Opinion

Medicare, like any other business (regardless of how you want to view it, it’s as much a business as any other insurance company), is dependent on cash flow. Money comes in from young people and their employers through withholding and taxes, and goes back out again in payments to doctors, hospitals, and all the others who bill Medicare for services and supplies in providing health care.

Unlike other businesses, it’s hampered by regulations and competing interests that affect its viability and capacity to adapt to changing markets and circumstances.

For a while, estimates were that Medicare would run out of cash in 2026, but with a stronger-then-expected COVID recovery, it’s been pushed back all the way to ... 2028.

Yeah.

The trouble here is that nobody wants to fix the system to keep it from happening. It’s easier to blame the other side for losing the game than it is to work together to win it. This isn’t a Republican or Democrat issue. Both of them are the problem.

Since Medicare started, the changes in American lifespan, population dynamics, and medical costs have meant that, as years go by, the spending on health care would eventually outstrip the cash coming in. Pushing it back 2 years doesn’t keep it from happening, though it does give more time to find a solution. But that’s only if you have people willing to do so.

Currently politicians favor a strategy of kicking the can down the road for the next congress to deal with. But we’re running out of road to kick it down, and the odds of the next generation of politicians being reasonable, functioning, adults seem to get lower each year.

Can you run your practice like that? In such a way that you know that in a few years your expenses will outweigh your income? And just figure that at some point you’ll get it figured out before your creditors come knocking?

Me neither.

If you were like me, or any other small business owner, you’d sit down and figure out what changes are needed so you’ll still have a viable business down the road.

Of course, that’s part of the issue. The people making these decisions for Medicare don’t have a vested interest in it. If it fails, they have other jobs and income sources to move on to, not to mention some pension-funded health insurance plan. It’s not their problem.

But for the patients, doctors, and other health care professionals who will be depending on it in 6 years, it is a problem, and a serious one.

Hopefully someone will listen before then.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Medicare, like any other business (regardless of how you want to view it, it’s as much a business as any other insurance company), is dependent on cash flow. Money comes in from young people and their employers through withholding and taxes, and goes back out again in payments to doctors, hospitals, and all the others who bill Medicare for services and supplies in providing health care.

Unlike other businesses, it’s hampered by regulations and competing interests that affect its viability and capacity to adapt to changing markets and circumstances.

For a while, estimates were that Medicare would run out of cash in 2026, but with a stronger-then-expected COVID recovery, it’s been pushed back all the way to ... 2028.

Yeah.

The trouble here is that nobody wants to fix the system to keep it from happening. It’s easier to blame the other side for losing the game than it is to work together to win it. This isn’t a Republican or Democrat issue. Both of them are the problem.

Since Medicare started, the changes in American lifespan, population dynamics, and medical costs have meant that, as years go by, the spending on health care would eventually outstrip the cash coming in. Pushing it back 2 years doesn’t keep it from happening, though it does give more time to find a solution. But that’s only if you have people willing to do so.

Currently politicians favor a strategy of kicking the can down the road for the next congress to deal with. But we’re running out of road to kick it down, and the odds of the next generation of politicians being reasonable, functioning, adults seem to get lower each year.

Can you run your practice like that? In such a way that you know that in a few years your expenses will outweigh your income? And just figure that at some point you’ll get it figured out before your creditors come knocking?

Me neither.

If you were like me, or any other small business owner, you’d sit down and figure out what changes are needed so you’ll still have a viable business down the road.

Of course, that’s part of the issue. The people making these decisions for Medicare don’t have a vested interest in it. If it fails, they have other jobs and income sources to move on to, not to mention some pension-funded health insurance plan. It’s not their problem.

But for the patients, doctors, and other health care professionals who will be depending on it in 6 years, it is a problem, and a serious one.

Hopefully someone will listen before then.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Medicare, like any other business (regardless of how you want to view it, it’s as much a business as any other insurance company), is dependent on cash flow. Money comes in from young people and their employers through withholding and taxes, and goes back out again in payments to doctors, hospitals, and all the others who bill Medicare for services and supplies in providing health care.

Unlike other businesses, it’s hampered by regulations and competing interests that affect its viability and capacity to adapt to changing markets and circumstances.

For a while, estimates were that Medicare would run out of cash in 2026, but with a stronger-then-expected COVID recovery, it’s been pushed back all the way to ... 2028.

Yeah.

The trouble here is that nobody wants to fix the system to keep it from happening. It’s easier to blame the other side for losing the game than it is to work together to win it. This isn’t a Republican or Democrat issue. Both of them are the problem.

Since Medicare started, the changes in American lifespan, population dynamics, and medical costs have meant that, as years go by, the spending on health care would eventually outstrip the cash coming in. Pushing it back 2 years doesn’t keep it from happening, though it does give more time to find a solution. But that’s only if you have people willing to do so.

Currently politicians favor a strategy of kicking the can down the road for the next congress to deal with. But we’re running out of road to kick it down, and the odds of the next generation of politicians being reasonable, functioning, adults seem to get lower each year.

Can you run your practice like that? In such a way that you know that in a few years your expenses will outweigh your income? And just figure that at some point you’ll get it figured out before your creditors come knocking?

Me neither.

If you were like me, or any other small business owner, you’d sit down and figure out what changes are needed so you’ll still have a viable business down the road.

Of course, that’s part of the issue. The people making these decisions for Medicare don’t have a vested interest in it. If it fails, they have other jobs and income sources to move on to, not to mention some pension-funded health insurance plan. It’s not their problem.

But for the patients, doctors, and other health care professionals who will be depending on it in 6 years, it is a problem, and a serious one.

Hopefully someone will listen before then.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

For younger generations, TikTok is a go-to site for those who like short and catchy video clips. As a social media platform that allows concise video sharing, TikTok has over 1 billion monthly global users. Because of its platform size, a plethora of resources, and influence on media discourse, TikTok is the place for content creators to share visual media. Its cursory, condensed content delivery with videos capped at 1-minute focuses on high-yield information and rapid identification of fundamental points that are both engaging and entertaining.

Currently, on TikTok, 40 billion views are associated with the hashtag #mentalhealth. Content creators and regular users are employing this platform to share their own experiences, opinions, and strategies to overcome their struggles. While it is understandable for creators to share their personal stories that may be abusive, traumatic, or violent, they may not be prepared for their video to “go viral.”

Like any other social media platform, hateful speech such as racism, sexism, or xenophobia can accumulate on TikTok, which may cause more self-harm than self-help. Oversharing about personal strategies may lead to misconceived advice for TikTok viewers, while watching these TikTok videos can have negative mental health effects, even though there are no malicious intentions behind the creators who post these videos.

Hence, public health should pay more attention to the potential health-related implications this platform can create, as the quality of the information and the qualifications of the creators are mostly unrevealed. The concerns include undisclosed conflicts of interest, unchecked spread of misinformation, difficulty identifying source credibility, and excessive false information that viewers must filter through.^1,2

Individual TikTok users may follow accounts and interpret these content creators as therapists and the content they see as therapy. They may also believe that a close relationship with the content creator exists when it does not. Specifically, these relationships may be defined as parasocial relationships, which are one-sided relationships where one person (the TikTok viewer) extends emotional energy, interest, and time, and the other party (the content creator) is completely unaware of the other’s existence.³ Additionally, Americans who are uninsured/underinsured may turn to this diluted version of therapy to compensate for the one-on-one or group therapy they need.

While TikTok may seem like a dangerous platform to browse through or post on, its growing influence cannot be underestimated. With 41% of TikTok users between the ages of 16 and 24, this is an ideal platform to disseminate public health information pertaining to this age group (for example, safe sex practices, substance abuse, and mental health issues).⁴ Because younger generations have incorporated social media into their daily lives, the medical community can harness TikTok’s potential to disseminate accurate information to potential patients for targeted medical education.

For example, Jake Goodman, MD, MBA, and Melissa Shepard, MD, each have more than a million TikTok followers and are notable psychiatrists who post a variety of content ranging from recognizing signs of depression to reducing stigma around mental health. Similarly, Justin Puder, PhD, is a licensed psychologist who advocates for ways to overcome mental health issues. By creating diverse content with appealing strategies, spreading accurate medical knowledge, and answering common medical questions for the public, these ‘mental health influencers’ educate potential patients to create patient-centered interactions.

Given the ever-changing digital media landscape, an emphasis must be placed on understanding how adolescents respond to social media in maladaptive or adaptive ways by pointing out the common strengths and weaknesses adolescents share. While there are many pros and cons to social media platforms, it is undeniable that these platforms – such as TikTok – are here to stay. It is crucial for members of the medical community to recognize the outlets that younger generations use to express themselves and to exploit these media channels therapeutically.
 

Ms. Wong is a fourth-year medical student at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y. Dr. Chua is a psychiatrist with the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia, and assistant professor of clinical psychiatry at the University of Pennsylvania, also in Philadelphia.

References

1. Gottlieb M and Dyer S. Information and Disinformation: Social Media in the COVID-19 Crisis. Acad Emerg Med. 2020 Jul;27(7):640-1. doi: 10.1111/acem.14036.

2. De Veirman M et al. Front Psychol. 2019;10:2685. doi: 10.3389/fpsyg.2019.02685.

3. Bennett N-K et al. “Parasocial Relationships: The Nature of Celebrity Fascinations.” National Register of Health Service Psychologists. https://www.findapsychologist.org/parasocial-relationships-the-nature-of-celebrity-fascinations/.

4. Eghtesadi M and Florea A. Can J Public Health. 2020 Jun;111(3):389-91. doi: 10.17269/s41997-020-00343-0.

For younger generations, TikTok is a go-to site for those who like short and catchy video clips. As a social media platform that allows concise video sharing, TikTok has over 1 billion monthly global users. Because of its platform size, a plethora of resources, and influence on media discourse, TikTok is the place for content creators to share visual media. Its cursory, condensed content delivery with videos capped at 1-minute focuses on high-yield information and rapid identification of fundamental points that are both engaging and entertaining.

Currently, on TikTok, 40 billion views are associated with the hashtag #mentalhealth. Content creators and regular users are employing this platform to share their own experiences, opinions, and strategies to overcome their struggles. While it is understandable for creators to share their personal stories that may be abusive, traumatic, or violent, they may not be prepared for their video to “go viral.”

Like any other social media platform, hateful speech such as racism, sexism, or xenophobia can accumulate on TikTok, which may cause more self-harm than self-help. Oversharing about personal strategies may lead to misconceived advice for TikTok viewers, while watching these TikTok videos can have negative mental health effects, even though there are no malicious intentions behind the creators who post these videos.

Hence, public health should pay more attention to the potential health-related implications this platform can create, as the quality of the information and the qualifications of the creators are mostly unrevealed. The concerns include undisclosed conflicts of interest, unchecked spread of misinformation, difficulty identifying source credibility, and excessive false information that viewers must filter through.^1,2

Individual TikTok users may follow accounts and interpret these content creators as therapists and the content they see as therapy. They may also believe that a close relationship with the content creator exists when it does not. Specifically, these relationships may be defined as parasocial relationships, which are one-sided relationships where one person (the TikTok viewer) extends emotional energy, interest, and time, and the other party (the content creator) is completely unaware of the other’s existence.³ Additionally, Americans who are uninsured/underinsured may turn to this diluted version of therapy to compensate for the one-on-one or group therapy they need.

While TikTok may seem like a dangerous platform to browse through or post on, its growing influence cannot be underestimated. With 41% of TikTok users between the ages of 16 and 24, this is an ideal platform to disseminate public health information pertaining to this age group (for example, safe sex practices, substance abuse, and mental health issues).⁴ Because younger generations have incorporated social media into their daily lives, the medical community can harness TikTok’s potential to disseminate accurate information to potential patients for targeted medical education.

For example, Jake Goodman, MD, MBA, and Melissa Shepard, MD, each have more than a million TikTok followers and are notable psychiatrists who post a variety of content ranging from recognizing signs of depression to reducing stigma around mental health. Similarly, Justin Puder, PhD, is a licensed psychologist who advocates for ways to overcome mental health issues. By creating diverse content with appealing strategies, spreading accurate medical knowledge, and answering common medical questions for the public, these ‘mental health influencers’ educate potential patients to create patient-centered interactions.

Given the ever-changing digital media landscape, an emphasis must be placed on understanding how adolescents respond to social media in maladaptive or adaptive ways by pointing out the common strengths and weaknesses adolescents share. While there are many pros and cons to social media platforms, it is undeniable that these platforms – such as TikTok – are here to stay. It is crucial for members of the medical community to recognize the outlets that younger generations use to express themselves and to exploit these media channels therapeutically.
 

Ms. Wong is a fourth-year medical student at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y. Dr. Chua is a psychiatrist with the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia, and assistant professor of clinical psychiatry at the University of Pennsylvania, also in Philadelphia.

References

1. Gottlieb M and Dyer S. Information and Disinformation: Social Media in the COVID-19 Crisis. Acad Emerg Med. 2020 Jul;27(7):640-1. doi: 10.1111/acem.14036.

2. De Veirman M et al. Front Psychol. 2019;10:2685. doi: 10.3389/fpsyg.2019.02685.

3. Bennett N-K et al. “Parasocial Relationships: The Nature of Celebrity Fascinations.” National Register of Health Service Psychologists. https://www.findapsychologist.org/parasocial-relationships-the-nature-of-celebrity-fascinations/.

4. Eghtesadi M and Florea A. Can J Public Health. 2020 Jun;111(3):389-91. doi: 10.17269/s41997-020-00343-0.

For younger generations, TikTok is a go-to site for those who like short and catchy video clips. As a social media platform that allows concise video sharing, TikTok has over 1 billion monthly global users. Because of its platform size, a plethora of resources, and influence on media discourse, TikTok is the place for content creators to share visual media. Its cursory, condensed content delivery with videos capped at 1-minute focuses on high-yield information and rapid identification of fundamental points that are both engaging and entertaining.

Currently, on TikTok, 40 billion views are associated with the hashtag #mentalhealth. Content creators and regular users are employing this platform to share their own experiences, opinions, and strategies to overcome their struggles. While it is understandable for creators to share their personal stories that may be abusive, traumatic, or violent, they may not be prepared for their video to “go viral.”

Like any other social media platform, hateful speech such as racism, sexism, or xenophobia can accumulate on TikTok, which may cause more self-harm than self-help. Oversharing about personal strategies may lead to misconceived advice for TikTok viewers, while watching these TikTok videos can have negative mental health effects, even though there are no malicious intentions behind the creators who post these videos.

Hence, public health should pay more attention to the potential health-related implications this platform can create, as the quality of the information and the qualifications of the creators are mostly unrevealed. The concerns include undisclosed conflicts of interest, unchecked spread of misinformation, difficulty identifying source credibility, and excessive false information that viewers must filter through.^1,2

Individual TikTok users may follow accounts and interpret these content creators as therapists and the content they see as therapy. They may also believe that a close relationship with the content creator exists when it does not. Specifically, these relationships may be defined as parasocial relationships, which are one-sided relationships where one person (the TikTok viewer) extends emotional energy, interest, and time, and the other party (the content creator) is completely unaware of the other’s existence.³ Additionally, Americans who are uninsured/underinsured may turn to this diluted version of therapy to compensate for the one-on-one or group therapy they need.

While TikTok may seem like a dangerous platform to browse through or post on, its growing influence cannot be underestimated. With 41% of TikTok users between the ages of 16 and 24, this is an ideal platform to disseminate public health information pertaining to this age group (for example, safe sex practices, substance abuse, and mental health issues).⁴ Because younger generations have incorporated social media into their daily lives, the medical community can harness TikTok’s potential to disseminate accurate information to potential patients for targeted medical education.

For example, Jake Goodman, MD, MBA, and Melissa Shepard, MD, each have more than a million TikTok followers and are notable psychiatrists who post a variety of content ranging from recognizing signs of depression to reducing stigma around mental health. Similarly, Justin Puder, PhD, is a licensed psychologist who advocates for ways to overcome mental health issues. By creating diverse content with appealing strategies, spreading accurate medical knowledge, and answering common medical questions for the public, these ‘mental health influencers’ educate potential patients to create patient-centered interactions.

Given the ever-changing digital media landscape, an emphasis must be placed on understanding how adolescents respond to social media in maladaptive or adaptive ways by pointing out the common strengths and weaknesses adolescents share. While there are many pros and cons to social media platforms, it is undeniable that these platforms – such as TikTok – are here to stay. It is crucial for members of the medical community to recognize the outlets that younger generations use to express themselves and to exploit these media channels therapeutically.
 

Ms. Wong is a fourth-year medical student at the New York Institute of Technology College of Osteopathic Medicine in Old Westbury, N.Y. Dr. Chua is a psychiatrist with the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia, and assistant professor of clinical psychiatry at the University of Pennsylvania, also in Philadelphia.

References

1. Gottlieb M and Dyer S. Information and Disinformation: Social Media in the COVID-19 Crisis. Acad Emerg Med. 2020 Jul;27(7):640-1. doi: 10.1111/acem.14036.

2. De Veirman M et al. Front Psychol. 2019;10:2685. doi: 10.3389/fpsyg.2019.02685.

3. Bennett N-K et al. “Parasocial Relationships: The Nature of Celebrity Fascinations.” National Register of Health Service Psychologists. https://www.findapsychologist.org/parasocial-relationships-the-nature-of-celebrity-fascinations/.

4. Eghtesadi M and Florea A. Can J Public Health. 2020 Jun;111(3):389-91. doi: 10.17269/s41997-020-00343-0.

It’s back to school time, and some may be wondering what the current availability of vaccines may mean and the effects of the ever-changing COVID-19 guidelines on their children’s education and day-to-day experiences as students this year.

Unlike last school year, there are now vaccines available for all over the age of 6 months, and home rapid antigen tests are more readily available. Additionally, many have now been exposed either by infection or vaccination to the virus.

The CDC has removed the recommendations for maintaining cohorts in the K-12 population. This changing landscape along with differing levels of personal risk make it challenging to counsel families about what to expect in terms of COVID this year.

The best defense that we currently have against COVID is the vaccine. Although it seems that many are susceptible to the virus despite the vaccine, those who have been vaccinated are less susceptible to serious disease, including young children.

As older children may be heading to college, it is important

to encourage them to isolate when they have symptoms, even when they test negative for COVID as we would all like to avoid being sick in general.

Additionally, they should pay attention to the COVID risk level in their area and wear masks, particularly when indoors, as the levels increase. College students should have a plan for where they can isolate when not feeling well. If anyone does test positive for COVID, they should follow the most recent quarantine guidelines, including wearing a well fitted mask when they do begin returning to activities.
 

Monkeypox

We now have a new health concern for this school year.

Monkeypox has come onto the scene with information changing as rapidly as information previously did for COVID. With this virus, we must particularly counsel those heading away to college to be careful to limit their exposure to this disease.

Dormitories and other congregate settings are high-risk locations for the spread of monkeypox. Particularly, students headed to stay in dormitories should be counseled about avoiding:

• sexual activity with those with lesions consistent with monkeypox;
• sharing eating and drinking utensils; and
• sleeping in the same bed as or sharing bedding or towels with anyone with a diagnosis of or lesions consistent with monkeypox.

Additionally, as with prevention of all infections, it is important to frequently wash hands or use alcohol-based sanitizer before eating, and avoid touching the face after using the restroom.

Guidance for those eligible for vaccines against monkeypox seems to be quickly changing as well.

At the time of this article, CDC guidance recommends the vaccine against monkeypox for:

• those considered to be at high risk for it, including those identified by public health officials as a contact of someone with monkeypox;
• those who are aware that a sexual partner had a diagnosis of monkeypox within the past 2 weeks;
• those with multiple sex partners in the past 2 weeks in an area with known monkeypox; and
• those whose jobs may expose them to monkeypox.

Currently, the CDC recommends the vaccine JYNNEOS, a two-dose vaccine that reaches maximum protection after fourteen days. Ultimately, guidance is likely to continue to quickly change for both COVID-19 and Monkeypox throughout the fall. It is possible that new vaccinations will become available, and families and physicians alike will have many questions.

Primary care offices should ensure that someone is keeping up to date with the latest guidance to share with the office so that physicians may share accurate information with their patients.

Families should be counseled that we anticipate information about monkeypox, particularly related to vaccinations, to continue to change, as it has during all stages of the COVID pandemic.

As always, patients should be reminded to continue regular routine vaccinations, including the annual influenza vaccine.

Dr. Wheat is a family physician at Erie Family Health Center and program director of Northwestern University’s McGaw Family Medicine residency program, both in Chicago. Dr. Wheat serves on the editorial advisory board of Family Practice News. You can contact her at [email protected].

It’s back to school time, and some may be wondering what the current availability of vaccines may mean and the effects of the ever-changing COVID-19 guidelines on their children’s education and day-to-day experiences as students this year.

Unlike last school year, there are now vaccines available for all over the age of 6 months, and home rapid antigen tests are more readily available. Additionally, many have now been exposed either by infection or vaccination to the virus.

The CDC has removed the recommendations for maintaining cohorts in the K-12 population. This changing landscape along with differing levels of personal risk make it challenging to counsel families about what to expect in terms of COVID this year.

The best defense that we currently have against COVID is the vaccine. Although it seems that many are susceptible to the virus despite the vaccine, those who have been vaccinated are less susceptible to serious disease, including young children.

As older children may be heading to college, it is important

to encourage them to isolate when they have symptoms, even when they test negative for COVID as we would all like to avoid being sick in general.

Additionally, they should pay attention to the COVID risk level in their area and wear masks, particularly when indoors, as the levels increase. College students should have a plan for where they can isolate when not feeling well. If anyone does test positive for COVID, they should follow the most recent quarantine guidelines, including wearing a well fitted mask when they do begin returning to activities.
 

Monkeypox

We now have a new health concern for this school year.

Monkeypox has come onto the scene with information changing as rapidly as information previously did for COVID. With this virus, we must particularly counsel those heading away to college to be careful to limit their exposure to this disease.

Dormitories and other congregate settings are high-risk locations for the spread of monkeypox. Particularly, students headed to stay in dormitories should be counseled about avoiding:

• sexual activity with those with lesions consistent with monkeypox;
• sharing eating and drinking utensils; and
• sleeping in the same bed as or sharing bedding or towels with anyone with a diagnosis of or lesions consistent with monkeypox.

Additionally, as with prevention of all infections, it is important to frequently wash hands or use alcohol-based sanitizer before eating, and avoid touching the face after using the restroom.

Guidance for those eligible for vaccines against monkeypox seems to be quickly changing as well.

At the time of this article, CDC guidance recommends the vaccine against monkeypox for:

• those considered to be at high risk for it, including those identified by public health officials as a contact of someone with monkeypox;
• those who are aware that a sexual partner had a diagnosis of monkeypox within the past 2 weeks;
• those with multiple sex partners in the past 2 weeks in an area with known monkeypox; and
• those whose jobs may expose them to monkeypox.

Currently, the CDC recommends the vaccine JYNNEOS, a two-dose vaccine that reaches maximum protection after fourteen days. Ultimately, guidance is likely to continue to quickly change for both COVID-19 and Monkeypox throughout the fall. It is possible that new vaccinations will become available, and families and physicians alike will have many questions.

Primary care offices should ensure that someone is keeping up to date with the latest guidance to share with the office so that physicians may share accurate information with their patients.

Families should be counseled that we anticipate information about monkeypox, particularly related to vaccinations, to continue to change, as it has during all stages of the COVID pandemic.

As always, patients should be reminded to continue regular routine vaccinations, including the annual influenza vaccine.

Dr. Wheat is a family physician at Erie Family Health Center and program director of Northwestern University’s McGaw Family Medicine residency program, both in Chicago. Dr. Wheat serves on the editorial advisory board of Family Practice News. You can contact her at [email protected].

It’s back to school time, and some may be wondering what the current availability of vaccines may mean and the effects of the ever-changing COVID-19 guidelines on their children’s education and day-to-day experiences as students this year.

Unlike last school year, there are now vaccines available for all over the age of 6 months, and home rapid antigen tests are more readily available. Additionally, many have now been exposed either by infection or vaccination to the virus.

The CDC has removed the recommendations for maintaining cohorts in the K-12 population. This changing landscape along with differing levels of personal risk make it challenging to counsel families about what to expect in terms of COVID this year.

The best defense that we currently have against COVID is the vaccine. Although it seems that many are susceptible to the virus despite the vaccine, those who have been vaccinated are less susceptible to serious disease, including young children.

As older children may be heading to college, it is important

to encourage them to isolate when they have symptoms, even when they test negative for COVID as we would all like to avoid being sick in general.

Additionally, they should pay attention to the COVID risk level in their area and wear masks, particularly when indoors, as the levels increase. College students should have a plan for where they can isolate when not feeling well. If anyone does test positive for COVID, they should follow the most recent quarantine guidelines, including wearing a well fitted mask when they do begin returning to activities.
 

Monkeypox

We now have a new health concern for this school year.

Monkeypox has come onto the scene with information changing as rapidly as information previously did for COVID. With this virus, we must particularly counsel those heading away to college to be careful to limit their exposure to this disease.

Dormitories and other congregate settings are high-risk locations for the spread of monkeypox. Particularly, students headed to stay in dormitories should be counseled about avoiding:

• sexual activity with those with lesions consistent with monkeypox;
• sharing eating and drinking utensils; and
• sleeping in the same bed as or sharing bedding or towels with anyone with a diagnosis of or lesions consistent with monkeypox.

Additionally, as with prevention of all infections, it is important to frequently wash hands or use alcohol-based sanitizer before eating, and avoid touching the face after using the restroom.

Guidance for those eligible for vaccines against monkeypox seems to be quickly changing as well.

At the time of this article, CDC guidance recommends the vaccine against monkeypox for:

• those considered to be at high risk for it, including those identified by public health officials as a contact of someone with monkeypox;
• those who are aware that a sexual partner had a diagnosis of monkeypox within the past 2 weeks;
• those with multiple sex partners in the past 2 weeks in an area with known monkeypox; and
• those whose jobs may expose them to monkeypox.

Currently, the CDC recommends the vaccine JYNNEOS, a two-dose vaccine that reaches maximum protection after fourteen days. Ultimately, guidance is likely to continue to quickly change for both COVID-19 and Monkeypox throughout the fall. It is possible that new vaccinations will become available, and families and physicians alike will have many questions.

Primary care offices should ensure that someone is keeping up to date with the latest guidance to share with the office so that physicians may share accurate information with their patients.

Families should be counseled that we anticipate information about monkeypox, particularly related to vaccinations, to continue to change, as it has during all stages of the COVID pandemic.

As always, patients should be reminded to continue regular routine vaccinations, including the annual influenza vaccine.

Dr. Wheat is a family physician at Erie Family Health Center and program director of Northwestern University’s McGaw Family Medicine residency program, both in Chicago. Dr. Wheat serves on the editorial advisory board of Family Practice News. You can contact her at [email protected].

The human pregnancy data reported for these 16 agents are very limited as only 8 of the drugs have this data. However, the 8 reports indicated that the use of these drugs was highly important for the mother and did not cause embryo/fetal harm.

• Acetylcysteine

The need for this antidote in a pregnant or lactating woman is most likely a rare requirement. However, the need for this agent does occur in women who have taken a potentially hepatic toxic dose of acetaminophen (e.g., Tylenol).

• Black widow spider antivenin

Only three reports of the use of this agent in a pregnant woman have been located. In each case, the symptoms from the spider bite did not respond to other therapies but did within 1 hour to the antivenin. There was no fetal harm in these cases.

• Deferasirox

This agent is an oral iron-chelating agent used for the treatment of chronic iron overload. Five case reports have described its use without causing any fetal harm.

• Deferoxamine

This agent has been used in more than 65 pregnancies for acute iron overdose or for transfusion-dependent thalassemia. No reports have observed adverse human developmental effects.

• Digoxin immune FAB (ovine)

Several reports have described the use of this agent in pregnancy. No fetal harm has been observed, but none of the reports involved exposure during organogenesis. However, in cases of digoxin overdose, the maternal benefits of therapy should take priority over the embryo/fetus.

• Dimercaprol

Although the limited animal data suggest low risk, there are no reports of the use of this drug in human organogenesis. The absence of data prevents an assessment of the embryo-fetal risk, but the maternal benefit and indirect embryo-fetal benefit appears to outweigh that risk.

• Edetate calcium disodium

This agent is used to treat acute or chronic lead poisoning. It is compatible in pregnancy because the maternal and possibly the embryo-fetal benefit appears to outweigh any unknown direct or indirect risks.

• Flumazenil

The use of this drug in the third trimester has been reported in two cases. Because the drug is indicated to reverse the effects of benzodiazepines on the central nervous system, the maternal benefit should far outweigh the unknown embryo-fetal risk.

• Glucagon

The embryo-fetal risks appear to be very low. Apparently, the drug does not cross the placenta.

• Glucarpidase

This drug is indicated for the treatment of methotrexate toxicity. There are no reports describing the use of this drug in pregnancy or during breastfeeding.

• Idarucizumab

This agent is a humanized monoclonal antibody fragment that is indicated for the reversal of the anticoagulant effects of dabigatran. No reports describing its use in human or animal pregnancy have been located. However, the maternal benefit appears to be high and probably outweighs the unknown risk to the embryo/fetus.

• Lanthanum carbonate

There are no human pregnancy or lactation data. It is used to reduce blood levels of phosphate in people with kidney disease.

• Pralidoxime

This agent relieves the paralysis of the muscles of respiration caused by an organophosphate pesticide or related compound. The human pregnancy experience is limited to two cases, one at 36 weeks and the other at 16 weeks, both of which delivered normal infants.

• Sapropterin

Four reports have described the use of sapropterin to lower blood phenylalanine levels in 31 pregnancies. There were no embryo-fetal adverse effects attributable to the drug.

• Sevelamer

Sevelamer is used to control high blood levels of phosphorus in people with chronic kidney disease who are on dialysis. There are no human pregnancy or breastfeeding data.

• Succimer

This drug is a heavy metal–chelating agent that is indicated for the treatment of lead poisoning in pediatric patients. The drug was teratogenic in rats and mice. Two reports described the use of the drug in two pregnant women for lead poisoning. It has also been used as an antidote for the treatment of arsenic, mercury, and cadmium poisoning in adults, but there have been no reports of this use in pregnant patients.

Mr. Briggs, now retired, was a clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs said he had no relevant financial disclosures. Email him at [email protected].

The human pregnancy data reported for these 16 agents are very limited as only 8 of the drugs have this data. However, the 8 reports indicated that the use of these drugs was highly important for the mother and did not cause embryo/fetal harm.

• Acetylcysteine

The need for this antidote in a pregnant or lactating woman is most likely a rare requirement. However, the need for this agent does occur in women who have taken a potentially hepatic toxic dose of acetaminophen (e.g., Tylenol).

• Black widow spider antivenin

Only three reports of the use of this agent in a pregnant woman have been located. In each case, the symptoms from the spider bite did not respond to other therapies but did within 1 hour to the antivenin. There was no fetal harm in these cases.

• Deferasirox

This agent is an oral iron-chelating agent used for the treatment of chronic iron overload. Five case reports have described its use without causing any fetal harm.

• Deferoxamine

This agent has been used in more than 65 pregnancies for acute iron overdose or for transfusion-dependent thalassemia. No reports have observed adverse human developmental effects.

• Digoxin immune FAB (ovine)

Several reports have described the use of this agent in pregnancy. No fetal harm has been observed, but none of the reports involved exposure during organogenesis. However, in cases of digoxin overdose, the maternal benefits of therapy should take priority over the embryo/fetus.

• Dimercaprol

Although the limited animal data suggest low risk, there are no reports of the use of this drug in human organogenesis. The absence of data prevents an assessment of the embryo-fetal risk, but the maternal benefit and indirect embryo-fetal benefit appears to outweigh that risk.

• Edetate calcium disodium

This agent is used to treat acute or chronic lead poisoning. It is compatible in pregnancy because the maternal and possibly the embryo-fetal benefit appears to outweigh any unknown direct or indirect risks.

• Flumazenil

The use of this drug in the third trimester has been reported in two cases. Because the drug is indicated to reverse the effects of benzodiazepines on the central nervous system, the maternal benefit should far outweigh the unknown embryo-fetal risk.

• Glucagon

The embryo-fetal risks appear to be very low. Apparently, the drug does not cross the placenta.

• Glucarpidase

This drug is indicated for the treatment of methotrexate toxicity. There are no reports describing the use of this drug in pregnancy or during breastfeeding.

• Idarucizumab

This agent is a humanized monoclonal antibody fragment that is indicated for the reversal of the anticoagulant effects of dabigatran. No reports describing its use in human or animal pregnancy have been located. However, the maternal benefit appears to be high and probably outweighs the unknown risk to the embryo/fetus.

• Lanthanum carbonate

There are no human pregnancy or lactation data. It is used to reduce blood levels of phosphate in people with kidney disease.

• Pralidoxime

This agent relieves the paralysis of the muscles of respiration caused by an organophosphate pesticide or related compound. The human pregnancy experience is limited to two cases, one at 36 weeks and the other at 16 weeks, both of which delivered normal infants.

• Sapropterin

Four reports have described the use of sapropterin to lower blood phenylalanine levels in 31 pregnancies. There were no embryo-fetal adverse effects attributable to the drug.

• Sevelamer

Sevelamer is used to control high blood levels of phosphorus in people with chronic kidney disease who are on dialysis. There are no human pregnancy or breastfeeding data.

• Succimer

This drug is a heavy metal–chelating agent that is indicated for the treatment of lead poisoning in pediatric patients. The drug was teratogenic in rats and mice. Two reports described the use of the drug in two pregnant women for lead poisoning. It has also been used as an antidote for the treatment of arsenic, mercury, and cadmium poisoning in adults, but there have been no reports of this use in pregnant patients.

Mr. Briggs, now retired, was a clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs said he had no relevant financial disclosures. Email him at [email protected].

The human pregnancy data reported for these 16 agents are very limited as only 8 of the drugs have this data. However, the 8 reports indicated that the use of these drugs was highly important for the mother and did not cause embryo/fetal harm.

• Acetylcysteine

The need for this antidote in a pregnant or lactating woman is most likely a rare requirement. However, the need for this agent does occur in women who have taken a potentially hepatic toxic dose of acetaminophen (e.g., Tylenol).

• Black widow spider antivenin

Only three reports of the use of this agent in a pregnant woman have been located. In each case, the symptoms from the spider bite did not respond to other therapies but did within 1 hour to the antivenin. There was no fetal harm in these cases.

• Deferasirox

This agent is an oral iron-chelating agent used for the treatment of chronic iron overload. Five case reports have described its use without causing any fetal harm.

• Deferoxamine

This agent has been used in more than 65 pregnancies for acute iron overdose or for transfusion-dependent thalassemia. No reports have observed adverse human developmental effects.

• Digoxin immune FAB (ovine)

Several reports have described the use of this agent in pregnancy. No fetal harm has been observed, but none of the reports involved exposure during organogenesis. However, in cases of digoxin overdose, the maternal benefits of therapy should take priority over the embryo/fetus.

• Dimercaprol

Although the limited animal data suggest low risk, there are no reports of the use of this drug in human organogenesis. The absence of data prevents an assessment of the embryo-fetal risk, but the maternal benefit and indirect embryo-fetal benefit appears to outweigh that risk.

• Edetate calcium disodium

This agent is used to treat acute or chronic lead poisoning. It is compatible in pregnancy because the maternal and possibly the embryo-fetal benefit appears to outweigh any unknown direct or indirect risks.

• Flumazenil

The use of this drug in the third trimester has been reported in two cases. Because the drug is indicated to reverse the effects of benzodiazepines on the central nervous system, the maternal benefit should far outweigh the unknown embryo-fetal risk.

• Glucagon

The embryo-fetal risks appear to be very low. Apparently, the drug does not cross the placenta.

• Glucarpidase

This drug is indicated for the treatment of methotrexate toxicity. There are no reports describing the use of this drug in pregnancy or during breastfeeding.

• Idarucizumab

This agent is a humanized monoclonal antibody fragment that is indicated for the reversal of the anticoagulant effects of dabigatran. No reports describing its use in human or animal pregnancy have been located. However, the maternal benefit appears to be high and probably outweighs the unknown risk to the embryo/fetus.

• Lanthanum carbonate

There are no human pregnancy or lactation data. It is used to reduce blood levels of phosphate in people with kidney disease.

• Pralidoxime

This agent relieves the paralysis of the muscles of respiration caused by an organophosphate pesticide or related compound. The human pregnancy experience is limited to two cases, one at 36 weeks and the other at 16 weeks, both of which delivered normal infants.

• Sapropterin

Four reports have described the use of sapropterin to lower blood phenylalanine levels in 31 pregnancies. There were no embryo-fetal adverse effects attributable to the drug.

• Sevelamer

Sevelamer is used to control high blood levels of phosphorus in people with chronic kidney disease who are on dialysis. There are no human pregnancy or breastfeeding data.

• Succimer

This drug is a heavy metal–chelating agent that is indicated for the treatment of lead poisoning in pediatric patients. The drug was teratogenic in rats and mice. Two reports described the use of the drug in two pregnant women for lead poisoning. It has also been used as an antidote for the treatment of arsenic, mercury, and cadmium poisoning in adults, but there have been no reports of this use in pregnant patients.

Mr. Briggs, now retired, was a clinical professor of pharmacy at the University of California, San Francisco, and adjunct professor of pharmacy at the University of Southern California, Los Angeles, as well as at Washington State University, Spokane. Mr. Briggs said he had no relevant financial disclosures. Email him at [email protected].

What is the real goal of weight loss? In health care, reducing excess body fat is known to improve many complications faced by patients with obesity. Even modest to moderate weight loss contributes to improvements in health. Normalizing body weight is not required.

While our culture promotes an ideal body size, in the health care setting, our attention must focus on achieving health improvement. We need to be more tolerant of variations in body size if patients are healthy. Of note, varying amounts of weight loss produce improvement in the different complications of obesity, so the amount of weight loss required for improving one condition differs from that required to improve another condition.

When we prescribe weight loss for health improvement, we are trying to reduce both the mechanical burden of fat and the excess ectopic and visceral body fat that is driving disease. The good news about the physiology of weight loss is that we do not need to attain a body mass index (BMI) of 25 or even 30 to have health improvement. The excess abnormal body fat is the first to go!

Losing weight causes a disproportional reduction in ectopic and visceral fat depots. With a 5% weight loss, visceral fat is reduced by 9%. With 16% weight loss, visceral fat is reduced by 30%. Clearing of liver fat is even more dramatic. With 16% weight loss, 65% of liver fat is cleared.

Because ectopic abnormal fat is cleared preferentially with weight loss, it affects different tissues with varying amounts of weight loss.
 

Weight loss and diabetes

A close relationship exists between weight loss and insulin sensitivity. With just 5% weight loss, insulin sensitivity in the liver and adipose tissue is greatly improved, but while muscle insulin sensitivity is improved at just 5% weight loss, it continues to improve with further weight loss. Indeed, weight loss has enormous benefits in improving glycemia in prediabetes and diabetes.

In patients with impaired glucose tolerance, weight loss of 10% can eliminate progression to type 2 diabetes. In patients with type 2 diabetes who still have beta-cell reserve, 15% weight loss can produce diabetes remission – normoglycemia without diabetes medications.
 

Weight loss and cardiovascular risk factors

Even very small amounts of weight loss – 3% – can improve triglycerides and glycemia. It takes 5% weight loss to show benefits in systolic and diastolic blood pressure, as well as in HDL and LDL cholesterol levels. For all of these, additional weight loss brings more improvement. Inflammatory markers are more difficult. It takes 10%-15% weight loss to improve most of these – for example, C-reactive protein.

Weight loss and other complications

It takes 10% or more weight loss to demonstrate improvements in symptoms in obstructive sleep apnea and gastroesophageal reflux disease. For knee pain, the relationship to improvement is not based on achieving a percentage loss. Each pound of weight lost can result in a fourfold reduction in the load exerted on the knee per step during daily activities, but it is important to reduce weight before there is structural damage, because weight loss can’t repair damaged knee joints. Moderate weight loss (5%-10%) produces improvements in quality-of-life measures, in urinary stress incontinence symptoms, and in measures of sexual function. It probably takes 15% or more weight loss to demonstrate improvement in cardiovascular events.

Must heavier patients lose more weight?

To answer this question, it is important to think in terms of percent weight loss rather than pounds or kilograms. In large studies of lifestyle intervention, of course individuals with higher BMI lost more weight. But the percentage weight loss was the same across BMI categories: class 1 (BMI 30-35), class 2 (BMI 35-40), class 3 (BMI > 40). Furthermore, the improvement in risk factors was the same across BMI categories. Those with class 3 obesity had the same improvements as those with class 1. This provides further rationale for thinking about weight loss as a percentage from baseline weight rather than as simply a weight-loss goal in pounds.

Goal setting is an important part of any behavioral intervention

At the start of a weight-loss intervention, the health care provider should raise the issue of the goal and the time course for achieving it. Patients often have unrealistic expectations, wanting to achieve large amounts of weight loss rapidly. Unfortunately, popular culture has reinforced this idea with advertisements using “lose 10 pounds the first week” and promoting before-and-after pictures of weight-loss results. The job of the health care provider is to coach and guide the patient in terms of achievable weight loss that can bring health improvement safely. Managing patient expectations is critical to long-term success.

Think in terms of percentage weight loss, not pounds, and set goals at achievable time points

Help patients translate a percent weight-loss goal to a pounds goal at 3, 6, and 12 months. With the emergence of medications approved for chronic weight management with robust weight-loss efficacy, it now is possible to achieve a weight-loss goal of 10% or 15% with regularity, and some patients will be able to achieve 20% or 25% weight loss with newer medications.

We should help our patients set a goal by calculating a goal for certain time points. A good goal for 3 months would be 5% weight loss. For our 200-lb patient, we would translate that to 10 lb in 3 months. For 6 months, the goal should be 10% (20 lb for our 200-lb patient). The usual trajectory of weight loss with lifestyle intervention alone is for a “plateau” at 6 months, although with newer medications, weight loss will continue for more than a year. That 1-year goal might be 15% (30 lb for our 200-lb patient) or even more, based on the patient’s baseline weight and body composition.

Weight-loss calculators can be useful tools for patients and health care providers. They can be found online and include the National Institutes of Health Body Weight Planner and the Pennington Biomedical Weight Loss Predictor Calculator. These tools give patients a realistic expectation of how fast weight loss can occur and provide guidelines to measure success.
 

Can patients lose too much weight?

In this patient population, losing too much weight is not typically a concern. However, newer medications are achieving average weight losses of 17% and 22% at 62 weeks, as reported by this news organization. There is a wide variation in response to these newer agents which target appetite, and many patients are losing more than the average percentages.

Remembering that the goal of weight loss is the reduction of excess abnormal body fat, we want patients to preserve as much lean mass as possible. Weight-bearing exercise can help during the weight-loss phase, but large or rapid weight loss can be concerning, especially in older individuals. When the BMI drops below 25, we want to watch patients carefully. Measurement of body composition, including bone mineral density, with dual-energy x-ray absorptiometry (DEXA) can help. This is a scenario where dose reduction of antiobesity medication can be indicated, and good clinical judgment is required to keep weight loss at healthy levels.
 

The future of weight loss

In the past, our strategy has been to promote as much weight loss as possible. With more effective medications, our strategy will have to change to a treat-to-target approach, such as we already use in hypertension and diabetes.

With the ability to produce powerful effects on appetite will come the need to not only target weight loss but to target preservation of lean mass and even to target different approaches for weight-loss maintenance. At present, we have no evidence that stopping medications results in anything other than weight regain. The study of different approaches to weight-loss maintenance will require our full attention.

Dr. Ryan has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, consultant, or trustee for: Altimmune; Amgen; Calibrate; Epitomee; Gila; Lilly; Novo Nordisk; Scientific Intake; Wondr Health; Xeno Biosciences; YSOPIA; Zealand. Received income in an amount equal to or greater than $250 from: Altimmune; Amgen; Calibrate; Epitomee; Gila; Lilly; Novo Nordisk; Scientific Intake; Wondr Health; Xeno Biosciences; YSOPIA; Zealand.

Donna Ryan, MD, is Professor Emerita, Pennington Biomedical Research Center, Louisiana State University, New Orleans.

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

What is the real goal of weight loss? In health care, reducing excess body fat is known to improve many complications faced by patients with obesity. Even modest to moderate weight loss contributes to improvements in health. Normalizing body weight is not required.

While our culture promotes an ideal body size, in the health care setting, our attention must focus on achieving health improvement. We need to be more tolerant of variations in body size if patients are healthy. Of note, varying amounts of weight loss produce improvement in the different complications of obesity, so the amount of weight loss required for improving one condition differs from that required to improve another condition.

When we prescribe weight loss for health improvement, we are trying to reduce both the mechanical burden of fat and the excess ectopic and visceral body fat that is driving disease. The good news about the physiology of weight loss is that we do not need to attain a body mass index (BMI) of 25 or even 30 to have health improvement. The excess abnormal body fat is the first to go!

Losing weight causes a disproportional reduction in ectopic and visceral fat depots. With a 5% weight loss, visceral fat is reduced by 9%. With 16% weight loss, visceral fat is reduced by 30%. Clearing of liver fat is even more dramatic. With 16% weight loss, 65% of liver fat is cleared.

Because ectopic abnormal fat is cleared preferentially with weight loss, it affects different tissues with varying amounts of weight loss.
 

Weight loss and diabetes

A close relationship exists between weight loss and insulin sensitivity. With just 5% weight loss, insulin sensitivity in the liver and adipose tissue is greatly improved, but while muscle insulin sensitivity is improved at just 5% weight loss, it continues to improve with further weight loss. Indeed, weight loss has enormous benefits in improving glycemia in prediabetes and diabetes.

In patients with impaired glucose tolerance, weight loss of 10% can eliminate progression to type 2 diabetes. In patients with type 2 diabetes who still have beta-cell reserve, 15% weight loss can produce diabetes remission – normoglycemia without diabetes medications.
 

Weight loss and cardiovascular risk factors

Even very small amounts of weight loss – 3% – can improve triglycerides and glycemia. It takes 5% weight loss to show benefits in systolic and diastolic blood pressure, as well as in HDL and LDL cholesterol levels. For all of these, additional weight loss brings more improvement. Inflammatory markers are more difficult. It takes 10%-15% weight loss to improve most of these – for example, C-reactive protein.

Weight loss and other complications

It takes 10% or more weight loss to demonstrate improvements in symptoms in obstructive sleep apnea and gastroesophageal reflux disease. For knee pain, the relationship to improvement is not based on achieving a percentage loss. Each pound of weight lost can result in a fourfold reduction in the load exerted on the knee per step during daily activities, but it is important to reduce weight before there is structural damage, because weight loss can’t repair damaged knee joints. Moderate weight loss (5%-10%) produces improvements in quality-of-life measures, in urinary stress incontinence symptoms, and in measures of sexual function. It probably takes 15% or more weight loss to demonstrate improvement in cardiovascular events.

Must heavier patients lose more weight?

To answer this question, it is important to think in terms of percent weight loss rather than pounds or kilograms. In large studies of lifestyle intervention, of course individuals with higher BMI lost more weight. But the percentage weight loss was the same across BMI categories: class 1 (BMI 30-35), class 2 (BMI 35-40), class 3 (BMI > 40). Furthermore, the improvement in risk factors was the same across BMI categories. Those with class 3 obesity had the same improvements as those with class 1. This provides further rationale for thinking about weight loss as a percentage from baseline weight rather than as simply a weight-loss goal in pounds.

Goal setting is an important part of any behavioral intervention

At the start of a weight-loss intervention, the health care provider should raise the issue of the goal and the time course for achieving it. Patients often have unrealistic expectations, wanting to achieve large amounts of weight loss rapidly. Unfortunately, popular culture has reinforced this idea with advertisements using “lose 10 pounds the first week” and promoting before-and-after pictures of weight-loss results. The job of the health care provider is to coach and guide the patient in terms of achievable weight loss that can bring health improvement safely. Managing patient expectations is critical to long-term success.

Think in terms of percentage weight loss, not pounds, and set goals at achievable time points

Help patients translate a percent weight-loss goal to a pounds goal at 3, 6, and 12 months. With the emergence of medications approved for chronic weight management with robust weight-loss efficacy, it now is possible to achieve a weight-loss goal of 10% or 15% with regularity, and some patients will be able to achieve 20% or 25% weight loss with newer medications.

We should help our patients set a goal by calculating a goal for certain time points. A good goal for 3 months would be 5% weight loss. For our 200-lb patient, we would translate that to 10 lb in 3 months. For 6 months, the goal should be 10% (20 lb for our 200-lb patient). The usual trajectory of weight loss with lifestyle intervention alone is for a “plateau” at 6 months, although with newer medications, weight loss will continue for more than a year. That 1-year goal might be 15% (30 lb for our 200-lb patient) or even more, based on the patient’s baseline weight and body composition.

Weight-loss calculators can be useful tools for patients and health care providers. They can be found online and include the National Institutes of Health Body Weight Planner and the Pennington Biomedical Weight Loss Predictor Calculator. These tools give patients a realistic expectation of how fast weight loss can occur and provide guidelines to measure success.
 

Can patients lose too much weight?

In this patient population, losing too much weight is not typically a concern. However, newer medications are achieving average weight losses of 17% and 22% at 62 weeks, as reported by this news organization. There is a wide variation in response to these newer agents which target appetite, and many patients are losing more than the average percentages.

Remembering that the goal of weight loss is the reduction of excess abnormal body fat, we want patients to preserve as much lean mass as possible. Weight-bearing exercise can help during the weight-loss phase, but large or rapid weight loss can be concerning, especially in older individuals. When the BMI drops below 25, we want to watch patients carefully. Measurement of body composition, including bone mineral density, with dual-energy x-ray absorptiometry (DEXA) can help. This is a scenario where dose reduction of antiobesity medication can be indicated, and good clinical judgment is required to keep weight loss at healthy levels.
 

The future of weight loss

In the past, our strategy has been to promote as much weight loss as possible. With more effective medications, our strategy will have to change to a treat-to-target approach, such as we already use in hypertension and diabetes.

With the ability to produce powerful effects on appetite will come the need to not only target weight loss but to target preservation of lean mass and even to target different approaches for weight-loss maintenance. At present, we have no evidence that stopping medications results in anything other than weight regain. The study of different approaches to weight-loss maintenance will require our full attention.

Dr. Ryan has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, consultant, or trustee for: Altimmune; Amgen; Calibrate; Epitomee; Gila; Lilly; Novo Nordisk; Scientific Intake; Wondr Health; Xeno Biosciences; YSOPIA; Zealand. Received income in an amount equal to or greater than $250 from: Altimmune; Amgen; Calibrate; Epitomee; Gila; Lilly; Novo Nordisk; Scientific Intake; Wondr Health; Xeno Biosciences; YSOPIA; Zealand.

Donna Ryan, MD, is Professor Emerita, Pennington Biomedical Research Center, Louisiana State University, New Orleans.

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

What is the real goal of weight loss? In health care, reducing excess body fat is known to improve many complications faced by patients with obesity. Even modest to moderate weight loss contributes to improvements in health. Normalizing body weight is not required.

While our culture promotes an ideal body size, in the health care setting, our attention must focus on achieving health improvement. We need to be more tolerant of variations in body size if patients are healthy. Of note, varying amounts of weight loss produce improvement in the different complications of obesity, so the amount of weight loss required for improving one condition differs from that required to improve another condition.

When we prescribe weight loss for health improvement, we are trying to reduce both the mechanical burden of fat and the excess ectopic and visceral body fat that is driving disease. The good news about the physiology of weight loss is that we do not need to attain a body mass index (BMI) of 25 or even 30 to have health improvement. The excess abnormal body fat is the first to go!

Losing weight causes a disproportional reduction in ectopic and visceral fat depots. With a 5% weight loss, visceral fat is reduced by 9%. With 16% weight loss, visceral fat is reduced by 30%. Clearing of liver fat is even more dramatic. With 16% weight loss, 65% of liver fat is cleared.

Because ectopic abnormal fat is cleared preferentially with weight loss, it affects different tissues with varying amounts of weight loss.
 

Weight loss and diabetes

A close relationship exists between weight loss and insulin sensitivity. With just 5% weight loss, insulin sensitivity in the liver and adipose tissue is greatly improved, but while muscle insulin sensitivity is improved at just 5% weight loss, it continues to improve with further weight loss. Indeed, weight loss has enormous benefits in improving glycemia in prediabetes and diabetes.

In patients with impaired glucose tolerance, weight loss of 10% can eliminate progression to type 2 diabetes. In patients with type 2 diabetes who still have beta-cell reserve, 15% weight loss can produce diabetes remission – normoglycemia without diabetes medications.
 

Weight loss and cardiovascular risk factors

Even very small amounts of weight loss – 3% – can improve triglycerides and glycemia. It takes 5% weight loss to show benefits in systolic and diastolic blood pressure, as well as in HDL and LDL cholesterol levels. For all of these, additional weight loss brings more improvement. Inflammatory markers are more difficult. It takes 10%-15% weight loss to improve most of these – for example, C-reactive protein.

Weight loss and other complications

It takes 10% or more weight loss to demonstrate improvements in symptoms in obstructive sleep apnea and gastroesophageal reflux disease. For knee pain, the relationship to improvement is not based on achieving a percentage loss. Each pound of weight lost can result in a fourfold reduction in the load exerted on the knee per step during daily activities, but it is important to reduce weight before there is structural damage, because weight loss can’t repair damaged knee joints. Moderate weight loss (5%-10%) produces improvements in quality-of-life measures, in urinary stress incontinence symptoms, and in measures of sexual function. It probably takes 15% or more weight loss to demonstrate improvement in cardiovascular events.

Must heavier patients lose more weight?

To answer this question, it is important to think in terms of percent weight loss rather than pounds or kilograms. In large studies of lifestyle intervention, of course individuals with higher BMI lost more weight. But the percentage weight loss was the same across BMI categories: class 1 (BMI 30-35), class 2 (BMI 35-40), class 3 (BMI > 40). Furthermore, the improvement in risk factors was the same across BMI categories. Those with class 3 obesity had the same improvements as those with class 1. This provides further rationale for thinking about weight loss as a percentage from baseline weight rather than as simply a weight-loss goal in pounds.

Goal setting is an important part of any behavioral intervention

At the start of a weight-loss intervention, the health care provider should raise the issue of the goal and the time course for achieving it. Patients often have unrealistic expectations, wanting to achieve large amounts of weight loss rapidly. Unfortunately, popular culture has reinforced this idea with advertisements using “lose 10 pounds the first week” and promoting before-and-after pictures of weight-loss results. The job of the health care provider is to coach and guide the patient in terms of achievable weight loss that can bring health improvement safely. Managing patient expectations is critical to long-term success.

Think in terms of percentage weight loss, not pounds, and set goals at achievable time points

Help patients translate a percent weight-loss goal to a pounds goal at 3, 6, and 12 months. With the emergence of medications approved for chronic weight management with robust weight-loss efficacy, it now is possible to achieve a weight-loss goal of 10% or 15% with regularity, and some patients will be able to achieve 20% or 25% weight loss with newer medications.

We should help our patients set a goal by calculating a goal for certain time points. A good goal for 3 months would be 5% weight loss. For our 200-lb patient, we would translate that to 10 lb in 3 months. For 6 months, the goal should be 10% (20 lb for our 200-lb patient). The usual trajectory of weight loss with lifestyle intervention alone is for a “plateau” at 6 months, although with newer medications, weight loss will continue for more than a year. That 1-year goal might be 15% (30 lb for our 200-lb patient) or even more, based on the patient’s baseline weight and body composition.

Weight-loss calculators can be useful tools for patients and health care providers. They can be found online and include the National Institutes of Health Body Weight Planner and the Pennington Biomedical Weight Loss Predictor Calculator. These tools give patients a realistic expectation of how fast weight loss can occur and provide guidelines to measure success.
 

Can patients lose too much weight?

In this patient population, losing too much weight is not typically a concern. However, newer medications are achieving average weight losses of 17% and 22% at 62 weeks, as reported by this news organization. There is a wide variation in response to these newer agents which target appetite, and many patients are losing more than the average percentages.

Remembering that the goal of weight loss is the reduction of excess abnormal body fat, we want patients to preserve as much lean mass as possible. Weight-bearing exercise can help during the weight-loss phase, but large or rapid weight loss can be concerning, especially in older individuals. When the BMI drops below 25, we want to watch patients carefully. Measurement of body composition, including bone mineral density, with dual-energy x-ray absorptiometry (DEXA) can help. This is a scenario where dose reduction of antiobesity medication can be indicated, and good clinical judgment is required to keep weight loss at healthy levels.
 

The future of weight loss

In the past, our strategy has been to promote as much weight loss as possible. With more effective medications, our strategy will have to change to a treat-to-target approach, such as we already use in hypertension and diabetes.

With the ability to produce powerful effects on appetite will come the need to not only target weight loss but to target preservation of lean mass and even to target different approaches for weight-loss maintenance. At present, we have no evidence that stopping medications results in anything other than weight regain. The study of different approaches to weight-loss maintenance will require our full attention.

Dr. Ryan has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, consultant, or trustee for: Altimmune; Amgen; Calibrate; Epitomee; Gila; Lilly; Novo Nordisk; Scientific Intake; Wondr Health; Xeno Biosciences; YSOPIA; Zealand. Received income in an amount equal to or greater than $250 from: Altimmune; Amgen; Calibrate; Epitomee; Gila; Lilly; Novo Nordisk; Scientific Intake; Wondr Health; Xeno Biosciences; YSOPIA; Zealand.

Donna Ryan, MD, is Professor Emerita, Pennington Biomedical Research Center, Louisiana State University, New Orleans.

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

Thursday night

It was 9 o’clock at night when my phone rang. I didn’t recognize the number but decided to answer it anyway. It was my doctor.

“Chase, I got your labs back and you have a critically low level. I spoke with someone at the hospital, I think I know what is happening, but I need you to go to the pharmacy right now and get a medicine.” She explained further and as I listened electric currents ran through my thighs until I could barely feel my legs.

“I’m so sorry, Chase. I missed it. It was low the last time we did your labs 9 months ago, and I missed it.”

In disbelief, I continued to listen as she instructed me about the next steps I was to take and prepared me for what was to come the next day.

“If you notice any changes overnight, go straight to the ED.”

My chest tingled and I could barely breathe. My mind struggled to comprehend what was happening. I looked at my husband sitting close by on the couch. He looked concerned. I tuned back in and heard her say: “Is your husband there? Can I talk to him?”

“Yes,” is all I could manage, and I handed him the phone. I sat while he listened and asked his questions. My breathing came back under my control, my legs felt wiry, and restlessness set in. “I have to get out of here,” I thought. “I have to go and pick up this medicine.”
 

Monday afternoon

I am sitting across from a PGY3 resident I have been treating since his intern year, as part of his treatment plan for managing a chronic mental illness that began in medical school. Earlier in the day, I received an urgent message from him requesting an emergency appointment.

Within a few minutes of sitting down, the story from his weekend call shift tumbled out of him. His speech became pressured, and his eyes welled with tears as he recounted in detail the steps he had taken to care for a very sick patient overnight.

“I missed it.” The dam broke and he sat sobbing in front of me, his body trembling.

I sat silently across from him. Willing him to breathe.

In time, his breathing came back under his control, and he slowly regained his composure. He continued: “I got the imaging, and I missed a bleed.”
 

Failure and shame

I can recall memorable moments from my training when I came to understand that what I initially perceived to be a mistake was instead part of the work. An example from our practice involves a patient whom I was comanaging with her primary care provider (PCP). She was not doing well following a critical work event. When I met with her after the event, she admitted having thoughts of suicide, refused a voluntary inpatient admission, and would not have met criteria for an involuntary admission. My hands were tied.

Together we created a plan to keep her safe, which included paging her PCP after hours if needed. I told her PCP before leaving that night that he might hear from her and that if she reached out, she would require hospitalization.

I arrived at work the following day, and her PCP shared with me that our patient had overdosed on medication, paged him, and was admitted to the unit.

He seemed forlorn.

I was both relieved by the news and confused by his reaction. I had hoped that she would choose a higher level of care than what we could provide her as an outpatient. I said: “This is good. She followed the plan.”

Her overdose was, of course, not part of the plan. She was struggling with several internal conflicts, including having mixed feelings about coming into the hospital; but, when the critical moment happened and she was faced with a decision to call for help or possibly die, she chose to call her PCP and have him paged as we had talked about.

I looked at her PCP. “You helped get her to where she needed to be.”

In the years of working side by side with medically trained colleagues, I have time and again needed to reframe for them that what they perceive to be a “failure” or a “crisis” is often a catalyst for change. The patient I comanaged with the PCP was a highly skilled caregiver and, as such, had been having a hard time asking for help. The hospitalization that her PCP facilitated allowed her to receive the care she needed and created an opportunity for family and friends to show up for her. Their support fed her, and she only made gains from that point on.

My training had taught me that respecting a patient’s autonomy was of the utmost importance. This instills confidence in patients as the authority in their lives. For a clinician to do this, a certain amount of helplessness must be tolerated. As I became better at identifying these moments of helplessness, feelings of failure and shame transformed.
 

Medical error

Sitting across from the PGY3 resident who I had met with weekly for the past 3 years, I thought about his error.

I thought about my phone call 4 nights earlier. My doctor was called at home by a lab technician, who never met their patients but was simply following protocol and alerted my doctor to the worsening number that she should have been aware of 9 months earlier.

Just like my doctor’s lapse of attention, my patient’s error was not a moment of helplessness to be tolerated. These were mistakes, and there was no way around it.

“People make mistakes.” I said simply.

We sat silently for a time.

I don’t remember who broke the silence. The conversation that followed was centered on our humanity and our capability for both compassion and fallibility. Afterward, I wondered who my doctor confided in and hoped she had a similar conversation.

Dr. Levesque is a clinical psychologist and clinical assistant professor of psychiatry at the Geisel School of Medicine at Dartmouth, Hanover, N.H., where she also serves on the Committee for a Respectful Learning Environment.

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

Thursday night

It was 9 o’clock at night when my phone rang. I didn’t recognize the number but decided to answer it anyway. It was my doctor.

“Chase, I got your labs back and you have a critically low level. I spoke with someone at the hospital, I think I know what is happening, but I need you to go to the pharmacy right now and get a medicine.” She explained further and as I listened electric currents ran through my thighs until I could barely feel my legs.

“I’m so sorry, Chase. I missed it. It was low the last time we did your labs 9 months ago, and I missed it.”

In disbelief, I continued to listen as she instructed me about the next steps I was to take and prepared me for what was to come the next day.

“If you notice any changes overnight, go straight to the ED.”

My chest tingled and I could barely breathe. My mind struggled to comprehend what was happening. I looked at my husband sitting close by on the couch. He looked concerned. I tuned back in and heard her say: “Is your husband there? Can I talk to him?”

“Yes,” is all I could manage, and I handed him the phone. I sat while he listened and asked his questions. My breathing came back under my control, my legs felt wiry, and restlessness set in. “I have to get out of here,” I thought. “I have to go and pick up this medicine.”
 

Monday afternoon

I am sitting across from a PGY3 resident I have been treating since his intern year, as part of his treatment plan for managing a chronic mental illness that began in medical school. Earlier in the day, I received an urgent message from him requesting an emergency appointment.

Within a few minutes of sitting down, the story from his weekend call shift tumbled out of him. His speech became pressured, and his eyes welled with tears as he recounted in detail the steps he had taken to care for a very sick patient overnight.

“I missed it.” The dam broke and he sat sobbing in front of me, his body trembling.

I sat silently across from him. Willing him to breathe.

In time, his breathing came back under his control, and he slowly regained his composure. He continued: “I got the imaging, and I missed a bleed.”
 

Failure and shame

I can recall memorable moments from my training when I came to understand that what I initially perceived to be a mistake was instead part of the work. An example from our practice involves a patient whom I was comanaging with her primary care provider (PCP). She was not doing well following a critical work event. When I met with her after the event, she admitted having thoughts of suicide, refused a voluntary inpatient admission, and would not have met criteria for an involuntary admission. My hands were tied.

Together we created a plan to keep her safe, which included paging her PCP after hours if needed. I told her PCP before leaving that night that he might hear from her and that if she reached out, she would require hospitalization.

I arrived at work the following day, and her PCP shared with me that our patient had overdosed on medication, paged him, and was admitted to the unit.

He seemed forlorn.

I was both relieved by the news and confused by his reaction. I had hoped that she would choose a higher level of care than what we could provide her as an outpatient. I said: “This is good. She followed the plan.”

Her overdose was, of course, not part of the plan. She was struggling with several internal conflicts, including having mixed feelings about coming into the hospital; but, when the critical moment happened and she was faced with a decision to call for help or possibly die, she chose to call her PCP and have him paged as we had talked about.

I looked at her PCP. “You helped get her to where she needed to be.”

In the years of working side by side with medically trained colleagues, I have time and again needed to reframe for them that what they perceive to be a “failure” or a “crisis” is often a catalyst for change. The patient I comanaged with the PCP was a highly skilled caregiver and, as such, had been having a hard time asking for help. The hospitalization that her PCP facilitated allowed her to receive the care she needed and created an opportunity for family and friends to show up for her. Their support fed her, and she only made gains from that point on.

My training had taught me that respecting a patient’s autonomy was of the utmost importance. This instills confidence in patients as the authority in their lives. For a clinician to do this, a certain amount of helplessness must be tolerated. As I became better at identifying these moments of helplessness, feelings of failure and shame transformed.
 

Medical error

Sitting across from the PGY3 resident who I had met with weekly for the past 3 years, I thought about his error.

I thought about my phone call 4 nights earlier. My doctor was called at home by a lab technician, who never met their patients but was simply following protocol and alerted my doctor to the worsening number that she should have been aware of 9 months earlier.

Just like my doctor’s lapse of attention, my patient’s error was not a moment of helplessness to be tolerated. These were mistakes, and there was no way around it.

“People make mistakes.” I said simply.

We sat silently for a time.

I don’t remember who broke the silence. The conversation that followed was centered on our humanity and our capability for both compassion and fallibility. Afterward, I wondered who my doctor confided in and hoped she had a similar conversation.

Dr. Levesque is a clinical psychologist and clinical assistant professor of psychiatry at the Geisel School of Medicine at Dartmouth, Hanover, N.H., where she also serves on the Committee for a Respectful Learning Environment.

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

Thursday night

It was 9 o’clock at night when my phone rang. I didn’t recognize the number but decided to answer it anyway. It was my doctor.

“Chase, I got your labs back and you have a critically low level. I spoke with someone at the hospital, I think I know what is happening, but I need you to go to the pharmacy right now and get a medicine.” She explained further and as I listened electric currents ran through my thighs until I could barely feel my legs.

“I’m so sorry, Chase. I missed it. It was low the last time we did your labs 9 months ago, and I missed it.”

In disbelief, I continued to listen as she instructed me about the next steps I was to take and prepared me for what was to come the next day.

“If you notice any changes overnight, go straight to the ED.”

My chest tingled and I could barely breathe. My mind struggled to comprehend what was happening. I looked at my husband sitting close by on the couch. He looked concerned. I tuned back in and heard her say: “Is your husband there? Can I talk to him?”

“Yes,” is all I could manage, and I handed him the phone. I sat while he listened and asked his questions. My breathing came back under my control, my legs felt wiry, and restlessness set in. “I have to get out of here,” I thought. “I have to go and pick up this medicine.”
 

Monday afternoon

I am sitting across from a PGY3 resident I have been treating since his intern year, as part of his treatment plan for managing a chronic mental illness that began in medical school. Earlier in the day, I received an urgent message from him requesting an emergency appointment.

Within a few minutes of sitting down, the story from his weekend call shift tumbled out of him. His speech became pressured, and his eyes welled with tears as he recounted in detail the steps he had taken to care for a very sick patient overnight.

“I missed it.” The dam broke and he sat sobbing in front of me, his body trembling.

I sat silently across from him. Willing him to breathe.

In time, his breathing came back under his control, and he slowly regained his composure. He continued: “I got the imaging, and I missed a bleed.”
 

Failure and shame

I can recall memorable moments from my training when I came to understand that what I initially perceived to be a mistake was instead part of the work. An example from our practice involves a patient whom I was comanaging with her primary care provider (PCP). She was not doing well following a critical work event. When I met with her after the event, she admitted having thoughts of suicide, refused a voluntary inpatient admission, and would not have met criteria for an involuntary admission. My hands were tied.

Together we created a plan to keep her safe, which included paging her PCP after hours if needed. I told her PCP before leaving that night that he might hear from her and that if she reached out, she would require hospitalization.

I arrived at work the following day, and her PCP shared with me that our patient had overdosed on medication, paged him, and was admitted to the unit.

He seemed forlorn.

I was both relieved by the news and confused by his reaction. I had hoped that she would choose a higher level of care than what we could provide her as an outpatient. I said: “This is good. She followed the plan.”

Her overdose was, of course, not part of the plan. She was struggling with several internal conflicts, including having mixed feelings about coming into the hospital; but, when the critical moment happened and she was faced with a decision to call for help or possibly die, she chose to call her PCP and have him paged as we had talked about.

I looked at her PCP. “You helped get her to where she needed to be.”

In the years of working side by side with medically trained colleagues, I have time and again needed to reframe for them that what they perceive to be a “failure” or a “crisis” is often a catalyst for change. The patient I comanaged with the PCP was a highly skilled caregiver and, as such, had been having a hard time asking for help. The hospitalization that her PCP facilitated allowed her to receive the care she needed and created an opportunity for family and friends to show up for her. Their support fed her, and she only made gains from that point on.

My training had taught me that respecting a patient’s autonomy was of the utmost importance. This instills confidence in patients as the authority in their lives. For a clinician to do this, a certain amount of helplessness must be tolerated. As I became better at identifying these moments of helplessness, feelings of failure and shame transformed.
 

Medical error

Sitting across from the PGY3 resident who I had met with weekly for the past 3 years, I thought about his error.

I thought about my phone call 4 nights earlier. My doctor was called at home by a lab technician, who never met their patients but was simply following protocol and alerted my doctor to the worsening number that she should have been aware of 9 months earlier.

Just like my doctor’s lapse of attention, my patient’s error was not a moment of helplessness to be tolerated. These were mistakes, and there was no way around it.

“People make mistakes.” I said simply.

We sat silently for a time.

I don’t remember who broke the silence. The conversation that followed was centered on our humanity and our capability for both compassion and fallibility. Afterward, I wondered who my doctor confided in and hoped she had a similar conversation.

Dr. Levesque is a clinical psychologist and clinical assistant professor of psychiatry at the Geisel School of Medicine at Dartmouth, Hanover, N.H., where she also serves on the Committee for a Respectful Learning Environment.

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

Recently I was reading an article on the histories behind great songs, and one section featured Procol Harem’s “A Whiter Shade of Pale.” It mentioned the verse that incorporated a reference to Chaucer (“As the Miller told his tale”).

This surprised me, as, since I’d first heard the song (1983, in “The Big Chill”) until I read this piece, I thought the line was “As the mirror told its tale.” The idea that it was a misheard Chaucer reference had never occurred to me.

These are called mondegreens. The brain translates the phrase into what it hears, often giving it an entirely different meaning. Manfred Mann’s version of “Blinded by the Light” is absolutely full of them. Even the national anthem isn’t immune (“José can you see by the donzerly light?”)

I’m sure there’s an interesting study idea about the brain and mondegreens, probably involving PET scans, somewhere in there.

The whole thing reminded me of an incident early in residency, I suppose you could call it a medical mondegreen.

During training I never went anywhere without a clipboard and notepad, frantically scribbling tidbits down during rounds, lectures, meetings, whatever. I’d go home and reread them over dinner, trying to commit them to memory.

And somewhere, on rounds early in my first year of training, an attending told me that you can sometimes see a Bell’s palsy cause a mild ipsilateral hemiparesis. This surprised me, but hey, I was the newly minted doctor, there to learn. So I wrote it down, memorized it, and moved on.

Even then, though, it made no sense to me. Of course, I was too afraid to ask other residents about it, for fear they’d think I was an idiot (a point that’s still debatable). And questioning the attending involved seemed unthinkable.

But I wandered through my hospital library (back then, young ones, we used paper textbooks and journals) trying to figure out why a peripheral VII palsy could cause an ipsilateral hemiparesis. It would not let me be.

Nothing.

Finally, one day after a lecture, I asked the attending involved. He had no recollection of having tossed the point out a few months ago, and said there was no reason. This confirmed what I’d already realized – a standard Bell’s palsy couldn’t possibly cause an ipsilateral hemiparesis (I’m not going into the crossed-brainstem syndromes here).

Maybe he’d misspoken and not realized it. Maybe I hadn’t heard him correctly. Maybe a little of both. Hospital hallways are anything but quiet. He also had a pending vacation to the coast which could have distracted him.

Like mondegreens in songs, it was just an error, and looking back on it with 30 years perspective, it’s kind of funny. Fortunately I never sent anyone with a hemiparesis home from the ER thinking they had a Bell’s palsy.

But it makes you realize how flawed human communication can be. By the time I asked the attending about it I’d realized it couldn’t possibly be right. It still leaves me wondering about how much we think we heard correctly but we didn’t – and that we don’t notice.

Sometimes you may think your ears are open, but they might just as well be closed if you don’t hear correctly. In medicine the consequences of such can be a lot worse than screwing up on karaoke night.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Recently I was reading an article on the histories behind great songs, and one section featured Procol Harem’s “A Whiter Shade of Pale.” It mentioned the verse that incorporated a reference to Chaucer (“As the Miller told his tale”).

This surprised me, as, since I’d first heard the song (1983, in “The Big Chill”) until I read this piece, I thought the line was “As the mirror told its tale.” The idea that it was a misheard Chaucer reference had never occurred to me.

These are called mondegreens. The brain translates the phrase into what it hears, often giving it an entirely different meaning. Manfred Mann’s version of “Blinded by the Light” is absolutely full of them. Even the national anthem isn’t immune (“José can you see by the donzerly light?”)

I’m sure there’s an interesting study idea about the brain and mondegreens, probably involving PET scans, somewhere in there.

The whole thing reminded me of an incident early in residency, I suppose you could call it a medical mondegreen.

During training I never went anywhere without a clipboard and notepad, frantically scribbling tidbits down during rounds, lectures, meetings, whatever. I’d go home and reread them over dinner, trying to commit them to memory.

And somewhere, on rounds early in my first year of training, an attending told me that you can sometimes see a Bell’s palsy cause a mild ipsilateral hemiparesis. This surprised me, but hey, I was the newly minted doctor, there to learn. So I wrote it down, memorized it, and moved on.

Even then, though, it made no sense to me. Of course, I was too afraid to ask other residents about it, for fear they’d think I was an idiot (a point that’s still debatable). And questioning the attending involved seemed unthinkable.

But I wandered through my hospital library (back then, young ones, we used paper textbooks and journals) trying to figure out why a peripheral VII palsy could cause an ipsilateral hemiparesis. It would not let me be.

Nothing.

Finally, one day after a lecture, I asked the attending involved. He had no recollection of having tossed the point out a few months ago, and said there was no reason. This confirmed what I’d already realized – a standard Bell’s palsy couldn’t possibly cause an ipsilateral hemiparesis (I’m not going into the crossed-brainstem syndromes here).

Maybe he’d misspoken and not realized it. Maybe I hadn’t heard him correctly. Maybe a little of both. Hospital hallways are anything but quiet. He also had a pending vacation to the coast which could have distracted him.

Like mondegreens in songs, it was just an error, and looking back on it with 30 years perspective, it’s kind of funny. Fortunately I never sent anyone with a hemiparesis home from the ER thinking they had a Bell’s palsy.

But it makes you realize how flawed human communication can be. By the time I asked the attending about it I’d realized it couldn’t possibly be right. It still leaves me wondering about how much we think we heard correctly but we didn’t – and that we don’t notice.

Sometimes you may think your ears are open, but they might just as well be closed if you don’t hear correctly. In medicine the consequences of such can be a lot worse than screwing up on karaoke night.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Recently I was reading an article on the histories behind great songs, and one section featured Procol Harem’s “A Whiter Shade of Pale.” It mentioned the verse that incorporated a reference to Chaucer (“As the Miller told his tale”).

This surprised me, as, since I’d first heard the song (1983, in “The Big Chill”) until I read this piece, I thought the line was “As the mirror told its tale.” The idea that it was a misheard Chaucer reference had never occurred to me.

These are called mondegreens. The brain translates the phrase into what it hears, often giving it an entirely different meaning. Manfred Mann’s version of “Blinded by the Light” is absolutely full of them. Even the national anthem isn’t immune (“José can you see by the donzerly light?”)

I’m sure there’s an interesting study idea about the brain and mondegreens, probably involving PET scans, somewhere in there.

The whole thing reminded me of an incident early in residency, I suppose you could call it a medical mondegreen.

During training I never went anywhere without a clipboard and notepad, frantically scribbling tidbits down during rounds, lectures, meetings, whatever. I’d go home and reread them over dinner, trying to commit them to memory.

And somewhere, on rounds early in my first year of training, an attending told me that you can sometimes see a Bell’s palsy cause a mild ipsilateral hemiparesis. This surprised me, but hey, I was the newly minted doctor, there to learn. So I wrote it down, memorized it, and moved on.

Even then, though, it made no sense to me. Of course, I was too afraid to ask other residents about it, for fear they’d think I was an idiot (a point that’s still debatable). And questioning the attending involved seemed unthinkable.

But I wandered through my hospital library (back then, young ones, we used paper textbooks and journals) trying to figure out why a peripheral VII palsy could cause an ipsilateral hemiparesis. It would not let me be.

Nothing.

Finally, one day after a lecture, I asked the attending involved. He had no recollection of having tossed the point out a few months ago, and said there was no reason. This confirmed what I’d already realized – a standard Bell’s palsy couldn’t possibly cause an ipsilateral hemiparesis (I’m not going into the crossed-brainstem syndromes here).

Maybe he’d misspoken and not realized it. Maybe I hadn’t heard him correctly. Maybe a little of both. Hospital hallways are anything but quiet. He also had a pending vacation to the coast which could have distracted him.

Like mondegreens in songs, it was just an error, and looking back on it with 30 years perspective, it’s kind of funny. Fortunately I never sent anyone with a hemiparesis home from the ER thinking they had a Bell’s palsy.

But it makes you realize how flawed human communication can be. By the time I asked the attending about it I’d realized it couldn’t possibly be right. It still leaves me wondering about how much we think we heard correctly but we didn’t – and that we don’t notice.

Sometimes you may think your ears are open, but they might just as well be closed if you don’t hear correctly. In medicine the consequences of such can be a lot worse than screwing up on karaoke night.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Many changes in the evolution of the treatment of diabetes have occurred during this year and 2021. Randomized controlled trials have resulted in updated guidelines for the use of glucagonlike peptide-1 receptor agonists (GLP1RAs) and continuous glucose monitoring (CGM) technology. I am hoping my discussion about these major advances in this edition of Highlights will be helpful to those caring for patients with diabetes.

Tirzepatide

The first GLP1RA, exenatide, was released in April 2005. Since then, numerous daily and weekly drugs of this class have been developed. We’ve learned they are effective glucose lowering drugs, and the weekly agents dulaglutide and semaglutide have shown impressive weight reduction properties as well as cardiovascular benefits.

Secondary outcomes have also shown renal benefits to these agents, and studies for primary renal efficacy are pending. Due to all of these properties, the GLP1RAs are recommended as the first injectable for the treatment of type 2 diabetes, prior to insulin initiation.¹

The next generation of these agents are a combination of a GLP1RA and a glucose-dependent insulinotropic polypeptide (GIP). Glucagonlike peptide-1 (GLP-1) stimulates insulin secretion, inhibits glucagon secretion, delays gastric emptying, and has central effects inducing satiety.

We now understand that GIP is the main incretin hormone in those without diabetes, causative of most of the incretin effects. But the insulin response after GIP secretion in type 2 diabetes is strongly reduced. It is now appreciated that this poor effect of GIP can be reduced when used in combination with a GLP1RA. This combination incretin, called by some a “twincretin,” is the basis for the drug tirzepatide which was approved by the Food and Drug Administration in May of 2022.

The data supporting this agent for both diabetes and obesity are impressive. For example, in a 40-week study with a baseline HbA1c of 8.0%, those randomized to tirzepatide at 5 mg, 10 mg, and 15 mg had HbA1c reductions of 1.87%, 1.89%, and 2.07% respectively.² Over 81% at all doses had HbA1c levels less than 6.5% at 40 weeks.

For the 5-mg, 10-mg, and 15-mg doses, weight change from baseline was 7.9%, 9.3%, and 11.0% respectively. Like older GLP1RAs, gastrointestinal side effects were the main problem. For the three doses, 3%, 5%, and 7%, respectively, had to stop the drug, compared with the 3% who stopped taking the placebo. In another study, tirzepatide was noninferior or superior at all three doses compared with semaglutide 1 mg weekly.³

In a population without diabetes, with 40% of patients having prediabetes, weight loss percentages for the three doses were 15.0%, 19.5%, and 20.9% respectively.⁴ Discontinuation percentages due to side effects were 4%-7%. The exciting part is we now have a drug that approaches weight loss from bariatric surgery. The cardiovascular and renal outcome trials are now underway, but the enthusiasm for this drug is clear from the data.

Like other GLP1RAs, the key is to start low and go slowly. It is recommended to start tirzepatide at 2.5 mg four times a week, then increase to 5 mg. Due to gastrointestinal side effects, some patients will do better at the lower dose before increasing. For those switching from another GLP1RA, there are no data to guide us but, in my practice, I start those patients at 5 mg weekly.
 

Continuous glucose monitoring

Data continue to accumulate that this form of glycemic self-monitoring is effective to reduce HbA1c levels and minimize hypoglycemia in both type 1 and type 2 diabetes. The most important change to the 2022 American Diabetes Association (ADA) standards of care is recognizing CGM as level A evidence for those receiving basal insulin without mealtime insulin.⁵ There are four CGMs on the market, but most of the market uses the Dexcom G6 or the Libre 2. Both of these devices will be updated within the next few months to newer generation sensors.

While there are similarities and differences between the two devices, by late 2022 and early 2023 changes to both will reduce the dissimilarities.

The next generation Libre (Libre 3) will be continuous, and “scanning” will no longer be required.  For those unable to get insurance to cover CGM, the Libre will continue to be more affordable than the Dexcom. Alerts will be present on both, but the Dexcom G7 will be approved for both the arm and the abdomen. The Dexcom also can communicate with several automated insulin delivery systems and data can be shared real-time with family members.

For clinicians just starting patients on this technology, my suggestion is to focus on one system so both the provider and staff can become familiar with it. It is key to review downloaded glucose metrics, in addition to the “ambulatory glucose profile,” a graphic overview of daily glycemia where patterns can be identified. It is also helpful to ask for assistance from endocrinologists who have experience with CGMs, in addition to the representatives of the companies.

COVID-19 and new-onset diabetes

From the beginning of the COVID 19 pandemic in 2020, it was clear that stress hyperglycemia and glucose dysregulation was an important observation for those infected. What was not known at the time is that for some, the hyperglycemia continued, and permanent diabetes ensued.

In one study of over 2.7 million U.S. veterans, men infected with COVID-19, but not women, were at a higher risk of new incident diabetes at 120 days after infection compared to no infection (odds ratio for men = 2.56).⁶

Another literature review using meta-analyses and cross-sectional studies concluded new-onset diabetes following COVID-19 infection can have a varied phenotype, with no risk factors, presenting from diabetic ketoacidosis to milder forms of diabetes.⁷

The current thought is that COVID-19 binds to the ACE2 and TMPRSS2 receptors which appear to be located on the beta-cells in the islet, resulting in insulin deficiency, in addition to the insulin resistance that seems to persist after the acute infection. Much more needs to be learned about this, but clinicians need to appreciate this appears to be a new form of diabetes and optimal treatments are not yet clear.

Dr. Hirsch is an endocrinologist, professor of medicine, and diabetes treatment and teaching chair at the University of Washington, Seattle. He has received research grant support from Dexcom and Insulet and has provided consulting to Abbott, Roche, Lifescan, and GWave. You can contact him at [email protected].

References

1. American Diabetes Association Professional Practice Committee. Pharmacologic approaches to glycemic treatment: Standards of Medical Care in Diabetes-2022. Diabetes Care. 2022;45(Suppl 1):S125-S143.

2. Rosenstock J et al. Efficacy and safety of a novel GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1): A double-blind, randomised, phase 3 trial. Lancet. 2021;398:143-55.

3. Frias JP et al. Tirzepatide versus semaglutide once weekly in patients with type 2 diabetes. N Engl J Med. 2021;385:503-15.

4. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity. N Engl J Med. 2022;387:205-16.

5. American Diabetes Association Professional Practice Committee. Diabetes technology: Standards of Medical Care in Diabetes–2022. Diabetes Care. 2022;45(Suppl 1):S97-S112.

6. Wander PL et al. The incidence of diabetes in 2,777,768 veterans with and without recent SARS-CoV-2 infection. Diabetes Care 2022;45:782-8.

7. Joshi SC and Pozzilli P. COVID-19 induced diabetes: A novel presentation. Diabetes Res Clin Pract. 2022 Aug 6;191:110034.

Many changes in the evolution of the treatment of diabetes have occurred during this year and 2021. Randomized controlled trials have resulted in updated guidelines for the use of glucagonlike peptide-1 receptor agonists (GLP1RAs) and continuous glucose monitoring (CGM) technology. I am hoping my discussion about these major advances in this edition of Highlights will be helpful to those caring for patients with diabetes.

Tirzepatide

The first GLP1RA, exenatide, was released in April 2005. Since then, numerous daily and weekly drugs of this class have been developed. We’ve learned they are effective glucose lowering drugs, and the weekly agents dulaglutide and semaglutide have shown impressive weight reduction properties as well as cardiovascular benefits.

Secondary outcomes have also shown renal benefits to these agents, and studies for primary renal efficacy are pending. Due to all of these properties, the GLP1RAs are recommended as the first injectable for the treatment of type 2 diabetes, prior to insulin initiation.¹

The next generation of these agents are a combination of a GLP1RA and a glucose-dependent insulinotropic polypeptide (GIP). Glucagonlike peptide-1 (GLP-1) stimulates insulin secretion, inhibits glucagon secretion, delays gastric emptying, and has central effects inducing satiety.

We now understand that GIP is the main incretin hormone in those without diabetes, causative of most of the incretin effects. But the insulin response after GIP secretion in type 2 diabetes is strongly reduced. It is now appreciated that this poor effect of GIP can be reduced when used in combination with a GLP1RA. This combination incretin, called by some a “twincretin,” is the basis for the drug tirzepatide which was approved by the Food and Drug Administration in May of 2022.

The data supporting this agent for both diabetes and obesity are impressive. For example, in a 40-week study with a baseline HbA1c of 8.0%, those randomized to tirzepatide at 5 mg, 10 mg, and 15 mg had HbA1c reductions of 1.87%, 1.89%, and 2.07% respectively.² Over 81% at all doses had HbA1c levels less than 6.5% at 40 weeks.

For the 5-mg, 10-mg, and 15-mg doses, weight change from baseline was 7.9%, 9.3%, and 11.0% respectively. Like older GLP1RAs, gastrointestinal side effects were the main problem. For the three doses, 3%, 5%, and 7%, respectively, had to stop the drug, compared with the 3% who stopped taking the placebo. In another study, tirzepatide was noninferior or superior at all three doses compared with semaglutide 1 mg weekly.³

In a population without diabetes, with 40% of patients having prediabetes, weight loss percentages for the three doses were 15.0%, 19.5%, and 20.9% respectively.⁴ Discontinuation percentages due to side effects were 4%-7%. The exciting part is we now have a drug that approaches weight loss from bariatric surgery. The cardiovascular and renal outcome trials are now underway, but the enthusiasm for this drug is clear from the data.

Like other GLP1RAs, the key is to start low and go slowly. It is recommended to start tirzepatide at 2.5 mg four times a week, then increase to 5 mg. Due to gastrointestinal side effects, some patients will do better at the lower dose before increasing. For those switching from another GLP1RA, there are no data to guide us but, in my practice, I start those patients at 5 mg weekly.
 

Continuous glucose monitoring

Data continue to accumulate that this form of glycemic self-monitoring is effective to reduce HbA1c levels and minimize hypoglycemia in both type 1 and type 2 diabetes. The most important change to the 2022 American Diabetes Association (ADA) standards of care is recognizing CGM as level A evidence for those receiving basal insulin without mealtime insulin.⁵ There are four CGMs on the market, but most of the market uses the Dexcom G6 or the Libre 2. Both of these devices will be updated within the next few months to newer generation sensors.

While there are similarities and differences between the two devices, by late 2022 and early 2023 changes to both will reduce the dissimilarities.

The next generation Libre (Libre 3) will be continuous, and “scanning” will no longer be required.  For those unable to get insurance to cover CGM, the Libre will continue to be more affordable than the Dexcom. Alerts will be present on both, but the Dexcom G7 will be approved for both the arm and the abdomen. The Dexcom also can communicate with several automated insulin delivery systems and data can be shared real-time with family members.

For clinicians just starting patients on this technology, my suggestion is to focus on one system so both the provider and staff can become familiar with it. It is key to review downloaded glucose metrics, in addition to the “ambulatory glucose profile,” a graphic overview of daily glycemia where patterns can be identified. It is also helpful to ask for assistance from endocrinologists who have experience with CGMs, in addition to the representatives of the companies.

COVID-19 and new-onset diabetes

From the beginning of the COVID 19 pandemic in 2020, it was clear that stress hyperglycemia and glucose dysregulation was an important observation for those infected. What was not known at the time is that for some, the hyperglycemia continued, and permanent diabetes ensued.

In one study of over 2.7 million U.S. veterans, men infected with COVID-19, but not women, were at a higher risk of new incident diabetes at 120 days after infection compared to no infection (odds ratio for men = 2.56).⁶

Another literature review using meta-analyses and cross-sectional studies concluded new-onset diabetes following COVID-19 infection can have a varied phenotype, with no risk factors, presenting from diabetic ketoacidosis to milder forms of diabetes.⁷

The current thought is that COVID-19 binds to the ACE2 and TMPRSS2 receptors which appear to be located on the beta-cells in the islet, resulting in insulin deficiency, in addition to the insulin resistance that seems to persist after the acute infection. Much more needs to be learned about this, but clinicians need to appreciate this appears to be a new form of diabetes and optimal treatments are not yet clear.

Dr. Hirsch is an endocrinologist, professor of medicine, and diabetes treatment and teaching chair at the University of Washington, Seattle. He has received research grant support from Dexcom and Insulet and has provided consulting to Abbott, Roche, Lifescan, and GWave. You can contact him at [email protected].

References

1. American Diabetes Association Professional Practice Committee. Pharmacologic approaches to glycemic treatment: Standards of Medical Care in Diabetes-2022. Diabetes Care. 2022;45(Suppl 1):S125-S143.

2. Rosenstock J et al. Efficacy and safety of a novel GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1): A double-blind, randomised, phase 3 trial. Lancet. 2021;398:143-55.

3. Frias JP et al. Tirzepatide versus semaglutide once weekly in patients with type 2 diabetes. N Engl J Med. 2021;385:503-15.

4. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity. N Engl J Med. 2022;387:205-16.

5. American Diabetes Association Professional Practice Committee. Diabetes technology: Standards of Medical Care in Diabetes–2022. Diabetes Care. 2022;45(Suppl 1):S97-S112.

6. Wander PL et al. The incidence of diabetes in 2,777,768 veterans with and without recent SARS-CoV-2 infection. Diabetes Care 2022;45:782-8.

7. Joshi SC and Pozzilli P. COVID-19 induced diabetes: A novel presentation. Diabetes Res Clin Pract. 2022 Aug 6;191:110034.

Many changes in the evolution of the treatment of diabetes have occurred during this year and 2021. Randomized controlled trials have resulted in updated guidelines for the use of glucagonlike peptide-1 receptor agonists (GLP1RAs) and continuous glucose monitoring (CGM) technology. I am hoping my discussion about these major advances in this edition of Highlights will be helpful to those caring for patients with diabetes.

Tirzepatide

The first GLP1RA, exenatide, was released in April 2005. Since then, numerous daily and weekly drugs of this class have been developed. We’ve learned they are effective glucose lowering drugs, and the weekly agents dulaglutide and semaglutide have shown impressive weight reduction properties as well as cardiovascular benefits.

Secondary outcomes have also shown renal benefits to these agents, and studies for primary renal efficacy are pending. Due to all of these properties, the GLP1RAs are recommended as the first injectable for the treatment of type 2 diabetes, prior to insulin initiation.¹

The next generation of these agents are a combination of a GLP1RA and a glucose-dependent insulinotropic polypeptide (GIP). Glucagonlike peptide-1 (GLP-1) stimulates insulin secretion, inhibits glucagon secretion, delays gastric emptying, and has central effects inducing satiety.

We now understand that GIP is the main incretin hormone in those without diabetes, causative of most of the incretin effects. But the insulin response after GIP secretion in type 2 diabetes is strongly reduced. It is now appreciated that this poor effect of GIP can be reduced when used in combination with a GLP1RA. This combination incretin, called by some a “twincretin,” is the basis for the drug tirzepatide which was approved by the Food and Drug Administration in May of 2022.

The data supporting this agent for both diabetes and obesity are impressive. For example, in a 40-week study with a baseline HbA1c of 8.0%, those randomized to tirzepatide at 5 mg, 10 mg, and 15 mg had HbA1c reductions of 1.87%, 1.89%, and 2.07% respectively.² Over 81% at all doses had HbA1c levels less than 6.5% at 40 weeks.

For the 5-mg, 10-mg, and 15-mg doses, weight change from baseline was 7.9%, 9.3%, and 11.0% respectively. Like older GLP1RAs, gastrointestinal side effects were the main problem. For the three doses, 3%, 5%, and 7%, respectively, had to stop the drug, compared with the 3% who stopped taking the placebo. In another study, tirzepatide was noninferior or superior at all three doses compared with semaglutide 1 mg weekly.³

In a population without diabetes, with 40% of patients having prediabetes, weight loss percentages for the three doses were 15.0%, 19.5%, and 20.9% respectively.⁴ Discontinuation percentages due to side effects were 4%-7%. The exciting part is we now have a drug that approaches weight loss from bariatric surgery. The cardiovascular and renal outcome trials are now underway, but the enthusiasm for this drug is clear from the data.

Like other GLP1RAs, the key is to start low and go slowly. It is recommended to start tirzepatide at 2.5 mg four times a week, then increase to 5 mg. Due to gastrointestinal side effects, some patients will do better at the lower dose before increasing. For those switching from another GLP1RA, there are no data to guide us but, in my practice, I start those patients at 5 mg weekly.
 

Continuous glucose monitoring

Data continue to accumulate that this form of glycemic self-monitoring is effective to reduce HbA1c levels and minimize hypoglycemia in both type 1 and type 2 diabetes. The most important change to the 2022 American Diabetes Association (ADA) standards of care is recognizing CGM as level A evidence for those receiving basal insulin without mealtime insulin.⁵ There are four CGMs on the market, but most of the market uses the Dexcom G6 or the Libre 2. Both of these devices will be updated within the next few months to newer generation sensors.

While there are similarities and differences between the two devices, by late 2022 and early 2023 changes to both will reduce the dissimilarities.

The next generation Libre (Libre 3) will be continuous, and “scanning” will no longer be required.  For those unable to get insurance to cover CGM, the Libre will continue to be more affordable than the Dexcom. Alerts will be present on both, but the Dexcom G7 will be approved for both the arm and the abdomen. The Dexcom also can communicate with several automated insulin delivery systems and data can be shared real-time with family members.

For clinicians just starting patients on this technology, my suggestion is to focus on one system so both the provider and staff can become familiar with it. It is key to review downloaded glucose metrics, in addition to the “ambulatory glucose profile,” a graphic overview of daily glycemia where patterns can be identified. It is also helpful to ask for assistance from endocrinologists who have experience with CGMs, in addition to the representatives of the companies.

COVID-19 and new-onset diabetes

From the beginning of the COVID 19 pandemic in 2020, it was clear that stress hyperglycemia and glucose dysregulation was an important observation for those infected. What was not known at the time is that for some, the hyperglycemia continued, and permanent diabetes ensued.

In one study of over 2.7 million U.S. veterans, men infected with COVID-19, but not women, were at a higher risk of new incident diabetes at 120 days after infection compared to no infection (odds ratio for men = 2.56).⁶

Another literature review using meta-analyses and cross-sectional studies concluded new-onset diabetes following COVID-19 infection can have a varied phenotype, with no risk factors, presenting from diabetic ketoacidosis to milder forms of diabetes.⁷

The current thought is that COVID-19 binds to the ACE2 and TMPRSS2 receptors which appear to be located on the beta-cells in the islet, resulting in insulin deficiency, in addition to the insulin resistance that seems to persist after the acute infection. Much more needs to be learned about this, but clinicians need to appreciate this appears to be a new form of diabetes and optimal treatments are not yet clear.

Dr. Hirsch is an endocrinologist, professor of medicine, and diabetes treatment and teaching chair at the University of Washington, Seattle. He has received research grant support from Dexcom and Insulet and has provided consulting to Abbott, Roche, Lifescan, and GWave. You can contact him at [email protected].

References

1. American Diabetes Association Professional Practice Committee. Pharmacologic approaches to glycemic treatment: Standards of Medical Care in Diabetes-2022. Diabetes Care. 2022;45(Suppl 1):S125-S143.

2. Rosenstock J et al. Efficacy and safety of a novel GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1): A double-blind, randomised, phase 3 trial. Lancet. 2021;398:143-55.

3. Frias JP et al. Tirzepatide versus semaglutide once weekly in patients with type 2 diabetes. N Engl J Med. 2021;385:503-15.

4. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity. N Engl J Med. 2022;387:205-16.

5. American Diabetes Association Professional Practice Committee. Diabetes technology: Standards of Medical Care in Diabetes–2022. Diabetes Care. 2022;45(Suppl 1):S97-S112.

6. Wander PL et al. The incidence of diabetes in 2,777,768 veterans with and without recent SARS-CoV-2 infection. Diabetes Care 2022;45:782-8.

7. Joshi SC and Pozzilli P. COVID-19 induced diabetes: A novel presentation. Diabetes Res Clin Pract. 2022 Aug 6;191:110034.

For many patients, sexual function is an important component of a healthy quality of life.¹ However, to many transgender individuals, their sexual organs are often a source of gender dysphoria, which can significantly inhibit sexual activity with their partners. Patients who seek gender-affirming surgery not only hope to have these feelings of dysphoria alleviated but also desire improvement in sexual function after surgery. While the medical and psychiatric criteria for patients seeking vaginoplasty procedures are well established by the World Professional Association for Transgender Health,² there is little guidance surrounding the discourse surgeons should have regarding sexual function pre- and postsurgery.

Setting realistic expectations is one of the major challenges surgeons and patients alike face in preoperative and postoperative encounters. Patients not only are tasked with recovering from a major surgical procedure, but must also now learn their new anatomy, which includes learning how to urinate, maintain proper neovaginal hygiene, and experience sexual pleasure.

Given the permanence of these procedures and the possibility of loss of sexual function, the surgeon must ensure that patients truly comprehend the nature of the procedure and its complications. During the preoperative consultation, the surgeon must inquire about any desire for future fertility, discuss any history of pelvic radiation, epispadias, hypospadias, current erectile dysfunction, libido, comorbid medical conditions (such as diabetes or smoking), current sexual practices, and overall patient goals regarding their surgical outcome.

The vast majority of patients state they will experience a significant decrease in gender dysphoria with the removal of their current natal male genitalia.¹ However, some patients have very specific preferences regarding the cosmetic appearance of vulvar structures. Others have more functional concerns about neovaginal depth and the ability to have receptive penetrative intercourse. It is important to note that not all transgender women have male partners. Furthermore, whether patients have male or female partners, some patients do not desire the ability to have penetrative intercourse and/or do not want to undergo the potential complications of a full-depth vaginoplasty. In these patients, offering a “shallow depth” vaginoplasty may be acceptable.

It is useful in the consultation to discuss a patient’s sexual partners and sexual practices in order to best determine the type of procedure that may be appropriate for a patient. In my practice, I emphasize that full-depth vaginoplasties require a lifelong commitment of dilation to maintain patency. Unlike cisgender women, patients must also douche to ensure appropriate vaginal hygiene. Regarding cosmetic preferences patients may have, it is essential to educate patients on the significant variation in the appearance of vulvar structures among both cisgender and transgender women.

During the surgical consultation, I review which structures from their natal genitalia are removed and which structures are utilized to create the neo–vulvar-vaginal anatomy. The testicles and spermatic cord are excised. The dorsal neurovascular bundle of the penile shaft and portion of the dorsal aspect of the glans penis are used to create the neoclitoris. A combination of penile shaft skin and scrotal skin is used to line the neovaginal canal. The erectile tissue of the penile shaft is also resected and the natal urethra is shortened and spatulated to create the urethral plate and urethral meatus. I also remind patients that the prostate remains intact during vaginoplasty procedures. Unless patients undergo the colonic interposition vaginoplasty and in some cases the peritoneal vaginoplasty, the neovaginal canal is not self-lubricating, nor will patients experience ejaculation after surgery. In the presurgical period, I often remind patients that the location of erogenous sensation after surgery will be altered and the method by which they self-stimulate will also be different. It is also essential to document whether patients can achieve satisfactory orgasms presurgically in order to determine adequate sexual function in the postoperative period.

It cannot be emphasized enough that the best predictor of unsatisfactory sexual function after genital gender-affirming surgery is poor sexual function prior to surgery.^1,3

Retention of sexual function after gender-affirming genital surgery is common, with studies citing a range of 70%-90% of patients reporting their ability to regularly achieve an orgasm after surgery.^1,4 In some cases, patients will report issues with sexual function after surgery despite having no prior history of sexual dysfunction. If patients present with complaints of postsurgical anorgasmia, the provider should rule out insufficient time for wound healing and resolution of surgery-site pain, and determine if there was an intraoperative injury to the neurovascular bundle or significant clitoral necrosis. A thorough genital exam should include a sensory examination of the neoclitoris and the introitus and neovaginal canal for signs of scarring, stenosis, loss of vaginal depth, or high-tone pelvic-floor dysfunction.

Unfortunately, if the neurovascular bundle is injured or if a patient experienced clitoral necrosis, the likelihood of a patient regaining sensation is decreased, although there are currently no studies examining the exact rates. It is also important to reassure patients that wound healing after surgery and relearning sexual function is not linear. I encourage patients to initially self-stimulate without a partner as they learn their new anatomy in order to remove any potential performance anxiety a partner could cause immediately after surgery. Similar to the approach to sexual dysfunction in cisgender patients, referral to a specialist in sexual health and/or pelvic floor physical therapy are useful adjuncts, depending on the findings from the physical exam and patient symptoms.
 

Dr. Brandt is an ob.gyn. and fellowship-trained gender-affirming surgeon in West Reading, Pa.

References

1. Garcia MM. Clin Plastic Surg. 2018;45:437-46.

2. Eli Coleman WB et al. “Standards of care for the health of transsexual, transgender, and gender non-conforming people” 7th version. World Professional Association for Transgender Health: 2012.

3. Garcia MM et al. Transl Androl Urol. 2014;3:156.

4. Ferrando CA, Bowers ML. “Genital gender confirmation surgery for patients assigned male at birth” In: Ferrando CA, ed. “Comprehensive care for the transgender patient” Philadelphia: Elsevier, 2020:82-92.

For many patients, sexual function is an important component of a healthy quality of life.¹ However, to many transgender individuals, their sexual organs are often a source of gender dysphoria, which can significantly inhibit sexual activity with their partners. Patients who seek gender-affirming surgery not only hope to have these feelings of dysphoria alleviated but also desire improvement in sexual function after surgery. While the medical and psychiatric criteria for patients seeking vaginoplasty procedures are well established by the World Professional Association for Transgender Health,² there is little guidance surrounding the discourse surgeons should have regarding sexual function pre- and postsurgery.

Setting realistic expectations is one of the major challenges surgeons and patients alike face in preoperative and postoperative encounters. Patients not only are tasked with recovering from a major surgical procedure, but must also now learn their new anatomy, which includes learning how to urinate, maintain proper neovaginal hygiene, and experience sexual pleasure.

Given the permanence of these procedures and the possibility of loss of sexual function, the surgeon must ensure that patients truly comprehend the nature of the procedure and its complications. During the preoperative consultation, the surgeon must inquire about any desire for future fertility, discuss any history of pelvic radiation, epispadias, hypospadias, current erectile dysfunction, libido, comorbid medical conditions (such as diabetes or smoking), current sexual practices, and overall patient goals regarding their surgical outcome.

The vast majority of patients state they will experience a significant decrease in gender dysphoria with the removal of their current natal male genitalia.¹ However, some patients have very specific preferences regarding the cosmetic appearance of vulvar structures. Others have more functional concerns about neovaginal depth and the ability to have receptive penetrative intercourse. It is important to note that not all transgender women have male partners. Furthermore, whether patients have male or female partners, some patients do not desire the ability to have penetrative intercourse and/or do not want to undergo the potential complications of a full-depth vaginoplasty. In these patients, offering a “shallow depth” vaginoplasty may be acceptable.

It is useful in the consultation to discuss a patient’s sexual partners and sexual practices in order to best determine the type of procedure that may be appropriate for a patient. In my practice, I emphasize that full-depth vaginoplasties require a lifelong commitment of dilation to maintain patency. Unlike cisgender women, patients must also douche to ensure appropriate vaginal hygiene. Regarding cosmetic preferences patients may have, it is essential to educate patients on the significant variation in the appearance of vulvar structures among both cisgender and transgender women.

During the surgical consultation, I review which structures from their natal genitalia are removed and which structures are utilized to create the neo–vulvar-vaginal anatomy. The testicles and spermatic cord are excised. The dorsal neurovascular bundle of the penile shaft and portion of the dorsal aspect of the glans penis are used to create the neoclitoris. A combination of penile shaft skin and scrotal skin is used to line the neovaginal canal. The erectile tissue of the penile shaft is also resected and the natal urethra is shortened and spatulated to create the urethral plate and urethral meatus. I also remind patients that the prostate remains intact during vaginoplasty procedures. Unless patients undergo the colonic interposition vaginoplasty and in some cases the peritoneal vaginoplasty, the neovaginal canal is not self-lubricating, nor will patients experience ejaculation after surgery. In the presurgical period, I often remind patients that the location of erogenous sensation after surgery will be altered and the method by which they self-stimulate will also be different. It is also essential to document whether patients can achieve satisfactory orgasms presurgically in order to determine adequate sexual function in the postoperative period.

It cannot be emphasized enough that the best predictor of unsatisfactory sexual function after genital gender-affirming surgery is poor sexual function prior to surgery.^1,3

Retention of sexual function after gender-affirming genital surgery is common, with studies citing a range of 70%-90% of patients reporting their ability to regularly achieve an orgasm after surgery.^1,4 In some cases, patients will report issues with sexual function after surgery despite having no prior history of sexual dysfunction. If patients present with complaints of postsurgical anorgasmia, the provider should rule out insufficient time for wound healing and resolution of surgery-site pain, and determine if there was an intraoperative injury to the neurovascular bundle or significant clitoral necrosis. A thorough genital exam should include a sensory examination of the neoclitoris and the introitus and neovaginal canal for signs of scarring, stenosis, loss of vaginal depth, or high-tone pelvic-floor dysfunction.

Unfortunately, if the neurovascular bundle is injured or if a patient experienced clitoral necrosis, the likelihood of a patient regaining sensation is decreased, although there are currently no studies examining the exact rates. It is also important to reassure patients that wound healing after surgery and relearning sexual function is not linear. I encourage patients to initially self-stimulate without a partner as they learn their new anatomy in order to remove any potential performance anxiety a partner could cause immediately after surgery. Similar to the approach to sexual dysfunction in cisgender patients, referral to a specialist in sexual health and/or pelvic floor physical therapy are useful adjuncts, depending on the findings from the physical exam and patient symptoms.
 

Dr. Brandt is an ob.gyn. and fellowship-trained gender-affirming surgeon in West Reading, Pa.

References

1. Garcia MM. Clin Plastic Surg. 2018;45:437-46.

2. Eli Coleman WB et al. “Standards of care for the health of transsexual, transgender, and gender non-conforming people” 7th version. World Professional Association for Transgender Health: 2012.

3. Garcia MM et al. Transl Androl Urol. 2014;3:156.

4. Ferrando CA, Bowers ML. “Genital gender confirmation surgery for patients assigned male at birth” In: Ferrando CA, ed. “Comprehensive care for the transgender patient” Philadelphia: Elsevier, 2020:82-92.

For many patients, sexual function is an important component of a healthy quality of life.¹ However, to many transgender individuals, their sexual organs are often a source of gender dysphoria, which can significantly inhibit sexual activity with their partners. Patients who seek gender-affirming surgery not only hope to have these feelings of dysphoria alleviated but also desire improvement in sexual function after surgery. While the medical and psychiatric criteria for patients seeking vaginoplasty procedures are well established by the World Professional Association for Transgender Health,² there is little guidance surrounding the discourse surgeons should have regarding sexual function pre- and postsurgery.

Setting realistic expectations is one of the major challenges surgeons and patients alike face in preoperative and postoperative encounters. Patients not only are tasked with recovering from a major surgical procedure, but must also now learn their new anatomy, which includes learning how to urinate, maintain proper neovaginal hygiene, and experience sexual pleasure.

Given the permanence of these procedures and the possibility of loss of sexual function, the surgeon must ensure that patients truly comprehend the nature of the procedure and its complications. During the preoperative consultation, the surgeon must inquire about any desire for future fertility, discuss any history of pelvic radiation, epispadias, hypospadias, current erectile dysfunction, libido, comorbid medical conditions (such as diabetes or smoking), current sexual practices, and overall patient goals regarding their surgical outcome.

The vast majority of patients state they will experience a significant decrease in gender dysphoria with the removal of their current natal male genitalia.¹ However, some patients have very specific preferences regarding the cosmetic appearance of vulvar structures. Others have more functional concerns about neovaginal depth and the ability to have receptive penetrative intercourse. It is important to note that not all transgender women have male partners. Furthermore, whether patients have male or female partners, some patients do not desire the ability to have penetrative intercourse and/or do not want to undergo the potential complications of a full-depth vaginoplasty. In these patients, offering a “shallow depth” vaginoplasty may be acceptable.

It is useful in the consultation to discuss a patient’s sexual partners and sexual practices in order to best determine the type of procedure that may be appropriate for a patient. In my practice, I emphasize that full-depth vaginoplasties require a lifelong commitment of dilation to maintain patency. Unlike cisgender women, patients must also douche to ensure appropriate vaginal hygiene. Regarding cosmetic preferences patients may have, it is essential to educate patients on the significant variation in the appearance of vulvar structures among both cisgender and transgender women.

During the surgical consultation, I review which structures from their natal genitalia are removed and which structures are utilized to create the neo–vulvar-vaginal anatomy. The testicles and spermatic cord are excised. The dorsal neurovascular bundle of the penile shaft and portion of the dorsal aspect of the glans penis are used to create the neoclitoris. A combination of penile shaft skin and scrotal skin is used to line the neovaginal canal. The erectile tissue of the penile shaft is also resected and the natal urethra is shortened and spatulated to create the urethral plate and urethral meatus. I also remind patients that the prostate remains intact during vaginoplasty procedures. Unless patients undergo the colonic interposition vaginoplasty and in some cases the peritoneal vaginoplasty, the neovaginal canal is not self-lubricating, nor will patients experience ejaculation after surgery. In the presurgical period, I often remind patients that the location of erogenous sensation after surgery will be altered and the method by which they self-stimulate will also be different. It is also essential to document whether patients can achieve satisfactory orgasms presurgically in order to determine adequate sexual function in the postoperative period.

It cannot be emphasized enough that the best predictor of unsatisfactory sexual function after genital gender-affirming surgery is poor sexual function prior to surgery.^1,3

Retention of sexual function after gender-affirming genital surgery is common, with studies citing a range of 70%-90% of patients reporting their ability to regularly achieve an orgasm after surgery.^1,4 In some cases, patients will report issues with sexual function after surgery despite having no prior history of sexual dysfunction. If patients present with complaints of postsurgical anorgasmia, the provider should rule out insufficient time for wound healing and resolution of surgery-site pain, and determine if there was an intraoperative injury to the neurovascular bundle or significant clitoral necrosis. A thorough genital exam should include a sensory examination of the neoclitoris and the introitus and neovaginal canal for signs of scarring, stenosis, loss of vaginal depth, or high-tone pelvic-floor dysfunction.

Unfortunately, if the neurovascular bundle is injured or if a patient experienced clitoral necrosis, the likelihood of a patient regaining sensation is decreased, although there are currently no studies examining the exact rates. It is also important to reassure patients that wound healing after surgery and relearning sexual function is not linear. I encourage patients to initially self-stimulate without a partner as they learn their new anatomy in order to remove any potential performance anxiety a partner could cause immediately after surgery. Similar to the approach to sexual dysfunction in cisgender patients, referral to a specialist in sexual health and/or pelvic floor physical therapy are useful adjuncts, depending on the findings from the physical exam and patient symptoms.
 

Dr. Brandt is an ob.gyn. and fellowship-trained gender-affirming surgeon in West Reading, Pa.

References

1. Garcia MM. Clin Plastic Surg. 2018;45:437-46.

2. Eli Coleman WB et al. “Standards of care for the health of transsexual, transgender, and gender non-conforming people” 7th version. World Professional Association for Transgender Health: 2012.

3. Garcia MM et al. Transl Androl Urol. 2014;3:156.

4. Ferrando CA, Bowers ML. “Genital gender confirmation surgery for patients assigned male at birth” In: Ferrando CA, ed. “Comprehensive care for the transgender patient” Philadelphia: Elsevier, 2020:82-92.

Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to noxious air particles. The physiologic results include varying degrees of gas-exchange abnormality and mechanical respiratory limitation, often in the form of dynamic hyperinflation. There’s a third major contributor, though – skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.

When your patients with COPD report dyspnea or exercise intolerance, what do you do? Do you attempt to determine its character to pinpoint its origin? Do you quiz them about their baseline activity levels to quantify their conditioning? I bet you get right to the point and order a cardiopulmonary exercise test (CPET). That way you’ll be able to tease out all the contributors. Nah. Most likely you add an inhaler before continuing to rush through your COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Smoking cessation? Check.

The physiology of dyspnea and exercise limitation in COPD has been extensively studied. Work-of-breathing, dynamic hyperinflation, and gas-exchange inefficiencies interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies the existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (AECOPD) and oral corticosteroids further aggravate skeletal muscle dysfunction.

The Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) Report directs clinicians to use inhalers to manage dyspnea. If they’re already on one inhaler, they get another. This continues until they’re stabilized on a long-acting beta-agonist (LABA), long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B through D disease. Unfortunately, the pulmonary rehabilitation recommendation is buried in the text and doesn’t appear within the popularized pharmacologic algorithms in the report’s figures.

The data for adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QOL) are good. However, although GOLD tells us to keep adding inhalers for the dyspneic patient with COPD, the authors acknowledge that this hasn’t been systematically tested. It’s important to remember that GOLD is a “statement” as opposed to a clinical practice guideline. The difference? A statement doesn’t require the same formal, rigorous scientific analysis known as the GRADE approach. Using this kind of analysis, a recent clinical practice guideline by the American Thoracic Society found no benefit in dyspnea or respiratory QOL with step-up from inhaler monotherapy.

Inhalers won’t do anything for gas-exchange inefficiencies and deconditioning, at least not directly. A recent CPET study from the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2-4 COPD patients. The numbers were higher for those who reported dyspnea. Skeletal muscle dysfunction rates are equally high.

Thus, dyspnea and exercise intolerance are major determinants of QOL in COPD, but inhalers will only get you so far. At a minimum, make sure you get an activity/exercise history from your patients with COPD. For those who are sedentary, provide an exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the complaint before doubling down. Finally, try to get the patient into a good pulmonary rehabilitation program. They’ll thank you afterwards.

Dr. Holley is Associate Professor, department of medicine, Uniformed Services University of the Health Sciences and Program Director, Pulmonary and Critical Care Medical Fellowship, department of medicine, Walter Reed National Military Medical Center, both in Bethesda, Md. He reported receiving research grants from Fisher-Paykel and receiving income from the American College of Chest Physicians.

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

Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to noxious air particles. The physiologic results include varying degrees of gas-exchange abnormality and mechanical respiratory limitation, often in the form of dynamic hyperinflation. There’s a third major contributor, though – skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.

When your patients with COPD report dyspnea or exercise intolerance, what do you do? Do you attempt to determine its character to pinpoint its origin? Do you quiz them about their baseline activity levels to quantify their conditioning? I bet you get right to the point and order a cardiopulmonary exercise test (CPET). That way you’ll be able to tease out all the contributors. Nah. Most likely you add an inhaler before continuing to rush through your COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Smoking cessation? Check.

The physiology of dyspnea and exercise limitation in COPD has been extensively studied. Work-of-breathing, dynamic hyperinflation, and gas-exchange inefficiencies interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies the existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (AECOPD) and oral corticosteroids further aggravate skeletal muscle dysfunction.

The Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) Report directs clinicians to use inhalers to manage dyspnea. If they’re already on one inhaler, they get another. This continues until they’re stabilized on a long-acting beta-agonist (LABA), long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B through D disease. Unfortunately, the pulmonary rehabilitation recommendation is buried in the text and doesn’t appear within the popularized pharmacologic algorithms in the report’s figures.

The data for adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QOL) are good. However, although GOLD tells us to keep adding inhalers for the dyspneic patient with COPD, the authors acknowledge that this hasn’t been systematically tested. It’s important to remember that GOLD is a “statement” as opposed to a clinical practice guideline. The difference? A statement doesn’t require the same formal, rigorous scientific analysis known as the GRADE approach. Using this kind of analysis, a recent clinical practice guideline by the American Thoracic Society found no benefit in dyspnea or respiratory QOL with step-up from inhaler monotherapy.

Inhalers won’t do anything for gas-exchange inefficiencies and deconditioning, at least not directly. A recent CPET study from the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2-4 COPD patients. The numbers were higher for those who reported dyspnea. Skeletal muscle dysfunction rates are equally high.

Thus, dyspnea and exercise intolerance are major determinants of QOL in COPD, but inhalers will only get you so far. At a minimum, make sure you get an activity/exercise history from your patients with COPD. For those who are sedentary, provide an exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the complaint before doubling down. Finally, try to get the patient into a good pulmonary rehabilitation program. They’ll thank you afterwards.

Dr. Holley is Associate Professor, department of medicine, Uniformed Services University of the Health Sciences and Program Director, Pulmonary and Critical Care Medical Fellowship, department of medicine, Walter Reed National Military Medical Center, both in Bethesda, Md. He reported receiving research grants from Fisher-Paykel and receiving income from the American College of Chest Physicians.

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

Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to noxious air particles. The physiologic results include varying degrees of gas-exchange abnormality and mechanical respiratory limitation, often in the form of dynamic hyperinflation. There’s a third major contributor, though – skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.

When your patients with COPD report dyspnea or exercise intolerance, what do you do? Do you attempt to determine its character to pinpoint its origin? Do you quiz them about their baseline activity levels to quantify their conditioning? I bet you get right to the point and order a cardiopulmonary exercise test (CPET). That way you’ll be able to tease out all the contributors. Nah. Most likely you add an inhaler before continuing to rush through your COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Smoking cessation? Check.

The physiology of dyspnea and exercise limitation in COPD has been extensively studied. Work-of-breathing, dynamic hyperinflation, and gas-exchange inefficiencies interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies the existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (AECOPD) and oral corticosteroids further aggravate skeletal muscle dysfunction.

The Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) Report directs clinicians to use inhalers to manage dyspnea. If they’re already on one inhaler, they get another. This continues until they’re stabilized on a long-acting beta-agonist (LABA), long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B through D disease. Unfortunately, the pulmonary rehabilitation recommendation is buried in the text and doesn’t appear within the popularized pharmacologic algorithms in the report’s figures.

The data for adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QOL) are good. However, although GOLD tells us to keep adding inhalers for the dyspneic patient with COPD, the authors acknowledge that this hasn’t been systematically tested. It’s important to remember that GOLD is a “statement” as opposed to a clinical practice guideline. The difference? A statement doesn’t require the same formal, rigorous scientific analysis known as the GRADE approach. Using this kind of analysis, a recent clinical practice guideline by the American Thoracic Society found no benefit in dyspnea or respiratory QOL with step-up from inhaler monotherapy.

Inhalers won’t do anything for gas-exchange inefficiencies and deconditioning, at least not directly. A recent CPET study from the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2-4 COPD patients. The numbers were higher for those who reported dyspnea. Skeletal muscle dysfunction rates are equally high.

Thus, dyspnea and exercise intolerance are major determinants of QOL in COPD, but inhalers will only get you so far. At a minimum, make sure you get an activity/exercise history from your patients with COPD. For those who are sedentary, provide an exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the complaint before doubling down. Finally, try to get the patient into a good pulmonary rehabilitation program. They’ll thank you afterwards.

Dr. Holley is Associate Professor, department of medicine, Uniformed Services University of the Health Sciences and Program Director, Pulmonary and Critical Care Medical Fellowship, department of medicine, Walter Reed National Military Medical Center, both in Bethesda, Md. He reported receiving research grants from Fisher-Paykel and receiving income from the American College of Chest Physicians.

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