalation. Some common tips include:

• Eat slowly.
• Eat a bland diet.
• Avoid fatty or fried foods.
• Avoid lying down immediately after eating.
• Prioritize water and fiber intake to mitigate constipation.
• Use over-the-counter treatments as needed (for example, laxative for constipation).

Most of these side effects are present only during dose escalation and resolve once the patient is on a stable dose.

Patients should be counseled about the less than 1% risk for gallbladder issues or pancreatitis. They should be instructed to go to an urgent care or emergency room if they develop severe abdominal pain, recurrent vomiting, or the inability to eat or drink.
 

Contraindications

We don’t prescribe GLP-1 receptor agonists, including semaglutide 2.4 mg, in patients with a personal or family history of medullary thyroid cancer. GLP-1 agonists are contraindicated in patients with a history of pancreatitis or gastroparesis. All FDA-approved antiobesity medications are contraindicated in women who are breastfeeding or trying for pregnancy. If this patient would like to pursue pregnancy again, semaglutide 2.4 mg should be stopped 2 months prior to conception.

Access

In this case, the patient’s insurance covered semaglutide 2.4 mg with a copay of $25 per month. Without insurance, semaglutide 2.4 mg (Wegovy) costs about $1,400 per month, and semaglutide 2.0 mg (Ozempic), the formulation approved for type 2 diabetes, costs up to $1,000 per month. These price ranges are often cost-prohibitive and unsustainable, especially because these medications are intended for long-term use.

Currently, Medicare does not cover antiobesity medications nor do most state Medicaid plans. Therefore, these medications are usually not considered by patients who have Medicare or Medicaid insurance.

Because insurance coverage varies and out-of-pocket costs can be prohibitive, many individuals seek other ways of acquiring semaglutide. The off-label use of semaglutide 2.0 mg (Ozempic) for obesity is scientifically supported and safe, whereas the use of compounded semaglutide is risky due to lack of regulation.

Compounded semaglutide should be avoided, given that these products are not controlled by the FDA, and adverse events have been reported in connection with compounded semaglutide.

In our clinical practice, patients have reported advertisements for “generic semaglutide” compounded with vitamins like vitamin B12 or B6. This is a significant area of concern because some vitamins (for instance, vitamin B6) are toxic at high doses.

We discussed the dangers of compounded semaglutide with our patient and told her that this isn’t something we recommend prescribing. If the patient didn’t want to wait for semaglutide 2.4 mg to be available at her pharmacy, we discussed alternative medications used for the management of obesity, such as other FDA-approved GLP-1 agonists (that is, liraglutide 3.0 mg) and off-label medications. In this case, the patient opted to wait for semaglutide 2.4 mg because she preferred a weekly injectable medication, given her busy lifestyle as a new mom.

Dr. Schmitz, of Weill Cornell Medicine, New York, disclosed no relevant financial relationships. Dr. Tchang, of Weill Cornell Medicine and the Iris Cantor Women's Health Center, both in New York, serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for Gelesis and Novo Nordisk, and has received income from Gelesis.

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

Good riddance COVID-19 pandemic? Alas, that’s wishful thinking.

Many assume the pandemic is in our rearview mirror, but its biological, psychological, and social impacts continue to unfold. Its repercussions are etched into our brain, mind, emotions, behaviors, cognition, and outlook on life. Welcome to Pandemic 2.0.

Think of people who survive a heart attack. They experience multiple changes. Their initial ephemeral thrill of beating death is rapidly tempered with anxiety and worry about a future myocardial infarction and health issues in general. They become more risk-averse and more prone to dysphoria, irritability, and impatience. These individuals adopt a healthy lifestyle (diet and exercise), which they had neglected before. They develop more disciplined personality traits, feel a greater appreciation for being alive, and develop a closer affinity to family and friends. Simple things they had overlooked become more meaningful. They reevaluate their life goals, including career vs personal fulfilment. Some may overindulge in pleasurable activities in case their heart fails again. Some of those changes may be abrupt or transient, while others may become permanent features of their lives. And some may seek psychotherapy, which they may never have considered before.

The pandemic is the equivalent of a “societal cardiac arrest.” Its immediate impact was devastating. Bustling cities suddenly became ghost towns. Schools were closed, and children were locked at home with their parents, who were laid off. Businesses shut down; the economy tanked. Anxiety about being infected and dying skyrocketed, triggering a universal acute stress reaction that worsened the mental health of the population, but especially of the millions with preexisting psychiatric disorders. Routine medical and dental care stopped. Television and social media disseminated alarming updates about massive intensive care unit admissions and morgues overflowing with corpses of COVID-19 victims. Posttraumatic stress disorder (PTSD) was brewing across the nation as everyone faced this life-threatening pandemic.

The warp-speed development of vaccines for COVID-19 was equivalent to a defibrillator for the societal asystole, but the turmoil continued among the frazzled population. Some refused the vaccine due to conspiracy theories about their dangerous adverse effects. Employees in the private sector, state and federal government, and even the military who refused the mandatory vaccination lost their jobs. Controversy about shuttering schools and depriving children of face-to-face learning and socializing prompted some states to keep schools open, in contrast to most other states. Anger escalated about wearing masks, social distancing, and avoiding gatherings such as at restaurants or houses of worship. Cynicism and mistrust sprouted about the competence and reliability of health “experts” due to some conflicting signals, precluding wide adherence to medical advice.

The lingering effects of the COVID-19 pandemic

Those were the immediate repercussions of the pandemic. But what are its lingering effects? The sequelae extend across 1) the health care system; 2) the mental and emotional wellness of the population; 3) education; 4) work culture; 5) the economy; 6) societal operations; 7) technological and digital transformations; 8) mistrust in various societal institutions; 9) lack of confidence in medical information; and 10) preparedness for another pandemic due to a new strain.

As all psychiatrists know, the demand for mental health services continues to surge well after the pandemic has subsided, straining access to outpatient and inpatient care. Multiple lines of evidence confirm a deterioration in the long-term psychological well-being of children and adolescents because of lockdowns, social isolation, and anxiety about their own health and the health of their loved ones, leading to a serious rise in depression and suicidal behavior.^1-3

Contunue to: Adults who survived pandemic...

Adults who survived the pandemic experienced grief during 2 very stressful years, with no peace of mind or “normal living.” Many began to contemplate the meaning of life and reevaluate the future, waxing more philosophical and embarking on “personal archeology.” The fragility of life suddenly became a ubiquitous epiphany that changed people’s habits. Working from home, which was necessary during the pandemic, became a preferred option for many, and home became an emotional refuge, not just a physical, brick-and-mortar refuge. Millions decided to quit working altogether (the “great resignation”).

Sexual activity declined precipitously during the pandemic for singles (French kissing became “the kiss of death”) but intercourse increased among couples, eventuating in a significant rise in births after the pandemic (a baby boomlet). Sexual interest among college students declined after the pandemic, which may be either due to fear of getting infected or a sublimation of libido to invest the energy in other, less risky activities.

At the societal level, the pandemic’s sequelae included a major shift to virtual communications, not just in health care (telepsychiatry and telemedicine) but also in business. Technology saved the day during the nadir of the pandemic by enabling psychiatrists and psychotherapists to treat their patients remotely. This was not technologically feasible during the past century’s influenza pandemics (1918, 1957, and 1968).

The intellectual and social development of an entire generation of children was stunted due to the COVID-19 pandemic. Consequences will continue to emerge in the years to come and may have ripple effects on this generation’s functioning. This may have particularly affected children of lower socioeconomic status, whose families cannot afford private schools and who are in dire need of good education to put them on the path of upward mobility.

As for adults who did not get infected by COVID-19, they suffered in 2 ways. First, they experienced a certain degree of brain atrophy, which is known to occur in chronic stress. This is attributed to persistent hypercortisolemia, which is toxic to the hippocampus. PTSD is well known to be associated with hippocampal atrophy.⁴ Additionally, a significant proportion of adults who contracted the COVID-19 virus and “recovered” were subsequently diagnosed with “long COVID,” with multiple neuropsychiatric symptoms, including psychosis, mania, depression, and panic attacks, as well as memory impairment and loss of the senses of smell and taste. For these individuals, the pandemic has not subsided; they will carry its neuropsychiatric scars for a long time.

Continue to: Economically, the pandemic...

Economically, the pandemic caused a horrific economic setback in its acute phase, which prompted the government to spend trillions to support the unemployed as well as blighted businesses. The economic sequalae of deficit spending of unprecedented proportions due to the pandemic triggered painful inflation that is ongoing. Interestingly, the numerical terms “billion” and “trillion” lost their loftiness as very huge numbers. Few people realize that counting to a billion (at one number per second) would take 31.7 years, while counting to a trillion would take 31,700 years! The inflationary impact of spending $6 trillion (which would take almost 200,000 years to count) becomes mathematically jarring. And despite the heroic measures to support the economy, some business perished, although others were created, changing the human architecture of the economy.

The pandemic drastically suppressed the “hunting and gathering” instinct of humans and demolished the fabled concept of work ethic. The “great resignation,” coupled with a desire to work from home on a mass scale, led to a glut of vacant office space in many large cities, lowering the value of commercial real estate. Following the pandemic, there was an uptick in moving away from urban areas, reflecting a creative destruction and reversal of a decades-long trend to gravitate to cities to work or live.

There was also political fallout from the pandemic. Staying at home is conducive to overdosing on television and social media, leading to an intensification and ossification of political hyperpartisanship and the further displacement of religious beliefs by passionately entrenched political beliefs. This continues to have seismic effects on political stability and harmony in our country. The pandemic may have instigated new models of national voting, which triggered further political friction.

Other examples of the pandemic’s aftereffects include a shortage of lifeguards and truck drivers, replacing the traditional handshake with a first bump, and increased spending on pleasurable activities (reminiscent of the Roaring 20s following the 1918 influenza pandemic), which may reflect an instinct to “live it up” before another deadly pandemic occurs.

Ironically, as I was finishing writing this article in early September 2023, the government announced that COVID-19 cases were again rising and a new vaccine was available for the new viral “strain.”

Here we go again: as the French saying goes: plus ça change, plus c’est la même chose…

Good riddance COVID-19 pandemic? Alas, that’s wishful thinking.

Many assume the pandemic is in our rearview mirror, but its biological, psychological, and social impacts continue to unfold. Its repercussions are etched into our brain, mind, emotions, behaviors, cognition, and outlook on life. Welcome to Pandemic 2.0.

Think of people who survive a heart attack. They experience multiple changes. Their initial ephemeral thrill of beating death is rapidly tempered with anxiety and worry about a future myocardial infarction and health issues in general. They become more risk-averse and more prone to dysphoria, irritability, and impatience. These individuals adopt a healthy lifestyle (diet and exercise), which they had neglected before. They develop more disciplined personality traits, feel a greater appreciation for being alive, and develop a closer affinity to family and friends. Simple things they had overlooked become more meaningful. They reevaluate their life goals, including career vs personal fulfilment. Some may overindulge in pleasurable activities in case their heart fails again. Some of those changes may be abrupt or transient, while others may become permanent features of their lives. And some may seek psychotherapy, which they may never have considered before.

The pandemic is the equivalent of a “societal cardiac arrest.” Its immediate impact was devastating. Bustling cities suddenly became ghost towns. Schools were closed, and children were locked at home with their parents, who were laid off. Businesses shut down; the economy tanked. Anxiety about being infected and dying skyrocketed, triggering a universal acute stress reaction that worsened the mental health of the population, but especially of the millions with preexisting psychiatric disorders. Routine medical and dental care stopped. Television and social media disseminated alarming updates about massive intensive care unit admissions and morgues overflowing with corpses of COVID-19 victims. Posttraumatic stress disorder (PTSD) was brewing across the nation as everyone faced this life-threatening pandemic.

The warp-speed development of vaccines for COVID-19 was equivalent to a defibrillator for the societal asystole, but the turmoil continued among the frazzled population. Some refused the vaccine due to conspiracy theories about their dangerous adverse effects. Employees in the private sector, state and federal government, and even the military who refused the mandatory vaccination lost their jobs. Controversy about shuttering schools and depriving children of face-to-face learning and socializing prompted some states to keep schools open, in contrast to most other states. Anger escalated about wearing masks, social distancing, and avoiding gatherings such as at restaurants or houses of worship. Cynicism and mistrust sprouted about the competence and reliability of health “experts” due to some conflicting signals, precluding wide adherence to medical advice.

The lingering effects of the COVID-19 pandemic

Those were the immediate repercussions of the pandemic. But what are its lingering effects? The sequelae extend across 1) the health care system; 2) the mental and emotional wellness of the population; 3) education; 4) work culture; 5) the economy; 6) societal operations; 7) technological and digital transformations; 8) mistrust in various societal institutions; 9) lack of confidence in medical information; and 10) preparedness for another pandemic due to a new strain.

As all psychiatrists know, the demand for mental health services continues to surge well after the pandemic has subsided, straining access to outpatient and inpatient care. Multiple lines of evidence confirm a deterioration in the long-term psychological well-being of children and adolescents because of lockdowns, social isolation, and anxiety about their own health and the health of their loved ones, leading to a serious rise in depression and suicidal behavior.^1-3

Contunue to: Adults who survived pandemic...

Adults who survived the pandemic experienced grief during 2 very stressful years, with no peace of mind or “normal living.” Many began to contemplate the meaning of life and reevaluate the future, waxing more philosophical and embarking on “personal archeology.” The fragility of life suddenly became a ubiquitous epiphany that changed people’s habits. Working from home, which was necessary during the pandemic, became a preferred option for many, and home became an emotional refuge, not just a physical, brick-and-mortar refuge. Millions decided to quit working altogether (the “great resignation”).

Sexual activity declined precipitously during the pandemic for singles (French kissing became “the kiss of death”) but intercourse increased among couples, eventuating in a significant rise in births after the pandemic (a baby boomlet). Sexual interest among college students declined after the pandemic, which may be either due to fear of getting infected or a sublimation of libido to invest the energy in other, less risky activities.

At the societal level, the pandemic’s sequelae included a major shift to virtual communications, not just in health care (telepsychiatry and telemedicine) but also in business. Technology saved the day during the nadir of the pandemic by enabling psychiatrists and psychotherapists to treat their patients remotely. This was not technologically feasible during the past century’s influenza pandemics (1918, 1957, and 1968).

The intellectual and social development of an entire generation of children was stunted due to the COVID-19 pandemic. Consequences will continue to emerge in the years to come and may have ripple effects on this generation’s functioning. This may have particularly affected children of lower socioeconomic status, whose families cannot afford private schools and who are in dire need of good education to put them on the path of upward mobility.

As for adults who did not get infected by COVID-19, they suffered in 2 ways. First, they experienced a certain degree of brain atrophy, which is known to occur in chronic stress. This is attributed to persistent hypercortisolemia, which is toxic to the hippocampus. PTSD is well known to be associated with hippocampal atrophy.⁴ Additionally, a significant proportion of adults who contracted the COVID-19 virus and “recovered” were subsequently diagnosed with “long COVID,” with multiple neuropsychiatric symptoms, including psychosis, mania, depression, and panic attacks, as well as memory impairment and loss of the senses of smell and taste. For these individuals, the pandemic has not subsided; they will carry its neuropsychiatric scars for a long time.

Continue to: Economically, the pandemic...

Economically, the pandemic caused a horrific economic setback in its acute phase, which prompted the government to spend trillions to support the unemployed as well as blighted businesses. The economic sequalae of deficit spending of unprecedented proportions due to the pandemic triggered painful inflation that is ongoing. Interestingly, the numerical terms “billion” and “trillion” lost their loftiness as very huge numbers. Few people realize that counting to a billion (at one number per second) would take 31.7 years, while counting to a trillion would take 31,700 years! The inflationary impact of spending $6 trillion (which would take almost 200,000 years to count) becomes mathematically jarring. And despite the heroic measures to support the economy, some business perished, although others were created, changing the human architecture of the economy.

The pandemic drastically suppressed the “hunting and gathering” instinct of humans and demolished the fabled concept of work ethic. The “great resignation,” coupled with a desire to work from home on a mass scale, led to a glut of vacant office space in many large cities, lowering the value of commercial real estate. Following the pandemic, there was an uptick in moving away from urban areas, reflecting a creative destruction and reversal of a decades-long trend to gravitate to cities to work or live.

There was also political fallout from the pandemic. Staying at home is conducive to overdosing on television and social media, leading to an intensification and ossification of political hyperpartisanship and the further displacement of religious beliefs by passionately entrenched political beliefs. This continues to have seismic effects on political stability and harmony in our country. The pandemic may have instigated new models of national voting, which triggered further political friction.

Other examples of the pandemic’s aftereffects include a shortage of lifeguards and truck drivers, replacing the traditional handshake with a first bump, and increased spending on pleasurable activities (reminiscent of the Roaring 20s following the 1918 influenza pandemic), which may reflect an instinct to “live it up” before another deadly pandemic occurs.

Ironically, as I was finishing writing this article in early September 2023, the government announced that COVID-19 cases were again rising and a new vaccine was available for the new viral “strain.”

Here we go again: as the French saying goes: plus ça change, plus c’est la même chose…

Good riddance COVID-19 pandemic? Alas, that’s wishful thinking.

Many assume the pandemic is in our rearview mirror, but its biological, psychological, and social impacts continue to unfold. Its repercussions are etched into our brain, mind, emotions, behaviors, cognition, and outlook on life. Welcome to Pandemic 2.0.

Think of people who survive a heart attack. They experience multiple changes. Their initial ephemeral thrill of beating death is rapidly tempered with anxiety and worry about a future myocardial infarction and health issues in general. They become more risk-averse and more prone to dysphoria, irritability, and impatience. These individuals adopt a healthy lifestyle (diet and exercise), which they had neglected before. They develop more disciplined personality traits, feel a greater appreciation for being alive, and develop a closer affinity to family and friends. Simple things they had overlooked become more meaningful. They reevaluate their life goals, including career vs personal fulfilment. Some may overindulge in pleasurable activities in case their heart fails again. Some of those changes may be abrupt or transient, while others may become permanent features of their lives. And some may seek psychotherapy, which they may never have considered before.

The pandemic is the equivalent of a “societal cardiac arrest.” Its immediate impact was devastating. Bustling cities suddenly became ghost towns. Schools were closed, and children were locked at home with their parents, who were laid off. Businesses shut down; the economy tanked. Anxiety about being infected and dying skyrocketed, triggering a universal acute stress reaction that worsened the mental health of the population, but especially of the millions with preexisting psychiatric disorders. Routine medical and dental care stopped. Television and social media disseminated alarming updates about massive intensive care unit admissions and morgues overflowing with corpses of COVID-19 victims. Posttraumatic stress disorder (PTSD) was brewing across the nation as everyone faced this life-threatening pandemic.

The warp-speed development of vaccines for COVID-19 was equivalent to a defibrillator for the societal asystole, but the turmoil continued among the frazzled population. Some refused the vaccine due to conspiracy theories about their dangerous adverse effects. Employees in the private sector, state and federal government, and even the military who refused the mandatory vaccination lost their jobs. Controversy about shuttering schools and depriving children of face-to-face learning and socializing prompted some states to keep schools open, in contrast to most other states. Anger escalated about wearing masks, social distancing, and avoiding gatherings such as at restaurants or houses of worship. Cynicism and mistrust sprouted about the competence and reliability of health “experts” due to some conflicting signals, precluding wide adherence to medical advice.

The lingering effects of the COVID-19 pandemic

Those were the immediate repercussions of the pandemic. But what are its lingering effects? The sequelae extend across 1) the health care system; 2) the mental and emotional wellness of the population; 3) education; 4) work culture; 5) the economy; 6) societal operations; 7) technological and digital transformations; 8) mistrust in various societal institutions; 9) lack of confidence in medical information; and 10) preparedness for another pandemic due to a new strain.

As all psychiatrists know, the demand for mental health services continues to surge well after the pandemic has subsided, straining access to outpatient and inpatient care. Multiple lines of evidence confirm a deterioration in the long-term psychological well-being of children and adolescents because of lockdowns, social isolation, and anxiety about their own health and the health of their loved ones, leading to a serious rise in depression and suicidal behavior.^1-3

Contunue to: Adults who survived pandemic...

Adults who survived the pandemic experienced grief during 2 very stressful years, with no peace of mind or “normal living.” Many began to contemplate the meaning of life and reevaluate the future, waxing more philosophical and embarking on “personal archeology.” The fragility of life suddenly became a ubiquitous epiphany that changed people’s habits. Working from home, which was necessary during the pandemic, became a preferred option for many, and home became an emotional refuge, not just a physical, brick-and-mortar refuge. Millions decided to quit working altogether (the “great resignation”).

Sexual activity declined precipitously during the pandemic for singles (French kissing became “the kiss of death”) but intercourse increased among couples, eventuating in a significant rise in births after the pandemic (a baby boomlet). Sexual interest among college students declined after the pandemic, which may be either due to fear of getting infected or a sublimation of libido to invest the energy in other, less risky activities.

At the societal level, the pandemic’s sequelae included a major shift to virtual communications, not just in health care (telepsychiatry and telemedicine) but also in business. Technology saved the day during the nadir of the pandemic by enabling psychiatrists and psychotherapists to treat their patients remotely. This was not technologically feasible during the past century’s influenza pandemics (1918, 1957, and 1968).

The intellectual and social development of an entire generation of children was stunted due to the COVID-19 pandemic. Consequences will continue to emerge in the years to come and may have ripple effects on this generation’s functioning. This may have particularly affected children of lower socioeconomic status, whose families cannot afford private schools and who are in dire need of good education to put them on the path of upward mobility.

As for adults who did not get infected by COVID-19, they suffered in 2 ways. First, they experienced a certain degree of brain atrophy, which is known to occur in chronic stress. This is attributed to persistent hypercortisolemia, which is toxic to the hippocampus. PTSD is well known to be associated with hippocampal atrophy.⁴ Additionally, a significant proportion of adults who contracted the COVID-19 virus and “recovered” were subsequently diagnosed with “long COVID,” with multiple neuropsychiatric symptoms, including psychosis, mania, depression, and panic attacks, as well as memory impairment and loss of the senses of smell and taste. For these individuals, the pandemic has not subsided; they will carry its neuropsychiatric scars for a long time.

Continue to: Economically, the pandemic...

Economically, the pandemic caused a horrific economic setback in its acute phase, which prompted the government to spend trillions to support the unemployed as well as blighted businesses. The economic sequalae of deficit spending of unprecedented proportions due to the pandemic triggered painful inflation that is ongoing. Interestingly, the numerical terms “billion” and “trillion” lost their loftiness as very huge numbers. Few people realize that counting to a billion (at one number per second) would take 31.7 years, while counting to a trillion would take 31,700 years! The inflationary impact of spending $6 trillion (which would take almost 200,000 years to count) becomes mathematically jarring. And despite the heroic measures to support the economy, some business perished, although others were created, changing the human architecture of the economy.

The pandemic drastically suppressed the “hunting and gathering” instinct of humans and demolished the fabled concept of work ethic. The “great resignation,” coupled with a desire to work from home on a mass scale, led to a glut of vacant office space in many large cities, lowering the value of commercial real estate. Following the pandemic, there was an uptick in moving away from urban areas, reflecting a creative destruction and reversal of a decades-long trend to gravitate to cities to work or live.

There was also political fallout from the pandemic. Staying at home is conducive to overdosing on television and social media, leading to an intensification and ossification of political hyperpartisanship and the further displacement of religious beliefs by passionately entrenched political beliefs. This continues to have seismic effects on political stability and harmony in our country. The pandemic may have instigated new models of national voting, which triggered further political friction.

Other examples of the pandemic’s aftereffects include a shortage of lifeguards and truck drivers, replacing the traditional handshake with a first bump, and increased spending on pleasurable activities (reminiscent of the Roaring 20s following the 1918 influenza pandemic), which may reflect an instinct to “live it up” before another deadly pandemic occurs.

Ironically, as I was finishing writing this article in early September 2023, the government announced that COVID-19 cases were again rising and a new vaccine was available for the new viral “strain.”

Here we go again: as the French saying goes: plus ça change, plus c’est la même chose…

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact [email protected].

Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common.

One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.

What smoking does for patients with schizophrenia

The high prevalence of smoking among patients with schizophrenia (50% to 88%) greatly exceeds the rates of smoking among patients with other psychiatric illnesses.^1,2 The role of smoking in relation to schizophrenia and other psychoses is multidimensional, and evidence implicates smoking as a risk factor for schizophrenia.^3,4

Two mechanisms may help explain tobacco use in patients with schizophrenia: reducing the adverse effects of antipsychotic medications and promoting neural transmission of dopamine. Second-generation antipsychotics (SGAs) are a first-line treatment, but they can produce EPS, metabolic dysregulation, and blood disorders such as hyponatremia and (rarely) agranulocytosis (1% with clozapine).⁵ Compared to those who are nonsmokers, patients with schizophrenia who smoke are more likely to experience more severe symptoms (eg, hallucinations and delusions) and less severe EPS.^5,6 Research suggests that exposure to polycyclic aromatic hydrocarbons released during smoking induces cytochrome P450 1A2, an enzyme that metabolizes antipsychotic medications such as haloperidol, clozapine, and olanzapine. Increased metabolism results in lower serum concentrations of antipsychotics, lower efficacy, and more severe positive symptoms.^5,6

Additionally, tobacco is an activator of nicotinic acetylcholine receptors (nAChR).⁶ When these receptors become activated, dopamine is released. Dopamine serves as a mediator of reward for nicotine use. In the context of schizophrenia, tobacco use opposes the mechanism of action of SGAs, which is to block neural transmission of dopamine.⁶ The etiology of EPS is related to the blockade of postsynaptic dopamine release in the striatum.⁶ By activating nAChR, smoking induces a downstream release of dopamine that can alleviate iatrogenic EPS by restoring neural transmission of dopamine.⁶ Nicotine may also modulate alpha-7 nicotinic receptor dysfunction, and improve the ability to filter out irrelevant environmental stimuli (impaired sensory gating), which can be overwhelming for patients with schizophrenia. It also can improve cognitive dysfunction and attention by inducing the release of dopamine in mesocortical pathways.⁷ The implications of this neural pathway are significant because smoking is significantly greater in tobacco users who are diagnosed with schizophrenia compared to tobacco users who lack a psychiatric diagnosis.^6,7 Smoking may enhance dopaminergic neural transmission to a far greater extent in tobacco users with schizophrenia compared to tobacco users who do not develop schizophrenia, which suggests intrinsic differences at the neuronal level. Neural differences between tobacco users with or without schizophrenia may synergize with smoking in clinically and biologically meaningful ways. These pathways require further research to support or disprove these hypotheses.

Aside from the dopaminergic system, mechanisms influencing tobacco use among patients with schizophrenia may also be related to nicotine’s mild antidepressant effects. Evidence suggests a clinically meaningful association between nicotine dependence and mood disorders, and this association may be due to the antidepressant effects of nicotine.^8-13 Patients with schizophrenia may experience respite from depressive symptoms through their tobacco use, eventually leading to nicotine dependence.

Continue to: Treatment of schizophrenia...

Treatment of schizophrenia involves multimodal management of a patient’s life, including reducing maladaptive habits that are harmful to health. Chronic smoking in patients with schizophrenia is associated not only with atherosclerosis and cardiovascular disease, but also with poor neurologic functioning, such as significant impairment in attention, working memory, learning, executive function, reasoning, problem-solving and speed of processing.¹⁴ One study found that in patients with schizophrenia, smoking increased the 20-year cardiovascular mortality risk by 86%.¹⁵

Despite challenges to abstinence, smoking cessation should be discussed with these patients, especially given the high prevalence of smoking among this vulnerable population. Bupropion and varenicline have been studied in the context of smoking cessation among patients with schizophrenia. Data on varenicline are mixed. Smokers with schizophrenia who received bupropion showed higher rates of abstinence from smoking compared to those who received placebo.¹⁶

As part of the biopsychosocial model of clinical care, sociodemographic factors must be considered in assessing the relationship between tobacco use and schizophrenia, because a large proportion of patients diagnosed with schizophrenia are members of underrepresented minority groups.¹⁷ A PubMed database search using keywords “African American” or “Black,” “tobacco,” and “schizophrenia” located only 12 studies, most of which lacked relevance to this question. Han et al¹⁸ is 1 of the few studies to investigate sociodemographic factors as they relate to tobacco use among adults with psychoses. Social determinants of health and other confounding variables also need defining to truly distinguish causation from correlation, especially regarding tobacco use and its association with other health risk behaviors.¹⁹

Without the street medicine component of the medical school training I received, the pattern of smoking among patients with schizophrenia may have remained invisible or insignificant to me, as tobacco use is not permitted in the inpatient and outpatient academic settings. This experience not only raised insightful questions, but also emphasized the clinical value of seeing patients within their living environment.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact [email protected].

Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common.

One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.

What smoking does for patients with schizophrenia

The high prevalence of smoking among patients with schizophrenia (50% to 88%) greatly exceeds the rates of smoking among patients with other psychiatric illnesses.^1,2 The role of smoking in relation to schizophrenia and other psychoses is multidimensional, and evidence implicates smoking as a risk factor for schizophrenia.^3,4

Two mechanisms may help explain tobacco use in patients with schizophrenia: reducing the adverse effects of antipsychotic medications and promoting neural transmission of dopamine. Second-generation antipsychotics (SGAs) are a first-line treatment, but they can produce EPS, metabolic dysregulation, and blood disorders such as hyponatremia and (rarely) agranulocytosis (1% with clozapine).⁵ Compared to those who are nonsmokers, patients with schizophrenia who smoke are more likely to experience more severe symptoms (eg, hallucinations and delusions) and less severe EPS.^5,6 Research suggests that exposure to polycyclic aromatic hydrocarbons released during smoking induces cytochrome P450 1A2, an enzyme that metabolizes antipsychotic medications such as haloperidol, clozapine, and olanzapine. Increased metabolism results in lower serum concentrations of antipsychotics, lower efficacy, and more severe positive symptoms.^5,6

Additionally, tobacco is an activator of nicotinic acetylcholine receptors (nAChR).⁶ When these receptors become activated, dopamine is released. Dopamine serves as a mediator of reward for nicotine use. In the context of schizophrenia, tobacco use opposes the mechanism of action of SGAs, which is to block neural transmission of dopamine.⁶ The etiology of EPS is related to the blockade of postsynaptic dopamine release in the striatum.⁶ By activating nAChR, smoking induces a downstream release of dopamine that can alleviate iatrogenic EPS by restoring neural transmission of dopamine.⁶ Nicotine may also modulate alpha-7 nicotinic receptor dysfunction, and improve the ability to filter out irrelevant environmental stimuli (impaired sensory gating), which can be overwhelming for patients with schizophrenia. It also can improve cognitive dysfunction and attention by inducing the release of dopamine in mesocortical pathways.⁷ The implications of this neural pathway are significant because smoking is significantly greater in tobacco users who are diagnosed with schizophrenia compared to tobacco users who lack a psychiatric diagnosis.^6,7 Smoking may enhance dopaminergic neural transmission to a far greater extent in tobacco users with schizophrenia compared to tobacco users who do not develop schizophrenia, which suggests intrinsic differences at the neuronal level. Neural differences between tobacco users with or without schizophrenia may synergize with smoking in clinically and biologically meaningful ways. These pathways require further research to support or disprove these hypotheses.

Aside from the dopaminergic system, mechanisms influencing tobacco use among patients with schizophrenia may also be related to nicotine’s mild antidepressant effects. Evidence suggests a clinically meaningful association between nicotine dependence and mood disorders, and this association may be due to the antidepressant effects of nicotine.^8-13 Patients with schizophrenia may experience respite from depressive symptoms through their tobacco use, eventually leading to nicotine dependence.

Continue to: Treatment of schizophrenia...

Treatment of schizophrenia involves multimodal management of a patient’s life, including reducing maladaptive habits that are harmful to health. Chronic smoking in patients with schizophrenia is associated not only with atherosclerosis and cardiovascular disease, but also with poor neurologic functioning, such as significant impairment in attention, working memory, learning, executive function, reasoning, problem-solving and speed of processing.¹⁴ One study found that in patients with schizophrenia, smoking increased the 20-year cardiovascular mortality risk by 86%.¹⁵

Despite challenges to abstinence, smoking cessation should be discussed with these patients, especially given the high prevalence of smoking among this vulnerable population. Bupropion and varenicline have been studied in the context of smoking cessation among patients with schizophrenia. Data on varenicline are mixed. Smokers with schizophrenia who received bupropion showed higher rates of abstinence from smoking compared to those who received placebo.¹⁶

As part of the biopsychosocial model of clinical care, sociodemographic factors must be considered in assessing the relationship between tobacco use and schizophrenia, because a large proportion of patients diagnosed with schizophrenia are members of underrepresented minority groups.¹⁷ A PubMed database search using keywords “African American” or “Black,” “tobacco,” and “schizophrenia” located only 12 studies, most of which lacked relevance to this question. Han et al¹⁸ is 1 of the few studies to investigate sociodemographic factors as they relate to tobacco use among adults with psychoses. Social determinants of health and other confounding variables also need defining to truly distinguish causation from correlation, especially regarding tobacco use and its association with other health risk behaviors.¹⁹

Without the street medicine component of the medical school training I received, the pattern of smoking among patients with schizophrenia may have remained invisible or insignificant to me, as tobacco use is not permitted in the inpatient and outpatient academic settings. This experience not only raised insightful questions, but also emphasized the clinical value of seeing patients within their living environment.

Editor’s note: Readers’ Forum is a department for correspondence from readers that is not in response to articles published in Current Psychiatry. All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact [email protected].

Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common.

One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.

What smoking does for patients with schizophrenia

The high prevalence of smoking among patients with schizophrenia (50% to 88%) greatly exceeds the rates of smoking among patients with other psychiatric illnesses.^1,2 The role of smoking in relation to schizophrenia and other psychoses is multidimensional, and evidence implicates smoking as a risk factor for schizophrenia.^3,4

Two mechanisms may help explain tobacco use in patients with schizophrenia: reducing the adverse effects of antipsychotic medications and promoting neural transmission of dopamine. Second-generation antipsychotics (SGAs) are a first-line treatment, but they can produce EPS, metabolic dysregulation, and blood disorders such as hyponatremia and (rarely) agranulocytosis (1% with clozapine).⁵ Compared to those who are nonsmokers, patients with schizophrenia who smoke are more likely to experience more severe symptoms (eg, hallucinations and delusions) and less severe EPS.^5,6 Research suggests that exposure to polycyclic aromatic hydrocarbons released during smoking induces cytochrome P450 1A2, an enzyme that metabolizes antipsychotic medications such as haloperidol, clozapine, and olanzapine. Increased metabolism results in lower serum concentrations of antipsychotics, lower efficacy, and more severe positive symptoms.^5,6

Additionally, tobacco is an activator of nicotinic acetylcholine receptors (nAChR).⁶ When these receptors become activated, dopamine is released. Dopamine serves as a mediator of reward for nicotine use. In the context of schizophrenia, tobacco use opposes the mechanism of action of SGAs, which is to block neural transmission of dopamine.⁶ The etiology of EPS is related to the blockade of postsynaptic dopamine release in the striatum.⁶ By activating nAChR, smoking induces a downstream release of dopamine that can alleviate iatrogenic EPS by restoring neural transmission of dopamine.⁶ Nicotine may also modulate alpha-7 nicotinic receptor dysfunction, and improve the ability to filter out irrelevant environmental stimuli (impaired sensory gating), which can be overwhelming for patients with schizophrenia. It also can improve cognitive dysfunction and attention by inducing the release of dopamine in mesocortical pathways.⁷ The implications of this neural pathway are significant because smoking is significantly greater in tobacco users who are diagnosed with schizophrenia compared to tobacco users who lack a psychiatric diagnosis.^6,7 Smoking may enhance dopaminergic neural transmission to a far greater extent in tobacco users with schizophrenia compared to tobacco users who do not develop schizophrenia, which suggests intrinsic differences at the neuronal level. Neural differences between tobacco users with or without schizophrenia may synergize with smoking in clinically and biologically meaningful ways. These pathways require further research to support or disprove these hypotheses.

Aside from the dopaminergic system, mechanisms influencing tobacco use among patients with schizophrenia may also be related to nicotine’s mild antidepressant effects. Evidence suggests a clinically meaningful association between nicotine dependence and mood disorders, and this association may be due to the antidepressant effects of nicotine.^8-13 Patients with schizophrenia may experience respite from depressive symptoms through their tobacco use, eventually leading to nicotine dependence.

Continue to: Treatment of schizophrenia...

Treatment of schizophrenia involves multimodal management of a patient’s life, including reducing maladaptive habits that are harmful to health. Chronic smoking in patients with schizophrenia is associated not only with atherosclerosis and cardiovascular disease, but also with poor neurologic functioning, such as significant impairment in attention, working memory, learning, executive function, reasoning, problem-solving and speed of processing.¹⁴ One study found that in patients with schizophrenia, smoking increased the 20-year cardiovascular mortality risk by 86%.¹⁵

Despite challenges to abstinence, smoking cessation should be discussed with these patients, especially given the high prevalence of smoking among this vulnerable population. Bupropion and varenicline have been studied in the context of smoking cessation among patients with schizophrenia. Data on varenicline are mixed. Smokers with schizophrenia who received bupropion showed higher rates of abstinence from smoking compared to those who received placebo.¹⁶

As part of the biopsychosocial model of clinical care, sociodemographic factors must be considered in assessing the relationship between tobacco use and schizophrenia, because a large proportion of patients diagnosed with schizophrenia are members of underrepresented minority groups.¹⁷ A PubMed database search using keywords “African American” or “Black,” “tobacco,” and “schizophrenia” located only 12 studies, most of which lacked relevance to this question. Han et al¹⁸ is 1 of the few studies to investigate sociodemographic factors as they relate to tobacco use among adults with psychoses. Social determinants of health and other confounding variables also need defining to truly distinguish causation from correlation, especially regarding tobacco use and its association with other health risk behaviors.¹⁹

Without the street medicine component of the medical school training I received, the pattern of smoking among patients with schizophrenia may have remained invisible or insignificant to me, as tobacco use is not permitted in the inpatient and outpatient academic settings. This experience not only raised insightful questions, but also emphasized the clinical value of seeing patients within their living environment.

Thank you very much to Drs. Vincent, Good, and El-Mallakh for their guest editorial on interventional psychiatry (“Interventional psychiatry: What are the next steps?” Current Psychiatry, July 2023, p. 7-9, doi:10.12788/cp.0378). Your addressing the “gap in training” regarding “evidence the growth of interventional psychiatry has exceeded the capacity of the current training infrastructure to provide trainees with adequate exposure to these procedures” is right on the mark, as is the observation that the Accreditation Council for Graduate Medical Education (ACGME) Psychiatry Milestones “do not indicate how competency in these therapies can be achieved.”

The Clinical Transcranial Magnetic Stimulation Society (CTMSS) is well aware of these issues and is actively addressing them:

1. We have increased the number of PULSES courses—designed to serve as intensive, introductory courses on TMS—we provide, and increased the number of members on our PULSES team to address this. We have also increased the number of PULSES scholarships for psychiatry residents that cover the costs of the conference and materials.

2. We created a standing Resident Subcommittee of our Education Committee that is focused on psychiatry resident training. We realize not all psychiatric residency programs have active TMS programs or attendings who are trained in TMS. Last year we presented lectures aimed at introducing TMS to PGY-1 and PGY-2 psychiatry residents. These were recorded and are available for free on the CTMSS website (www.clinicaltmssociety.org).

3. The Resident Subcommittee presented the American Association of Directors of Psychiatric Residency Training with a curriculum submission that was accepted and will be available to all psychiatric residents across the country free of charge. (Current Psychiatry Associate Editor Phillip G. Janicak, MD was very helpful to our subcommittee with this project.)

4. The topic of resident/fellow training in all forms of neuromodulation was discussed during our monthly Grand Rounds webinar and at our annual meeting.

5. The issue of having a broader base of knowledge and training in neuromodulation was a topic at a recent Education Committee meeting, and this year we are adding lectures on electroconvulsive therapy and esketamine to our Grand Rounds webinars. Many CTMSS members are trained and knowledgeable in multiple neuromodulation modalities.

Continue to: 6. Many CTMSS members...

6. Many CTMSS members are involved in academic programs or are invited to training programs to teach psychiatric residents as guest lecturers.

7. The UK's Royal College of Psychiatrists has requested access to our prerecorded lectures, and CTMSS members are working on translating our lectures into Spanish.

Resident education is a key component of the main goals of the CTMSS. Our Board of Directors is fully committed to resident education and has directed the Education Committee to address it. We look forward to moving forward on educating psychiatric residents, with the hope of eventually engaging the ACGME to acknowledge TMS by name in the ACGME guidelines, provide residents with at least basic information on TMS, and clarify how competency in these therapies can be achieved.

Thank you very much to Drs. Vincent, Good, and El-Mallakh for their guest editorial on interventional psychiatry (“Interventional psychiatry: What are the next steps?” Current Psychiatry, July 2023, p. 7-9, doi:10.12788/cp.0378). Your addressing the “gap in training” regarding “evidence the growth of interventional psychiatry has exceeded the capacity of the current training infrastructure to provide trainees with adequate exposure to these procedures” is right on the mark, as is the observation that the Accreditation Council for Graduate Medical Education (ACGME) Psychiatry Milestones “do not indicate how competency in these therapies can be achieved.”

The Clinical Transcranial Magnetic Stimulation Society (CTMSS) is well aware of these issues and is actively addressing them:

1. We have increased the number of PULSES courses—designed to serve as intensive, introductory courses on TMS—we provide, and increased the number of members on our PULSES team to address this. We have also increased the number of PULSES scholarships for psychiatry residents that cover the costs of the conference and materials.

2. We created a standing Resident Subcommittee of our Education Committee that is focused on psychiatry resident training. We realize not all psychiatric residency programs have active TMS programs or attendings who are trained in TMS. Last year we presented lectures aimed at introducing TMS to PGY-1 and PGY-2 psychiatry residents. These were recorded and are available for free on the CTMSS website (www.clinicaltmssociety.org).

3. The Resident Subcommittee presented the American Association of Directors of Psychiatric Residency Training with a curriculum submission that was accepted and will be available to all psychiatric residents across the country free of charge. (Current Psychiatry Associate Editor Phillip G. Janicak, MD was very helpful to our subcommittee with this project.)

4. The topic of resident/fellow training in all forms of neuromodulation was discussed during our monthly Grand Rounds webinar and at our annual meeting.

5. The issue of having a broader base of knowledge and training in neuromodulation was a topic at a recent Education Committee meeting, and this year we are adding lectures on electroconvulsive therapy and esketamine to our Grand Rounds webinars. Many CTMSS members are trained and knowledgeable in multiple neuromodulation modalities.

Continue to: 6. Many CTMSS members...

6. Many CTMSS members are involved in academic programs or are invited to training programs to teach psychiatric residents as guest lecturers.

7. The UK's Royal College of Psychiatrists has requested access to our prerecorded lectures, and CTMSS members are working on translating our lectures into Spanish.

Resident education is a key component of the main goals of the CTMSS. Our Board of Directors is fully committed to resident education and has directed the Education Committee to address it. We look forward to moving forward on educating psychiatric residents, with the hope of eventually engaging the ACGME to acknowledge TMS by name in the ACGME guidelines, provide residents with at least basic information on TMS, and clarify how competency in these therapies can be achieved.

Thank you very much to Drs. Vincent, Good, and El-Mallakh for their guest editorial on interventional psychiatry (“Interventional psychiatry: What are the next steps?” Current Psychiatry, July 2023, p. 7-9, doi:10.12788/cp.0378). Your addressing the “gap in training” regarding “evidence the growth of interventional psychiatry has exceeded the capacity of the current training infrastructure to provide trainees with adequate exposure to these procedures” is right on the mark, as is the observation that the Accreditation Council for Graduate Medical Education (ACGME) Psychiatry Milestones “do not indicate how competency in these therapies can be achieved.”

The Clinical Transcranial Magnetic Stimulation Society (CTMSS) is well aware of these issues and is actively addressing them:

1. We have increased the number of PULSES courses—designed to serve as intensive, introductory courses on TMS—we provide, and increased the number of members on our PULSES team to address this. We have also increased the number of PULSES scholarships for psychiatry residents that cover the costs of the conference and materials.

2. We created a standing Resident Subcommittee of our Education Committee that is focused on psychiatry resident training. We realize not all psychiatric residency programs have active TMS programs or attendings who are trained in TMS. Last year we presented lectures aimed at introducing TMS to PGY-1 and PGY-2 psychiatry residents. These were recorded and are available for free on the CTMSS website (www.clinicaltmssociety.org).

3. The Resident Subcommittee presented the American Association of Directors of Psychiatric Residency Training with a curriculum submission that was accepted and will be available to all psychiatric residents across the country free of charge. (Current Psychiatry Associate Editor Phillip G. Janicak, MD was very helpful to our subcommittee with this project.)

4. The topic of resident/fellow training in all forms of neuromodulation was discussed during our monthly Grand Rounds webinar and at our annual meeting.

5. The issue of having a broader base of knowledge and training in neuromodulation was a topic at a recent Education Committee meeting, and this year we are adding lectures on electroconvulsive therapy and esketamine to our Grand Rounds webinars. Many CTMSS members are trained and knowledgeable in multiple neuromodulation modalities.

Continue to: 6. Many CTMSS members...

6. Many CTMSS members are involved in academic programs or are invited to training programs to teach psychiatric residents as guest lecturers.

7. The UK's Royal College of Psychiatrists has requested access to our prerecorded lectures, and CTMSS members are working on translating our lectures into Spanish.

Resident education is a key component of the main goals of the CTMSS. Our Board of Directors is fully committed to resident education and has directed the Education Committee to address it. We look forward to moving forward on educating psychiatric residents, with the hope of eventually engaging the ACGME to acknowledge TMS by name in the ACGME guidelines, provide residents with at least basic information on TMS, and clarify how competency in these therapies can be achieved.

AGA has long been a powerful voice in advocating locally and nationally for issues of critical importance to our profession and patients.

While AGA’s advocacy efforts related to access to colorectal cancer screening are frequently highlighted, this is one aspect of a larger advocacy agenda.

This month, I wish to highlight AGA’s extensive advocacy efforts focused on expanding access to obesity treatment. More than 2 in 5 adults in the U.S. have obesity, and weight management has been shown to be beneficial in patients with comorbid gastrointestinal diseases, such as metabolic dysfunction–associated steatotic liver disease, gastroesophageal reflux disease, gallbladder disease, pancreatitis, and GI malignancy.

In 2022, Inside Scope, a podcast by AGA, featured a 6-part seriescalled “Obesity in GI.” In July, Drs. Octavia Pickett-Blakely and Naresh Gunaratnam moderated a Gastro Bites lunch-and-learn session on “Obesity in GI Care – Embracing and Putting It into Practice” in which they discussed models of care delivery supporting obesity management in GI practice.

In November 2022, AGA released “AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity,” (https://shorturl.at/bDNOV) to aid clinicians in appropriately prescribing obesity pharmacotherapy on the front lines of care.

On the policy front, in June, AGA held a Capitol Hill briefing in support of H.R.1577 - Treat and Reduce Obesity Act of 2021 (TROA), a bipartisan bill that would improve access to obesity treatment and care by expanding coverage under Medicare Part D for FDA-approved obesity pharmacotherapy, as well as related services such as behavioral, nutrition, and other counseling. Please check out our new obesity advocacy toolkit for more information.

This month we update you on important multi-society guidance regarding peri-endoscopic management of GLP-1 receptor agonists. We highlight new AGA Clinical Practice Updates on ostomy management and use of gastric POEM for treatment of gastroparesis, as well as a randomized controlled trial from Gastroenterology showing the effectiveness of hemostatic powder in the management of malignant GI bleeding as compared with standard care.

In our Member Spotlight, we feature gastroenterologist Sameer Berry, MD, MBA, who discusses his role as a physician-entrepreneur seeking to transform GI care delivery through his AGA GI Opportunity Fund–supported company, Oshi Health.

This issue includes our annual supplement, “Gastroenterology Data Trends.” It features a collection of contributions on GI and climate change, long COVID and the GI tract, and the evolution of targeted therapies for C. difficile, among others.

We hope you enjoy this, and all the exciting content included in our October issue.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

AGA has long been a powerful voice in advocating locally and nationally for issues of critical importance to our profession and patients.

While AGA’s advocacy efforts related to access to colorectal cancer screening are frequently highlighted, this is one aspect of a larger advocacy agenda.

This month, I wish to highlight AGA’s extensive advocacy efforts focused on expanding access to obesity treatment. More than 2 in 5 adults in the U.S. have obesity, and weight management has been shown to be beneficial in patients with comorbid gastrointestinal diseases, such as metabolic dysfunction–associated steatotic liver disease, gastroesophageal reflux disease, gallbladder disease, pancreatitis, and GI malignancy.

In 2022, Inside Scope, a podcast by AGA, featured a 6-part seriescalled “Obesity in GI.” In July, Drs. Octavia Pickett-Blakely and Naresh Gunaratnam moderated a Gastro Bites lunch-and-learn session on “Obesity in GI Care – Embracing and Putting It into Practice” in which they discussed models of care delivery supporting obesity management in GI practice.

In November 2022, AGA released “AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity,” (https://shorturl.at/bDNOV) to aid clinicians in appropriately prescribing obesity pharmacotherapy on the front lines of care.

On the policy front, in June, AGA held a Capitol Hill briefing in support of H.R.1577 - Treat and Reduce Obesity Act of 2021 (TROA), a bipartisan bill that would improve access to obesity treatment and care by expanding coverage under Medicare Part D for FDA-approved obesity pharmacotherapy, as well as related services such as behavioral, nutrition, and other counseling. Please check out our new obesity advocacy toolkit for more information.

This month we update you on important multi-society guidance regarding peri-endoscopic management of GLP-1 receptor agonists. We highlight new AGA Clinical Practice Updates on ostomy management and use of gastric POEM for treatment of gastroparesis, as well as a randomized controlled trial from Gastroenterology showing the effectiveness of hemostatic powder in the management of malignant GI bleeding as compared with standard care.

In our Member Spotlight, we feature gastroenterologist Sameer Berry, MD, MBA, who discusses his role as a physician-entrepreneur seeking to transform GI care delivery through his AGA GI Opportunity Fund–supported company, Oshi Health.

This issue includes our annual supplement, “Gastroenterology Data Trends.” It features a collection of contributions on GI and climate change, long COVID and the GI tract, and the evolution of targeted therapies for C. difficile, among others.

We hope you enjoy this, and all the exciting content included in our October issue.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

AGA has long been a powerful voice in advocating locally and nationally for issues of critical importance to our profession and patients.

While AGA’s advocacy efforts related to access to colorectal cancer screening are frequently highlighted, this is one aspect of a larger advocacy agenda.

This month, I wish to highlight AGA’s extensive advocacy efforts focused on expanding access to obesity treatment. More than 2 in 5 adults in the U.S. have obesity, and weight management has been shown to be beneficial in patients with comorbid gastrointestinal diseases, such as metabolic dysfunction–associated steatotic liver disease, gastroesophageal reflux disease, gallbladder disease, pancreatitis, and GI malignancy.

In 2022, Inside Scope, a podcast by AGA, featured a 6-part seriescalled “Obesity in GI.” In July, Drs. Octavia Pickett-Blakely and Naresh Gunaratnam moderated a Gastro Bites lunch-and-learn session on “Obesity in GI Care – Embracing and Putting It into Practice” in which they discussed models of care delivery supporting obesity management in GI practice.

In November 2022, AGA released “AGA Clinical Practice Guideline on Pharmacological Interventions for Adults With Obesity,” (https://shorturl.at/bDNOV) to aid clinicians in appropriately prescribing obesity pharmacotherapy on the front lines of care.

On the policy front, in June, AGA held a Capitol Hill briefing in support of H.R.1577 - Treat and Reduce Obesity Act of 2021 (TROA), a bipartisan bill that would improve access to obesity treatment and care by expanding coverage under Medicare Part D for FDA-approved obesity pharmacotherapy, as well as related services such as behavioral, nutrition, and other counseling. Please check out our new obesity advocacy toolkit for more information.

This month we update you on important multi-society guidance regarding peri-endoscopic management of GLP-1 receptor agonists. We highlight new AGA Clinical Practice Updates on ostomy management and use of gastric POEM for treatment of gastroparesis, as well as a randomized controlled trial from Gastroenterology showing the effectiveness of hemostatic powder in the management of malignant GI bleeding as compared with standard care.

In our Member Spotlight, we feature gastroenterologist Sameer Berry, MD, MBA, who discusses his role as a physician-entrepreneur seeking to transform GI care delivery through his AGA GI Opportunity Fund–supported company, Oshi Health.

This issue includes our annual supplement, “Gastroenterology Data Trends.” It features a collection of contributions on GI and climate change, long COVID and the GI tract, and the evolution of targeted therapies for C. difficile, among others.

We hope you enjoy this, and all the exciting content included in our October issue.

Megan A. Adams, MD, JD, MSc
Editor-in-Chief

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Massachusetts General Hospital

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

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

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Massachusetts General Hospital

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

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

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Massachusetts General Hospital

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

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

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.