The US Preventive Services Task Force (USPSTF) recently released draft recommendations on screening for tuberculosis (TB).¹ The USPSTF continues to recommend screening for latent TB infection (LTBI) in those at high risk.

Why is this important? Up to one-quarter of the world’s population has been infected with TB, according to World Health Organization (WHO) estimates. In 2021, active TB was diagnosed in 10.6 million people, and it caused 1.6 million deaths.² Worldwide, TB is still a major cause of mortality: It is the 13th leading cause of death and is the leading cause of infectious disease mortality in non-COVID years.

Although the rate of active TB in the United States has been declining for decades (from 30.7/100,000 in 1960 to 2.4/100,000 in 2021), 7882 cases were reported in 2021, and an estimated 13 million people in the United States have LTBI.³ If not treated, 5% to 10% of LTBI cases will progress to active TB. This risk is higher in those with certain medical conditions.³ People born outside the United States currently account for 71.4% of reported TB cases in the United States.³

To reduce the morbidity and mortality of TB, the Centers for Disease Control and Prevention (CDC), WHO, and USPSTF all recommend screening for and treating LTBI. An effective approach to TB control also includes early detection and completion of treatment for active TB, as well as testing contacts of active TB cases.

Who should be screened? Those at high risk for LTBI include those who were born in, or who have resided in, countries with high rates of TB (eg, Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia); those who have lived in a correctional facility or homeless shelter; household and other close contacts of active TB cases; and health care workers who provide care to patients with TB.

Some chronic medical conditions can increase risk for progression to active TB in those with LTBI. Patients who should be tested for LTBI as part of their routine care include those who are HIV positive; are receiving immunosuppressive therapy (chemotherapy, biological immune suppressants); have received an organ transplant; have silicosis; use illicit injected drugs; and/or have had a gastrectomy or jejunoileal bypass.

In addition, local communities may have populations or geographic regions in which TB rates are high. Family physicians can obtain this information from their state or local health departments.

There are 2 screening tests for LTBI: TB blood tests (interferon-gamma release assays [IGRAs]) and the Mantoux tuberculin skin test (TST). Two TB blood tests are available in the United States: QuantiFERON-TB Gold Plus (QFT-Plus) and T-SPOT.TB test (T-Spot).

There are advantages and disadvantages to both types of tests. A TST requires accurate administration and interpretation and 2 clinic visits, 48 to 72 hours apart. The cutoff on a positive test (5, 10, or 15 mm) depends on the patient’s age and risk.⁴ An IGRA should be processed within 8 to 32 hours and is more expensive. However, a major advantage is that it is more specific, because it is unaffected by previous vaccination with bacille Calmette-Guérin or by most nontuberculous mycobacteria infections.

To rule out active TB ... If a TB screening test is positive, the recommended work-up is to ask about TB symptoms and perform a chest x-ray to rule out active pulmonary TB. Sputum collection for acid-fast smear and culture should be ordered for anyone with a suspicious chest x-ray, respiratory symptoms consistent with TB, or HIV infection.

Treatment for LTBI markedly reduces the risk for active TB. There are 4 options:

• Isoniazid (INH) plus rifapentine (RPT) once per week for 3 months.
• Rifampin (RIF) daily for 4 months.
• INH plus RIF daily for 3 months.
• INH daily for 6 or 9 months.

Details about the variables to consider in choosing a regimen are described on the CDC website.^4,5

Know your resources. Local and state public health departments should have TB control programs and are sources of information on TB diagnosis and treatment; they also can assist with follow-up of TB contacts.⁶ Although LTBI is a reportable condition only in young children, any suspicion of community spread of active TB should be reported to the public health department.

The US Preventive Services Task Force (USPSTF) recently released draft recommendations on screening for tuberculosis (TB).¹ The USPSTF continues to recommend screening for latent TB infection (LTBI) in those at high risk.

Why is this important? Up to one-quarter of the world’s population has been infected with TB, according to World Health Organization (WHO) estimates. In 2021, active TB was diagnosed in 10.6 million people, and it caused 1.6 million deaths.² Worldwide, TB is still a major cause of mortality: It is the 13th leading cause of death and is the leading cause of infectious disease mortality in non-COVID years.

Although the rate of active TB in the United States has been declining for decades (from 30.7/100,000 in 1960 to 2.4/100,000 in 2021), 7882 cases were reported in 2021, and an estimated 13 million people in the United States have LTBI.³ If not treated, 5% to 10% of LTBI cases will progress to active TB. This risk is higher in those with certain medical conditions.³ People born outside the United States currently account for 71.4% of reported TB cases in the United States.³

To reduce the morbidity and mortality of TB, the Centers for Disease Control and Prevention (CDC), WHO, and USPSTF all recommend screening for and treating LTBI. An effective approach to TB control also includes early detection and completion of treatment for active TB, as well as testing contacts of active TB cases.

Who should be screened? Those at high risk for LTBI include those who were born in, or who have resided in, countries with high rates of TB (eg, Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia); those who have lived in a correctional facility or homeless shelter; household and other close contacts of active TB cases; and health care workers who provide care to patients with TB.

Some chronic medical conditions can increase risk for progression to active TB in those with LTBI. Patients who should be tested for LTBI as part of their routine care include those who are HIV positive; are receiving immunosuppressive therapy (chemotherapy, biological immune suppressants); have received an organ transplant; have silicosis; use illicit injected drugs; and/or have had a gastrectomy or jejunoileal bypass.

In addition, local communities may have populations or geographic regions in which TB rates are high. Family physicians can obtain this information from their state or local health departments.

There are 2 screening tests for LTBI: TB blood tests (interferon-gamma release assays [IGRAs]) and the Mantoux tuberculin skin test (TST). Two TB blood tests are available in the United States: QuantiFERON-TB Gold Plus (QFT-Plus) and T-SPOT.TB test (T-Spot).

There are advantages and disadvantages to both types of tests. A TST requires accurate administration and interpretation and 2 clinic visits, 48 to 72 hours apart. The cutoff on a positive test (5, 10, or 15 mm) depends on the patient’s age and risk.⁴ An IGRA should be processed within 8 to 32 hours and is more expensive. However, a major advantage is that it is more specific, because it is unaffected by previous vaccination with bacille Calmette-Guérin or by most nontuberculous mycobacteria infections.

To rule out active TB ... If a TB screening test is positive, the recommended work-up is to ask about TB symptoms and perform a chest x-ray to rule out active pulmonary TB. Sputum collection for acid-fast smear and culture should be ordered for anyone with a suspicious chest x-ray, respiratory symptoms consistent with TB, or HIV infection.

Treatment for LTBI markedly reduces the risk for active TB. There are 4 options:

• Isoniazid (INH) plus rifapentine (RPT) once per week for 3 months.
• Rifampin (RIF) daily for 4 months.
• INH plus RIF daily for 3 months.
• INH daily for 6 or 9 months.

Details about the variables to consider in choosing a regimen are described on the CDC website.^4,5

Know your resources. Local and state public health departments should have TB control programs and are sources of information on TB diagnosis and treatment; they also can assist with follow-up of TB contacts.⁶ Although LTBI is a reportable condition only in young children, any suspicion of community spread of active TB should be reported to the public health department.

The US Preventive Services Task Force (USPSTF) recently released draft recommendations on screening for tuberculosis (TB).¹ The USPSTF continues to recommend screening for latent TB infection (LTBI) in those at high risk.

Why is this important? Up to one-quarter of the world’s population has been infected with TB, according to World Health Organization (WHO) estimates. In 2021, active TB was diagnosed in 10.6 million people, and it caused 1.6 million deaths.² Worldwide, TB is still a major cause of mortality: It is the 13th leading cause of death and is the leading cause of infectious disease mortality in non-COVID years.

Although the rate of active TB in the United States has been declining for decades (from 30.7/100,000 in 1960 to 2.4/100,000 in 2021), 7882 cases were reported in 2021, and an estimated 13 million people in the United States have LTBI.³ If not treated, 5% to 10% of LTBI cases will progress to active TB. This risk is higher in those with certain medical conditions.³ People born outside the United States currently account for 71.4% of reported TB cases in the United States.³

To reduce the morbidity and mortality of TB, the Centers for Disease Control and Prevention (CDC), WHO, and USPSTF all recommend screening for and treating LTBI. An effective approach to TB control also includes early detection and completion of treatment for active TB, as well as testing contacts of active TB cases.

Who should be screened? Those at high risk for LTBI include those who were born in, or who have resided in, countries with high rates of TB (eg, Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia); those who have lived in a correctional facility or homeless shelter; household and other close contacts of active TB cases; and health care workers who provide care to patients with TB.

Some chronic medical conditions can increase risk for progression to active TB in those with LTBI. Patients who should be tested for LTBI as part of their routine care include those who are HIV positive; are receiving immunosuppressive therapy (chemotherapy, biological immune suppressants); have received an organ transplant; have silicosis; use illicit injected drugs; and/or have had a gastrectomy or jejunoileal bypass.

In addition, local communities may have populations or geographic regions in which TB rates are high. Family physicians can obtain this information from their state or local health departments.

There are 2 screening tests for LTBI: TB blood tests (interferon-gamma release assays [IGRAs]) and the Mantoux tuberculin skin test (TST). Two TB blood tests are available in the United States: QuantiFERON-TB Gold Plus (QFT-Plus) and T-SPOT.TB test (T-Spot).

There are advantages and disadvantages to both types of tests. A TST requires accurate administration and interpretation and 2 clinic visits, 48 to 72 hours apart. The cutoff on a positive test (5, 10, or 15 mm) depends on the patient’s age and risk.⁴ An IGRA should be processed within 8 to 32 hours and is more expensive. However, a major advantage is that it is more specific, because it is unaffected by previous vaccination with bacille Calmette-Guérin or by most nontuberculous mycobacteria infections.

To rule out active TB ... If a TB screening test is positive, the recommended work-up is to ask about TB symptoms and perform a chest x-ray to rule out active pulmonary TB. Sputum collection for acid-fast smear and culture should be ordered for anyone with a suspicious chest x-ray, respiratory symptoms consistent with TB, or HIV infection.

Treatment for LTBI markedly reduces the risk for active TB. There are 4 options:

• Isoniazid (INH) plus rifapentine (RPT) once per week for 3 months.
• Rifampin (RIF) daily for 4 months.
• INH plus RIF daily for 3 months.
• INH daily for 6 or 9 months.

Details about the variables to consider in choosing a regimen are described on the CDC website.^4,5

Know your resources. Local and state public health departments should have TB control programs and are sources of information on TB diagnosis and treatment; they also can assist with follow-up of TB contacts.⁶ Although LTBI is a reportable condition only in young children, any suspicion of community spread of active TB should be reported to the public health department.

Leave the mouthwash. Take the yogurt

Most of us have experienced some sort of bad breath. It’s common in the morning right after waking up, but it also may be a sign for underlying medical issues like dental problems or acid reflux. Wherever it comes from, we always want to get rid of it. A recent meta-analysis in BMJ Open may have found the answer in some common foods.

Mladenovic/iStock/Getty Images

For those with halitosis, the basic problem is that the bacteria in their mouths are not happy about where they are. The researchers looked at 130 studies and found seven that suggested fermented food has some effect in combating bad breath.

Now when we say fermented food, we’re not talking about that science project waiting to happen in the back of the refrigerator. Think yogurt, sourdough bread, or miso soup. Anything that contains probiotic bacteria.

Matthew J. Messina, DDS, assistant professor of dentistry at Ohio State University, who was not involved with the study, told Healthline that “the whole idea behind probiotics is [bacteria replacement]. Supplant the ‘bad guys’ with the ‘good guys,’ then we’ll end up with a better result.” Essentially balancing the scales in your mouth.

It may not be a long-term solution, Dr. Messina said, but the short-term data are positive. So if you experience bad breath from time to time, try a little bowl of yogurt instead of chewing gum. If nothing else, the bacteria in your mouth will thank you.

You can talk the silly talk, but can you walk the silly walk?

The Ministry of Silly Walks sketch from Monty Python is an enduring comedy classic, and one of surprising relevance for doctors. After all, this isn’t the first time a study has analyzed the unusual strides of Mr. Putey and Mr. Teabag.

The BMJ Christmas edition truly is the gift that keeps on giving. For this plunge into the Flying Circus, the study authors recruited a small group of fairly average adults and had them walk normally around a track for 5 minutes, monitoring their oxygen intake and energy expenditure. After that, the study participants imitated Mr. Putey’s walk and then Mr. Teabag’s.

Michael Blann/DigitalVision

In the sketch, Mr. Teabag notes that Mr. Putey’s walk is “not particularly silly,” which is borne out in the research. When imitating Mr. Putey’s walk, oxygen intake and energy expenditure were barely higher than a normal walk, not enough to achieve a meaningful difference. Hopefully he’ll get that government grant to further develop his silly walk, because right now Mr. Putey’s walk simply doesn’t cut it.

Mr. Teabag’s walk is a different story and the very image of inefficiency. Oxygen intake was 2.5 times higher than during the normal walk, and energy expenditure was noticeably higher (8 kcal in men and 5.2 kcal in women). In fact, the walk was so inefficient and its effect so drastic it actually reached the level of vigorous exercise. Thanks to this, the study authors noted that just 11 minutes a day of walking like Mr. Teabag would be enough to reach the general goal of 75 minutes of vigorous exercise per week. Boosting that to 12-19 minutes would increase daily energy expenditure by 100 kcal.

The study authors wrote, “Had an initiative to promote inefficient movement been adopted in the early 1970s, we might now be living among a healthier society. Efforts to promote higher energy – and perhaps more joyful – walking should ensure inclusivity and inefficiency for all.” We think they just advocated for a real-life Ministry of Silly Walks. Well, there have been worse ideas. Just look at Twitter.
 

When efficient gut microbes go bad

With the latest news from the Ministry of Silly Walks, is it time for humans to embrace all things inefficient? Maybe.

ChrisChrisW/Getty Images

Turns out that individuals with more efficient digestive systems – those that extract more energy from the fuel supplied to them by the busy mouths above – tend to gain more weight than those with less efficient guts, even when they eat the same food, according to a recent study published in Microbiome.

The researchers took a look at the composition of gut microbes in a group of 85 volunteers and found that about 40% had microbiomes dominated by Bacteroides bacteria, which are more effective at extracting nutrients from food. That group also weighed 10% more on average, amounting to an extra 9 kg.

In a rather blatant demonstration of efficiency, the investigators also measured the speed of the participants’ digestion, as they had hypothesized that those with the longest digestive travel times would be the ones who harvested the most nutrition from their food. That was not the case.

The study subjects with the most efficient gut bacteria “also have the fastest passage through the gastrointestinal system, which has given us something to think about,” senior author Henrik Roager of the University of Copenhagen said in a written statement.

You know what gives us something to think about? Stool energy density and intestinal transit time and faecal bacterial cell counts, that’s what. Ick. Sometimes science is gross.

Here’s another thought, though: Seeing faecal instead of fecal is kind of funny to our American eyes, but adding that extra letter is also inefficient, which could mean that it’s good. So, in the spirit of embracing the inefficient as a new year begins, we’re resolving to wrap our editorial arms around faecal and the faeces it represents. Well, not literally, of course. More like we’re embracing the spirit of faeces.

Leave the mouthwash. Take the yogurt

Most of us have experienced some sort of bad breath. It’s common in the morning right after waking up, but it also may be a sign for underlying medical issues like dental problems or acid reflux. Wherever it comes from, we always want to get rid of it. A recent meta-analysis in BMJ Open may have found the answer in some common foods.

Mladenovic/iStock/Getty Images

For those with halitosis, the basic problem is that the bacteria in their mouths are not happy about where they are. The researchers looked at 130 studies and found seven that suggested fermented food has some effect in combating bad breath.

Now when we say fermented food, we’re not talking about that science project waiting to happen in the back of the refrigerator. Think yogurt, sourdough bread, or miso soup. Anything that contains probiotic bacteria.

Matthew J. Messina, DDS, assistant professor of dentistry at Ohio State University, who was not involved with the study, told Healthline that “the whole idea behind probiotics is [bacteria replacement]. Supplant the ‘bad guys’ with the ‘good guys,’ then we’ll end up with a better result.” Essentially balancing the scales in your mouth.

It may not be a long-term solution, Dr. Messina said, but the short-term data are positive. So if you experience bad breath from time to time, try a little bowl of yogurt instead of chewing gum. If nothing else, the bacteria in your mouth will thank you.

You can talk the silly talk, but can you walk the silly walk?

The Ministry of Silly Walks sketch from Monty Python is an enduring comedy classic, and one of surprising relevance for doctors. After all, this isn’t the first time a study has analyzed the unusual strides of Mr. Putey and Mr. Teabag.

The BMJ Christmas edition truly is the gift that keeps on giving. For this plunge into the Flying Circus, the study authors recruited a small group of fairly average adults and had them walk normally around a track for 5 minutes, monitoring their oxygen intake and energy expenditure. After that, the study participants imitated Mr. Putey’s walk and then Mr. Teabag’s.

Michael Blann/DigitalVision

In the sketch, Mr. Teabag notes that Mr. Putey’s walk is “not particularly silly,” which is borne out in the research. When imitating Mr. Putey’s walk, oxygen intake and energy expenditure were barely higher than a normal walk, not enough to achieve a meaningful difference. Hopefully he’ll get that government grant to further develop his silly walk, because right now Mr. Putey’s walk simply doesn’t cut it.

Mr. Teabag’s walk is a different story and the very image of inefficiency. Oxygen intake was 2.5 times higher than during the normal walk, and energy expenditure was noticeably higher (8 kcal in men and 5.2 kcal in women). In fact, the walk was so inefficient and its effect so drastic it actually reached the level of vigorous exercise. Thanks to this, the study authors noted that just 11 minutes a day of walking like Mr. Teabag would be enough to reach the general goal of 75 minutes of vigorous exercise per week. Boosting that to 12-19 minutes would increase daily energy expenditure by 100 kcal.

The study authors wrote, “Had an initiative to promote inefficient movement been adopted in the early 1970s, we might now be living among a healthier society. Efforts to promote higher energy – and perhaps more joyful – walking should ensure inclusivity and inefficiency for all.” We think they just advocated for a real-life Ministry of Silly Walks. Well, there have been worse ideas. Just look at Twitter.
 

When efficient gut microbes go bad

With the latest news from the Ministry of Silly Walks, is it time for humans to embrace all things inefficient? Maybe.

ChrisChrisW/Getty Images

Turns out that individuals with more efficient digestive systems – those that extract more energy from the fuel supplied to them by the busy mouths above – tend to gain more weight than those with less efficient guts, even when they eat the same food, according to a recent study published in Microbiome.

The researchers took a look at the composition of gut microbes in a group of 85 volunteers and found that about 40% had microbiomes dominated by Bacteroides bacteria, which are more effective at extracting nutrients from food. That group also weighed 10% more on average, amounting to an extra 9 kg.

In a rather blatant demonstration of efficiency, the investigators also measured the speed of the participants’ digestion, as they had hypothesized that those with the longest digestive travel times would be the ones who harvested the most nutrition from their food. That was not the case.

The study subjects with the most efficient gut bacteria “also have the fastest passage through the gastrointestinal system, which has given us something to think about,” senior author Henrik Roager of the University of Copenhagen said in a written statement.

You know what gives us something to think about? Stool energy density and intestinal transit time and faecal bacterial cell counts, that’s what. Ick. Sometimes science is gross.

Here’s another thought, though: Seeing faecal instead of fecal is kind of funny to our American eyes, but adding that extra letter is also inefficient, which could mean that it’s good. So, in the spirit of embracing the inefficient as a new year begins, we’re resolving to wrap our editorial arms around faecal and the faeces it represents. Well, not literally, of course. More like we’re embracing the spirit of faeces.

Leave the mouthwash. Take the yogurt

Most of us have experienced some sort of bad breath. It’s common in the morning right after waking up, but it also may be a sign for underlying medical issues like dental problems or acid reflux. Wherever it comes from, we always want to get rid of it. A recent meta-analysis in BMJ Open may have found the answer in some common foods.

Mladenovic/iStock/Getty Images

For those with halitosis, the basic problem is that the bacteria in their mouths are not happy about where they are. The researchers looked at 130 studies and found seven that suggested fermented food has some effect in combating bad breath.

Now when we say fermented food, we’re not talking about that science project waiting to happen in the back of the refrigerator. Think yogurt, sourdough bread, or miso soup. Anything that contains probiotic bacteria.

Matthew J. Messina, DDS, assistant professor of dentistry at Ohio State University, who was not involved with the study, told Healthline that “the whole idea behind probiotics is [bacteria replacement]. Supplant the ‘bad guys’ with the ‘good guys,’ then we’ll end up with a better result.” Essentially balancing the scales in your mouth.

It may not be a long-term solution, Dr. Messina said, but the short-term data are positive. So if you experience bad breath from time to time, try a little bowl of yogurt instead of chewing gum. If nothing else, the bacteria in your mouth will thank you.

You can talk the silly talk, but can you walk the silly walk?

The Ministry of Silly Walks sketch from Monty Python is an enduring comedy classic, and one of surprising relevance for doctors. After all, this isn’t the first time a study has analyzed the unusual strides of Mr. Putey and Mr. Teabag.

The BMJ Christmas edition truly is the gift that keeps on giving. For this plunge into the Flying Circus, the study authors recruited a small group of fairly average adults and had them walk normally around a track for 5 minutes, monitoring their oxygen intake and energy expenditure. After that, the study participants imitated Mr. Putey’s walk and then Mr. Teabag’s.

Michael Blann/DigitalVision

In the sketch, Mr. Teabag notes that Mr. Putey’s walk is “not particularly silly,” which is borne out in the research. When imitating Mr. Putey’s walk, oxygen intake and energy expenditure were barely higher than a normal walk, not enough to achieve a meaningful difference. Hopefully he’ll get that government grant to further develop his silly walk, because right now Mr. Putey’s walk simply doesn’t cut it.

Mr. Teabag’s walk is a different story and the very image of inefficiency. Oxygen intake was 2.5 times higher than during the normal walk, and energy expenditure was noticeably higher (8 kcal in men and 5.2 kcal in women). In fact, the walk was so inefficient and its effect so drastic it actually reached the level of vigorous exercise. Thanks to this, the study authors noted that just 11 minutes a day of walking like Mr. Teabag would be enough to reach the general goal of 75 minutes of vigorous exercise per week. Boosting that to 12-19 minutes would increase daily energy expenditure by 100 kcal.

The study authors wrote, “Had an initiative to promote inefficient movement been adopted in the early 1970s, we might now be living among a healthier society. Efforts to promote higher energy – and perhaps more joyful – walking should ensure inclusivity and inefficiency for all.” We think they just advocated for a real-life Ministry of Silly Walks. Well, there have been worse ideas. Just look at Twitter.
 

When efficient gut microbes go bad

With the latest news from the Ministry of Silly Walks, is it time for humans to embrace all things inefficient? Maybe.

ChrisChrisW/Getty Images

Turns out that individuals with more efficient digestive systems – those that extract more energy from the fuel supplied to them by the busy mouths above – tend to gain more weight than those with less efficient guts, even when they eat the same food, according to a recent study published in Microbiome.

The researchers took a look at the composition of gut microbes in a group of 85 volunteers and found that about 40% had microbiomes dominated by Bacteroides bacteria, which are more effective at extracting nutrients from food. That group also weighed 10% more on average, amounting to an extra 9 kg.

In a rather blatant demonstration of efficiency, the investigators also measured the speed of the participants’ digestion, as they had hypothesized that those with the longest digestive travel times would be the ones who harvested the most nutrition from their food. That was not the case.

The study subjects with the most efficient gut bacteria “also have the fastest passage through the gastrointestinal system, which has given us something to think about,” senior author Henrik Roager of the University of Copenhagen said in a written statement.

You know what gives us something to think about? Stool energy density and intestinal transit time and faecal bacterial cell counts, that’s what. Ick. Sometimes science is gross.

Here’s another thought, though: Seeing faecal instead of fecal is kind of funny to our American eyes, but adding that extra letter is also inefficient, which could mean that it’s good. So, in the spirit of embracing the inefficient as a new year begins, we’re resolving to wrap our editorial arms around faecal and the faeces it represents. Well, not literally, of course. More like we’re embracing the spirit of faeces.

Two new papers published recently provide evidence of the efficacy and safety of bimekizumab in psoriatic arthritis (PsA). Bimekizumab is a novel bispecific monoclonal antibody targeting interleukin (IL)-17A and IL-17F and is already approved for the treatment of chronic plaque psoriasis. McInnes and colleagues reported the results of the phase 3 BE OPTIMAL study, which included 852 patients with active PsA who were naive to biologic disease-modifying antirheumatic drugs (bDMARD) and were randomly assigned to receive bimekizumab, placebo, or adalimumab. At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥ 50% improvement in American College of Rheumatology response (ACR50; 44% vs 10%; odds ratio [OR] 7.1; P < .0001). Compared with placebo, significant improvements were also noted in psoriasis, enthesitis, and dactylitis in the bimekizumab group and there was less progression of radiographic damage.

Bimekizumab was also demonstrated to be beneficial in PsA patients with inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi). In the phase 3 BE COMPLETE study, which included 400 patients with active PsA and previous inadequate response or intolerance to TNFi, patients were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo. Merola and colleagues reported that at week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ACR50 response (43% vs 7%; OR 11.1; P < .0001). Thus, bimekizumab is a welcome addition to the treatment portfolio we have for PsA. In regard to side effects of special concern when inhibiting IL-17, bimekizumab was associated with higher risk for oral and genital candidiasis, occurring in 4% of the treated patients within 16 weeks in the two studies; however, no cases of systemic fungal infections occurred. The incidence of inflammatory bowel disease was also very low, but head-to-head studies against other available agents would be required to help rheumatologists decide the place of bimekizumab in PsA management.

A common clinical question is whether axial PsA is similar to ankylosing spondylitis (AS) with psoriasis. Assuming that it is, clinicians have used treatments approved for AS for managing axial PsA. Recent studies have questioned this assumption, however. Michelena and colleagues conducted a cross-sectional study that included 109 patients with axial PsA and 127 patients with AS and psoriasis from the REGISPONSER registry. Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27–negative axial PsA had less inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001), along with a higher prevalence of nail disease (P = .009). Patients with HLA-B27–positive axial PsA vs AS and psoriasis were similar but had less structural damage to the spine (P < .001). Thus, there seem to be significant clinical and genetic differences between these two diseases that require further investigation. Lack of an accepted definition of axial PsA, however, is a hindrance to multiple high-quality genetic, clinical, and interventional studies comparing axial PsA and AS with psoriasis.

Observational studies have recognized the clinical and familial association between psoriatic disease and Crohn's disease (CD), but such cross-sectional or retrospective studies cannot identify causal relationships. Mendelian randomization is a method used to identify causal relationships. Using this method, Sun and colleagues demonstrated that PsA was associated with a 31.9% increased risk for CD (P < .001) and genetically predicted CD was linked to a 44.8% higher risk for PsA (P = .001). No such association was found with ulcerative colitis. Thus, there is a bidirectional causal relationship between the two diseases. Patients with PsA should be evaluated for symptoms of CD, and those with CD for psoriatic disease, to facilitate early diagnosis and better long-term outcomes.

Two new papers published recently provide evidence of the efficacy and safety of bimekizumab in psoriatic arthritis (PsA). Bimekizumab is a novel bispecific monoclonal antibody targeting interleukin (IL)-17A and IL-17F and is already approved for the treatment of chronic plaque psoriasis. McInnes and colleagues reported the results of the phase 3 BE OPTIMAL study, which included 852 patients with active PsA who were naive to biologic disease-modifying antirheumatic drugs (bDMARD) and were randomly assigned to receive bimekizumab, placebo, or adalimumab. At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥ 50% improvement in American College of Rheumatology response (ACR50; 44% vs 10%; odds ratio [OR] 7.1; P < .0001). Compared with placebo, significant improvements were also noted in psoriasis, enthesitis, and dactylitis in the bimekizumab group and there was less progression of radiographic damage.

Bimekizumab was also demonstrated to be beneficial in PsA patients with inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi). In the phase 3 BE COMPLETE study, which included 400 patients with active PsA and previous inadequate response or intolerance to TNFi, patients were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo. Merola and colleagues reported that at week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ACR50 response (43% vs 7%; OR 11.1; P < .0001). Thus, bimekizumab is a welcome addition to the treatment portfolio we have for PsA. In regard to side effects of special concern when inhibiting IL-17, bimekizumab was associated with higher risk for oral and genital candidiasis, occurring in 4% of the treated patients within 16 weeks in the two studies; however, no cases of systemic fungal infections occurred. The incidence of inflammatory bowel disease was also very low, but head-to-head studies against other available agents would be required to help rheumatologists decide the place of bimekizumab in PsA management.

A common clinical question is whether axial PsA is similar to ankylosing spondylitis (AS) with psoriasis. Assuming that it is, clinicians have used treatments approved for AS for managing axial PsA. Recent studies have questioned this assumption, however. Michelena and colleagues conducted a cross-sectional study that included 109 patients with axial PsA and 127 patients with AS and psoriasis from the REGISPONSER registry. Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27–negative axial PsA had less inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001), along with a higher prevalence of nail disease (P = .009). Patients with HLA-B27–positive axial PsA vs AS and psoriasis were similar but had less structural damage to the spine (P < .001). Thus, there seem to be significant clinical and genetic differences between these two diseases that require further investigation. Lack of an accepted definition of axial PsA, however, is a hindrance to multiple high-quality genetic, clinical, and interventional studies comparing axial PsA and AS with psoriasis.

Observational studies have recognized the clinical and familial association between psoriatic disease and Crohn's disease (CD), but such cross-sectional or retrospective studies cannot identify causal relationships. Mendelian randomization is a method used to identify causal relationships. Using this method, Sun and colleagues demonstrated that PsA was associated with a 31.9% increased risk for CD (P < .001) and genetically predicted CD was linked to a 44.8% higher risk for PsA (P = .001). No such association was found with ulcerative colitis. Thus, there is a bidirectional causal relationship between the two diseases. Patients with PsA should be evaluated for symptoms of CD, and those with CD for psoriatic disease, to facilitate early diagnosis and better long-term outcomes.

Two new papers published recently provide evidence of the efficacy and safety of bimekizumab in psoriatic arthritis (PsA). Bimekizumab is a novel bispecific monoclonal antibody targeting interleukin (IL)-17A and IL-17F and is already approved for the treatment of chronic plaque psoriasis. McInnes and colleagues reported the results of the phase 3 BE OPTIMAL study, which included 852 patients with active PsA who were naive to biologic disease-modifying antirheumatic drugs (bDMARD) and were randomly assigned to receive bimekizumab, placebo, or adalimumab. At week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ≥ 50% improvement in American College of Rheumatology response (ACR50; 44% vs 10%; odds ratio [OR] 7.1; P < .0001). Compared with placebo, significant improvements were also noted in psoriasis, enthesitis, and dactylitis in the bimekizumab group and there was less progression of radiographic damage.

Bimekizumab was also demonstrated to be beneficial in PsA patients with inadequate response or intolerance to tumor necrosis factor inhibitors (TNFi). In the phase 3 BE COMPLETE study, which included 400 patients with active PsA and previous inadequate response or intolerance to TNFi, patients were randomly assigned to receive 160 mg subcutaneous bimekizumab every 4 weeks or placebo. Merola and colleagues reported that at week 16, a significantly higher proportion of patients receiving bimekizumab vs placebo achieved ACR50 response (43% vs 7%; OR 11.1; P < .0001). Thus, bimekizumab is a welcome addition to the treatment portfolio we have for PsA. In regard to side effects of special concern when inhibiting IL-17, bimekizumab was associated with higher risk for oral and genital candidiasis, occurring in 4% of the treated patients within 16 weeks in the two studies; however, no cases of systemic fungal infections occurred. The incidence of inflammatory bowel disease was also very low, but head-to-head studies against other available agents would be required to help rheumatologists decide the place of bimekizumab in PsA management.

A common clinical question is whether axial PsA is similar to ankylosing spondylitis (AS) with psoriasis. Assuming that it is, clinicians have used treatments approved for AS for managing axial PsA. Recent studies have questioned this assumption, however. Michelena and colleagues conducted a cross-sectional study that included 109 patients with axial PsA and 127 patients with AS and psoriasis from the REGISPONSER registry. Compared with patients with AS and psoriasis, patients with human leukocyte antigen (HLA)-B27–negative axial PsA had less inflammatory pain (P = .002), anterior uveitis (P = .014), and structural damage (P < .001), along with a higher prevalence of nail disease (P = .009). Patients with HLA-B27–positive axial PsA vs AS and psoriasis were similar but had less structural damage to the spine (P < .001). Thus, there seem to be significant clinical and genetic differences between these two diseases that require further investigation. Lack of an accepted definition of axial PsA, however, is a hindrance to multiple high-quality genetic, clinical, and interventional studies comparing axial PsA and AS with psoriasis.

Observational studies have recognized the clinical and familial association between psoriatic disease and Crohn's disease (CD), but such cross-sectional or retrospective studies cannot identify causal relationships. Mendelian randomization is a method used to identify causal relationships. Using this method, Sun and colleagues demonstrated that PsA was associated with a 31.9% increased risk for CD (P < .001) and genetically predicted CD was linked to a 44.8% higher risk for PsA (P = .001). No such association was found with ulcerative colitis. Thus, there is a bidirectional causal relationship between the two diseases. Patients with PsA should be evaluated for symptoms of CD, and those with CD for psoriatic disease, to facilitate early diagnosis and better long-term outcomes.

January's theme is migraine triggers. We'll take a look at three recent studies that have tried to better determine the nature of specific triggers for headache.

One of the most common and reportedly consistent migraine triggers is exposure to alcohol, and the International Classification of Headache Disorders (ICHD-3) includes alcohol-induced headache as a secondary headache. Little is known regarding the association between migraine and alcohol. Vives-Mestres and colleagues investigated the alcohol intake of people using a digital health diary for headache. They specifically looked at the 48 hours preceding a migraine attack and whether alcohol was consumed, and also the number of beverages consumed. This was further adjusted for sex, age, and average weekly alcohol intake.

The N1-Headache Tracker is a digital headache diary that patients use to track their daily headache symptoms and inform them of potential migraine risk factors. Over a 90-day period, this study followed patients that did not meet the criteria for a diagnosis of chronic migraine. They also reported on their intake to the platform that they regularly consume alcohol. Of note, persons who never tracked alcohol consumption were excluded from this study. On intake to the platform, alcohol exposure was characterized both as whether daily consumption of alcohol was occurring and as the total daily number of alcoholic beverages.

The primary outcome of this study was migraine attack 1 day after alcohol consumption. Participants were specifically asked if their headaches were diagnosed as migraine by a physician. Migraine attack onset was considered binary, and a logistic model was used to estimate the probability of having a migraine attack on any given day with the association of alcohol intake for up to 48 hours prior to that day.

A total of 487 people with migraine were included in this trial and they collectively contributed over 43,000 diary days; almost 6000 were first days of a migraine attack. Overall alcohol consumption was not considered high and was noted to vary between groups; people with lower frequency migraine tended to have higher rates of alcohol intake. No significant correlation was observed between the presence of migraine attacks within 48 hours after alcohol consumption. This did not vary among different probability models; a population-level model showed that the probability of a migraine attack 2 days after alcohol intake was 25% lower than the probability of an attack with no alcohol consumption. This was also true after adjustment for age, sex, and average number of alcoholic beverages per week.

The association between migraine and alcohol is complicated, and the concept of migraine triggers in general is very complex. Although over 70% of people with migraine say that they have a consistent trigger, and alcohol is consistently at the top of the list of those reported triggers, there does not appear to be a direct correlation between migraine and alcohol exposure. The greatest caveat of this study is the fact that people with chronic migraine were excluded. Further research should specifically investigate triggers such as alcohol in this population.

The use of proton pump inhibitors (PPI) has been shown in previous studies over the past few years to be associated with a number of neurologic events and risks, including impaired hearing, vision, and memory, as well as migraine occurrence. The specifics of this association are not well known — specifically, whether the duration of use is the main factor, or whether it is acute exposure to a PPI medication that is a trigger. Kang and colleagues reviewed data in the Korean national database and developed a case-control model to study this association specifically.

The migraine and control groups were equally matched: They had the same demographics, smoking status, alcohol consumption, blood pressure range, fasting glucose, and total cholesterol. Past and current PPI use and comparisons of migraine occurrence were further differentiated among patients who were exposed to PPI medications for < 30 days, 30-365 days, and > 365 days.

The use of PPI treatments was noted to be linked to increased migraine regardless of duration, and regardless of the acute presence of the PPI. Even a history of prior PPI use was noted to increase the odds ratio of migraine development. This was significant among all subgroups, independent of age, sex, and other comorbidities. There was no difference in the presence of aura associated with migraine.

As we noted above, the concept of migraine triggers is overall poorly understood. This is even more the case when it comes to historical exposures. Although the use of PPI medications appears to be associated with the occurrence of migraine in this population, these medications are necessary in many instances, including in patients with severe gastritis and gastroesophageal reflux refractory to diet changes. It remains to be seen precisely how PPI medications would potentially lead to a higher incidence of migraine.

Among many of the triggers discussed, specific foods are commonly thought to be associated with migraine. Although there is scant evidence for a specific diet to improve migraine frequency, many patients are very interested in potential dietary changes that may help them. Prior studies and reviews have looked at gluten-free, dairy-free, low-carbohydrate, low-tyramine, and elimination diets — all of which were not associated with a significant improvement in migraine frequency or severity. Bakıran and colleagues sought to investigate an antioxidant-rich diet that included polyphenols and carotenoids — substances that may improve systemic inflammation, glucose metabolism, and oxidative stress.

Phytochemical-rich foods include fruits and vegetables (excluding potatoes) as well as nuts, whole grains, pulses, and olive oil. The phytochemical index is a tool used by dietitians and nutritionists to assess the phytochemical content in a diet.

A total of 90 patients who had a diagnosis of episodic migraine by a neurologist were enrolled. Individuals were excluded if they had a body mass index > 40 or < 18 or had other significant chronic comorbidities, such as hypertension, diabetes, hepatic or renal disease, or other neurologic conditions. Participants filled out a headache diary over 3 months; the Migraine Disability Assessment (MIDAS) questionnaire was also followed in order to assess migraine-related disability. Diet quality was cataloged as per patient records; patients also filled out a 3-day nonconsecutive food diary. This information was added to a food software program that calculated specific nutrients, including the phytochemical index.

Participants were divided into groups with good diet quality and poor diet quality based on their phytochemical index. No differences were seen in migraine frequency or disability between these groups, although mean attack duration was lower in those with poor diet quality. Severity was noted to be higher in those with poor diet quality; 75% of participants with poor diet quality experienced severe attacks.

Overall, the results of this study are very mixed. Participants on the recommended high phytochemical diet were seen to have lower severity of migraine but a prolonged duration of attack. There also was no correlation between this diet and either frequency or disability. This was a small study, and further research should focus on this among other diet changes that have the possibility to improve the quality of life of people with migraine.

January's theme is migraine triggers. We'll take a look at three recent studies that have tried to better determine the nature of specific triggers for headache.

One of the most common and reportedly consistent migraine triggers is exposure to alcohol, and the International Classification of Headache Disorders (ICHD-3) includes alcohol-induced headache as a secondary headache. Little is known regarding the association between migraine and alcohol. Vives-Mestres and colleagues investigated the alcohol intake of people using a digital health diary for headache. They specifically looked at the 48 hours preceding a migraine attack and whether alcohol was consumed, and also the number of beverages consumed. This was further adjusted for sex, age, and average weekly alcohol intake.

The N1-Headache Tracker is a digital headache diary that patients use to track their daily headache symptoms and inform them of potential migraine risk factors. Over a 90-day period, this study followed patients that did not meet the criteria for a diagnosis of chronic migraine. They also reported on their intake to the platform that they regularly consume alcohol. Of note, persons who never tracked alcohol consumption were excluded from this study. On intake to the platform, alcohol exposure was characterized both as whether daily consumption of alcohol was occurring and as the total daily number of alcoholic beverages.

The primary outcome of this study was migraine attack 1 day after alcohol consumption. Participants were specifically asked if their headaches were diagnosed as migraine by a physician. Migraine attack onset was considered binary, and a logistic model was used to estimate the probability of having a migraine attack on any given day with the association of alcohol intake for up to 48 hours prior to that day.

A total of 487 people with migraine were included in this trial and they collectively contributed over 43,000 diary days; almost 6000 were first days of a migraine attack. Overall alcohol consumption was not considered high and was noted to vary between groups; people with lower frequency migraine tended to have higher rates of alcohol intake. No significant correlation was observed between the presence of migraine attacks within 48 hours after alcohol consumption. This did not vary among different probability models; a population-level model showed that the probability of a migraine attack 2 days after alcohol intake was 25% lower than the probability of an attack with no alcohol consumption. This was also true after adjustment for age, sex, and average number of alcoholic beverages per week.

The association between migraine and alcohol is complicated, and the concept of migraine triggers in general is very complex. Although over 70% of people with migraine say that they have a consistent trigger, and alcohol is consistently at the top of the list of those reported triggers, there does not appear to be a direct correlation between migraine and alcohol exposure. The greatest caveat of this study is the fact that people with chronic migraine were excluded. Further research should specifically investigate triggers such as alcohol in this population.

The use of proton pump inhibitors (PPI) has been shown in previous studies over the past few years to be associated with a number of neurologic events and risks, including impaired hearing, vision, and memory, as well as migraine occurrence. The specifics of this association are not well known — specifically, whether the duration of use is the main factor, or whether it is acute exposure to a PPI medication that is a trigger. Kang and colleagues reviewed data in the Korean national database and developed a case-control model to study this association specifically.

The migraine and control groups were equally matched: They had the same demographics, smoking status, alcohol consumption, blood pressure range, fasting glucose, and total cholesterol. Past and current PPI use and comparisons of migraine occurrence were further differentiated among patients who were exposed to PPI medications for < 30 days, 30-365 days, and > 365 days.

The use of PPI treatments was noted to be linked to increased migraine regardless of duration, and regardless of the acute presence of the PPI. Even a history of prior PPI use was noted to increase the odds ratio of migraine development. This was significant among all subgroups, independent of age, sex, and other comorbidities. There was no difference in the presence of aura associated with migraine.

As we noted above, the concept of migraine triggers is overall poorly understood. This is even more the case when it comes to historical exposures. Although the use of PPI medications appears to be associated with the occurrence of migraine in this population, these medications are necessary in many instances, including in patients with severe gastritis and gastroesophageal reflux refractory to diet changes. It remains to be seen precisely how PPI medications would potentially lead to a higher incidence of migraine.

Among many of the triggers discussed, specific foods are commonly thought to be associated with migraine. Although there is scant evidence for a specific diet to improve migraine frequency, many patients are very interested in potential dietary changes that may help them. Prior studies and reviews have looked at gluten-free, dairy-free, low-carbohydrate, low-tyramine, and elimination diets — all of which were not associated with a significant improvement in migraine frequency or severity. Bakıran and colleagues sought to investigate an antioxidant-rich diet that included polyphenols and carotenoids — substances that may improve systemic inflammation, glucose metabolism, and oxidative stress.

Phytochemical-rich foods include fruits and vegetables (excluding potatoes) as well as nuts, whole grains, pulses, and olive oil. The phytochemical index is a tool used by dietitians and nutritionists to assess the phytochemical content in a diet.

A total of 90 patients who had a diagnosis of episodic migraine by a neurologist were enrolled. Individuals were excluded if they had a body mass index > 40 or < 18 or had other significant chronic comorbidities, such as hypertension, diabetes, hepatic or renal disease, or other neurologic conditions. Participants filled out a headache diary over 3 months; the Migraine Disability Assessment (MIDAS) questionnaire was also followed in order to assess migraine-related disability. Diet quality was cataloged as per patient records; patients also filled out a 3-day nonconsecutive food diary. This information was added to a food software program that calculated specific nutrients, including the phytochemical index.

Participants were divided into groups with good diet quality and poor diet quality based on their phytochemical index. No differences were seen in migraine frequency or disability between these groups, although mean attack duration was lower in those with poor diet quality. Severity was noted to be higher in those with poor diet quality; 75% of participants with poor diet quality experienced severe attacks.

Overall, the results of this study are very mixed. Participants on the recommended high phytochemical diet were seen to have lower severity of migraine but a prolonged duration of attack. There also was no correlation between this diet and either frequency or disability. This was a small study, and further research should focus on this among other diet changes that have the possibility to improve the quality of life of people with migraine.

January's theme is migraine triggers. We'll take a look at three recent studies that have tried to better determine the nature of specific triggers for headache.

One of the most common and reportedly consistent migraine triggers is exposure to alcohol, and the International Classification of Headache Disorders (ICHD-3) includes alcohol-induced headache as a secondary headache. Little is known regarding the association between migraine and alcohol. Vives-Mestres and colleagues investigated the alcohol intake of people using a digital health diary for headache. They specifically looked at the 48 hours preceding a migraine attack and whether alcohol was consumed, and also the number of beverages consumed. This was further adjusted for sex, age, and average weekly alcohol intake.

The N1-Headache Tracker is a digital headache diary that patients use to track their daily headache symptoms and inform them of potential migraine risk factors. Over a 90-day period, this study followed patients that did not meet the criteria for a diagnosis of chronic migraine. They also reported on their intake to the platform that they regularly consume alcohol. Of note, persons who never tracked alcohol consumption were excluded from this study. On intake to the platform, alcohol exposure was characterized both as whether daily consumption of alcohol was occurring and as the total daily number of alcoholic beverages.

The primary outcome of this study was migraine attack 1 day after alcohol consumption. Participants were specifically asked if their headaches were diagnosed as migraine by a physician. Migraine attack onset was considered binary, and a logistic model was used to estimate the probability of having a migraine attack on any given day with the association of alcohol intake for up to 48 hours prior to that day.

A total of 487 people with migraine were included in this trial and they collectively contributed over 43,000 diary days; almost 6000 were first days of a migraine attack. Overall alcohol consumption was not considered high and was noted to vary between groups; people with lower frequency migraine tended to have higher rates of alcohol intake. No significant correlation was observed between the presence of migraine attacks within 48 hours after alcohol consumption. This did not vary among different probability models; a population-level model showed that the probability of a migraine attack 2 days after alcohol intake was 25% lower than the probability of an attack with no alcohol consumption. This was also true after adjustment for age, sex, and average number of alcoholic beverages per week.

The association between migraine and alcohol is complicated, and the concept of migraine triggers in general is very complex. Although over 70% of people with migraine say that they have a consistent trigger, and alcohol is consistently at the top of the list of those reported triggers, there does not appear to be a direct correlation between migraine and alcohol exposure. The greatest caveat of this study is the fact that people with chronic migraine were excluded. Further research should specifically investigate triggers such as alcohol in this population.

The use of proton pump inhibitors (PPI) has been shown in previous studies over the past few years to be associated with a number of neurologic events and risks, including impaired hearing, vision, and memory, as well as migraine occurrence. The specifics of this association are not well known — specifically, whether the duration of use is the main factor, or whether it is acute exposure to a PPI medication that is a trigger. Kang and colleagues reviewed data in the Korean national database and developed a case-control model to study this association specifically.

The migraine and control groups were equally matched: They had the same demographics, smoking status, alcohol consumption, blood pressure range, fasting glucose, and total cholesterol. Past and current PPI use and comparisons of migraine occurrence were further differentiated among patients who were exposed to PPI medications for < 30 days, 30-365 days, and > 365 days.

The use of PPI treatments was noted to be linked to increased migraine regardless of duration, and regardless of the acute presence of the PPI. Even a history of prior PPI use was noted to increase the odds ratio of migraine development. This was significant among all subgroups, independent of age, sex, and other comorbidities. There was no difference in the presence of aura associated with migraine.

As we noted above, the concept of migraine triggers is overall poorly understood. This is even more the case when it comes to historical exposures. Although the use of PPI medications appears to be associated with the occurrence of migraine in this population, these medications are necessary in many instances, including in patients with severe gastritis and gastroesophageal reflux refractory to diet changes. It remains to be seen precisely how PPI medications would potentially lead to a higher incidence of migraine.

Among many of the triggers discussed, specific foods are commonly thought to be associated with migraine. Although there is scant evidence for a specific diet to improve migraine frequency, many patients are very interested in potential dietary changes that may help them. Prior studies and reviews have looked at gluten-free, dairy-free, low-carbohydrate, low-tyramine, and elimination diets — all of which were not associated with a significant improvement in migraine frequency or severity. Bakıran and colleagues sought to investigate an antioxidant-rich diet that included polyphenols and carotenoids — substances that may improve systemic inflammation, glucose metabolism, and oxidative stress.

Phytochemical-rich foods include fruits and vegetables (excluding potatoes) as well as nuts, whole grains, pulses, and olive oil. The phytochemical index is a tool used by dietitians and nutritionists to assess the phytochemical content in a diet.

A total of 90 patients who had a diagnosis of episodic migraine by a neurologist were enrolled. Individuals were excluded if they had a body mass index > 40 or < 18 or had other significant chronic comorbidities, such as hypertension, diabetes, hepatic or renal disease, or other neurologic conditions. Participants filled out a headache diary over 3 months; the Migraine Disability Assessment (MIDAS) questionnaire was also followed in order to assess migraine-related disability. Diet quality was cataloged as per patient records; patients also filled out a 3-day nonconsecutive food diary. This information was added to a food software program that calculated specific nutrients, including the phytochemical index.

Participants were divided into groups with good diet quality and poor diet quality based on their phytochemical index. No differences were seen in migraine frequency or disability between these groups, although mean attack duration was lower in those with poor diet quality. Severity was noted to be higher in those with poor diet quality; 75% of participants with poor diet quality experienced severe attacks.

Overall, the results of this study are very mixed. Participants on the recommended high phytochemical diet were seen to have lower severity of migraine but a prolonged duration of attack. There also was no correlation between this diet and either frequency or disability. This was a small study, and further research should focus on this among other diet changes that have the possibility to improve the quality of life of people with migraine.

The Diagnosis: Atypical Mycobacterial Infection

The history of rapid growth followed by shrinkage as well as the craterlike clinical appearance of our patient’s lesion were suspicious for the keratoacanthoma variant of squamous cell carcinoma (SCC). Periodic acid–Schiff green staining was negative for fungal or bacterial organisms, and the biopsy findings of keratinocyte atypia and irregular epidermal proliferation seemed to confirm our suspicion for well-differentiated SCC (Figure 1). Our patient subsequently was scheduled for Mohs micrographic surgery. Fortunately, a sample of tissue had been sent for panculture—bacterial, fungal, and mycobacterial—to rule out infectious etiologies, given the history of possible traumatic inoculation, and returned positive for Mycobacterium marinum infection prior to the surgery. Mohs surgery was canceled, and he was referred to an infectious disease specialist who started antibiotic treatment with azithromycin, ethambutol, and rifabutin. After 1 month of treatment the lesion substantially improved (Figure 2), further supporting the diagnosis of M marinum infection over SCC.

The differential diagnosis also included sporotrichosis, leishmaniasis, and chromoblastomycosis. Sporotrichosis lesions typically develop as multiple nodules and ulcers along a path of lymphatic drainage and can exhibit asteroid bodies and cigar-shaped yeast forms on histology. Chromoblastomycosis may display pseudoepitheliomatous hyperplasia and granulomatous inflammation; however, pathognomonic pigmented Medlar bodies also likely would be present.¹ Leishmaniasis has a wide variety of presentations; however, it typically occurs in patients with exposure to endemic areas outside of the United States. Although leishmaniasis may demonstrate pseudoepitheliomatous hyperplasia, ulceration, and mixed inflammation on histology, it also likely would show amastigotes within dermal macrophages.²

Atypical mycobacterial infections initially may be misdiagnosed as SCC due to their tendency to induce irregular acanthosis in the form of pseudoepitheliomatous hyperplasia as well as mild keratinocyte atypia secondary to inflammation.^3,4 Our case is unique because it occurred with M marinum infection specifically. The histopathologic findings of M marinum infections are variable and may additionally include granulomas, most commonly suppurative; intraepithelial abscesses; small vessel proliferation; dermal fibrosis; multinucleated giant cells; and transepidermal elimination.^4,5 Periodic acid–Schiff, Ziehl-Neelsen (acid-fast bacilli), and Fite staining may be used to distinguish M marinum infection from SCC but have low sensitivities (approximately 30%). Culture remains the most reliable test, with a sensitivity of nearly 80%.^5-7 In our patient, a Periodic acid–Schiff stain was obtained prior to receiving culture results, and acid-fast bacilli and Fite staining were added after the culture returned positive; however, all 3 stains failed to highlight any mycobacteria.

The primary risk factor for infection with M marinum is contact with aquatic environments or marine animals, and most cases involve the fingers or the hand.⁶ After we reached the diagnosis and further discussed the patient’s history, he recalled fishing for and cleaning raw shrimp around the time that he had a splinter. The Infectious Diseases Society of America recommends a treatment course extending 1 to 2 months after clinical symptoms resolve with ethambutol in addition to clarithromycin or azithromycin.⁸ If the infection is near a joint, rifampin should be empirically added to account for a potentially deeper infection. Imaging should be obtained to evaluate for joint space involvement, with magnetic resonance imaging being the preferred modality. If joint space involvement is confirmed, surgical debridement is indicated. Surgical debridement also is indicated for infections that fail to respond to antibiotic therapy.⁸

This case highlights M marinum infection as a potential mimicker of SCC, particularly if the biopsy is relatively superficial, as often occurs when obtained via the common shave technique. The distinction is critical, as M marinum infection is highly treatable and inappropriate surgery on the typical hand and finger locations may subject patients to substantial morbidity, such as the need for a skin graft, reduced mobility from scarring, or risk for serious wound infection.⁹ For superficial biopsies of an atypical squamous process, pathologists also may consider routinely recommending tissue culture, especially for hand and finger locations or when a history of local trauma is reported, instead of recommending complete excision or repeat biopsy alone.

The Diagnosis: Atypical Mycobacterial Infection

The history of rapid growth followed by shrinkage as well as the craterlike clinical appearance of our patient’s lesion were suspicious for the keratoacanthoma variant of squamous cell carcinoma (SCC). Periodic acid–Schiff green staining was negative for fungal or bacterial organisms, and the biopsy findings of keratinocyte atypia and irregular epidermal proliferation seemed to confirm our suspicion for well-differentiated SCC (Figure 1). Our patient subsequently was scheduled for Mohs micrographic surgery. Fortunately, a sample of tissue had been sent for panculture—bacterial, fungal, and mycobacterial—to rule out infectious etiologies, given the history of possible traumatic inoculation, and returned positive for Mycobacterium marinum infection prior to the surgery. Mohs surgery was canceled, and he was referred to an infectious disease specialist who started antibiotic treatment with azithromycin, ethambutol, and rifabutin. After 1 month of treatment the lesion substantially improved (Figure 2), further supporting the diagnosis of M marinum infection over SCC.

The differential diagnosis also included sporotrichosis, leishmaniasis, and chromoblastomycosis. Sporotrichosis lesions typically develop as multiple nodules and ulcers along a path of lymphatic drainage and can exhibit asteroid bodies and cigar-shaped yeast forms on histology. Chromoblastomycosis may display pseudoepitheliomatous hyperplasia and granulomatous inflammation; however, pathognomonic pigmented Medlar bodies also likely would be present.¹ Leishmaniasis has a wide variety of presentations; however, it typically occurs in patients with exposure to endemic areas outside of the United States. Although leishmaniasis may demonstrate pseudoepitheliomatous hyperplasia, ulceration, and mixed inflammation on histology, it also likely would show amastigotes within dermal macrophages.²

Atypical mycobacterial infections initially may be misdiagnosed as SCC due to their tendency to induce irregular acanthosis in the form of pseudoepitheliomatous hyperplasia as well as mild keratinocyte atypia secondary to inflammation.^3,4 Our case is unique because it occurred with M marinum infection specifically. The histopathologic findings of M marinum infections are variable and may additionally include granulomas, most commonly suppurative; intraepithelial abscesses; small vessel proliferation; dermal fibrosis; multinucleated giant cells; and transepidermal elimination.^4,5 Periodic acid–Schiff, Ziehl-Neelsen (acid-fast bacilli), and Fite staining may be used to distinguish M marinum infection from SCC but have low sensitivities (approximately 30%). Culture remains the most reliable test, with a sensitivity of nearly 80%.^5-7 In our patient, a Periodic acid–Schiff stain was obtained prior to receiving culture results, and acid-fast bacilli and Fite staining were added after the culture returned positive; however, all 3 stains failed to highlight any mycobacteria.

The primary risk factor for infection with M marinum is contact with aquatic environments or marine animals, and most cases involve the fingers or the hand.⁶ After we reached the diagnosis and further discussed the patient’s history, he recalled fishing for and cleaning raw shrimp around the time that he had a splinter. The Infectious Diseases Society of America recommends a treatment course extending 1 to 2 months after clinical symptoms resolve with ethambutol in addition to clarithromycin or azithromycin.⁸ If the infection is near a joint, rifampin should be empirically added to account for a potentially deeper infection. Imaging should be obtained to evaluate for joint space involvement, with magnetic resonance imaging being the preferred modality. If joint space involvement is confirmed, surgical debridement is indicated. Surgical debridement also is indicated for infections that fail to respond to antibiotic therapy.⁸

This case highlights M marinum infection as a potential mimicker of SCC, particularly if the biopsy is relatively superficial, as often occurs when obtained via the common shave technique. The distinction is critical, as M marinum infection is highly treatable and inappropriate surgery on the typical hand and finger locations may subject patients to substantial morbidity, such as the need for a skin graft, reduced mobility from scarring, or risk for serious wound infection.⁹ For superficial biopsies of an atypical squamous process, pathologists also may consider routinely recommending tissue culture, especially for hand and finger locations or when a history of local trauma is reported, instead of recommending complete excision or repeat biopsy alone.

The Diagnosis: Atypical Mycobacterial Infection

The history of rapid growth followed by shrinkage as well as the craterlike clinical appearance of our patient’s lesion were suspicious for the keratoacanthoma variant of squamous cell carcinoma (SCC). Periodic acid–Schiff green staining was negative for fungal or bacterial organisms, and the biopsy findings of keratinocyte atypia and irregular epidermal proliferation seemed to confirm our suspicion for well-differentiated SCC (Figure 1). Our patient subsequently was scheduled for Mohs micrographic surgery. Fortunately, a sample of tissue had been sent for panculture—bacterial, fungal, and mycobacterial—to rule out infectious etiologies, given the history of possible traumatic inoculation, and returned positive for Mycobacterium marinum infection prior to the surgery. Mohs surgery was canceled, and he was referred to an infectious disease specialist who started antibiotic treatment with azithromycin, ethambutol, and rifabutin. After 1 month of treatment the lesion substantially improved (Figure 2), further supporting the diagnosis of M marinum infection over SCC.

The differential diagnosis also included sporotrichosis, leishmaniasis, and chromoblastomycosis. Sporotrichosis lesions typically develop as multiple nodules and ulcers along a path of lymphatic drainage and can exhibit asteroid bodies and cigar-shaped yeast forms on histology. Chromoblastomycosis may display pseudoepitheliomatous hyperplasia and granulomatous inflammation; however, pathognomonic pigmented Medlar bodies also likely would be present.¹ Leishmaniasis has a wide variety of presentations; however, it typically occurs in patients with exposure to endemic areas outside of the United States. Although leishmaniasis may demonstrate pseudoepitheliomatous hyperplasia, ulceration, and mixed inflammation on histology, it also likely would show amastigotes within dermal macrophages.²

Atypical mycobacterial infections initially may be misdiagnosed as SCC due to their tendency to induce irregular acanthosis in the form of pseudoepitheliomatous hyperplasia as well as mild keratinocyte atypia secondary to inflammation.^3,4 Our case is unique because it occurred with M marinum infection specifically. The histopathologic findings of M marinum infections are variable and may additionally include granulomas, most commonly suppurative; intraepithelial abscesses; small vessel proliferation; dermal fibrosis; multinucleated giant cells; and transepidermal elimination.^4,5 Periodic acid–Schiff, Ziehl-Neelsen (acid-fast bacilli), and Fite staining may be used to distinguish M marinum infection from SCC but have low sensitivities (approximately 30%). Culture remains the most reliable test, with a sensitivity of nearly 80%.^5-7 In our patient, a Periodic acid–Schiff stain was obtained prior to receiving culture results, and acid-fast bacilli and Fite staining were added after the culture returned positive; however, all 3 stains failed to highlight any mycobacteria.

The primary risk factor for infection with M marinum is contact with aquatic environments or marine animals, and most cases involve the fingers or the hand.⁶ After we reached the diagnosis and further discussed the patient’s history, he recalled fishing for and cleaning raw shrimp around the time that he had a splinter. The Infectious Diseases Society of America recommends a treatment course extending 1 to 2 months after clinical symptoms resolve with ethambutol in addition to clarithromycin or azithromycin.⁸ If the infection is near a joint, rifampin should be empirically added to account for a potentially deeper infection. Imaging should be obtained to evaluate for joint space involvement, with magnetic resonance imaging being the preferred modality. If joint space involvement is confirmed, surgical debridement is indicated. Surgical debridement also is indicated for infections that fail to respond to antibiotic therapy.⁸

This case highlights M marinum infection as a potential mimicker of SCC, particularly if the biopsy is relatively superficial, as often occurs when obtained via the common shave technique. The distinction is critical, as M marinum infection is highly treatable and inappropriate surgery on the typical hand and finger locations may subject patients to substantial morbidity, such as the need for a skin graft, reduced mobility from scarring, or risk for serious wound infection.⁹ For superficial biopsies of an atypical squamous process, pathologists also may consider routinely recommending tissue culture, especially for hand and finger locations or when a history of local trauma is reported, instead of recommending complete excision or repeat biopsy alone.

A dermatology resident has more education and experience than a medical student or intern but less than a fellow or attending physician. Because of this position, residents have a unique opportunity to provide feedback and education to those with less knowledge and experience as a teacher and also to provide feedback to their more senior colleagues about their teaching effectiveness while simultaneously learning from them. The reciprocal exchange of information—from patients and colleagues in clinic, co-residents or attendings in lectures, or in other environments such as pathology at the microscope or skills during simulation training sessions—is the cornerstone of medical education. Being able to give effective feedback while also learning to accept it is one of the most vital skills a resident can learn to thrive in medical education.

The importance of feedback cannot be understated. The art of medicine involves the scientific knowledge needed to treat disease, as well as the social ability to educate, comfort, and heal those afflicted. Mastering this art takes a lifetime. The direct imparting of knowledge from those more experienced to those learning occurs via feedback. In addition, the desire to better oneself leads to more satisfaction with work and improved performance.¹ The ability to give and receive feedback is vital for the field of dermatology and medicine in general.

Types and Implementation of Feedback

Feedback comes in many forms and can be classified via different characteristics such as formal vs informal, written vs spoken, real time vs delayed, and single observer vs pooled data. Each style of feedback has positive and negative aspects, and a feedback provider will need to weigh the pros and cons when deciding the most appropriate one. Although there is no one correct way to provide feedback, the literature shows that some forms of feedback may be more effective and better received than others. This can depend on the context of what is being evaluated.

Many dermatology residencies employ formal scheduled feedback as part of their curricula, ensuring that residents will receive feedback at preset time intervals and providing residency directors with information to assess improvement and areas where more growth is needed. The Accreditation Council for Graduate Medical Education provides a reference for programs on how to give this formal standardized feedback in The Milestones Guidebook.² This feedback is a minimum required amount, with a survey of residents showing preference for frequent informal feedback sessions in addition to standardized formal feedback.³ Another study showed that residents want feedback that is confidential, in person, shortly after experiences, and specific to their actions.⁴ Medical students also voiced a need for frequent, transparent, and actionable feedback during protected, predetermined, and communicated times.⁵ Clearly, learners appreciate spoken intentional feedback as opposed to the traditional formal model of feedback.

Finally, a study was performed analyzing how prior generations of physician educators view millennial trainees.⁶ Because most current dermatology residents were born between 1981 and 1996, this study seemed to pinpoint thoughts toward teaching current residents. The study found that although negative judgments such as millennial entitlement (P<.001), impoliteness (P<.001), oversensitivity (P<.001), and inferior work ethic (P<.001) reached significance, millennial ideals of social justice (P<.001) and savviness with technology (P<.001) also were notable. Overall, millennials were thought to be good colleagues (P<.001), were equally competent to more experienced clinicians (P<.001), and would lead medicine to a good future (P=.039).⁶

Identifying and Maximizing the Impact of Feedback

In addition to how and when to provide feedback, there are discrepancies between attending and resident perception of what is considered feedback. This disconnect can be seen in a study of 122 respondents (67 residents and 55 attendings) that showed 31% of attendings reported giving feedback daily, as opposed to only 9% of residents who reported receiving daily feedback.⁴ When feedback is to be performed, it may be important to specifically announce the process so that it can be properly acknowledged.⁷

Beach⁸ provided a systematic breakdown of clinical teaching to those who may be unfamiliar with the process. This method is divided into preclinic, in-clinic, and postclinic strategies to maximize learning. The author recommended establishing the objectives of the rotation from the teacher’s perspective and inquiring about the objectives of the learner. Both perspectives should inform the lessons to be learned; for example, if a medical student expresses specific interest in psoriasis (a well-established part of a medical student curriculum), all efforts should be placed on arranging for that student to see those specific patients. Beach⁸ also recommended providing resources and creating a positive supportive learning environment to better utilize precious clinic time and create investment in all learning parties. The author recommended matching trainees during clinic to competence-specific challenges in clinical practice where appropriate technical skill is needed. Appropriate autonomy also is promoted, as it requires higher levels of learning and knowledge consolidation. Group discussions can be facilitated by asking questions of increasing levels of difficulty as experience increases. Finally, postclinic feedback should be timely and constructive.⁸

One technique discussed by Beach⁸ is the “1-minute preceptor plus” approach. In this approach, the teacher wants to establish 5 “micro-skills” by first getting a commitment, then checking for supportive evidence of this initial plan, teaching a general principle, reinforcing what was properly performed, and correcting errors. The “plus” comes from trying to take that lesson and apply it to a broader concept. Although this concept is meant to be used in a time-limited setting, it can be expanded to larger conversations. A common example could be made when residents teach rotating medical students through direct observation and supervision during clinic. In this hypothetical situation, the resident and medical student see a patient with erythematous silver-scaled plaques on the elbows and knees. During the patient encounter, the student then inquires about any personal history of cardiovascular disease, diabetes mellitus, and hypertension. After leaving the examination room, the medical student asserts the diagnosis is plaque psoriasis because of the physical examination findings and distribution of lesions. A discussion about the relationship between psoriasis and metabolic syndrome commences, emphasizing the pathophysiology of type 1 helper T-cell–mediated and type 17 helper T-cell–mediated inflammation with vascular damage and growth from inflammatory cytokines.⁹ The student subsequently is praised on inquiring about relevant comorbidities, and a relevant journal article is retrieved for the student’s future studies. Teaching points regarding the Koebner phenomenon, such as that it is not an instantaneous process and comes with a differential diagnosis, are then provided.

Situation-Behavior-Impact is another teaching method developed by the Center for Creative Leadership. In this technique, one will identify what specifically happened, how the learner responded, and what occurred because of the response.¹⁰ This technique is exemplified in the following mock conversation between an attending and their resident following a challenging patient situation: “When you walked into the room and asked the patient coming in for a follow-up appointment ‘What brings you in today?,’ they immediately tensed up and responded that you should already know and check your electronic medical record. This tension could be ameliorated by reviewing the patient’s medical record and addressing what they initially presented for, followed by inquiring if there are other skin problems they want to discuss afterwards.” By identifying the cause-and-effect relationship, helpful and unhelpful responses can be identified and ways to mitigate or continue behaviors can be brainstormed.

The Learning Process

Brodell et all¹¹ outlined techniques to augment the education process that are specific to dermatology. They recommended learning general applicable concepts instead of contextless memorization, mnemonic devices to assist memory for associations and lists, and repetition and practice of learned material. For teaching, they divided techniques into Aristotelian or Socratic; Aristotelian teaching is the formal lecture style, whereas Socratic is conversation based. Both have a place in teaching—as fundamental knowledge grows via Aristotelian teaching, critical thinking can be enhanced via the Socratic method. The authors then outlined tips to create the most conducive learning environment for students.¹¹

Feedback is a reciprocal process with information being given and received by both the teacher and the learner. This is paramount because perfecting the art of teaching is a career-long process and can only be achieved via correction of oversights and mistakes. A questionnaire-based study found that when critiquing the teacher, a combination of self-assessment with assessment from learners was effective in stimulating the greatest level of change in the teacher.¹² This finding likely is because the educator was able to see the juxtaposition of how they think they performed with how students interpreted the same situation. Another survey-based study showed that of 68 attending physicians, 28 attendings saw utility in specialized feedback training; an additional 11 attendings agreed with online modules to improve their feedback skills. A recommendation that trainees receive training on the acceptance feedback also was proposed.¹³ Specialized training to give and receive feedback could be initiated for both attending and resident physicians to fully create an environment emphasizing improvement and teamwork.

Final Thoughts

The art of giving and receiving feedback is a deliberate process that develops with experience and training. Because residents are early in their medical career, being familiar with techniques such as those outlined in this article can enhance teaching and the reception of feedback. Residents are in a unique position, as residency itself is a time of dramatic learning and teaching. Providing feedback gives us a way to advance medicine and better ourselves by solidifying good habits and knowledge.

Acknowledgment—I thank Warren R. Heymann, MD (Camden, New Jersey), for assisting in the creation of this topic and reviewing this article.

A dermatology resident has more education and experience than a medical student or intern but less than a fellow or attending physician. Because of this position, residents have a unique opportunity to provide feedback and education to those with less knowledge and experience as a teacher and also to provide feedback to their more senior colleagues about their teaching effectiveness while simultaneously learning from them. The reciprocal exchange of information—from patients and colleagues in clinic, co-residents or attendings in lectures, or in other environments such as pathology at the microscope or skills during simulation training sessions—is the cornerstone of medical education. Being able to give effective feedback while also learning to accept it is one of the most vital skills a resident can learn to thrive in medical education.

The importance of feedback cannot be understated. The art of medicine involves the scientific knowledge needed to treat disease, as well as the social ability to educate, comfort, and heal those afflicted. Mastering this art takes a lifetime. The direct imparting of knowledge from those more experienced to those learning occurs via feedback. In addition, the desire to better oneself leads to more satisfaction with work and improved performance.¹ The ability to give and receive feedback is vital for the field of dermatology and medicine in general.

Types and Implementation of Feedback

Feedback comes in many forms and can be classified via different characteristics such as formal vs informal, written vs spoken, real time vs delayed, and single observer vs pooled data. Each style of feedback has positive and negative aspects, and a feedback provider will need to weigh the pros and cons when deciding the most appropriate one. Although there is no one correct way to provide feedback, the literature shows that some forms of feedback may be more effective and better received than others. This can depend on the context of what is being evaluated.

Many dermatology residencies employ formal scheduled feedback as part of their curricula, ensuring that residents will receive feedback at preset time intervals and providing residency directors with information to assess improvement and areas where more growth is needed. The Accreditation Council for Graduate Medical Education provides a reference for programs on how to give this formal standardized feedback in The Milestones Guidebook.² This feedback is a minimum required amount, with a survey of residents showing preference for frequent informal feedback sessions in addition to standardized formal feedback.³ Another study showed that residents want feedback that is confidential, in person, shortly after experiences, and specific to their actions.⁴ Medical students also voiced a need for frequent, transparent, and actionable feedback during protected, predetermined, and communicated times.⁵ Clearly, learners appreciate spoken intentional feedback as opposed to the traditional formal model of feedback.

Finally, a study was performed analyzing how prior generations of physician educators view millennial trainees.⁶ Because most current dermatology residents were born between 1981 and 1996, this study seemed to pinpoint thoughts toward teaching current residents. The study found that although negative judgments such as millennial entitlement (P<.001), impoliteness (P<.001), oversensitivity (P<.001), and inferior work ethic (P<.001) reached significance, millennial ideals of social justice (P<.001) and savviness with technology (P<.001) also were notable. Overall, millennials were thought to be good colleagues (P<.001), were equally competent to more experienced clinicians (P<.001), and would lead medicine to a good future (P=.039).⁶

Identifying and Maximizing the Impact of Feedback

In addition to how and when to provide feedback, there are discrepancies between attending and resident perception of what is considered feedback. This disconnect can be seen in a study of 122 respondents (67 residents and 55 attendings) that showed 31% of attendings reported giving feedback daily, as opposed to only 9% of residents who reported receiving daily feedback.⁴ When feedback is to be performed, it may be important to specifically announce the process so that it can be properly acknowledged.⁷

Beach⁸ provided a systematic breakdown of clinical teaching to those who may be unfamiliar with the process. This method is divided into preclinic, in-clinic, and postclinic strategies to maximize learning. The author recommended establishing the objectives of the rotation from the teacher’s perspective and inquiring about the objectives of the learner. Both perspectives should inform the lessons to be learned; for example, if a medical student expresses specific interest in psoriasis (a well-established part of a medical student curriculum), all efforts should be placed on arranging for that student to see those specific patients. Beach⁸ also recommended providing resources and creating a positive supportive learning environment to better utilize precious clinic time and create investment in all learning parties. The author recommended matching trainees during clinic to competence-specific challenges in clinical practice where appropriate technical skill is needed. Appropriate autonomy also is promoted, as it requires higher levels of learning and knowledge consolidation. Group discussions can be facilitated by asking questions of increasing levels of difficulty as experience increases. Finally, postclinic feedback should be timely and constructive.⁸

One technique discussed by Beach⁸ is the “1-minute preceptor plus” approach. In this approach, the teacher wants to establish 5 “micro-skills” by first getting a commitment, then checking for supportive evidence of this initial plan, teaching a general principle, reinforcing what was properly performed, and correcting errors. The “plus” comes from trying to take that lesson and apply it to a broader concept. Although this concept is meant to be used in a time-limited setting, it can be expanded to larger conversations. A common example could be made when residents teach rotating medical students through direct observation and supervision during clinic. In this hypothetical situation, the resident and medical student see a patient with erythematous silver-scaled plaques on the elbows and knees. During the patient encounter, the student then inquires about any personal history of cardiovascular disease, diabetes mellitus, and hypertension. After leaving the examination room, the medical student asserts the diagnosis is plaque psoriasis because of the physical examination findings and distribution of lesions. A discussion about the relationship between psoriasis and metabolic syndrome commences, emphasizing the pathophysiology of type 1 helper T-cell–mediated and type 17 helper T-cell–mediated inflammation with vascular damage and growth from inflammatory cytokines.⁹ The student subsequently is praised on inquiring about relevant comorbidities, and a relevant journal article is retrieved for the student’s future studies. Teaching points regarding the Koebner phenomenon, such as that it is not an instantaneous process and comes with a differential diagnosis, are then provided.

Situation-Behavior-Impact is another teaching method developed by the Center for Creative Leadership. In this technique, one will identify what specifically happened, how the learner responded, and what occurred because of the response.¹⁰ This technique is exemplified in the following mock conversation between an attending and their resident following a challenging patient situation: “When you walked into the room and asked the patient coming in for a follow-up appointment ‘What brings you in today?,’ they immediately tensed up and responded that you should already know and check your electronic medical record. This tension could be ameliorated by reviewing the patient’s medical record and addressing what they initially presented for, followed by inquiring if there are other skin problems they want to discuss afterwards.” By identifying the cause-and-effect relationship, helpful and unhelpful responses can be identified and ways to mitigate or continue behaviors can be brainstormed.

The Learning Process

Brodell et all¹¹ outlined techniques to augment the education process that are specific to dermatology. They recommended learning general applicable concepts instead of contextless memorization, mnemonic devices to assist memory for associations and lists, and repetition and practice of learned material. For teaching, they divided techniques into Aristotelian or Socratic; Aristotelian teaching is the formal lecture style, whereas Socratic is conversation based. Both have a place in teaching—as fundamental knowledge grows via Aristotelian teaching, critical thinking can be enhanced via the Socratic method. The authors then outlined tips to create the most conducive learning environment for students.¹¹

Feedback is a reciprocal process with information being given and received by both the teacher and the learner. This is paramount because perfecting the art of teaching is a career-long process and can only be achieved via correction of oversights and mistakes. A questionnaire-based study found that when critiquing the teacher, a combination of self-assessment with assessment from learners was effective in stimulating the greatest level of change in the teacher.¹² This finding likely is because the educator was able to see the juxtaposition of how they think they performed with how students interpreted the same situation. Another survey-based study showed that of 68 attending physicians, 28 attendings saw utility in specialized feedback training; an additional 11 attendings agreed with online modules to improve their feedback skills. A recommendation that trainees receive training on the acceptance feedback also was proposed.¹³ Specialized training to give and receive feedback could be initiated for both attending and resident physicians to fully create an environment emphasizing improvement and teamwork.

Final Thoughts

The art of giving and receiving feedback is a deliberate process that develops with experience and training. Because residents are early in their medical career, being familiar with techniques such as those outlined in this article can enhance teaching and the reception of feedback. Residents are in a unique position, as residency itself is a time of dramatic learning and teaching. Providing feedback gives us a way to advance medicine and better ourselves by solidifying good habits and knowledge.

Acknowledgment—I thank Warren R. Heymann, MD (Camden, New Jersey), for assisting in the creation of this topic and reviewing this article.

A dermatology resident has more education and experience than a medical student or intern but less than a fellow or attending physician. Because of this position, residents have a unique opportunity to provide feedback and education to those with less knowledge and experience as a teacher and also to provide feedback to their more senior colleagues about their teaching effectiveness while simultaneously learning from them. The reciprocal exchange of information—from patients and colleagues in clinic, co-residents or attendings in lectures, or in other environments such as pathology at the microscope or skills during simulation training sessions—is the cornerstone of medical education. Being able to give effective feedback while also learning to accept it is one of the most vital skills a resident can learn to thrive in medical education.

The importance of feedback cannot be understated. The art of medicine involves the scientific knowledge needed to treat disease, as well as the social ability to educate, comfort, and heal those afflicted. Mastering this art takes a lifetime. The direct imparting of knowledge from those more experienced to those learning occurs via feedback. In addition, the desire to better oneself leads to more satisfaction with work and improved performance.¹ The ability to give and receive feedback is vital for the field of dermatology and medicine in general.

Types and Implementation of Feedback

Feedback comes in many forms and can be classified via different characteristics such as formal vs informal, written vs spoken, real time vs delayed, and single observer vs pooled data. Each style of feedback has positive and negative aspects, and a feedback provider will need to weigh the pros and cons when deciding the most appropriate one. Although there is no one correct way to provide feedback, the literature shows that some forms of feedback may be more effective and better received than others. This can depend on the context of what is being evaluated.

Many dermatology residencies employ formal scheduled feedback as part of their curricula, ensuring that residents will receive feedback at preset time intervals and providing residency directors with information to assess improvement and areas where more growth is needed. The Accreditation Council for Graduate Medical Education provides a reference for programs on how to give this formal standardized feedback in The Milestones Guidebook.² This feedback is a minimum required amount, with a survey of residents showing preference for frequent informal feedback sessions in addition to standardized formal feedback.³ Another study showed that residents want feedback that is confidential, in person, shortly after experiences, and specific to their actions.⁴ Medical students also voiced a need for frequent, transparent, and actionable feedback during protected, predetermined, and communicated times.⁵ Clearly, learners appreciate spoken intentional feedback as opposed to the traditional formal model of feedback.

Finally, a study was performed analyzing how prior generations of physician educators view millennial trainees.⁶ Because most current dermatology residents were born between 1981 and 1996, this study seemed to pinpoint thoughts toward teaching current residents. The study found that although negative judgments such as millennial entitlement (P<.001), impoliteness (P<.001), oversensitivity (P<.001), and inferior work ethic (P<.001) reached significance, millennial ideals of social justice (P<.001) and savviness with technology (P<.001) also were notable. Overall, millennials were thought to be good colleagues (P<.001), were equally competent to more experienced clinicians (P<.001), and would lead medicine to a good future (P=.039).⁶

Identifying and Maximizing the Impact of Feedback

In addition to how and when to provide feedback, there are discrepancies between attending and resident perception of what is considered feedback. This disconnect can be seen in a study of 122 respondents (67 residents and 55 attendings) that showed 31% of attendings reported giving feedback daily, as opposed to only 9% of residents who reported receiving daily feedback.⁴ When feedback is to be performed, it may be important to specifically announce the process so that it can be properly acknowledged.⁷

Beach⁸ provided a systematic breakdown of clinical teaching to those who may be unfamiliar with the process. This method is divided into preclinic, in-clinic, and postclinic strategies to maximize learning. The author recommended establishing the objectives of the rotation from the teacher’s perspective and inquiring about the objectives of the learner. Both perspectives should inform the lessons to be learned; for example, if a medical student expresses specific interest in psoriasis (a well-established part of a medical student curriculum), all efforts should be placed on arranging for that student to see those specific patients. Beach⁸ also recommended providing resources and creating a positive supportive learning environment to better utilize precious clinic time and create investment in all learning parties. The author recommended matching trainees during clinic to competence-specific challenges in clinical practice where appropriate technical skill is needed. Appropriate autonomy also is promoted, as it requires higher levels of learning and knowledge consolidation. Group discussions can be facilitated by asking questions of increasing levels of difficulty as experience increases. Finally, postclinic feedback should be timely and constructive.⁸

One technique discussed by Beach⁸ is the “1-minute preceptor plus” approach. In this approach, the teacher wants to establish 5 “micro-skills” by first getting a commitment, then checking for supportive evidence of this initial plan, teaching a general principle, reinforcing what was properly performed, and correcting errors. The “plus” comes from trying to take that lesson and apply it to a broader concept. Although this concept is meant to be used in a time-limited setting, it can be expanded to larger conversations. A common example could be made when residents teach rotating medical students through direct observation and supervision during clinic. In this hypothetical situation, the resident and medical student see a patient with erythematous silver-scaled plaques on the elbows and knees. During the patient encounter, the student then inquires about any personal history of cardiovascular disease, diabetes mellitus, and hypertension. After leaving the examination room, the medical student asserts the diagnosis is plaque psoriasis because of the physical examination findings and distribution of lesions. A discussion about the relationship between psoriasis and metabolic syndrome commences, emphasizing the pathophysiology of type 1 helper T-cell–mediated and type 17 helper T-cell–mediated inflammation with vascular damage and growth from inflammatory cytokines.⁹ The student subsequently is praised on inquiring about relevant comorbidities, and a relevant journal article is retrieved for the student’s future studies. Teaching points regarding the Koebner phenomenon, such as that it is not an instantaneous process and comes with a differential diagnosis, are then provided.

Situation-Behavior-Impact is another teaching method developed by the Center for Creative Leadership. In this technique, one will identify what specifically happened, how the learner responded, and what occurred because of the response.¹⁰ This technique is exemplified in the following mock conversation between an attending and their resident following a challenging patient situation: “When you walked into the room and asked the patient coming in for a follow-up appointment ‘What brings you in today?,’ they immediately tensed up and responded that you should already know and check your electronic medical record. This tension could be ameliorated by reviewing the patient’s medical record and addressing what they initially presented for, followed by inquiring if there are other skin problems they want to discuss afterwards.” By identifying the cause-and-effect relationship, helpful and unhelpful responses can be identified and ways to mitigate or continue behaviors can be brainstormed.

The Learning Process

Brodell et all¹¹ outlined techniques to augment the education process that are specific to dermatology. They recommended learning general applicable concepts instead of contextless memorization, mnemonic devices to assist memory for associations and lists, and repetition and practice of learned material. For teaching, they divided techniques into Aristotelian or Socratic; Aristotelian teaching is the formal lecture style, whereas Socratic is conversation based. Both have a place in teaching—as fundamental knowledge grows via Aristotelian teaching, critical thinking can be enhanced via the Socratic method. The authors then outlined tips to create the most conducive learning environment for students.¹¹

Feedback is a reciprocal process with information being given and received by both the teacher and the learner. This is paramount because perfecting the art of teaching is a career-long process and can only be achieved via correction of oversights and mistakes. A questionnaire-based study found that when critiquing the teacher, a combination of self-assessment with assessment from learners was effective in stimulating the greatest level of change in the teacher.¹² This finding likely is because the educator was able to see the juxtaposition of how they think they performed with how students interpreted the same situation. Another survey-based study showed that of 68 attending physicians, 28 attendings saw utility in specialized feedback training; an additional 11 attendings agreed with online modules to improve their feedback skills. A recommendation that trainees receive training on the acceptance feedback also was proposed.¹³ Specialized training to give and receive feedback could be initiated for both attending and resident physicians to fully create an environment emphasizing improvement and teamwork.

Final Thoughts

The art of giving and receiving feedback is a deliberate process that develops with experience and training. Because residents are early in their medical career, being familiar with techniques such as those outlined in this article can enhance teaching and the reception of feedback. Residents are in a unique position, as residency itself is a time of dramatic learning and teaching. Providing feedback gives us a way to advance medicine and better ourselves by solidifying good habits and knowledge.

Acknowledgment—I thank Warren R. Heymann, MD (Camden, New Jersey), for assisting in the creation of this topic and reviewing this article.

Congress averted bigger reductions in Medicare’s future payments for clinicians in its massive, year-end spending bill, but physicians will still see a 2% cut in a key payment variable in 2023.

The bill also authorizes new policies regarding accelerated drug approvals and substance use disorder treatment.

The House voted 225-201 to clear a wide-ranging legislative package, known as an omnibus, for President Joe Biden’s signature. The Senate voted 68-29 to approve the measure.

Clinicians had been facing as much as 8.5% in cuts to certain factors that set their Medicare payment. The American Medical Association credited an advocacy campaign it joined with more than 150 organizations with fending off the much-feared reimbursement cuts. The 2% trim for 2023 will decline to 1.25% for 2024.

These reductions will hit as many clinicians face the toll on rising costs for running their practices, as Congress has not included inflation-based payment adjustments in Medicare’s physician payment rule, the AMA said.

“Congress must immediately begin the work of long-overdue Medicare physician payment reform that will lead to the program stability that beneficiaries and physicians need,” AMA President Jack Resneck, MD, said in a statement.

While the omnibus bill blocks 6.5% of Medicare payment cuts originally slated to take effect in 2023, it still puts “untenable strain” on primary care clinicians, said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians, in a statement.

“However, we’re pleased to see several provisions that will improve access to care, including bolstering mental health services, extending telehealth, and expanding Medicaid and CHIP coverage,” Dr. Iroku-Malize added.
 

New health care policies in omnibus

Lawmakers adopted many health care policy changes in the omnibus package, which contained 12 overdue spending bills for fiscal year 2023. (Much of the federal government has been funded through stop-gap measures since this budget year began on Oct. 1.) The final measure runs to more than 4,100 pages in PDF form.

House Energy and Commerce Chairman Frank Pallone Jr. (D-NJ) said the health care provisions will:

• Expand patient access to opioid addiction treatment by making it easier for clinicians to dispense buprenorphine for opioid use disorder maintenance or detoxification treatment
• Require health care providers to complete a training requirement on identifying and treating patients with substance use disorders
• Guarantee 12 months of continuous Medicaid coverage for 40 million children
• Provide 2 years of additional Children’s Health Insurance Program (CHIP) funding
• Permanently extend the option for states to offer 12 months of Medicaid coverage to new mothers
• Continue Medicare’s expanded access to telehealth by extending COVID-19 telehealth flexibilities through Dec. 31, 2024.

FDA’s accelerated approval

The omnibus also will shorten the period of uncertainty patients and clinicians face with medicines cleared under the accelerated approval pathway.

The Food and Drug Administration uses accelerated approvals to give conditional clearances to medicines for fatal and serious conditions based on limited evidence signaling a potential benefit. Companies are expected to continue research needed to prove whether promising signals, such as stemming tumor growth, benefits patients.

Concerns have mounted when companies delay confirmatory trials or try to maintain accelerated approvals for drugs that fail those trials.

Mr. Pallone said the omnibus contains provisions that:

• Require the FDA to specify conditions for required post-approval studies
• Authorize the FDA to require post-approval studies to be underway at the time of approval or within a specified time period following approval.
• Clarify and streamline current FDA authority to withdraw approvals when sponsors fail to conduct studies with due diligence.

Reshma Ramachandran, MD, MPP, MHS, who serves as the chair of the Doctors for America’s FDA Task Force, told this news organization that she was pleased to see these provisions pass. She had been disappointed they were not included earlier this year in the latest Prescription Drug User Fee Act reauthorization.

The provisions in the omnibus make “clear what steps the FDA can take to remove an unproven drug off the market should manufacturers fail to complete these studies or demonstrate meaningful clinical benefit,” Dr. Ramachandran wrote in an email.

Dr. Ramachandran said she hopes lawmakers build on these steps in the future. She suggested Congress add a mandate to require drug labels to clearly state when the FDA is still waiting for evidence needed to confirm benefits of medicines cleared by accelerated approval.

“Nevertheless, Congress in including and, hopefully, passing these reforms has made it clear that drug companies need to provide meaningful evidence that their accelerated approval drugs work in patients and FDA can take action to protect patients should this not occur,” Dr. Ramachandran wrote.

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

Congress averted bigger reductions in Medicare’s future payments for clinicians in its massive, year-end spending bill, but physicians will still see a 2% cut in a key payment variable in 2023.

The bill also authorizes new policies regarding accelerated drug approvals and substance use disorder treatment.

The House voted 225-201 to clear a wide-ranging legislative package, known as an omnibus, for President Joe Biden’s signature. The Senate voted 68-29 to approve the measure.

Clinicians had been facing as much as 8.5% in cuts to certain factors that set their Medicare payment. The American Medical Association credited an advocacy campaign it joined with more than 150 organizations with fending off the much-feared reimbursement cuts. The 2% trim for 2023 will decline to 1.25% for 2024.

These reductions will hit as many clinicians face the toll on rising costs for running their practices, as Congress has not included inflation-based payment adjustments in Medicare’s physician payment rule, the AMA said.

“Congress must immediately begin the work of long-overdue Medicare physician payment reform that will lead to the program stability that beneficiaries and physicians need,” AMA President Jack Resneck, MD, said in a statement.

While the omnibus bill blocks 6.5% of Medicare payment cuts originally slated to take effect in 2023, it still puts “untenable strain” on primary care clinicians, said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians, in a statement.

“However, we’re pleased to see several provisions that will improve access to care, including bolstering mental health services, extending telehealth, and expanding Medicaid and CHIP coverage,” Dr. Iroku-Malize added.
 

New health care policies in omnibus

Lawmakers adopted many health care policy changes in the omnibus package, which contained 12 overdue spending bills for fiscal year 2023. (Much of the federal government has been funded through stop-gap measures since this budget year began on Oct. 1.) The final measure runs to more than 4,100 pages in PDF form.

House Energy and Commerce Chairman Frank Pallone Jr. (D-NJ) said the health care provisions will:

• Expand patient access to opioid addiction treatment by making it easier for clinicians to dispense buprenorphine for opioid use disorder maintenance or detoxification treatment
• Require health care providers to complete a training requirement on identifying and treating patients with substance use disorders
• Guarantee 12 months of continuous Medicaid coverage for 40 million children
• Provide 2 years of additional Children’s Health Insurance Program (CHIP) funding
• Permanently extend the option for states to offer 12 months of Medicaid coverage to new mothers
• Continue Medicare’s expanded access to telehealth by extending COVID-19 telehealth flexibilities through Dec. 31, 2024.

FDA’s accelerated approval

The omnibus also will shorten the period of uncertainty patients and clinicians face with medicines cleared under the accelerated approval pathway.

The Food and Drug Administration uses accelerated approvals to give conditional clearances to medicines for fatal and serious conditions based on limited evidence signaling a potential benefit. Companies are expected to continue research needed to prove whether promising signals, such as stemming tumor growth, benefits patients.

Concerns have mounted when companies delay confirmatory trials or try to maintain accelerated approvals for drugs that fail those trials.

Mr. Pallone said the omnibus contains provisions that:

• Require the FDA to specify conditions for required post-approval studies
• Authorize the FDA to require post-approval studies to be underway at the time of approval or within a specified time period following approval.
• Clarify and streamline current FDA authority to withdraw approvals when sponsors fail to conduct studies with due diligence.

Reshma Ramachandran, MD, MPP, MHS, who serves as the chair of the Doctors for America’s FDA Task Force, told this news organization that she was pleased to see these provisions pass. She had been disappointed they were not included earlier this year in the latest Prescription Drug User Fee Act reauthorization.

The provisions in the omnibus make “clear what steps the FDA can take to remove an unproven drug off the market should manufacturers fail to complete these studies or demonstrate meaningful clinical benefit,” Dr. Ramachandran wrote in an email.

Dr. Ramachandran said she hopes lawmakers build on these steps in the future. She suggested Congress add a mandate to require drug labels to clearly state when the FDA is still waiting for evidence needed to confirm benefits of medicines cleared by accelerated approval.

“Nevertheless, Congress in including and, hopefully, passing these reforms has made it clear that drug companies need to provide meaningful evidence that their accelerated approval drugs work in patients and FDA can take action to protect patients should this not occur,” Dr. Ramachandran wrote.

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

Congress averted bigger reductions in Medicare’s future payments for clinicians in its massive, year-end spending bill, but physicians will still see a 2% cut in a key payment variable in 2023.

The bill also authorizes new policies regarding accelerated drug approvals and substance use disorder treatment.

The House voted 225-201 to clear a wide-ranging legislative package, known as an omnibus, for President Joe Biden’s signature. The Senate voted 68-29 to approve the measure.

Clinicians had been facing as much as 8.5% in cuts to certain factors that set their Medicare payment. The American Medical Association credited an advocacy campaign it joined with more than 150 organizations with fending off the much-feared reimbursement cuts. The 2% trim for 2023 will decline to 1.25% for 2024.

These reductions will hit as many clinicians face the toll on rising costs for running their practices, as Congress has not included inflation-based payment adjustments in Medicare’s physician payment rule, the AMA said.

“Congress must immediately begin the work of long-overdue Medicare physician payment reform that will lead to the program stability that beneficiaries and physicians need,” AMA President Jack Resneck, MD, said in a statement.

While the omnibus bill blocks 6.5% of Medicare payment cuts originally slated to take effect in 2023, it still puts “untenable strain” on primary care clinicians, said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians, in a statement.

“However, we’re pleased to see several provisions that will improve access to care, including bolstering mental health services, extending telehealth, and expanding Medicaid and CHIP coverage,” Dr. Iroku-Malize added.
 

New health care policies in omnibus

Lawmakers adopted many health care policy changes in the omnibus package, which contained 12 overdue spending bills for fiscal year 2023. (Much of the federal government has been funded through stop-gap measures since this budget year began on Oct. 1.) The final measure runs to more than 4,100 pages in PDF form.

House Energy and Commerce Chairman Frank Pallone Jr. (D-NJ) said the health care provisions will:

• Expand patient access to opioid addiction treatment by making it easier for clinicians to dispense buprenorphine for opioid use disorder maintenance or detoxification treatment
• Require health care providers to complete a training requirement on identifying and treating patients with substance use disorders
• Guarantee 12 months of continuous Medicaid coverage for 40 million children
• Provide 2 years of additional Children’s Health Insurance Program (CHIP) funding
• Permanently extend the option for states to offer 12 months of Medicaid coverage to new mothers
• Continue Medicare’s expanded access to telehealth by extending COVID-19 telehealth flexibilities through Dec. 31, 2024.

FDA’s accelerated approval

The omnibus also will shorten the period of uncertainty patients and clinicians face with medicines cleared under the accelerated approval pathway.

The Food and Drug Administration uses accelerated approvals to give conditional clearances to medicines for fatal and serious conditions based on limited evidence signaling a potential benefit. Companies are expected to continue research needed to prove whether promising signals, such as stemming tumor growth, benefits patients.

Concerns have mounted when companies delay confirmatory trials or try to maintain accelerated approvals for drugs that fail those trials.

Mr. Pallone said the omnibus contains provisions that:

• Require the FDA to specify conditions for required post-approval studies
• Authorize the FDA to require post-approval studies to be underway at the time of approval or within a specified time period following approval.
• Clarify and streamline current FDA authority to withdraw approvals when sponsors fail to conduct studies with due diligence.

Reshma Ramachandran, MD, MPP, MHS, who serves as the chair of the Doctors for America’s FDA Task Force, told this news organization that she was pleased to see these provisions pass. She had been disappointed they were not included earlier this year in the latest Prescription Drug User Fee Act reauthorization.

The provisions in the omnibus make “clear what steps the FDA can take to remove an unproven drug off the market should manufacturers fail to complete these studies or demonstrate meaningful clinical benefit,” Dr. Ramachandran wrote in an email.

Dr. Ramachandran said she hopes lawmakers build on these steps in the future. She suggested Congress add a mandate to require drug labels to clearly state when the FDA is still waiting for evidence needed to confirm benefits of medicines cleared by accelerated approval.

“Nevertheless, Congress in including and, hopefully, passing these reforms has made it clear that drug companies need to provide meaningful evidence that their accelerated approval drugs work in patients and FDA can take action to protect patients should this not occur,” Dr. Ramachandran wrote.

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

PARIS – All the way back in 1907, The Lancet published an article on a gonorrhea vaccine trial. Today, after continuous research throughout the intervening 110-plus years, scientists may finally have achieved success. Sébastien Fouéré, MD, discussed the details at a press conference that focused on the highlights of the Dermatology Days of Paris conference. Dr. Fouéré is the head of the genital dermatology and sexually transmitted infections unit at Saint-Louis Hospital, Paris.

Twin bacteria

Although the gonorrhea vaccine has long been the subject of research, Dr. Fouéré views 2017 as a turning point. This was when the results of a study led by Helen Petousis-Harris, PhD, were published.

“She tried to formalize the not completely indisputable results published by Cuba, where it seemed there were fewer gonococci in individuals vaccinated against meningococcal group B,” he noted.

Dr. Petousis-Harris, an immunologist, conducted a retrospective case-control study involving 11 clinics in New Zealand. The participants were aged 15-30 years, were eligible to receive the meningococcal B vaccine, and had been diagnosed with gonorrhea, chlamydia, or both. The researchers found that receiving the meningococcal B vaccine in childhood provides around 30% protection against Neisseria gonorrhoeae infections.

“It’s not perhaps a coincidence that a meningococcal B vaccine would be protective against gonorrhea,” Dr. Fouéré pointed out. He considers this protection logical, even expected, insofar as “meningococcus and gonococcus are almost twins.” There is 90% and 100% homology between membrane proteins of the two bacteria.
 

Vaccine is effective

Two retrospective case-control studies confirm that the vaccine is protective. One of the studies, carried out by an Australian team, found that the effectiveness was 32%, quite close to that reported by Petousis-Harris. In the other study, a U.S. team brought to light a dose-response relationship. A partial vaccination series (single serogroup B meningococcal outer membrane vesicle vaccine dose) was 26% effective against gonorrhea, while a complete vaccination series (two MenB-4C doses) was 40% effective.

Prospective studies are in progress, which will provide a higher level of evidence. The ANRS DOXYVAC trial has been underway since January 2021. The participants are men who have sex with men, who are highly exposed to the risk of sexually transmitted infections, and who presented with at least one STI in the year before their participation in the study. “The study is being conducted by Jean-Michel Molina of Saint-Louis Hospital. What they’re trying to do is protect our cohort of pre-exposure prophylaxis patients with meningococcal vaccine,” explained Dr. Fouéré.

Initial findings demonstrated the efficacy of a meningococcal B vaccine in reducing the risk of gonorrhea and the efficacy of doxycycline as preventive intervention for STIs when taken within 72 hours after sexual intercourse. In light of these results, a decision was made at the end of October to discontinue the trial and to recommend providing both interventions to all ANRS DOXYVAC participants. The follow-up of the participants will continue until the end of 2023. The results that led to stopping the study in its current form will be presented in early 2023.

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

PARIS – All the way back in 1907, The Lancet published an article on a gonorrhea vaccine trial. Today, after continuous research throughout the intervening 110-plus years, scientists may finally have achieved success. Sébastien Fouéré, MD, discussed the details at a press conference that focused on the highlights of the Dermatology Days of Paris conference. Dr. Fouéré is the head of the genital dermatology and sexually transmitted infections unit at Saint-Louis Hospital, Paris.

Twin bacteria

Although the gonorrhea vaccine has long been the subject of research, Dr. Fouéré views 2017 as a turning point. This was when the results of a study led by Helen Petousis-Harris, PhD, were published.

“She tried to formalize the not completely indisputable results published by Cuba, where it seemed there were fewer gonococci in individuals vaccinated against meningococcal group B,” he noted.

Dr. Petousis-Harris, an immunologist, conducted a retrospective case-control study involving 11 clinics in New Zealand. The participants were aged 15-30 years, were eligible to receive the meningococcal B vaccine, and had been diagnosed with gonorrhea, chlamydia, or both. The researchers found that receiving the meningococcal B vaccine in childhood provides around 30% protection against Neisseria gonorrhoeae infections.

“It’s not perhaps a coincidence that a meningococcal B vaccine would be protective against gonorrhea,” Dr. Fouéré pointed out. He considers this protection logical, even expected, insofar as “meningococcus and gonococcus are almost twins.” There is 90% and 100% homology between membrane proteins of the two bacteria.
 

Vaccine is effective

Two retrospective case-control studies confirm that the vaccine is protective. One of the studies, carried out by an Australian team, found that the effectiveness was 32%, quite close to that reported by Petousis-Harris. In the other study, a U.S. team brought to light a dose-response relationship. A partial vaccination series (single serogroup B meningococcal outer membrane vesicle vaccine dose) was 26% effective against gonorrhea, while a complete vaccination series (two MenB-4C doses) was 40% effective.

Prospective studies are in progress, which will provide a higher level of evidence. The ANRS DOXYVAC trial has been underway since January 2021. The participants are men who have sex with men, who are highly exposed to the risk of sexually transmitted infections, and who presented with at least one STI in the year before their participation in the study. “The study is being conducted by Jean-Michel Molina of Saint-Louis Hospital. What they’re trying to do is protect our cohort of pre-exposure prophylaxis patients with meningococcal vaccine,” explained Dr. Fouéré.

Initial findings demonstrated the efficacy of a meningococcal B vaccine in reducing the risk of gonorrhea and the efficacy of doxycycline as preventive intervention for STIs when taken within 72 hours after sexual intercourse. In light of these results, a decision was made at the end of October to discontinue the trial and to recommend providing both interventions to all ANRS DOXYVAC participants. The follow-up of the participants will continue until the end of 2023. The results that led to stopping the study in its current form will be presented in early 2023.

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

PARIS – All the way back in 1907, The Lancet published an article on a gonorrhea vaccine trial. Today, after continuous research throughout the intervening 110-plus years, scientists may finally have achieved success. Sébastien Fouéré, MD, discussed the details at a press conference that focused on the highlights of the Dermatology Days of Paris conference. Dr. Fouéré is the head of the genital dermatology and sexually transmitted infections unit at Saint-Louis Hospital, Paris.

Twin bacteria

Although the gonorrhea vaccine has long been the subject of research, Dr. Fouéré views 2017 as a turning point. This was when the results of a study led by Helen Petousis-Harris, PhD, were published.

“She tried to formalize the not completely indisputable results published by Cuba, where it seemed there were fewer gonococci in individuals vaccinated against meningococcal group B,” he noted.

Dr. Petousis-Harris, an immunologist, conducted a retrospective case-control study involving 11 clinics in New Zealand. The participants were aged 15-30 years, were eligible to receive the meningococcal B vaccine, and had been diagnosed with gonorrhea, chlamydia, or both. The researchers found that receiving the meningococcal B vaccine in childhood provides around 30% protection against Neisseria gonorrhoeae infections.

“It’s not perhaps a coincidence that a meningococcal B vaccine would be protective against gonorrhea,” Dr. Fouéré pointed out. He considers this protection logical, even expected, insofar as “meningococcus and gonococcus are almost twins.” There is 90% and 100% homology between membrane proteins of the two bacteria.
 

Vaccine is effective

Two retrospective case-control studies confirm that the vaccine is protective. One of the studies, carried out by an Australian team, found that the effectiveness was 32%, quite close to that reported by Petousis-Harris. In the other study, a U.S. team brought to light a dose-response relationship. A partial vaccination series (single serogroup B meningococcal outer membrane vesicle vaccine dose) was 26% effective against gonorrhea, while a complete vaccination series (two MenB-4C doses) was 40% effective.

Prospective studies are in progress, which will provide a higher level of evidence. The ANRS DOXYVAC trial has been underway since January 2021. The participants are men who have sex with men, who are highly exposed to the risk of sexually transmitted infections, and who presented with at least one STI in the year before their participation in the study. “The study is being conducted by Jean-Michel Molina of Saint-Louis Hospital. What they’re trying to do is protect our cohort of pre-exposure prophylaxis patients with meningococcal vaccine,” explained Dr. Fouéré.

Initial findings demonstrated the efficacy of a meningococcal B vaccine in reducing the risk of gonorrhea and the efficacy of doxycycline as preventive intervention for STIs when taken within 72 hours after sexual intercourse. In light of these results, a decision was made at the end of October to discontinue the trial and to recommend providing both interventions to all ANRS DOXYVAC participants. The follow-up of the participants will continue until the end of 2023. The results that led to stopping the study in its current form will be presented in early 2023.

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

People who follow a vegetarian lifestyle have around twice as many depressive episodes as those who eat meat, according to the Brazilian Longitudinal Study of Adult Health.

What to know

The high incidence of depression among vegetarians is not caused by nutrition but possibly by several factors, including the vegetarian social experience; depression itself may increase the likelihood of becoming vegetarian, or both vegetarianism and depression may be associated with guilt through factors involving the meat industry.

Adopting a vegetarian diet might affect one’s relationship with others and involvement in social activities and may sometimes be associated with teasing or other forms of social ostracism.

It is possible that being depressed and dwelling on negative thoughts cause people to be more likely to become vegetarian rather than the other way around.

Videos depicting violence and cruelty in the meat industry may affect depressed people, causing them to dwell on the images, feel guilty for their part in creating the demand for meat, and become vegetarian.

Survey data were collected in Brazil, a country famous for its meat-heavy diet, and while there has been a sharp increase in vegetarianism, vegetarians still account for less than 0.5%.

This is a summary of the article, “Association Between Meatless Diet and Depressive Episodes: A Cross-sectional Analysis of Baseline Data From the Longitudinal Study of Adult Health (ELSA-Brasil),” published in the Journal of Affective Disorders. The full article can be found at sciencedirect.com.

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

People who follow a vegetarian lifestyle have around twice as many depressive episodes as those who eat meat, according to the Brazilian Longitudinal Study of Adult Health.

What to know

The high incidence of depression among vegetarians is not caused by nutrition but possibly by several factors, including the vegetarian social experience; depression itself may increase the likelihood of becoming vegetarian, or both vegetarianism and depression may be associated with guilt through factors involving the meat industry.

Adopting a vegetarian diet might affect one’s relationship with others and involvement in social activities and may sometimes be associated with teasing or other forms of social ostracism.

It is possible that being depressed and dwelling on negative thoughts cause people to be more likely to become vegetarian rather than the other way around.

Videos depicting violence and cruelty in the meat industry may affect depressed people, causing them to dwell on the images, feel guilty for their part in creating the demand for meat, and become vegetarian.

Survey data were collected in Brazil, a country famous for its meat-heavy diet, and while there has been a sharp increase in vegetarianism, vegetarians still account for less than 0.5%.

This is a summary of the article, “Association Between Meatless Diet and Depressive Episodes: A Cross-sectional Analysis of Baseline Data From the Longitudinal Study of Adult Health (ELSA-Brasil),” published in the Journal of Affective Disorders. The full article can be found at sciencedirect.com.

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

People who follow a vegetarian lifestyle have around twice as many depressive episodes as those who eat meat, according to the Brazilian Longitudinal Study of Adult Health.

What to know

The high incidence of depression among vegetarians is not caused by nutrition but possibly by several factors, including the vegetarian social experience; depression itself may increase the likelihood of becoming vegetarian, or both vegetarianism and depression may be associated with guilt through factors involving the meat industry.

Adopting a vegetarian diet might affect one’s relationship with others and involvement in social activities and may sometimes be associated with teasing or other forms of social ostracism.

It is possible that being depressed and dwelling on negative thoughts cause people to be more likely to become vegetarian rather than the other way around.

Videos depicting violence and cruelty in the meat industry may affect depressed people, causing them to dwell on the images, feel guilty for their part in creating the demand for meat, and become vegetarian.

Survey data were collected in Brazil, a country famous for its meat-heavy diet, and while there has been a sharp increase in vegetarianism, vegetarians still account for less than 0.5%.

This is a summary of the article, “Association Between Meatless Diet and Depressive Episodes: A Cross-sectional Analysis of Baseline Data From the Longitudinal Study of Adult Health (ELSA-Brasil),” published in the Journal of Affective Disorders. The full article can be found at sciencedirect.com.

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

OBG Management caught up with Drs. Jan Shifren and Genevieve Neal-Perry while they were attending the annual meeting of The North American Menopause Society (NAMS), held October 12-15, 2022, in Atlanta, Georgia. Dr. Shifren presented on the “Ins and Outs of Hormone Therapy,” while Dr. Neal-Perry focused on “Menopause Physiology.” 

Evaluating symptomatic patients for appropriate hormone therapy

OBG Management: In your presentation to the group at the NAMS meeting, you described a 51-year-old patient with the principal symptoms of frequent hot flashes and night sweats, sleep disruption, fatigue, irritability, vaginal dryness, and dyspareunia. As she reported already trying several lifestyle modification approaches, what are your questions for her to determine whether hormone therapy (HT), systemic or low-dose vaginal, is advisable?

Jan Shifren, MD: As with every patient, you need to begin with a thorough history and confirm her physical exam is up to date. If there are concerns related to genitourinary symptoms of menopause (GSM), then a pelvic exam is indicated. This patient is a healthy menopausal woman with bothersome hot flashes, night sweats, and vaginal dryness. Sleep disruption from night sweats is likely the cause of her fatigue and irritability, and her dyspareunia due to atrophic vulvovaginal changes. The principal indication for systemic HT is bothersome vasomotor symptoms (VMS), and a healthy woman who is under age 60 or within 10 years of the onset of menopause is generally a very good candidate for hormones. For this healthy 51-year-old with bothersome VMS unresponsive to lifestyle modification, the benefits of HT should outweigh potential risks. As low-dose vaginal estrogen therapy is minimally absorbed and very safe, this would be recommended instead of systemic HT if her only menopause symptoms were vaginal dryness and dyspareunia.

HT types and formulations

OBG Management: For this patient, low-dose vaginal estrogen is appropriate. In general, how do you decide on recommendations for combination therapy or estrogen only, and what formulations and dosages do you recommend?

Dr. Shifren: Any woman with a uterus needs to take a progestogen together with estrogen to protect her uterus from estrogen-induced endometrial overgrowth. With low dose vaginal estrogen therapy, however, concurrent progestogen is not needed.

Continue to: Estrogen options...

Many of our patients like the idea that they are using “natural” HT. I inform them that bioidentical is a marketing term rather than a medical term, but if their goal is to take the same hormones that their ovaries made when they were younger, they should use FDA-approved formulations of estradiol and progesterone for their menopausal HT symptoms. I do not recommend compounded bioidentical HT due to concerns regarding product quality and safety. The combination of FDA-approved estradiol patches and oral micronized progesterone provides a high quality, carefully regulated bioidentical HT regimen. For women greatly preferring an oral estrogen, oral estradiol with micronized progesterone is an option.

In addition to patient preference for natural HT, the reasons that I encourage women to consider the estradiol transdermal patch for their menopausal HT include:

1. no increased risk of venous thromboembolic events when physiologically dosed menopausal estradiol therapy is provided by a skin patch (observational data).¹ With oral estrogens, even when dosed for menopause, VTE risk increases, as coagulation factors increase due to the first-pass hepatic effect. This does not occur with non-oral menopausal estrogens.
2. no increased risk of gallbladder disease, which occurs with oral estrogen therapy (observational data)²
3. possibly lower risk of stroke when low-dose menopausal HT is provided via skin patch (observational data)³
4. convenience—the patches are changed once or twice weekly
5. wide range of doses available, which optimizes identifying the lowest effective dose and decreasing the dose over time.

Progestogen options. Progestogens may be given daily or cyclically. Use of daily progestogen typically results in amenorrhea, which is preferred by most women. Cyclic use of a progestogen for 12-14 days each month results in a monthly withdrawal bleed, which is a good option for a woman experiencing bothersome breakthrough bleeding with daily progestogen. Use of a progestogen-releasing IUD is an off-label alternative for endometrial protection with menopausal HT. As discussed earlier, as many women prefer bioidentical HT, one of our preferred regimens is to provide transdermal estradiol with FDA-approved oral micronized progesterone. There are several patches that combine estradiol with a progestogen, but there is not a lot of dosing flexibility and product choice. There also is an approved product available that combines oral estradiol and micronized progesterone in one tablet.

Scheduling follow-up

OBG Management: Now that you have started the opening case patient on HT, how often are you going to monitor her for treatment?

Dr. Shifren: Women will not experience maximum efficacy for hot flash relief from their estrogen therapy for 3 months, so I typically see a patient back at 3 to 4 months to assess side effects and symptom control. I encourage women to reach out sooner if they are having a bothersome side effect. Once she is doing well on an HT regimen, we assess risks and benefits of ongoing treatment annually. The goal is to be certain she is on the lowest dose of estrogen that treats her symptoms, and we slowly decrease the estrogen dose over time.

Breast cancer risk

OBG Management: In your presentation, you mentioned that the risk of breast cancer does not increase appreciably with short-term use of HT. Is it possible to define short term?

Dr. Shifren: In the Women’s Health Initiative (WHI), a large double-blind, randomized, placebo-controlled trial of menopausal HT, there was a slight increase in breast cancer risk after approximately 4 to 5 years of use in women using estrogen with progestogen.⁴ I share with patients that this increased risk is about the same as that of obesity or drinking more than 1 alcoholic beverage daily. As an increased risk of breast cancer does not occur for several years, a woman may be able to take hormones for bothersome symptoms, feel well, and slowly come off without incurring significant breast cancer risk. In the WHI, there was no increase in breast cancer risk in women without a uterus randomized to estrogen alone.

Regarding cardiovascular risk, in the WHI, an increased risk of cardiovascular events generally was not seen in healthy women younger than age 60 and within 10 years of the onset of menopause.⁵ Benefits of HT may not outweigh risks for women with significant underlying cardiovascular risk factors, even if they are younger and close to menopause onset.

Continue to: The importance of shared decision making...

Dr. Shifren: As with any important health care decision, women should be involved in an individualized discussion of risks and benefits, with shared decision making about whether HT is the right choice. Women also should be involved in ongoing decisions regarding HT formulation, dose, and duration of use.

A nonhormonal option for hot flashes

OBG Management: How many women experience VMS around the time of menopause?

Dr. Genevieve Neal-Perry, MD, PhD: About 60% to 70% of individuals will experience hot flashes around the time of the menopause.⁶ Of those, about 40% are what we would call moderate to severe hot flashes—which are typically the most disruptive in terms of quality of life.⁷ The window of time in which they are likely to have them, at typically their most intense timeframe, is 2 years before the final menstrual period and the year after.⁷ In terms of the average duration, however, it’s about 7 years, which is a lot longer than what we previously thought.⁸ Moreover, there are disparities in that women of color, particularly African American women, can have them as long as 10 years.⁸
 

OBG Management: Can you explain why the VMS occur, and specifically around the time of menopause?

Dr. Neal-Perry: For many years we did not understand the basic biology of hot flashes. When you think about it, it’s completely amazing—when half of our population experiences hot flashes, and we don’t understand why, and we don’t have therapy that specifically targets hot flashes.

What we now know from work completed by Naomi Rance, in particular, is that a specific region of the brain, the hypothalamus, exhibited changes in number of neurons that seemed to be increased in size in menopausal people and smaller in size in people who were not menopausal.⁹ That started the journey to understanding the biology, and eventual mechanism, of hot flashes. It took about 10-15 years before we really began to understand why.

What we know now is that estrogen, a hormone that is made by the ovaries, activates and inactivates neurons located in the hypothalamus, a brain region that controls our thermoregulation—the way your body perceives temperature. The hypothalamus controls your response to temperature, either you experience chills or you dissipate heat by vasodilating (hot flush) and sweating.

The thermoregulatory region of the hypothalamus houses cells that receive messages from KNDy neurons, neurons also located in the hypothalamus that express kisspeptin, neurokinin, and dynorphin. Importantly, KNDy neurons express estrogen receptors. (The way that I like to think about estrogen and estrogen receptors is that estrogen is like the ball and the receptor is like the catcher’s mitt.) When estrogen interacts with this receptor, it keeps KNDy neurons quiet. But the increased variability and loss of estrogen that occurs around the time of menopause “disinhibits” KNDy neurons—meaning that they are no longer being reined in by estrogen. In response to decreased estrogen regulation, KNDy neurons become hypertrophied with neurotransmitters and more active. Specifically, KNDy neurons release neurokinin, a neuropeptide that self-stimulates KNDy neurons and activates neurons in the thermoregulatory zone of the brain—it’s a speed-forward feed-backward mechanism. The thermoregulatory neurons interpret this signal as “I feel hot,” and the body begins a series of functions to cool things down.

ILLUSTRATION: KIMBERLY MARTENS FOR OBG MANAGEMENT

Continue to: Treatments that act on the thermoregulatory region

Dr. Neal-Perry: I have described what happens in the brain around the time of menopause, and what triggers those hot flashes.

Estrogen. The reason that estrogen worked to treat the hot flashes is because estrogen inhibits and calms the neurons that become hyperactive during the menopause.

Fezolinetant. Fezolinetant is unique because it specifically targets the hormone receptor that triggers hot flashes, the neurokinin receptor. Fezolinetant is a nonhormone therapy that not only reduces the activity of KNDy neurons but also blocks the effects of neurons in the thermoregulatory zone, thereby reducing the sensation of the hot flashes. We are in such a special time in medical history for individuals who experience hot flashes because now we understand the basic biology of hot flashes, and we can generate targeted therapy to manage hot flashes—that is for both individuals who identify as women and individuals who identify as men, because both experience hot flashes.
 

OBG Management: Is there a particular threshold of hot flash symptoms that is considered important to treat, or is treatment based on essentially the bother to patients?

Dr. Neal-Perry: Treatment is solely based on if it bothers the patient. But we do know that people who have lots of bothersome hot flashes have a higher risk for heart disease and may have sleep disruption, reduced cognitive function, and poorer quality of life. Sleep dysfunction can impact the ability to think and function and can put those affected at increased risk for accidents.

For people who are having these symptoms that are disruptive to their life, you do want to treat them. You might say, “Well, we’ve had estrogen, why not use estrogen,” right? Well estrogen works very well, but there are lots of people who can’t use estrogen—individuals who have breast cancer, blood clotting disorders, significant heart disease, or diabetes. Then there are just some people who don’t feel comfortable using estrogen.

We have had a huge gap in care for individuals who experience hot flashes and who are ineligible for menopausal HT. While there are other nonhormonal options, they often have side effects like sexual dysfunction, hypersomnolence, or insomnia. Some people choose not to use these nonhormonal treatments because the side effects are worse for them than to trying to manage the hot flashes. The introduction to a nonhormonal therapy that is effective and does not have lots of side effects is exciting and will be welcomed by many who have not found relief.
 

OBG Management: Is fezolinetant available now for patients?

Dr. Neal-Perry: It is not available yet. Hopefully, it will be approved within the next year. Astellas recently completed a double blind randomized cross over design phase 3 study that found fezolinetant is highly effective for the management of hot flashes and that it has a low side effect profile.¹⁰ Fezolinetant’s most common side effect was COVID-19, a reflection of the fact that the trial was done during the COVID pandemic. The other most common side effect was headache. Everything else was minimal.

Other drugs in the same class as fezolinetant have been under development for the management of hot flashes; however, they encountered liver function challenges, and studies were stopped. Fezolinetant did not cause liver dysfunction.

Hot flash modifiers

OBG Management: Referring to that neuropathway, are there physiologic differences among women who do and do not experience hot flashes, and are there particular mechanisms that may protect patients against being bothered by hot flashes?

Dr. Neal-Perry: Well, there are some things that we can control, and there are things that we cannot control (like our genetic background). Some of the processes that are important for estrogen receptor function and estrogen metabolism, as well as some other receptor systems, can work differently. When estrogen metabolism is slightly different, it could result in reduced estrogen receptor activity and more hot flashes. Then there are some receptor polymorphisms that can increase or reduce the risk for hot flashes—the genetic piece.¹¹

There are things that can modify your risk for hot flashes and the duration of hot flashes. Individuals who are obese or smoke may experience more hot flashes. Women of color, especially African American women, tend to have hot flashes occur earlier in their reproductive life and last for a longer duration; hot flashes may occur up to 2 years before menopause, last for more than 10 years, and be more disruptive. By contrast, Asian women tend to report fewer and less disruptive hot flashes.⁸
 

OBG Management: If fezolinetant were to be FDA approved, will there be particular patients that it will most appropriate for, since it is an estrogen alternative?

Dr. Neal-Perry: Yes, there may be different patients who might benefit from fezolinetant. This will depend on what the situation is—patients who have breast cancer, poorly controlled diabetes, or heart disease, and those patients who prefer not to use estrogen will benefit from fezolinetant, as we are going to look for other treatment options for those individuals. It will be important for medical providers to listen to their patients and understand the medical background of that individual to really define what is the best next step for the management of their hot flashes.

This is an exciting time for individuals affected by menopausal hot flashes; to understand the biology of hot flashes gives us real opportunities to bridge gaps around how to manage them. Individuals who experience hot flashes will know that they don’t have to suffer, that there are other options that are safe, that can help meet their needs and put them in a better place. ●

Multiethnic differences in the menopause experience

---

Excerpted from the presentation, “Do you see me? Culturally responsive care in menopause,” by Makeba Williams, MD, NCMP, at The North American Menopause Society meeting in Atlanta, Georgia, October 12-15, 2022.

Dr. Williams is Vice Chair of Professional Development and Wellness, Associate Professor, Washington University School of Medicine

The Study of Women’s Health Across the Nation (SWAN) challenged the notion that there is a universal menopausal experience.¹ Up until that time, we had been using this universal experience that is based largely on the experiences of White women and applying that data to the experiences of women of color. Other research has shown that African American women have poorer quality of life and health status, and that they receive less treatment for a number of conditions.^2,3

In a recent review of more than 20 years of literature, we found only 17 articles that met the inclusion criteria, reflecting the invisibility of African American women and other ethnic and racial minorities in the menopause literature and research. Key findings included that African American women^1,4:

• experience an earlier age of onset of menopause
• have higher rates of premature menopause and early menopause, which is a risk factor for cardiovascular disease
• experience a longer time of the menopausal transition, with variability in the average age of menopause onset
• overall report lower rates of vaginal symptoms
• are less likely to report sleep disturbances than White women or Hispanic women, but more likely to report these symptoms than Asian women
• experience a higher prevalence, frequency, and severity of vasomotor symptoms (VMS), and were more bothered by those symptoms

− 48.4 years in the Healthy Women’s Study

− 50.9 years in the Penn Ovarian Aging Study

− 51.4 years in SWAN

• reported lower educational attainment, experiencing more socioeconomic disadvantage and exposure to more adverse life effects
• receive less treatment for VMS, hypertension, and depression, and are less likely to be prescribed statin drugs
• experience more discrimination
• use cigarettes and tobacco more, but are less likely to use alcohol and less likely to have physical activity.

Cultural influences on menopause

Im and colleagues have published many studies looking at cultural influences on African American, Hispanic, and Asian American women, and comparing them to White women.⁵ Notable differences were found regarding education level, family income, employment, number of children, and greater perceived health (which is associated with fewer menopausal symptoms). They identified 5 qualitative ideas:

1. Positive acceptance. Minority women, or racial and ethnic women, perceived the transition to menopause more positively, and generally took on a posture of acceptance, reporting feeling liberated from many of the challenges associated with the reproductive period. In addition, many associated a greater sense of maturity and respect within their communities with the natural aging process.
2. Optimism. Ethnic women tended to embrace menopause, using humor and laughter to express emotions during stressful life changes. This runs counter to many of the perspectives reported by White women, who often viewed the menopausal transition and aging negatively, as we equate aging with the loss of youthfulness in the United States.
3. Unique, not universal. Most of the ethnic minority women thought that there was something unique about their menopausal experiences, and that they were influenced by immigration transition, financial situations, etc. Many White woman perceived that the menopausal experience was shared among all women.
4. Closed, not open. There were differences in how we talk about symptoms, or whether or not we talk about them at all. Ethnic women tended to be silent about their symptoms. By contrast, White women tended to be more open and talkative and communicative about their symptoms.
5. Minimizing, not controlling. No symptom management was the strategy of choice for most women. Minority women tended to manage their symptoms by tolerating and normalizing them. Only those women with the most serious symptoms sought out medication for temporary relief. Some expressed a tendency to downplay their symptoms because many of them had more important things that they were dealing with in their lives.

What is an individual social identity?

An individual social identity reflects the many groups to which one belongs. It is how one shows up, and yet it is much more than how they physically show up. When you pass your eye on patients, you are only seeing the tip of the iceberg. The full social identity of a patient resides below the surface. Social identity is complex, on a continuum, and can change depending on time and place. How we prioritize our social identities may change, depending on the context and the situation.

Our intersecting social identities give rise to our cultural identity, and it is through the prism of intersectionality that we can understand the ways in which our social identities converge to give rise to disparities in health care in midlife and menopausal women. Holding space for cultural identity, we can impact how our patients are perceiving their menopause, how they are moving through decision making about taking care of themselves in menopause. And we can provide more responsive care to their cultural identities, and hopefully at the end of the day we reduce some of these disparities that we are seeing in our menopausal patients and also are reducing our unconscious bias in our patient interactions.

Culturally responsive care

There are several components to home in on when we are trying to provide culturally responsive care to patients.

1. A commitment to being culturally curious. We have to accept what the literature is sharing with us, that there is not a universal menopausal experience. We have for far too long applied this universal experience of menopause that has largely been based on White women to different racial and ethnic populations.
2. Recognizing. I appreciate that my identity as a Black woman may be very different from other Black women in the room, or whatever their social identity. I am not expected to understand all of the others’ experiences, and I don’t expect that for you either.
3. Acknowledge unconscious implicit biases. Acknowledge the groups to which you have a strong implicit bias, and allow it to drive you to reduce barriers to engaging with patients.
4. Connecting with the individual patient. It is through a process of individuating that we learn from our patients’ unique characteristics, rather than relying on assumptions and stereotypes. We have a window of opportunity to see our patient and move beyond thinking of them in terms of racial and ethnic stereotypes or particular social groups. It is through this process of individualizing that we can seek answers to key questions.

The ultimate goal is to understand our individual patients’ perceptions, outlook on menopause, and contextual factors in their lives that influence the menopause journey.

CASE ENCOUNTER

I quickly look at the patient-filled form before I knock on the exam door, and I see that the patient has checked off that she has hot flashes, night sweats, and I make a mental note, she’s menopausal. I already have a preliminary plan to give this patient hormone therapy. I open the door, and I see that she’s Black. I know, based upon the data from SWAN and others, that her menopause means longer duration, more severe vasomotor symptoms. I have already teed up a prescription to go to the pharmacy.

The problem is, I have not even talked to her. She may actually nod her head, saying that she is going to go to the pharmacy, but she may never pick up that prescription. She likely leaves my office feeling unheard; her needs are unmet. I move onto the next patient. I feel good, but in actuality, I didn’t hear her. I have provided her bias and stereotyped care. I missed an opportunity to truly engage this patient and her care, and my good intentions of following the literature about her experience in menopause have contributed quite likely to her increased morbidity and mortality, her increased cardiovascular disease risk, all because I have not held space for her cultural identity.

References

1. Harlow SD, Burnett-Bowie SM, Greendale GA, et al. Disparities in reproductive aging and midlife health between Black and White women: the Study of Women’s Health Across the Nation (SWAN). Women’s Midlife Health. 2022;8:3. doi: 10.1186/s40695-022-00073-y.
2. Chlebowski RT, Aragaki AK, Anderson GL, et al. Forty-year trends in menopausal hormone therapy use and breast cancer incidence among postmenopausal black and white women. Cancer. 2020;126:2956-2964. doi: 10.1002/ cncr.32846.
3. Weng HH, McBride CM, Bosworth HB, et al. Racial differences in physician recommendation of hormone replacement therapy. Prev Med. 2001;33:668673. doi: 10.1006/pmed.2001.0943.
4. Williams M, Richard-Davis G, Williams PL, et al. A review of African American women’s experiences in menopause. Menopause. 2022;29:1331-1337. doi: 10.1097/GME.0000000000002060.
5. Im EO. Ethnic differences in symptoms experienced during the menopausal transition. Health Care Women Int. 2009;30:339-355. doi: 10.1080/07399330802695002.

OBG Management caught up with Drs. Jan Shifren and Genevieve Neal-Perry while they were attending the annual meeting of The North American Menopause Society (NAMS), held October 12-15, 2022, in Atlanta, Georgia. Dr. Shifren presented on the “Ins and Outs of Hormone Therapy,” while Dr. Neal-Perry focused on “Menopause Physiology.” 

Evaluating symptomatic patients for appropriate hormone therapy

OBG Management: In your presentation to the group at the NAMS meeting, you described a 51-year-old patient with the principal symptoms of frequent hot flashes and night sweats, sleep disruption, fatigue, irritability, vaginal dryness, and dyspareunia. As she reported already trying several lifestyle modification approaches, what are your questions for her to determine whether hormone therapy (HT), systemic or low-dose vaginal, is advisable?

Jan Shifren, MD: As with every patient, you need to begin with a thorough history and confirm her physical exam is up to date. If there are concerns related to genitourinary symptoms of menopause (GSM), then a pelvic exam is indicated. This patient is a healthy menopausal woman with bothersome hot flashes, night sweats, and vaginal dryness. Sleep disruption from night sweats is likely the cause of her fatigue and irritability, and her dyspareunia due to atrophic vulvovaginal changes. The principal indication for systemic HT is bothersome vasomotor symptoms (VMS), and a healthy woman who is under age 60 or within 10 years of the onset of menopause is generally a very good candidate for hormones. For this healthy 51-year-old with bothersome VMS unresponsive to lifestyle modification, the benefits of HT should outweigh potential risks. As low-dose vaginal estrogen therapy is minimally absorbed and very safe, this would be recommended instead of systemic HT if her only menopause symptoms were vaginal dryness and dyspareunia.

HT types and formulations

OBG Management: For this patient, low-dose vaginal estrogen is appropriate. In general, how do you decide on recommendations for combination therapy or estrogen only, and what formulations and dosages do you recommend?

Dr. Shifren: Any woman with a uterus needs to take a progestogen together with estrogen to protect her uterus from estrogen-induced endometrial overgrowth. With low dose vaginal estrogen therapy, however, concurrent progestogen is not needed.

Continue to: Estrogen options...

Many of our patients like the idea that they are using “natural” HT. I inform them that bioidentical is a marketing term rather than a medical term, but if their goal is to take the same hormones that their ovaries made when they were younger, they should use FDA-approved formulations of estradiol and progesterone for their menopausal HT symptoms. I do not recommend compounded bioidentical HT due to concerns regarding product quality and safety. The combination of FDA-approved estradiol patches and oral micronized progesterone provides a high quality, carefully regulated bioidentical HT regimen. For women greatly preferring an oral estrogen, oral estradiol with micronized progesterone is an option.

In addition to patient preference for natural HT, the reasons that I encourage women to consider the estradiol transdermal patch for their menopausal HT include:

1. no increased risk of venous thromboembolic events when physiologically dosed menopausal estradiol therapy is provided by a skin patch (observational data).¹ With oral estrogens, even when dosed for menopause, VTE risk increases, as coagulation factors increase due to the first-pass hepatic effect. This does not occur with non-oral menopausal estrogens.
2. no increased risk of gallbladder disease, which occurs with oral estrogen therapy (observational data)²
3. possibly lower risk of stroke when low-dose menopausal HT is provided via skin patch (observational data)³
4. convenience—the patches are changed once or twice weekly
5. wide range of doses available, which optimizes identifying the lowest effective dose and decreasing the dose over time.

Progestogen options. Progestogens may be given daily or cyclically. Use of daily progestogen typically results in amenorrhea, which is preferred by most women. Cyclic use of a progestogen for 12-14 days each month results in a monthly withdrawal bleed, which is a good option for a woman experiencing bothersome breakthrough bleeding with daily progestogen. Use of a progestogen-releasing IUD is an off-label alternative for endometrial protection with menopausal HT. As discussed earlier, as many women prefer bioidentical HT, one of our preferred regimens is to provide transdermal estradiol with FDA-approved oral micronized progesterone. There are several patches that combine estradiol with a progestogen, but there is not a lot of dosing flexibility and product choice. There also is an approved product available that combines oral estradiol and micronized progesterone in one tablet.

Scheduling follow-up

OBG Management: Now that you have started the opening case patient on HT, how often are you going to monitor her for treatment?

Dr. Shifren: Women will not experience maximum efficacy for hot flash relief from their estrogen therapy for 3 months, so I typically see a patient back at 3 to 4 months to assess side effects and symptom control. I encourage women to reach out sooner if they are having a bothersome side effect. Once she is doing well on an HT regimen, we assess risks and benefits of ongoing treatment annually. The goal is to be certain she is on the lowest dose of estrogen that treats her symptoms, and we slowly decrease the estrogen dose over time.

Breast cancer risk

OBG Management: In your presentation, you mentioned that the risk of breast cancer does not increase appreciably with short-term use of HT. Is it possible to define short term?

Dr. Shifren: In the Women’s Health Initiative (WHI), a large double-blind, randomized, placebo-controlled trial of menopausal HT, there was a slight increase in breast cancer risk after approximately 4 to 5 years of use in women using estrogen with progestogen.⁴ I share with patients that this increased risk is about the same as that of obesity or drinking more than 1 alcoholic beverage daily. As an increased risk of breast cancer does not occur for several years, a woman may be able to take hormones for bothersome symptoms, feel well, and slowly come off without incurring significant breast cancer risk. In the WHI, there was no increase in breast cancer risk in women without a uterus randomized to estrogen alone.

Regarding cardiovascular risk, in the WHI, an increased risk of cardiovascular events generally was not seen in healthy women younger than age 60 and within 10 years of the onset of menopause.⁵ Benefits of HT may not outweigh risks for women with significant underlying cardiovascular risk factors, even if they are younger and close to menopause onset.

Continue to: The importance of shared decision making...

Dr. Shifren: As with any important health care decision, women should be involved in an individualized discussion of risks and benefits, with shared decision making about whether HT is the right choice. Women also should be involved in ongoing decisions regarding HT formulation, dose, and duration of use.

A nonhormonal option for hot flashes

OBG Management: How many women experience VMS around the time of menopause?

Dr. Genevieve Neal-Perry, MD, PhD: About 60% to 70% of individuals will experience hot flashes around the time of the menopause.⁶ Of those, about 40% are what we would call moderate to severe hot flashes—which are typically the most disruptive in terms of quality of life.⁷ The window of time in which they are likely to have them, at typically their most intense timeframe, is 2 years before the final menstrual period and the year after.⁷ In terms of the average duration, however, it’s about 7 years, which is a lot longer than what we previously thought.⁸ Moreover, there are disparities in that women of color, particularly African American women, can have them as long as 10 years.⁸
 

OBG Management: Can you explain why the VMS occur, and specifically around the time of menopause?

Dr. Neal-Perry: For many years we did not understand the basic biology of hot flashes. When you think about it, it’s completely amazing—when half of our population experiences hot flashes, and we don’t understand why, and we don’t have therapy that specifically targets hot flashes.

What we now know from work completed by Naomi Rance, in particular, is that a specific region of the brain, the hypothalamus, exhibited changes in number of neurons that seemed to be increased in size in menopausal people and smaller in size in people who were not menopausal.⁹ That started the journey to understanding the biology, and eventual mechanism, of hot flashes. It took about 10-15 years before we really began to understand why.

What we know now is that estrogen, a hormone that is made by the ovaries, activates and inactivates neurons located in the hypothalamus, a brain region that controls our thermoregulation—the way your body perceives temperature. The hypothalamus controls your response to temperature, either you experience chills or you dissipate heat by vasodilating (hot flush) and sweating.

The thermoregulatory region of the hypothalamus houses cells that receive messages from KNDy neurons, neurons also located in the hypothalamus that express kisspeptin, neurokinin, and dynorphin. Importantly, KNDy neurons express estrogen receptors. (The way that I like to think about estrogen and estrogen receptors is that estrogen is like the ball and the receptor is like the catcher’s mitt.) When estrogen interacts with this receptor, it keeps KNDy neurons quiet. But the increased variability and loss of estrogen that occurs around the time of menopause “disinhibits” KNDy neurons—meaning that they are no longer being reined in by estrogen. In response to decreased estrogen regulation, KNDy neurons become hypertrophied with neurotransmitters and more active. Specifically, KNDy neurons release neurokinin, a neuropeptide that self-stimulates KNDy neurons and activates neurons in the thermoregulatory zone of the brain—it’s a speed-forward feed-backward mechanism. The thermoregulatory neurons interpret this signal as “I feel hot,” and the body begins a series of functions to cool things down.

ILLUSTRATION: KIMBERLY MARTENS FOR OBG MANAGEMENT

Continue to: Treatments that act on the thermoregulatory region

Dr. Neal-Perry: I have described what happens in the brain around the time of menopause, and what triggers those hot flashes.

Estrogen. The reason that estrogen worked to treat the hot flashes is because estrogen inhibits and calms the neurons that become hyperactive during the menopause.

Fezolinetant. Fezolinetant is unique because it specifically targets the hormone receptor that triggers hot flashes, the neurokinin receptor. Fezolinetant is a nonhormone therapy that not only reduces the activity of KNDy neurons but also blocks the effects of neurons in the thermoregulatory zone, thereby reducing the sensation of the hot flashes. We are in such a special time in medical history for individuals who experience hot flashes because now we understand the basic biology of hot flashes, and we can generate targeted therapy to manage hot flashes—that is for both individuals who identify as women and individuals who identify as men, because both experience hot flashes.
 

OBG Management: Is there a particular threshold of hot flash symptoms that is considered important to treat, or is treatment based on essentially the bother to patients?

Dr. Neal-Perry: Treatment is solely based on if it bothers the patient. But we do know that people who have lots of bothersome hot flashes have a higher risk for heart disease and may have sleep disruption, reduced cognitive function, and poorer quality of life. Sleep dysfunction can impact the ability to think and function and can put those affected at increased risk for accidents.

For people who are having these symptoms that are disruptive to their life, you do want to treat them. You might say, “Well, we’ve had estrogen, why not use estrogen,” right? Well estrogen works very well, but there are lots of people who can’t use estrogen—individuals who have breast cancer, blood clotting disorders, significant heart disease, or diabetes. Then there are just some people who don’t feel comfortable using estrogen.

We have had a huge gap in care for individuals who experience hot flashes and who are ineligible for menopausal HT. While there are other nonhormonal options, they often have side effects like sexual dysfunction, hypersomnolence, or insomnia. Some people choose not to use these nonhormonal treatments because the side effects are worse for them than to trying to manage the hot flashes. The introduction to a nonhormonal therapy that is effective and does not have lots of side effects is exciting and will be welcomed by many who have not found relief.
 

OBG Management: Is fezolinetant available now for patients?

Dr. Neal-Perry: It is not available yet. Hopefully, it will be approved within the next year. Astellas recently completed a double blind randomized cross over design phase 3 study that found fezolinetant is highly effective for the management of hot flashes and that it has a low side effect profile.¹⁰ Fezolinetant’s most common side effect was COVID-19, a reflection of the fact that the trial was done during the COVID pandemic. The other most common side effect was headache. Everything else was minimal.

Other drugs in the same class as fezolinetant have been under development for the management of hot flashes; however, they encountered liver function challenges, and studies were stopped. Fezolinetant did not cause liver dysfunction.

Hot flash modifiers

OBG Management: Referring to that neuropathway, are there physiologic differences among women who do and do not experience hot flashes, and are there particular mechanisms that may protect patients against being bothered by hot flashes?

Dr. Neal-Perry: Well, there are some things that we can control, and there are things that we cannot control (like our genetic background). Some of the processes that are important for estrogen receptor function and estrogen metabolism, as well as some other receptor systems, can work differently. When estrogen metabolism is slightly different, it could result in reduced estrogen receptor activity and more hot flashes. Then there are some receptor polymorphisms that can increase or reduce the risk for hot flashes—the genetic piece.¹¹

There are things that can modify your risk for hot flashes and the duration of hot flashes. Individuals who are obese or smoke may experience more hot flashes. Women of color, especially African American women, tend to have hot flashes occur earlier in their reproductive life and last for a longer duration; hot flashes may occur up to 2 years before menopause, last for more than 10 years, and be more disruptive. By contrast, Asian women tend to report fewer and less disruptive hot flashes.⁸
 

OBG Management: If fezolinetant were to be FDA approved, will there be particular patients that it will most appropriate for, since it is an estrogen alternative?

Dr. Neal-Perry: Yes, there may be different patients who might benefit from fezolinetant. This will depend on what the situation is—patients who have breast cancer, poorly controlled diabetes, or heart disease, and those patients who prefer not to use estrogen will benefit from fezolinetant, as we are going to look for other treatment options for those individuals. It will be important for medical providers to listen to their patients and understand the medical background of that individual to really define what is the best next step for the management of their hot flashes.

This is an exciting time for individuals affected by menopausal hot flashes; to understand the biology of hot flashes gives us real opportunities to bridge gaps around how to manage them. Individuals who experience hot flashes will know that they don’t have to suffer, that there are other options that are safe, that can help meet their needs and put them in a better place. ●

Multiethnic differences in the menopause experience

---

Excerpted from the presentation, “Do you see me? Culturally responsive care in menopause,” by Makeba Williams, MD, NCMP, at The North American Menopause Society meeting in Atlanta, Georgia, October 12-15, 2022.

Dr. Williams is Vice Chair of Professional Development and Wellness, Associate Professor, Washington University School of Medicine

The Study of Women’s Health Across the Nation (SWAN) challenged the notion that there is a universal menopausal experience.¹ Up until that time, we had been using this universal experience that is based largely on the experiences of White women and applying that data to the experiences of women of color. Other research has shown that African American women have poorer quality of life and health status, and that they receive less treatment for a number of conditions.^2,3

In a recent review of more than 20 years of literature, we found only 17 articles that met the inclusion criteria, reflecting the invisibility of African American women and other ethnic and racial minorities in the menopause literature and research. Key findings included that African American women^1,4:

• experience an earlier age of onset of menopause
• have higher rates of premature menopause and early menopause, which is a risk factor for cardiovascular disease
• experience a longer time of the menopausal transition, with variability in the average age of menopause onset
• overall report lower rates of vaginal symptoms
• are less likely to report sleep disturbances than White women or Hispanic women, but more likely to report these symptoms than Asian women
• experience a higher prevalence, frequency, and severity of vasomotor symptoms (VMS), and were more bothered by those symptoms

− 48.4 years in the Healthy Women’s Study

− 50.9 years in the Penn Ovarian Aging Study

− 51.4 years in SWAN

• reported lower educational attainment, experiencing more socioeconomic disadvantage and exposure to more adverse life effects
• receive less treatment for VMS, hypertension, and depression, and are less likely to be prescribed statin drugs
• experience more discrimination
• use cigarettes and tobacco more, but are less likely to use alcohol and less likely to have physical activity.

Cultural influences on menopause

Im and colleagues have published many studies looking at cultural influences on African American, Hispanic, and Asian American women, and comparing them to White women.⁵ Notable differences were found regarding education level, family income, employment, number of children, and greater perceived health (which is associated with fewer menopausal symptoms). They identified 5 qualitative ideas:

1. Positive acceptance. Minority women, or racial and ethnic women, perceived the transition to menopause more positively, and generally took on a posture of acceptance, reporting feeling liberated from many of the challenges associated with the reproductive period. In addition, many associated a greater sense of maturity and respect within their communities with the natural aging process.
2. Optimism. Ethnic women tended to embrace menopause, using humor and laughter to express emotions during stressful life changes. This runs counter to many of the perspectives reported by White women, who often viewed the menopausal transition and aging negatively, as we equate aging with the loss of youthfulness in the United States.
3. Unique, not universal. Most of the ethnic minority women thought that there was something unique about their menopausal experiences, and that they were influenced by immigration transition, financial situations, etc. Many White woman perceived that the menopausal experience was shared among all women.
4. Closed, not open. There were differences in how we talk about symptoms, or whether or not we talk about them at all. Ethnic women tended to be silent about their symptoms. By contrast, White women tended to be more open and talkative and communicative about their symptoms.
5. Minimizing, not controlling. No symptom management was the strategy of choice for most women. Minority women tended to manage their symptoms by tolerating and normalizing them. Only those women with the most serious symptoms sought out medication for temporary relief. Some expressed a tendency to downplay their symptoms because many of them had more important things that they were dealing with in their lives.

What is an individual social identity?

An individual social identity reflects the many groups to which one belongs. It is how one shows up, and yet it is much more than how they physically show up. When you pass your eye on patients, you are only seeing the tip of the iceberg. The full social identity of a patient resides below the surface. Social identity is complex, on a continuum, and can change depending on time and place. How we prioritize our social identities may change, depending on the context and the situation.

Our intersecting social identities give rise to our cultural identity, and it is through the prism of intersectionality that we can understand the ways in which our social identities converge to give rise to disparities in health care in midlife and menopausal women. Holding space for cultural identity, we can impact how our patients are perceiving their menopause, how they are moving through decision making about taking care of themselves in menopause. And we can provide more responsive care to their cultural identities, and hopefully at the end of the day we reduce some of these disparities that we are seeing in our menopausal patients and also are reducing our unconscious bias in our patient interactions.

Culturally responsive care

There are several components to home in on when we are trying to provide culturally responsive care to patients.

1. A commitment to being culturally curious. We have to accept what the literature is sharing with us, that there is not a universal menopausal experience. We have for far too long applied this universal experience of menopause that has largely been based on White women to different racial and ethnic populations.
2. Recognizing. I appreciate that my identity as a Black woman may be very different from other Black women in the room, or whatever their social identity. I am not expected to understand all of the others’ experiences, and I don’t expect that for you either.
3. Acknowledge unconscious implicit biases. Acknowledge the groups to which you have a strong implicit bias, and allow it to drive you to reduce barriers to engaging with patients.
4. Connecting with the individual patient. It is through a process of individuating that we learn from our patients’ unique characteristics, rather than relying on assumptions and stereotypes. We have a window of opportunity to see our patient and move beyond thinking of them in terms of racial and ethnic stereotypes or particular social groups. It is through this process of individualizing that we can seek answers to key questions.

The ultimate goal is to understand our individual patients’ perceptions, outlook on menopause, and contextual factors in their lives that influence the menopause journey.

CASE ENCOUNTER

I quickly look at the patient-filled form before I knock on the exam door, and I see that the patient has checked off that she has hot flashes, night sweats, and I make a mental note, she’s menopausal. I already have a preliminary plan to give this patient hormone therapy. I open the door, and I see that she’s Black. I know, based upon the data from SWAN and others, that her menopause means longer duration, more severe vasomotor symptoms. I have already teed up a prescription to go to the pharmacy.

The problem is, I have not even talked to her. She may actually nod her head, saying that she is going to go to the pharmacy, but she may never pick up that prescription. She likely leaves my office feeling unheard; her needs are unmet. I move onto the next patient. I feel good, but in actuality, I didn’t hear her. I have provided her bias and stereotyped care. I missed an opportunity to truly engage this patient and her care, and my good intentions of following the literature about her experience in menopause have contributed quite likely to her increased morbidity and mortality, her increased cardiovascular disease risk, all because I have not held space for her cultural identity.

References

1. Harlow SD, Burnett-Bowie SM, Greendale GA, et al. Disparities in reproductive aging and midlife health between Black and White women: the Study of Women’s Health Across the Nation (SWAN). Women’s Midlife Health. 2022;8:3. doi: 10.1186/s40695-022-00073-y.
2. Chlebowski RT, Aragaki AK, Anderson GL, et al. Forty-year trends in menopausal hormone therapy use and breast cancer incidence among postmenopausal black and white women. Cancer. 2020;126:2956-2964. doi: 10.1002/ cncr.32846.
3. Weng HH, McBride CM, Bosworth HB, et al. Racial differences in physician recommendation of hormone replacement therapy. Prev Med. 2001;33:668673. doi: 10.1006/pmed.2001.0943.
4. Williams M, Richard-Davis G, Williams PL, et al. A review of African American women’s experiences in menopause. Menopause. 2022;29:1331-1337. doi: 10.1097/GME.0000000000002060.
5. Im EO. Ethnic differences in symptoms experienced during the menopausal transition. Health Care Women Int. 2009;30:339-355. doi: 10.1080/07399330802695002.

OBG Management caught up with Drs. Jan Shifren and Genevieve Neal-Perry while they were attending the annual meeting of The North American Menopause Society (NAMS), held October 12-15, 2022, in Atlanta, Georgia. Dr. Shifren presented on the “Ins and Outs of Hormone Therapy,” while Dr. Neal-Perry focused on “Menopause Physiology.” 

Evaluating symptomatic patients for appropriate hormone therapy

OBG Management: In your presentation to the group at the NAMS meeting, you described a 51-year-old patient with the principal symptoms of frequent hot flashes and night sweats, sleep disruption, fatigue, irritability, vaginal dryness, and dyspareunia. As she reported already trying several lifestyle modification approaches, what are your questions for her to determine whether hormone therapy (HT), systemic or low-dose vaginal, is advisable?

Jan Shifren, MD: As with every patient, you need to begin with a thorough history and confirm her physical exam is up to date. If there are concerns related to genitourinary symptoms of menopause (GSM), then a pelvic exam is indicated. This patient is a healthy menopausal woman with bothersome hot flashes, night sweats, and vaginal dryness. Sleep disruption from night sweats is likely the cause of her fatigue and irritability, and her dyspareunia due to atrophic vulvovaginal changes. The principal indication for systemic HT is bothersome vasomotor symptoms (VMS), and a healthy woman who is under age 60 or within 10 years of the onset of menopause is generally a very good candidate for hormones. For this healthy 51-year-old with bothersome VMS unresponsive to lifestyle modification, the benefits of HT should outweigh potential risks. As low-dose vaginal estrogen therapy is minimally absorbed and very safe, this would be recommended instead of systemic HT if her only menopause symptoms were vaginal dryness and dyspareunia.

HT types and formulations

OBG Management: For this patient, low-dose vaginal estrogen is appropriate. In general, how do you decide on recommendations for combination therapy or estrogen only, and what formulations and dosages do you recommend?

Dr. Shifren: Any woman with a uterus needs to take a progestogen together with estrogen to protect her uterus from estrogen-induced endometrial overgrowth. With low dose vaginal estrogen therapy, however, concurrent progestogen is not needed.

Continue to: Estrogen options...

Many of our patients like the idea that they are using “natural” HT. I inform them that bioidentical is a marketing term rather than a medical term, but if their goal is to take the same hormones that their ovaries made when they were younger, they should use FDA-approved formulations of estradiol and progesterone for their menopausal HT symptoms. I do not recommend compounded bioidentical HT due to concerns regarding product quality and safety. The combination of FDA-approved estradiol patches and oral micronized progesterone provides a high quality, carefully regulated bioidentical HT regimen. For women greatly preferring an oral estrogen, oral estradiol with micronized progesterone is an option.

In addition to patient preference for natural HT, the reasons that I encourage women to consider the estradiol transdermal patch for their menopausal HT include:

1. no increased risk of venous thromboembolic events when physiologically dosed menopausal estradiol therapy is provided by a skin patch (observational data).¹ With oral estrogens, even when dosed for menopause, VTE risk increases, as coagulation factors increase due to the first-pass hepatic effect. This does not occur with non-oral menopausal estrogens.
2. no increased risk of gallbladder disease, which occurs with oral estrogen therapy (observational data)²
3. possibly lower risk of stroke when low-dose menopausal HT is provided via skin patch (observational data)³
4. convenience—the patches are changed once or twice weekly
5. wide range of doses available, which optimizes identifying the lowest effective dose and decreasing the dose over time.

Progestogen options. Progestogens may be given daily or cyclically. Use of daily progestogen typically results in amenorrhea, which is preferred by most women. Cyclic use of a progestogen for 12-14 days each month results in a monthly withdrawal bleed, which is a good option for a woman experiencing bothersome breakthrough bleeding with daily progestogen. Use of a progestogen-releasing IUD is an off-label alternative for endometrial protection with menopausal HT. As discussed earlier, as many women prefer bioidentical HT, one of our preferred regimens is to provide transdermal estradiol with FDA-approved oral micronized progesterone. There are several patches that combine estradiol with a progestogen, but there is not a lot of dosing flexibility and product choice. There also is an approved product available that combines oral estradiol and micronized progesterone in one tablet.

Scheduling follow-up

OBG Management: Now that you have started the opening case patient on HT, how often are you going to monitor her for treatment?

Dr. Shifren: Women will not experience maximum efficacy for hot flash relief from their estrogen therapy for 3 months, so I typically see a patient back at 3 to 4 months to assess side effects and symptom control. I encourage women to reach out sooner if they are having a bothersome side effect. Once she is doing well on an HT regimen, we assess risks and benefits of ongoing treatment annually. The goal is to be certain she is on the lowest dose of estrogen that treats her symptoms, and we slowly decrease the estrogen dose over time.

Breast cancer risk

OBG Management: In your presentation, you mentioned that the risk of breast cancer does not increase appreciably with short-term use of HT. Is it possible to define short term?

Dr. Shifren: In the Women’s Health Initiative (WHI), a large double-blind, randomized, placebo-controlled trial of menopausal HT, there was a slight increase in breast cancer risk after approximately 4 to 5 years of use in women using estrogen with progestogen.⁴ I share with patients that this increased risk is about the same as that of obesity or drinking more than 1 alcoholic beverage daily. As an increased risk of breast cancer does not occur for several years, a woman may be able to take hormones for bothersome symptoms, feel well, and slowly come off without incurring significant breast cancer risk. In the WHI, there was no increase in breast cancer risk in women without a uterus randomized to estrogen alone.

Regarding cardiovascular risk, in the WHI, an increased risk of cardiovascular events generally was not seen in healthy women younger than age 60 and within 10 years of the onset of menopause.⁵ Benefits of HT may not outweigh risks for women with significant underlying cardiovascular risk factors, even if they are younger and close to menopause onset.

Continue to: The importance of shared decision making...

Dr. Shifren: As with any important health care decision, women should be involved in an individualized discussion of risks and benefits, with shared decision making about whether HT is the right choice. Women also should be involved in ongoing decisions regarding HT formulation, dose, and duration of use.

A nonhormonal option for hot flashes

OBG Management: How many women experience VMS around the time of menopause?

Dr. Genevieve Neal-Perry, MD, PhD: About 60% to 70% of individuals will experience hot flashes around the time of the menopause.⁶ Of those, about 40% are what we would call moderate to severe hot flashes—which are typically the most disruptive in terms of quality of life.⁷ The window of time in which they are likely to have them, at typically their most intense timeframe, is 2 years before the final menstrual period and the year after.⁷ In terms of the average duration, however, it’s about 7 years, which is a lot longer than what we previously thought.⁸ Moreover, there are disparities in that women of color, particularly African American women, can have them as long as 10 years.⁸
 

OBG Management: Can you explain why the VMS occur, and specifically around the time of menopause?

Dr. Neal-Perry: For many years we did not understand the basic biology of hot flashes. When you think about it, it’s completely amazing—when half of our population experiences hot flashes, and we don’t understand why, and we don’t have therapy that specifically targets hot flashes.

What we now know from work completed by Naomi Rance, in particular, is that a specific region of the brain, the hypothalamus, exhibited changes in number of neurons that seemed to be increased in size in menopausal people and smaller in size in people who were not menopausal.⁹ That started the journey to understanding the biology, and eventual mechanism, of hot flashes. It took about 10-15 years before we really began to understand why.

What we know now is that estrogen, a hormone that is made by the ovaries, activates and inactivates neurons located in the hypothalamus, a brain region that controls our thermoregulation—the way your body perceives temperature. The hypothalamus controls your response to temperature, either you experience chills or you dissipate heat by vasodilating (hot flush) and sweating.

The thermoregulatory region of the hypothalamus houses cells that receive messages from KNDy neurons, neurons also located in the hypothalamus that express kisspeptin, neurokinin, and dynorphin. Importantly, KNDy neurons express estrogen receptors. (The way that I like to think about estrogen and estrogen receptors is that estrogen is like the ball and the receptor is like the catcher’s mitt.) When estrogen interacts with this receptor, it keeps KNDy neurons quiet. But the increased variability and loss of estrogen that occurs around the time of menopause “disinhibits” KNDy neurons—meaning that they are no longer being reined in by estrogen. In response to decreased estrogen regulation, KNDy neurons become hypertrophied with neurotransmitters and more active. Specifically, KNDy neurons release neurokinin, a neuropeptide that self-stimulates KNDy neurons and activates neurons in the thermoregulatory zone of the brain—it’s a speed-forward feed-backward mechanism. The thermoregulatory neurons interpret this signal as “I feel hot,” and the body begins a series of functions to cool things down.

ILLUSTRATION: KIMBERLY MARTENS FOR OBG MANAGEMENT

Continue to: Treatments that act on the thermoregulatory region

Dr. Neal-Perry: I have described what happens in the brain around the time of menopause, and what triggers those hot flashes.

Estrogen. The reason that estrogen worked to treat the hot flashes is because estrogen inhibits and calms the neurons that become hyperactive during the menopause.

Fezolinetant. Fezolinetant is unique because it specifically targets the hormone receptor that triggers hot flashes, the neurokinin receptor. Fezolinetant is a nonhormone therapy that not only reduces the activity of KNDy neurons but also blocks the effects of neurons in the thermoregulatory zone, thereby reducing the sensation of the hot flashes. We are in such a special time in medical history for individuals who experience hot flashes because now we understand the basic biology of hot flashes, and we can generate targeted therapy to manage hot flashes—that is for both individuals who identify as women and individuals who identify as men, because both experience hot flashes.
 

OBG Management: Is there a particular threshold of hot flash symptoms that is considered important to treat, or is treatment based on essentially the bother to patients?

Dr. Neal-Perry: Treatment is solely based on if it bothers the patient. But we do know that people who have lots of bothersome hot flashes have a higher risk for heart disease and may have sleep disruption, reduced cognitive function, and poorer quality of life. Sleep dysfunction can impact the ability to think and function and can put those affected at increased risk for accidents.

For people who are having these symptoms that are disruptive to their life, you do want to treat them. You might say, “Well, we’ve had estrogen, why not use estrogen,” right? Well estrogen works very well, but there are lots of people who can’t use estrogen—individuals who have breast cancer, blood clotting disorders, significant heart disease, or diabetes. Then there are just some people who don’t feel comfortable using estrogen.

We have had a huge gap in care for individuals who experience hot flashes and who are ineligible for menopausal HT. While there are other nonhormonal options, they often have side effects like sexual dysfunction, hypersomnolence, or insomnia. Some people choose not to use these nonhormonal treatments because the side effects are worse for them than to trying to manage the hot flashes. The introduction to a nonhormonal therapy that is effective and does not have lots of side effects is exciting and will be welcomed by many who have not found relief.
 

OBG Management: Is fezolinetant available now for patients?

Dr. Neal-Perry: It is not available yet. Hopefully, it will be approved within the next year. Astellas recently completed a double blind randomized cross over design phase 3 study that found fezolinetant is highly effective for the management of hot flashes and that it has a low side effect profile.¹⁰ Fezolinetant’s most common side effect was COVID-19, a reflection of the fact that the trial was done during the COVID pandemic. The other most common side effect was headache. Everything else was minimal.

Other drugs in the same class as fezolinetant have been under development for the management of hot flashes; however, they encountered liver function challenges, and studies were stopped. Fezolinetant did not cause liver dysfunction.

Hot flash modifiers

OBG Management: Referring to that neuropathway, are there physiologic differences among women who do and do not experience hot flashes, and are there particular mechanisms that may protect patients against being bothered by hot flashes?

Dr. Neal-Perry: Well, there are some things that we can control, and there are things that we cannot control (like our genetic background). Some of the processes that are important for estrogen receptor function and estrogen metabolism, as well as some other receptor systems, can work differently. When estrogen metabolism is slightly different, it could result in reduced estrogen receptor activity and more hot flashes. Then there are some receptor polymorphisms that can increase or reduce the risk for hot flashes—the genetic piece.¹¹

There are things that can modify your risk for hot flashes and the duration of hot flashes. Individuals who are obese or smoke may experience more hot flashes. Women of color, especially African American women, tend to have hot flashes occur earlier in their reproductive life and last for a longer duration; hot flashes may occur up to 2 years before menopause, last for more than 10 years, and be more disruptive. By contrast, Asian women tend to report fewer and less disruptive hot flashes.⁸
 

OBG Management: If fezolinetant were to be FDA approved, will there be particular patients that it will most appropriate for, since it is an estrogen alternative?

Dr. Neal-Perry: Yes, there may be different patients who might benefit from fezolinetant. This will depend on what the situation is—patients who have breast cancer, poorly controlled diabetes, or heart disease, and those patients who prefer not to use estrogen will benefit from fezolinetant, as we are going to look for other treatment options for those individuals. It will be important for medical providers to listen to their patients and understand the medical background of that individual to really define what is the best next step for the management of their hot flashes.

This is an exciting time for individuals affected by menopausal hot flashes; to understand the biology of hot flashes gives us real opportunities to bridge gaps around how to manage them. Individuals who experience hot flashes will know that they don’t have to suffer, that there are other options that are safe, that can help meet their needs and put them in a better place. ●

Multiethnic differences in the menopause experience

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Excerpted from the presentation, “Do you see me? Culturally responsive care in menopause,” by Makeba Williams, MD, NCMP, at The North American Menopause Society meeting in Atlanta, Georgia, October 12-15, 2022.

Dr. Williams is Vice Chair of Professional Development and Wellness, Associate Professor, Washington University School of Medicine

The Study of Women’s Health Across the Nation (SWAN) challenged the notion that there is a universal menopausal experience.¹ Up until that time, we had been using this universal experience that is based largely on the experiences of White women and applying that data to the experiences of women of color. Other research has shown that African American women have poorer quality of life and health status, and that they receive less treatment for a number of conditions.^2,3

In a recent review of more than 20 years of literature, we found only 17 articles that met the inclusion criteria, reflecting the invisibility of African American women and other ethnic and racial minorities in the menopause literature and research. Key findings included that African American women^1,4:

• experience an earlier age of onset of menopause
• have higher rates of premature menopause and early menopause, which is a risk factor for cardiovascular disease
• experience a longer time of the menopausal transition, with variability in the average age of menopause onset
• overall report lower rates of vaginal symptoms
• are less likely to report sleep disturbances than White women or Hispanic women, but more likely to report these symptoms than Asian women
• experience a higher prevalence, frequency, and severity of vasomotor symptoms (VMS), and were more bothered by those symptoms

− 48.4 years in the Healthy Women’s Study

− 50.9 years in the Penn Ovarian Aging Study

− 51.4 years in SWAN

• reported lower educational attainment, experiencing more socioeconomic disadvantage and exposure to more adverse life effects
• receive less treatment for VMS, hypertension, and depression, and are less likely to be prescribed statin drugs
• experience more discrimination
• use cigarettes and tobacco more, but are less likely to use alcohol and less likely to have physical activity.

Cultural influences on menopause

Im and colleagues have published many studies looking at cultural influences on African American, Hispanic, and Asian American women, and comparing them to White women.⁵ Notable differences were found regarding education level, family income, employment, number of children, and greater perceived health (which is associated with fewer menopausal symptoms). They identified 5 qualitative ideas:

1. Positive acceptance. Minority women, or racial and ethnic women, perceived the transition to menopause more positively, and generally took on a posture of acceptance, reporting feeling liberated from many of the challenges associated with the reproductive period. In addition, many associated a greater sense of maturity and respect within their communities with the natural aging process.
2. Optimism. Ethnic women tended to embrace menopause, using humor and laughter to express emotions during stressful life changes. This runs counter to many of the perspectives reported by White women, who often viewed the menopausal transition and aging negatively, as we equate aging with the loss of youthfulness in the United States.
3. Unique, not universal. Most of the ethnic minority women thought that there was something unique about their menopausal experiences, and that they were influenced by immigration transition, financial situations, etc. Many White woman perceived that the menopausal experience was shared among all women.
4. Closed, not open. There were differences in how we talk about symptoms, or whether or not we talk about them at all. Ethnic women tended to be silent about their symptoms. By contrast, White women tended to be more open and talkative and communicative about their symptoms.
5. Minimizing, not controlling. No symptom management was the strategy of choice for most women. Minority women tended to manage their symptoms by tolerating and normalizing them. Only those women with the most serious symptoms sought out medication for temporary relief. Some expressed a tendency to downplay their symptoms because many of them had more important things that they were dealing with in their lives.

What is an individual social identity?

An individual social identity reflects the many groups to which one belongs. It is how one shows up, and yet it is much more than how they physically show up. When you pass your eye on patients, you are only seeing the tip of the iceberg. The full social identity of a patient resides below the surface. Social identity is complex, on a continuum, and can change depending on time and place. How we prioritize our social identities may change, depending on the context and the situation.

Our intersecting social identities give rise to our cultural identity, and it is through the prism of intersectionality that we can understand the ways in which our social identities converge to give rise to disparities in health care in midlife and menopausal women. Holding space for cultural identity, we can impact how our patients are perceiving their menopause, how they are moving through decision making about taking care of themselves in menopause. And we can provide more responsive care to their cultural identities, and hopefully at the end of the day we reduce some of these disparities that we are seeing in our menopausal patients and also are reducing our unconscious bias in our patient interactions.

Culturally responsive care

There are several components to home in on when we are trying to provide culturally responsive care to patients.

1. A commitment to being culturally curious. We have to accept what the literature is sharing with us, that there is not a universal menopausal experience. We have for far too long applied this universal experience of menopause that has largely been based on White women to different racial and ethnic populations.
2. Recognizing. I appreciate that my identity as a Black woman may be very different from other Black women in the room, or whatever their social identity. I am not expected to understand all of the others’ experiences, and I don’t expect that for you either.
3. Acknowledge unconscious implicit biases. Acknowledge the groups to which you have a strong implicit bias, and allow it to drive you to reduce barriers to engaging with patients.
4. Connecting with the individual patient. It is through a process of individuating that we learn from our patients’ unique characteristics, rather than relying on assumptions and stereotypes. We have a window of opportunity to see our patient and move beyond thinking of them in terms of racial and ethnic stereotypes or particular social groups. It is through this process of individualizing that we can seek answers to key questions.

The ultimate goal is to understand our individual patients’ perceptions, outlook on menopause, and contextual factors in their lives that influence the menopause journey.

CASE ENCOUNTER

I quickly look at the patient-filled form before I knock on the exam door, and I see that the patient has checked off that she has hot flashes, night sweats, and I make a mental note, she’s menopausal. I already have a preliminary plan to give this patient hormone therapy. I open the door, and I see that she’s Black. I know, based upon the data from SWAN and others, that her menopause means longer duration, more severe vasomotor symptoms. I have already teed up a prescription to go to the pharmacy.

The problem is, I have not even talked to her. She may actually nod her head, saying that she is going to go to the pharmacy, but she may never pick up that prescription. She likely leaves my office feeling unheard; her needs are unmet. I move onto the next patient. I feel good, but in actuality, I didn’t hear her. I have provided her bias and stereotyped care. I missed an opportunity to truly engage this patient and her care, and my good intentions of following the literature about her experience in menopause have contributed quite likely to her increased morbidity and mortality, her increased cardiovascular disease risk, all because I have not held space for her cultural identity.

References

1. Harlow SD, Burnett-Bowie SM, Greendale GA, et al. Disparities in reproductive aging and midlife health between Black and White women: the Study of Women’s Health Across the Nation (SWAN). Women’s Midlife Health. 2022;8:3. doi: 10.1186/s40695-022-00073-y.
2. Chlebowski RT, Aragaki AK, Anderson GL, et al. Forty-year trends in menopausal hormone therapy use and breast cancer incidence among postmenopausal black and white women. Cancer. 2020;126:2956-2964. doi: 10.1002/ cncr.32846.
3. Weng HH, McBride CM, Bosworth HB, et al. Racial differences in physician recommendation of hormone replacement therapy. Prev Med. 2001;33:668673. doi: 10.1006/pmed.2001.0943.
4. Williams M, Richard-Davis G, Williams PL, et al. A review of African American women’s experiences in menopause. Menopause. 2022;29:1331-1337. doi: 10.1097/GME.0000000000002060.
5. Im EO. Ethnic differences in symptoms experienced during the menopausal transition. Health Care Women Int. 2009;30:339-355. doi: 10.1080/07399330802695002.