Clinicians in Portugal say a 31-year-old man with confirmed monkeypox developed acute myocarditis roughly 1 week after the eruption of the characteristic skin lesions of the disease.

“This case highlights cardiac involvement as a potential complication associated with monkeypox infection,” Ana Isabel Pinho, MD, department of cardiology, São João University Hospital Centre, Porto, Portugal, said in a news release.

“We believe that reporting this potential causal relationship can raise more awareness of the scientific community and health professionals for acute myocarditis as a possible complication associated with monkeypox and might be helpful for close monitoring of affected patients for further recognition of other complications in the future,” Dr. Pinho adds.

Dr. Pinho and colleagues describe the case in a report published in JACC: Case Reports.
 

Case details

The patient presented with a 5-day history of malaise, myalgias, and fever followed by the eruption of multiple swollen skin lesions on his face, hands, and genitalia.

Monkeypox was confirmed by positive polymerase chain reaction assay of a swab sample from a skin lesion.

Three days later, the patient developed chest tightness that radiated through the left arm and which awoke him during the night. He was admitted to an intensive care unit with clinical suspicion of acute myocarditis.

The patient’s initial electrocardiogram showed sinus rhythm with nonspecific ventricular repolarization abnormalities.

On chest x-ray, the cardiothoracic index was normal, with no interstitial infiltrates, pleural effusion, or masses. On transthoracic echocardigraphy, biventricular systolic function was preserved, and there was no pericardial effusion.

Routine laboratory tests revealed elevated levels of C-reactive protein, creatine phosphokinase, high-sensitivity troponin I, and brain natriuretic peptide, suggesting stress injury to the heart.

Findings on cardiac magnetic resonance were consistent with myocardial inflammation and acute myocarditis.

The patient was treated with supportive care, and he made a full clinical recovery. He was discharged after 1 week. On discharge, cardiac enzymes were within the normal range. The patient showed sustained electric and hemodynamic stability, and the skin lesions had healed.

“Through this important case study, we are developing a deeper understanding of monkeypox, viral myocarditis, and how to accurately diagnose and manage this disease,” Julia Grapsa, MD, PhD, editor-in-chief of JACC: Case Reports, commented in the news release.

“I commend the authors on this valuable clinical case during a critical time as monkeypox continues to spread globally,” Dr. Grapsa added.

The researchers say further research is needed to identify the pathologic mechanism underlying monkeypox-associated cardiac injury.
 

By the numbers

According to the latest data, California has reported 3,629 cases, followed closely by New York with 3,367 cases, Florida with 1,957 cases, Texas with 1,698, Georgia with 1,418, and Illinois with 1,081. The other states have reported fewer than 600 cases.

The CDC says that globally, more than 52,000 monkeypox cases have been reported.

Monkeypox case counts appear to be slowing in the United States and globally.

Last week, the World Health Organization said the number of new cases worldwide declined by 21% between Aug. 15 and 21 after increasing for 4 straight weeks.

The research had no funding. Dr. Pinho and colleagues have disclosed no relevant financial relationships.

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

Clinicians in Portugal say a 31-year-old man with confirmed monkeypox developed acute myocarditis roughly 1 week after the eruption of the characteristic skin lesions of the disease.

“This case highlights cardiac involvement as a potential complication associated with monkeypox infection,” Ana Isabel Pinho, MD, department of cardiology, São João University Hospital Centre, Porto, Portugal, said in a news release.

“We believe that reporting this potential causal relationship can raise more awareness of the scientific community and health professionals for acute myocarditis as a possible complication associated with monkeypox and might be helpful for close monitoring of affected patients for further recognition of other complications in the future,” Dr. Pinho adds.

Dr. Pinho and colleagues describe the case in a report published in JACC: Case Reports.
 

Case details

The patient presented with a 5-day history of malaise, myalgias, and fever followed by the eruption of multiple swollen skin lesions on his face, hands, and genitalia.

Monkeypox was confirmed by positive polymerase chain reaction assay of a swab sample from a skin lesion.

Three days later, the patient developed chest tightness that radiated through the left arm and which awoke him during the night. He was admitted to an intensive care unit with clinical suspicion of acute myocarditis.

The patient’s initial electrocardiogram showed sinus rhythm with nonspecific ventricular repolarization abnormalities.

On chest x-ray, the cardiothoracic index was normal, with no interstitial infiltrates, pleural effusion, or masses. On transthoracic echocardigraphy, biventricular systolic function was preserved, and there was no pericardial effusion.

Routine laboratory tests revealed elevated levels of C-reactive protein, creatine phosphokinase, high-sensitivity troponin I, and brain natriuretic peptide, suggesting stress injury to the heart.

Findings on cardiac magnetic resonance were consistent with myocardial inflammation and acute myocarditis.

The patient was treated with supportive care, and he made a full clinical recovery. He was discharged after 1 week. On discharge, cardiac enzymes were within the normal range. The patient showed sustained electric and hemodynamic stability, and the skin lesions had healed.

“Through this important case study, we are developing a deeper understanding of monkeypox, viral myocarditis, and how to accurately diagnose and manage this disease,” Julia Grapsa, MD, PhD, editor-in-chief of JACC: Case Reports, commented in the news release.

“I commend the authors on this valuable clinical case during a critical time as monkeypox continues to spread globally,” Dr. Grapsa added.

The researchers say further research is needed to identify the pathologic mechanism underlying monkeypox-associated cardiac injury.
 

By the numbers

According to the latest data, California has reported 3,629 cases, followed closely by New York with 3,367 cases, Florida with 1,957 cases, Texas with 1,698, Georgia with 1,418, and Illinois with 1,081. The other states have reported fewer than 600 cases.

The CDC says that globally, more than 52,000 monkeypox cases have been reported.

Monkeypox case counts appear to be slowing in the United States and globally.

Last week, the World Health Organization said the number of new cases worldwide declined by 21% between Aug. 15 and 21 after increasing for 4 straight weeks.

The research had no funding. Dr. Pinho and colleagues have disclosed no relevant financial relationships.

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

Clinicians in Portugal say a 31-year-old man with confirmed monkeypox developed acute myocarditis roughly 1 week after the eruption of the characteristic skin lesions of the disease.

“This case highlights cardiac involvement as a potential complication associated with monkeypox infection,” Ana Isabel Pinho, MD, department of cardiology, São João University Hospital Centre, Porto, Portugal, said in a news release.

“We believe that reporting this potential causal relationship can raise more awareness of the scientific community and health professionals for acute myocarditis as a possible complication associated with monkeypox and might be helpful for close monitoring of affected patients for further recognition of other complications in the future,” Dr. Pinho adds.

Dr. Pinho and colleagues describe the case in a report published in JACC: Case Reports.
 

Case details

The patient presented with a 5-day history of malaise, myalgias, and fever followed by the eruption of multiple swollen skin lesions on his face, hands, and genitalia.

Monkeypox was confirmed by positive polymerase chain reaction assay of a swab sample from a skin lesion.

Three days later, the patient developed chest tightness that radiated through the left arm and which awoke him during the night. He was admitted to an intensive care unit with clinical suspicion of acute myocarditis.

The patient’s initial electrocardiogram showed sinus rhythm with nonspecific ventricular repolarization abnormalities.

On chest x-ray, the cardiothoracic index was normal, with no interstitial infiltrates, pleural effusion, or masses. On transthoracic echocardigraphy, biventricular systolic function was preserved, and there was no pericardial effusion.

Routine laboratory tests revealed elevated levels of C-reactive protein, creatine phosphokinase, high-sensitivity troponin I, and brain natriuretic peptide, suggesting stress injury to the heart.

Findings on cardiac magnetic resonance were consistent with myocardial inflammation and acute myocarditis.

The patient was treated with supportive care, and he made a full clinical recovery. He was discharged after 1 week. On discharge, cardiac enzymes were within the normal range. The patient showed sustained electric and hemodynamic stability, and the skin lesions had healed.

“Through this important case study, we are developing a deeper understanding of monkeypox, viral myocarditis, and how to accurately diagnose and manage this disease,” Julia Grapsa, MD, PhD, editor-in-chief of JACC: Case Reports, commented in the news release.

“I commend the authors on this valuable clinical case during a critical time as monkeypox continues to spread globally,” Dr. Grapsa added.

The researchers say further research is needed to identify the pathologic mechanism underlying monkeypox-associated cardiac injury.
 

By the numbers

According to the latest data, California has reported 3,629 cases, followed closely by New York with 3,367 cases, Florida with 1,957 cases, Texas with 1,698, Georgia with 1,418, and Illinois with 1,081. The other states have reported fewer than 600 cases.

The CDC says that globally, more than 52,000 monkeypox cases have been reported.

Monkeypox case counts appear to be slowing in the United States and globally.

Last week, the World Health Organization said the number of new cases worldwide declined by 21% between Aug. 15 and 21 after increasing for 4 straight weeks.

The research had no funding. Dr. Pinho and colleagues have disclosed no relevant financial relationships.

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

The Diagnosis: Chemical Leukoderma

A clinical diagnosis of chemical leukoderma was made. In our patient, the observed linear hypopigmentation likely resulted from the prior treatment for De Quervain tenosynovitis in which an intralesional corticosteroid entered the lymphatic channel causing a linear distribution of chemical leukoderma. The hypopigmentation self-resolved at 6-month follow-up, and the patient was counseled to continue steroid injections if indicated.

Chemical leukoderma is an acquired depigmenting dermatosis that displays vitiligolike patterning. Detailed personal and family history in addition to complete physical examination are crucial given the inability to distinguish chemical leukoderma from vitiligo on histopathology. A set of clinical criteria proposed by Ghosh and Mukhopadhyay¹ includes the presence of acquired depigmented macules and patches resembling vitiligo, history of repeat exposure to certain chemical substances, hypopigmentation at the site of exposure, and/ or confettilike white macules. Three of these 4 clinical findings must be present to establish a diagnosis of chemical leukoderma. The extent of disease involvement may be graded as follows: Stage I is defined as leukoderma only at the site of contact to the offending agent. Stage II involvement is characterized by local spread beyond the exposure site via the lymphatic system. Stages IIIA and IIIB leukoderma entail hematogenous spread distant to the site of chemical exposure. Although stage IIIA leukoderma is limited to cutaneous involvement, stage IIIB findings are marked by systemic organ involvement. Stage IV disease is defined by the distant spread of hypopigmented macules and patches that continues following 1 year of strict avoidance of the causative agent.¹

The pathogenesis behind chemical leukoderma is not completely understood. Studies have suggested that individuals with certain genetic susceptibilities are predisposed to developing the condition after being exposed to chemicals with melanocytotoxic properties.^2,3 It has been proposed that the chemicals accelerate pre-existing cellular stress cascades within melanocytes to levels higher than what healthy cells can tolerate. Genetic factors can increase an individual’s total melanocytic stress or establish a lower cellular threshold for stress than what the immune system can manage.⁴ These influences culminate in an inflammatory response that results in melanocytic destruction and subsequent cutaneous hypopigmentation.

The most well-known offending chemical agents are phenol and catechol derivatives, such as hydroquinone, which is used in topical bleaching agents to treat diseases of hyperpigmentation, including melasma.² Potent topical or intralesional corticosteroids also may precipitate chemical leukoderma, most notably in individuals with darker skin tones. Hypomelanosis induced by intralesional steroids frequently occurs weeks to months after administration and commonly is observed in a stellate or linear pattern with an irregular outline.⁵ Other offending chemical agents include sulfhydryls, mercurials, arsenic, benzoyl peroxide, azelaic acid, imiquimod, chloroquine, and tyrosine kinase inhibitors.^2,5

Segmental vitiligo is characterized by unilateral hypopigmentation in a linear or blocklike distribution that does not cross the midline. However, onset of segmental vitiligo classically occurs prior to 30 years of age and frequently is related with early leukotrichia.⁶ Additionally, the hypomelanosis associated with segmental vitiligo more often presents as broad bands or patches that occasionally have a blaschkoid distribution and most commonly appear on the face.⁵ Lichen striatus is a lichenoid dermatosis that presents as asymptomatic pink or hypopigmented papules that follow the Blaschko lines, often favoring the extremities. Postinflammatory hypopigmentation also may occur as an associated sequela of resolved lichen striatus. Although the disease onset of lichen striatus may occur in adulthood, it typically appears in childhood and is triggered by factors such as trauma, hypersensitivity reactions, viral infections, and medications. Physical injuries such as trauma following surgical procedures also can lead to hypomelanosis; however, our patient denied any relevant surgical history. Progressive macular hypomelanosis is a skin condition presenting as ill-defined, nummular, hypopigmented macules or patches that commonly affects women with darker skin tones with an ethnic background from a tropical location or residing in a tropical environment.⁵ Lesions frequently appear on the trunk and rarely progress to the proximal extremities, making it an unlikely diagnosis for our patient.

In most cases of chemical leukoderma, spontaneous repigmentation often occurs within 12 months after the elimination of the offending substance; however, hypopigmented lesions may persist or continue to develop at sites distant from the initial site despite discontinuing the causative agent.1 Therapies for vitiligo, such as topical corticosteroids, topical immunosuppressants, narrowband UVB phototherapy, and psoralen plus UVA photochemotherapy, may be utilized for chemical leukoderma that does not self-resolve.

The Diagnosis: Chemical Leukoderma

A clinical diagnosis of chemical leukoderma was made. In our patient, the observed linear hypopigmentation likely resulted from the prior treatment for De Quervain tenosynovitis in which an intralesional corticosteroid entered the lymphatic channel causing a linear distribution of chemical leukoderma. The hypopigmentation self-resolved at 6-month follow-up, and the patient was counseled to continue steroid injections if indicated.

Chemical leukoderma is an acquired depigmenting dermatosis that displays vitiligolike patterning. Detailed personal and family history in addition to complete physical examination are crucial given the inability to distinguish chemical leukoderma from vitiligo on histopathology. A set of clinical criteria proposed by Ghosh and Mukhopadhyay¹ includes the presence of acquired depigmented macules and patches resembling vitiligo, history of repeat exposure to certain chemical substances, hypopigmentation at the site of exposure, and/ or confettilike white macules. Three of these 4 clinical findings must be present to establish a diagnosis of chemical leukoderma. The extent of disease involvement may be graded as follows: Stage I is defined as leukoderma only at the site of contact to the offending agent. Stage II involvement is characterized by local spread beyond the exposure site via the lymphatic system. Stages IIIA and IIIB leukoderma entail hematogenous spread distant to the site of chemical exposure. Although stage IIIA leukoderma is limited to cutaneous involvement, stage IIIB findings are marked by systemic organ involvement. Stage IV disease is defined by the distant spread of hypopigmented macules and patches that continues following 1 year of strict avoidance of the causative agent.¹

The pathogenesis behind chemical leukoderma is not completely understood. Studies have suggested that individuals with certain genetic susceptibilities are predisposed to developing the condition after being exposed to chemicals with melanocytotoxic properties.^2,3 It has been proposed that the chemicals accelerate pre-existing cellular stress cascades within melanocytes to levels higher than what healthy cells can tolerate. Genetic factors can increase an individual’s total melanocytic stress or establish a lower cellular threshold for stress than what the immune system can manage.⁴ These influences culminate in an inflammatory response that results in melanocytic destruction and subsequent cutaneous hypopigmentation.

The most well-known offending chemical agents are phenol and catechol derivatives, such as hydroquinone, which is used in topical bleaching agents to treat diseases of hyperpigmentation, including melasma.² Potent topical or intralesional corticosteroids also may precipitate chemical leukoderma, most notably in individuals with darker skin tones. Hypomelanosis induced by intralesional steroids frequently occurs weeks to months after administration and commonly is observed in a stellate or linear pattern with an irregular outline.⁵ Other offending chemical agents include sulfhydryls, mercurials, arsenic, benzoyl peroxide, azelaic acid, imiquimod, chloroquine, and tyrosine kinase inhibitors.^2,5

Segmental vitiligo is characterized by unilateral hypopigmentation in a linear or blocklike distribution that does not cross the midline. However, onset of segmental vitiligo classically occurs prior to 30 years of age and frequently is related with early leukotrichia.⁶ Additionally, the hypomelanosis associated with segmental vitiligo more often presents as broad bands or patches that occasionally have a blaschkoid distribution and most commonly appear on the face.⁵ Lichen striatus is a lichenoid dermatosis that presents as asymptomatic pink or hypopigmented papules that follow the Blaschko lines, often favoring the extremities. Postinflammatory hypopigmentation also may occur as an associated sequela of resolved lichen striatus. Although the disease onset of lichen striatus may occur in adulthood, it typically appears in childhood and is triggered by factors such as trauma, hypersensitivity reactions, viral infections, and medications. Physical injuries such as trauma following surgical procedures also can lead to hypomelanosis; however, our patient denied any relevant surgical history. Progressive macular hypomelanosis is a skin condition presenting as ill-defined, nummular, hypopigmented macules or patches that commonly affects women with darker skin tones with an ethnic background from a tropical location or residing in a tropical environment.⁵ Lesions frequently appear on the trunk and rarely progress to the proximal extremities, making it an unlikely diagnosis for our patient.

In most cases of chemical leukoderma, spontaneous repigmentation often occurs within 12 months after the elimination of the offending substance; however, hypopigmented lesions may persist or continue to develop at sites distant from the initial site despite discontinuing the causative agent.1 Therapies for vitiligo, such as topical corticosteroids, topical immunosuppressants, narrowband UVB phototherapy, and psoralen plus UVA photochemotherapy, may be utilized for chemical leukoderma that does not self-resolve.

The Diagnosis: Chemical Leukoderma

A clinical diagnosis of chemical leukoderma was made. In our patient, the observed linear hypopigmentation likely resulted from the prior treatment for De Quervain tenosynovitis in which an intralesional corticosteroid entered the lymphatic channel causing a linear distribution of chemical leukoderma. The hypopigmentation self-resolved at 6-month follow-up, and the patient was counseled to continue steroid injections if indicated.

Chemical leukoderma is an acquired depigmenting dermatosis that displays vitiligolike patterning. Detailed personal and family history in addition to complete physical examination are crucial given the inability to distinguish chemical leukoderma from vitiligo on histopathology. A set of clinical criteria proposed by Ghosh and Mukhopadhyay¹ includes the presence of acquired depigmented macules and patches resembling vitiligo, history of repeat exposure to certain chemical substances, hypopigmentation at the site of exposure, and/ or confettilike white macules. Three of these 4 clinical findings must be present to establish a diagnosis of chemical leukoderma. The extent of disease involvement may be graded as follows: Stage I is defined as leukoderma only at the site of contact to the offending agent. Stage II involvement is characterized by local spread beyond the exposure site via the lymphatic system. Stages IIIA and IIIB leukoderma entail hematogenous spread distant to the site of chemical exposure. Although stage IIIA leukoderma is limited to cutaneous involvement, stage IIIB findings are marked by systemic organ involvement. Stage IV disease is defined by the distant spread of hypopigmented macules and patches that continues following 1 year of strict avoidance of the causative agent.¹

The pathogenesis behind chemical leukoderma is not completely understood. Studies have suggested that individuals with certain genetic susceptibilities are predisposed to developing the condition after being exposed to chemicals with melanocytotoxic properties.^2,3 It has been proposed that the chemicals accelerate pre-existing cellular stress cascades within melanocytes to levels higher than what healthy cells can tolerate. Genetic factors can increase an individual’s total melanocytic stress or establish a lower cellular threshold for stress than what the immune system can manage.⁴ These influences culminate in an inflammatory response that results in melanocytic destruction and subsequent cutaneous hypopigmentation.

The most well-known offending chemical agents are phenol and catechol derivatives, such as hydroquinone, which is used in topical bleaching agents to treat diseases of hyperpigmentation, including melasma.² Potent topical or intralesional corticosteroids also may precipitate chemical leukoderma, most notably in individuals with darker skin tones. Hypomelanosis induced by intralesional steroids frequently occurs weeks to months after administration and commonly is observed in a stellate or linear pattern with an irregular outline.⁵ Other offending chemical agents include sulfhydryls, mercurials, arsenic, benzoyl peroxide, azelaic acid, imiquimod, chloroquine, and tyrosine kinase inhibitors.^2,5

Segmental vitiligo is characterized by unilateral hypopigmentation in a linear or blocklike distribution that does not cross the midline. However, onset of segmental vitiligo classically occurs prior to 30 years of age and frequently is related with early leukotrichia.⁶ Additionally, the hypomelanosis associated with segmental vitiligo more often presents as broad bands or patches that occasionally have a blaschkoid distribution and most commonly appear on the face.⁵ Lichen striatus is a lichenoid dermatosis that presents as asymptomatic pink or hypopigmented papules that follow the Blaschko lines, often favoring the extremities. Postinflammatory hypopigmentation also may occur as an associated sequela of resolved lichen striatus. Although the disease onset of lichen striatus may occur in adulthood, it typically appears in childhood and is triggered by factors such as trauma, hypersensitivity reactions, viral infections, and medications. Physical injuries such as trauma following surgical procedures also can lead to hypomelanosis; however, our patient denied any relevant surgical history. Progressive macular hypomelanosis is a skin condition presenting as ill-defined, nummular, hypopigmented macules or patches that commonly affects women with darker skin tones with an ethnic background from a tropical location or residing in a tropical environment.⁵ Lesions frequently appear on the trunk and rarely progress to the proximal extremities, making it an unlikely diagnosis for our patient.

In most cases of chemical leukoderma, spontaneous repigmentation often occurs within 12 months after the elimination of the offending substance; however, hypopigmented lesions may persist or continue to develop at sites distant from the initial site despite discontinuing the causative agent.1 Therapies for vitiligo, such as topical corticosteroids, topical immunosuppressants, narrowband UVB phototherapy, and psoralen plus UVA photochemotherapy, may be utilized for chemical leukoderma that does not self-resolve.

If you want your skin to show fewer signs of aging, like wrinkles, then you’d do well to put down the cell phone, a new study conducted in fruit flies suggests.

Blue light from screens on smartphones, computers, and other gadgets “may have detrimental effects on a wide range of cells in our body, from skin and fat cells to sensory neurons,” Oregon State University scientist Jadwiga Giebultowicz, PhD, said of the study, which was published in the journal Frontiers in Aging.

“Our study suggests that avoidance of excessive blue light exposure may be a good anti-aging strategy,” Dr. Giebultowicz added.

Ultraviolet rays from the sun harm skin appearance and health. Doctors are continuing to study the damage caused by the screens of devices that most people are exposed to throughout the day. These devices emit blue light.

“Aging occurs in various ways, but on a cellular level, we age when cells stop repairing and producing new healthy cells. And cells that aren’t functioning properly are more likely to self destruct – which has ramifications not only in terms of appearance but for the whole body,” the New York Post wrote. “It’s the reason why the elderly take longer to heal, and their bones and organs begin to deteriorate.”

Dr. Giebultowicz said the study shows that certain substances in the body, called metabolites, are essential indicators of how a cell functions. These metabolites are naturally occurring as the body converts food and drinks into energy. Research indicates that these substances are altered by blue light exposure.

More specifically, researchers found that levels of succinate, or succinic acid, in fruit flies increased under excessive blue light, while glutamate decreased, the newspaper wrote.

Researchers said the insects “make an appropriate analog for humans” because the same signaling devices are shared.

The flies were exposed with more blue light than people usually get. Dr. Giebultowicz said future research is needed on human cells.

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

If you want your skin to show fewer signs of aging, like wrinkles, then you’d do well to put down the cell phone, a new study conducted in fruit flies suggests.

Blue light from screens on smartphones, computers, and other gadgets “may have detrimental effects on a wide range of cells in our body, from skin and fat cells to sensory neurons,” Oregon State University scientist Jadwiga Giebultowicz, PhD, said of the study, which was published in the journal Frontiers in Aging.

“Our study suggests that avoidance of excessive blue light exposure may be a good anti-aging strategy,” Dr. Giebultowicz added.

Ultraviolet rays from the sun harm skin appearance and health. Doctors are continuing to study the damage caused by the screens of devices that most people are exposed to throughout the day. These devices emit blue light.

“Aging occurs in various ways, but on a cellular level, we age when cells stop repairing and producing new healthy cells. And cells that aren’t functioning properly are more likely to self destruct – which has ramifications not only in terms of appearance but for the whole body,” the New York Post wrote. “It’s the reason why the elderly take longer to heal, and their bones and organs begin to deteriorate.”

Dr. Giebultowicz said the study shows that certain substances in the body, called metabolites, are essential indicators of how a cell functions. These metabolites are naturally occurring as the body converts food and drinks into energy. Research indicates that these substances are altered by blue light exposure.

More specifically, researchers found that levels of succinate, or succinic acid, in fruit flies increased under excessive blue light, while glutamate decreased, the newspaper wrote.

Researchers said the insects “make an appropriate analog for humans” because the same signaling devices are shared.

The flies were exposed with more blue light than people usually get. Dr. Giebultowicz said future research is needed on human cells.

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

If you want your skin to show fewer signs of aging, like wrinkles, then you’d do well to put down the cell phone, a new study conducted in fruit flies suggests.

Blue light from screens on smartphones, computers, and other gadgets “may have detrimental effects on a wide range of cells in our body, from skin and fat cells to sensory neurons,” Oregon State University scientist Jadwiga Giebultowicz, PhD, said of the study, which was published in the journal Frontiers in Aging.

“Our study suggests that avoidance of excessive blue light exposure may be a good anti-aging strategy,” Dr. Giebultowicz added.

Ultraviolet rays from the sun harm skin appearance and health. Doctors are continuing to study the damage caused by the screens of devices that most people are exposed to throughout the day. These devices emit blue light.

“Aging occurs in various ways, but on a cellular level, we age when cells stop repairing and producing new healthy cells. And cells that aren’t functioning properly are more likely to self destruct – which has ramifications not only in terms of appearance but for the whole body,” the New York Post wrote. “It’s the reason why the elderly take longer to heal, and their bones and organs begin to deteriorate.”

Dr. Giebultowicz said the study shows that certain substances in the body, called metabolites, are essential indicators of how a cell functions. These metabolites are naturally occurring as the body converts food and drinks into energy. Research indicates that these substances are altered by blue light exposure.

More specifically, researchers found that levels of succinate, or succinic acid, in fruit flies increased under excessive blue light, while glutamate decreased, the newspaper wrote.

Researchers said the insects “make an appropriate analog for humans” because the same signaling devices are shared.

The flies were exposed with more blue light than people usually get. Dr. Giebultowicz said future research is needed on human cells.

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

Reduced physical function is an independent risk factor for composite and individual cardiovascular events, including coronary heart disease (CHD), stroke, and heart failure (HF) in older adults, according to new observational data from the Atherosclerosis Risk in Communities (ARIC) study.

“We found that physical function in older adults predicts future cardiovascular disease (CVD) beyond traditional heart disease risk factors, regardless of whether an individual has a history of cardiovascular disease,” senior author Kunihiro Matsushita, MD, PhD, division of cardiology, Johns Hopkins University, Baltimore, said in a news release.

The study was published online in the Journal of the American Heart Association.
 

Keeping fit with age

The researchers analyzed health data collected between 2011 and 2013 for 5,570 ARIC participants (mean age, 75 years; 58% women, 22% Black persons). They assessed physical function using the Short Physical Performance Battery (SPPB), which measures walking speed, leg strength, and balance.

On the basis of the results, participants were categorized into three physical function groups: low (score, 0-6; 13% of the cohort), intermediate (score, 7-9; 30%) and high (score, 10-12; 57%).

During a median follow up of 7 years, there were 930 composite CVD events (386 CHD, 251 stroke, and 529 HF).

Adults with lower SPPB scores had a higher cumulative incidence of composite CVD outcomes.

The 5-year cumulative incidence of the composite CVD outcome in the low- and intermediate-SPPB categories was about three times (23.4%) and two times (15.3%) higher than in the high-SPPB category (8.6%), the researchers reported.

In addition, continuous SPPB scores showed significant associations with composite and individual CVD outcomes in all models. A 1-point lower SPPB score was associated with 6%-10% higher risk for CVD events after adjusting for potential confounders.

In the fully adjusted model, the risk for composite CVD outcomes was 47% higher (hazard ratio, 1.47; 95% confidence interval, 1.20-1.79) in those with low physical function and 25% higher in those with intermediate physical function (HR, 1.25; 95% CI, 1.07-1.46) compared with peers with high physical function.

For the individual outcomes, low physical function was associated with higher risk for stroke (HR, 1.81; 95% CI, 1.24-2.64) and HF (HR, 1.33; 95% CI, 1.02-1.73), whereas the association for CHD was not significant.

The associations were largely consistent across subgroups, including those with CVD at baseline.

The addition of SPPB scores significantly improved risk prediction of CVD events beyond traditional CVD risk factors in adults regardless of prior CVD history, suggesting that this tool may be useful for classifying CVD risk in older adults, the researchers said.
 

Meaningful impact on care?

“Our findings highlight the value of assessing the physical function level of older adults in clinical practice,” lead author Xiao Hu, MHS, with the department of epidemiology at Johns Hopkins, said in the news release. “In addition to heart health, older adults are at higher risk for falls and disability. The assessment of physical function may also inform the risk of these concerning conditions in older adults.”

Weighing in on the study, Jonathan Halperin, MD, cardiologist at Mount Sinai Heart and professor of medicine (cardiology) at the Icahn School of Medicine at Mount Sinai, both in New York, said that “It’s known that cardiorespiratory fitness is an important predictor of cardiovascular risk, but it is one of the few physiological risk factors that are subjectively queried but not objectively assessed in routine clinical practice.”

In this study, Dr. Halperin noted, the investigators found that a battery of physical performance assessments, including a walk test, chair standing, and balance testing, improved cardiovascular risk prediction.

Dr. Halperin cautioned, however, that “since even the short sequence of tests takes time to perform and interpret, and is not currently reimbursed under most health insurance policies, it is not clear whether the report will have a meaningful impact on patient care.”

This research was funded by the National Institutes of Health. Dr. Matsushita and Dr. Halperin have no relevant disclosures.

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

Reduced physical function is an independent risk factor for composite and individual cardiovascular events, including coronary heart disease (CHD), stroke, and heart failure (HF) in older adults, according to new observational data from the Atherosclerosis Risk in Communities (ARIC) study.

“We found that physical function in older adults predicts future cardiovascular disease (CVD) beyond traditional heart disease risk factors, regardless of whether an individual has a history of cardiovascular disease,” senior author Kunihiro Matsushita, MD, PhD, division of cardiology, Johns Hopkins University, Baltimore, said in a news release.

The study was published online in the Journal of the American Heart Association.
 

Keeping fit with age

The researchers analyzed health data collected between 2011 and 2013 for 5,570 ARIC participants (mean age, 75 years; 58% women, 22% Black persons). They assessed physical function using the Short Physical Performance Battery (SPPB), which measures walking speed, leg strength, and balance.

On the basis of the results, participants were categorized into three physical function groups: low (score, 0-6; 13% of the cohort), intermediate (score, 7-9; 30%) and high (score, 10-12; 57%).

During a median follow up of 7 years, there were 930 composite CVD events (386 CHD, 251 stroke, and 529 HF).

Adults with lower SPPB scores had a higher cumulative incidence of composite CVD outcomes.

The 5-year cumulative incidence of the composite CVD outcome in the low- and intermediate-SPPB categories was about three times (23.4%) and two times (15.3%) higher than in the high-SPPB category (8.6%), the researchers reported.

In addition, continuous SPPB scores showed significant associations with composite and individual CVD outcomes in all models. A 1-point lower SPPB score was associated with 6%-10% higher risk for CVD events after adjusting for potential confounders.

In the fully adjusted model, the risk for composite CVD outcomes was 47% higher (hazard ratio, 1.47; 95% confidence interval, 1.20-1.79) in those with low physical function and 25% higher in those with intermediate physical function (HR, 1.25; 95% CI, 1.07-1.46) compared with peers with high physical function.

For the individual outcomes, low physical function was associated with higher risk for stroke (HR, 1.81; 95% CI, 1.24-2.64) and HF (HR, 1.33; 95% CI, 1.02-1.73), whereas the association for CHD was not significant.

The associations were largely consistent across subgroups, including those with CVD at baseline.

The addition of SPPB scores significantly improved risk prediction of CVD events beyond traditional CVD risk factors in adults regardless of prior CVD history, suggesting that this tool may be useful for classifying CVD risk in older adults, the researchers said.
 

Meaningful impact on care?

“Our findings highlight the value of assessing the physical function level of older adults in clinical practice,” lead author Xiao Hu, MHS, with the department of epidemiology at Johns Hopkins, said in the news release. “In addition to heart health, older adults are at higher risk for falls and disability. The assessment of physical function may also inform the risk of these concerning conditions in older adults.”

Weighing in on the study, Jonathan Halperin, MD, cardiologist at Mount Sinai Heart and professor of medicine (cardiology) at the Icahn School of Medicine at Mount Sinai, both in New York, said that “It’s known that cardiorespiratory fitness is an important predictor of cardiovascular risk, but it is one of the few physiological risk factors that are subjectively queried but not objectively assessed in routine clinical practice.”

In this study, Dr. Halperin noted, the investigators found that a battery of physical performance assessments, including a walk test, chair standing, and balance testing, improved cardiovascular risk prediction.

Dr. Halperin cautioned, however, that “since even the short sequence of tests takes time to perform and interpret, and is not currently reimbursed under most health insurance policies, it is not clear whether the report will have a meaningful impact on patient care.”

This research was funded by the National Institutes of Health. Dr. Matsushita and Dr. Halperin have no relevant disclosures.

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

Reduced physical function is an independent risk factor for composite and individual cardiovascular events, including coronary heart disease (CHD), stroke, and heart failure (HF) in older adults, according to new observational data from the Atherosclerosis Risk in Communities (ARIC) study.

“We found that physical function in older adults predicts future cardiovascular disease (CVD) beyond traditional heart disease risk factors, regardless of whether an individual has a history of cardiovascular disease,” senior author Kunihiro Matsushita, MD, PhD, division of cardiology, Johns Hopkins University, Baltimore, said in a news release.

The study was published online in the Journal of the American Heart Association.
 

Keeping fit with age

The researchers analyzed health data collected between 2011 and 2013 for 5,570 ARIC participants (mean age, 75 years; 58% women, 22% Black persons). They assessed physical function using the Short Physical Performance Battery (SPPB), which measures walking speed, leg strength, and balance.

On the basis of the results, participants were categorized into three physical function groups: low (score, 0-6; 13% of the cohort), intermediate (score, 7-9; 30%) and high (score, 10-12; 57%).

During a median follow up of 7 years, there were 930 composite CVD events (386 CHD, 251 stroke, and 529 HF).

Adults with lower SPPB scores had a higher cumulative incidence of composite CVD outcomes.

The 5-year cumulative incidence of the composite CVD outcome in the low- and intermediate-SPPB categories was about three times (23.4%) and two times (15.3%) higher than in the high-SPPB category (8.6%), the researchers reported.

In addition, continuous SPPB scores showed significant associations with composite and individual CVD outcomes in all models. A 1-point lower SPPB score was associated with 6%-10% higher risk for CVD events after adjusting for potential confounders.

In the fully adjusted model, the risk for composite CVD outcomes was 47% higher (hazard ratio, 1.47; 95% confidence interval, 1.20-1.79) in those with low physical function and 25% higher in those with intermediate physical function (HR, 1.25; 95% CI, 1.07-1.46) compared with peers with high physical function.

For the individual outcomes, low physical function was associated with higher risk for stroke (HR, 1.81; 95% CI, 1.24-2.64) and HF (HR, 1.33; 95% CI, 1.02-1.73), whereas the association for CHD was not significant.

The associations were largely consistent across subgroups, including those with CVD at baseline.

The addition of SPPB scores significantly improved risk prediction of CVD events beyond traditional CVD risk factors in adults regardless of prior CVD history, suggesting that this tool may be useful for classifying CVD risk in older adults, the researchers said.
 

Meaningful impact on care?

“Our findings highlight the value of assessing the physical function level of older adults in clinical practice,” lead author Xiao Hu, MHS, with the department of epidemiology at Johns Hopkins, said in the news release. “In addition to heart health, older adults are at higher risk for falls and disability. The assessment of physical function may also inform the risk of these concerning conditions in older adults.”

Weighing in on the study, Jonathan Halperin, MD, cardiologist at Mount Sinai Heart and professor of medicine (cardiology) at the Icahn School of Medicine at Mount Sinai, both in New York, said that “It’s known that cardiorespiratory fitness is an important predictor of cardiovascular risk, but it is one of the few physiological risk factors that are subjectively queried but not objectively assessed in routine clinical practice.”

In this study, Dr. Halperin noted, the investigators found that a battery of physical performance assessments, including a walk test, chair standing, and balance testing, improved cardiovascular risk prediction.

Dr. Halperin cautioned, however, that “since even the short sequence of tests takes time to perform and interpret, and is not currently reimbursed under most health insurance policies, it is not clear whether the report will have a meaningful impact on patient care.”

This research was funded by the National Institutes of Health. Dr. Matsushita and Dr. Halperin have no relevant disclosures.

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

Robots can be better at detecting mental well-being issues in children than parent-reported or self-reported testing, say U.K. researchers.

The researchers behind a new study, presented at the 31st IEEE International Conference on Robot & Human Interactive Communication (RO-MAN) in Naples, Italy, have suggested that robots could be a useful addition to traditional methods of mental health assessment.

“There are times when traditional methods aren’t able to catch mental well-being lapses in children, as sometimes the changes are incredibly subtle,” said Nida Itrat Abbasi, a PhD student at Cambridge (England) Affective Computing and Robotics Group, University of Cambridge, and the study’s first author. “We wanted to see whether robots might be able to help with this process,” she explained.

The authors highlighted how, during the COVID-19 pandemic, home schooling, financial pressures, and isolation from peers and friends impacted the mental health of many children. Even before the pandemic however, anxiety and depression among children in the United Kingdom has been on the rise, but the resources and support to address mental well-being are severely limited.
 

Children engage with robots

For their study the research team – which comprised roboticists, computer scientists, and psychiatrists from the University of Cambridge – enrolled 28 participants between ages 8 and 13 years. While being observed from an adjacent room by a parent or guardian, along with members of the research team, the participants  took part in a one-to-one 45-minute session with a Nao robot – a humanoid robot about 60 cm tall – that administered a series of standard psychological questionnaires to assess the mental well-being of each participant.

Participants interacted with the robot throughout the session by speaking with it or by touching sensors on the robot’s hands and feet. Additional sensors tracked participants’ heartbeat, head, and eye movements during the session.

Professor Hatice Gunes, affective intelligence and robotics laboratory, department of computer science, University of Cambridge, said: “Children are quite tactile, and they’re drawn to technology. If they’re using a screen-based tool, they’re withdrawn from the physical world,” she said. “But robots are perfect because they’re in the physical world – they’re more interactive, so the children are more engaged.”

Prior to each session the children and their parent or guardian completed standard online questionnaires to assess each child’s mental well-being.

During each session, the robot performed four different tasks:

• Asked open-ended questions about happy and sad memories over the last week.
• Administered the Short Mood and Feelings Questionnaire (SMFQ).
• Administered a picture task inspired by the Children’s Apperception Test (CAT), where children are asked to answer questions related to pictures shown.
• Administered the Revised Children’s Anxiety and Depression Scale (RCADS) for generalized anxiety, panic disorder, and low mood.

Following the SMFQ children were divided into three different groups according to how likely they were to be struggling with their mental well-being.

The researchers found that children with varying levels of well-being concerns interacted differently with the robot. For children that might not be experiencing mental well-being–related problems, the researchers found that interacting with the robot led to more positive response ratings to the questionnaires. However, for children that might be experiencing well-being–related concerns, the robot may have enabled them to divulge their true feelings and experiences, leading to more negative response ratings to the questionnaire.
 

Robots an addition not a replacement

“Since the robot we use is child-sized, and completely nonthreatening, children might see the robot as a confidant – they feel like they won’t get into trouble if they share secrets with it,” said Ms. Abbasi. “Other researchers have found that children are more likely to divulge private information – like that they’re being bullied, for example – to a robot than they would be to an adult,” she said.

Study participants all said they “enjoyed talking with the robot,” commented the authors, who added that, “the children were willing to confide in the robot, in some cases sharing information with the robot that they had not yet shared via the standard assessment method of online or in-person questionnaires.”

This is the first time that robots have been used to assess mental well-being in children, the researchers pointed out. “Robots could be a useful addition to traditional methods of mental health assessment,” they said, though they emphasized that robots are “not intended to be a substitute for professional mental health support.”

“We don’t have any intention of replacing psychologists or other mental health professionals with robots, since their expertise far surpasses anything a robot can do,” said Dr. Micol Spitale, affective computing and robotics laboratory, University of Cambridge, and study coauthor. “However, our work suggests that robots could be a useful tool in helping children to open up and share things they might not be comfortable sharing at first.”

The researchers say that they hope to expand their survey in future by including more participants and following them over time. They are also investigating whether similar results could be achieved if children interact with the robot via video chat.

A version of this article first appeared on Medscape UK.

Robots can be better at detecting mental well-being issues in children than parent-reported or self-reported testing, say U.K. researchers.

The researchers behind a new study, presented at the 31st IEEE International Conference on Robot & Human Interactive Communication (RO-MAN) in Naples, Italy, have suggested that robots could be a useful addition to traditional methods of mental health assessment.

“There are times when traditional methods aren’t able to catch mental well-being lapses in children, as sometimes the changes are incredibly subtle,” said Nida Itrat Abbasi, a PhD student at Cambridge (England) Affective Computing and Robotics Group, University of Cambridge, and the study’s first author. “We wanted to see whether robots might be able to help with this process,” she explained.

The authors highlighted how, during the COVID-19 pandemic, home schooling, financial pressures, and isolation from peers and friends impacted the mental health of many children. Even before the pandemic however, anxiety and depression among children in the United Kingdom has been on the rise, but the resources and support to address mental well-being are severely limited.
 

Children engage with robots

For their study the research team – which comprised roboticists, computer scientists, and psychiatrists from the University of Cambridge – enrolled 28 participants between ages 8 and 13 years. While being observed from an adjacent room by a parent or guardian, along with members of the research team, the participants  took part in a one-to-one 45-minute session with a Nao robot – a humanoid robot about 60 cm tall – that administered a series of standard psychological questionnaires to assess the mental well-being of each participant.

Participants interacted with the robot throughout the session by speaking with it or by touching sensors on the robot’s hands and feet. Additional sensors tracked participants’ heartbeat, head, and eye movements during the session.

Professor Hatice Gunes, affective intelligence and robotics laboratory, department of computer science, University of Cambridge, said: “Children are quite tactile, and they’re drawn to technology. If they’re using a screen-based tool, they’re withdrawn from the physical world,” she said. “But robots are perfect because they’re in the physical world – they’re more interactive, so the children are more engaged.”

Prior to each session the children and their parent or guardian completed standard online questionnaires to assess each child’s mental well-being.

During each session, the robot performed four different tasks:

• Asked open-ended questions about happy and sad memories over the last week.
• Administered the Short Mood and Feelings Questionnaire (SMFQ).
• Administered a picture task inspired by the Children’s Apperception Test (CAT), where children are asked to answer questions related to pictures shown.
• Administered the Revised Children’s Anxiety and Depression Scale (RCADS) for generalized anxiety, panic disorder, and low mood.

Following the SMFQ children were divided into three different groups according to how likely they were to be struggling with their mental well-being.

The researchers found that children with varying levels of well-being concerns interacted differently with the robot. For children that might not be experiencing mental well-being–related problems, the researchers found that interacting with the robot led to more positive response ratings to the questionnaires. However, for children that might be experiencing well-being–related concerns, the robot may have enabled them to divulge their true feelings and experiences, leading to more negative response ratings to the questionnaire.
 

Robots an addition not a replacement

“Since the robot we use is child-sized, and completely nonthreatening, children might see the robot as a confidant – they feel like they won’t get into trouble if they share secrets with it,” said Ms. Abbasi. “Other researchers have found that children are more likely to divulge private information – like that they’re being bullied, for example – to a robot than they would be to an adult,” she said.

Study participants all said they “enjoyed talking with the robot,” commented the authors, who added that, “the children were willing to confide in the robot, in some cases sharing information with the robot that they had not yet shared via the standard assessment method of online or in-person questionnaires.”

This is the first time that robots have been used to assess mental well-being in children, the researchers pointed out. “Robots could be a useful addition to traditional methods of mental health assessment,” they said, though they emphasized that robots are “not intended to be a substitute for professional mental health support.”

“We don’t have any intention of replacing psychologists or other mental health professionals with robots, since their expertise far surpasses anything a robot can do,” said Dr. Micol Spitale, affective computing and robotics laboratory, University of Cambridge, and study coauthor. “However, our work suggests that robots could be a useful tool in helping children to open up and share things they might not be comfortable sharing at first.”

The researchers say that they hope to expand their survey in future by including more participants and following them over time. They are also investigating whether similar results could be achieved if children interact with the robot via video chat.

A version of this article first appeared on Medscape UK.

Robots can be better at detecting mental well-being issues in children than parent-reported or self-reported testing, say U.K. researchers.

The researchers behind a new study, presented at the 31st IEEE International Conference on Robot & Human Interactive Communication (RO-MAN) in Naples, Italy, have suggested that robots could be a useful addition to traditional methods of mental health assessment.

“There are times when traditional methods aren’t able to catch mental well-being lapses in children, as sometimes the changes are incredibly subtle,” said Nida Itrat Abbasi, a PhD student at Cambridge (England) Affective Computing and Robotics Group, University of Cambridge, and the study’s first author. “We wanted to see whether robots might be able to help with this process,” she explained.

The authors highlighted how, during the COVID-19 pandemic, home schooling, financial pressures, and isolation from peers and friends impacted the mental health of many children. Even before the pandemic however, anxiety and depression among children in the United Kingdom has been on the rise, but the resources and support to address mental well-being are severely limited.
 

Children engage with robots

For their study the research team – which comprised roboticists, computer scientists, and psychiatrists from the University of Cambridge – enrolled 28 participants between ages 8 and 13 years. While being observed from an adjacent room by a parent or guardian, along with members of the research team, the participants  took part in a one-to-one 45-minute session with a Nao robot – a humanoid robot about 60 cm tall – that administered a series of standard psychological questionnaires to assess the mental well-being of each participant.

Participants interacted with the robot throughout the session by speaking with it or by touching sensors on the robot’s hands and feet. Additional sensors tracked participants’ heartbeat, head, and eye movements during the session.

Professor Hatice Gunes, affective intelligence and robotics laboratory, department of computer science, University of Cambridge, said: “Children are quite tactile, and they’re drawn to technology. If they’re using a screen-based tool, they’re withdrawn from the physical world,” she said. “But robots are perfect because they’re in the physical world – they’re more interactive, so the children are more engaged.”

Prior to each session the children and their parent or guardian completed standard online questionnaires to assess each child’s mental well-being.

During each session, the robot performed four different tasks:

• Asked open-ended questions about happy and sad memories over the last week.
• Administered the Short Mood and Feelings Questionnaire (SMFQ).
• Administered a picture task inspired by the Children’s Apperception Test (CAT), where children are asked to answer questions related to pictures shown.
• Administered the Revised Children’s Anxiety and Depression Scale (RCADS) for generalized anxiety, panic disorder, and low mood.

Following the SMFQ children were divided into three different groups according to how likely they were to be struggling with their mental well-being.

The researchers found that children with varying levels of well-being concerns interacted differently with the robot. For children that might not be experiencing mental well-being–related problems, the researchers found that interacting with the robot led to more positive response ratings to the questionnaires. However, for children that might be experiencing well-being–related concerns, the robot may have enabled them to divulge their true feelings and experiences, leading to more negative response ratings to the questionnaire.
 

Robots an addition not a replacement

“Since the robot we use is child-sized, and completely nonthreatening, children might see the robot as a confidant – they feel like they won’t get into trouble if they share secrets with it,” said Ms. Abbasi. “Other researchers have found that children are more likely to divulge private information – like that they’re being bullied, for example – to a robot than they would be to an adult,” she said.

Study participants all said they “enjoyed talking with the robot,” commented the authors, who added that, “the children were willing to confide in the robot, in some cases sharing information with the robot that they had not yet shared via the standard assessment method of online or in-person questionnaires.”

This is the first time that robots have been used to assess mental well-being in children, the researchers pointed out. “Robots could be a useful addition to traditional methods of mental health assessment,” they said, though they emphasized that robots are “not intended to be a substitute for professional mental health support.”

“We don’t have any intention of replacing psychologists or other mental health professionals with robots, since their expertise far surpasses anything a robot can do,” said Dr. Micol Spitale, affective computing and robotics laboratory, University of Cambridge, and study coauthor. “However, our work suggests that robots could be a useful tool in helping children to open up and share things they might not be comfortable sharing at first.”

The researchers say that they hope to expand their survey in future by including more participants and following them over time. They are also investigating whether similar results could be achieved if children interact with the robot via video chat.

A version of this article first appeared on Medscape UK.

Lauren G. Cliffel, MSW, looks forward to the upcoming 2022 Association of VA Hematology/Oncology (AVAHO) annual meeting and the opportunity to connect in-person with social workers, physicians, nurses, cancer navigators, and other cancer care providers who share a mission to establish and expand oncology programs for veterans. 

The theme of this year's annual meeting is "Your Best Version: Self-care in Cancer Care." Sessions include a discussion by a cancer care provider who was also a cancer patient, as well as presentations on the VA Whole Health initiative, survivorship, palliative care, and the Schwartz Rounds initiative. In addition, there will be sessions on self-care that include methods to address burnout and compassion fatigue.

Lauren G. Cliffel, MSW, looks forward to the upcoming 2022 Association of VA Hematology/Oncology (AVAHO) annual meeting and the opportunity to connect in-person with social workers, physicians, nurses, cancer navigators, and other cancer care providers who share a mission to establish and expand oncology programs for veterans. 

The theme of this year's annual meeting is "Your Best Version: Self-care in Cancer Care." Sessions include a discussion by a cancer care provider who was also a cancer patient, as well as presentations on the VA Whole Health initiative, survivorship, palliative care, and the Schwartz Rounds initiative. In addition, there will be sessions on self-care that include methods to address burnout and compassion fatigue.

Lauren G. Cliffel, MSW, looks forward to the upcoming 2022 Association of VA Hematology/Oncology (AVAHO) annual meeting and the opportunity to connect in-person with social workers, physicians, nurses, cancer navigators, and other cancer care providers who share a mission to establish and expand oncology programs for veterans. 

The theme of this year's annual meeting is "Your Best Version: Self-care in Cancer Care." Sessions include a discussion by a cancer care provider who was also a cancer patient, as well as presentations on the VA Whole Health initiative, survivorship, palliative care, and the Schwartz Rounds initiative. In addition, there will be sessions on self-care that include methods to address burnout and compassion fatigue.

Bernadette Heron, PharmD, provides a glance at activities planned for the approaching AVAHO 2022 annual meeting and announces with enthusiasm this year's theme: "Your Best Version: Self-care in Cancer Care."

Bringing self-care into the theater of clinically relevant issues is central to optimizing the care of patients with cancer, Dr Heron suggests. To this purpose, the structured sessions and interventions to be presented at AVAHO 2022 include a deep dive into burnout among practitioners as well as everyday clinical care issues.

Bernadette Heron, PharmD, provides a glance at activities planned for the approaching AVAHO 2022 annual meeting and announces with enthusiasm this year's theme: "Your Best Version: Self-care in Cancer Care."

Bringing self-care into the theater of clinically relevant issues is central to optimizing the care of patients with cancer, Dr Heron suggests. To this purpose, the structured sessions and interventions to be presented at AVAHO 2022 include a deep dive into burnout among practitioners as well as everyday clinical care issues.

Bernadette Heron, PharmD, provides a glance at activities planned for the approaching AVAHO 2022 annual meeting and announces with enthusiasm this year's theme: "Your Best Version: Self-care in Cancer Care."

Bringing self-care into the theater of clinically relevant issues is central to optimizing the care of patients with cancer, Dr Heron suggests. To this purpose, the structured sessions and interventions to be presented at AVAHO 2022 include a deep dive into burnout among practitioners as well as everyday clinical care issues.

Nick Burwick, MD, summarizes a series of topics to be addressed at the AVAHO 2022 annual meeting, including provider well-being, patient experience, multidisciplinary reflective care, and precision oncology.

In addition to the exciting presentations and sessions, Dr Burwick invokes the more informal aspects of AVAHO 2022, such as meeting colleagues and friends and taking the time to appreciate the host city of San Diego. Above all, Dr Burwick underscores this year’s theme of self-care and resilience in the cancer care setting.

Nick Burwick, MD, summarizes a series of topics to be addressed at the AVAHO 2022 annual meeting, including provider well-being, patient experience, multidisciplinary reflective care, and precision oncology.

In addition to the exciting presentations and sessions, Dr Burwick invokes the more informal aspects of AVAHO 2022, such as meeting colleagues and friends and taking the time to appreciate the host city of San Diego. Above all, Dr Burwick underscores this year’s theme of self-care and resilience in the cancer care setting.

Nick Burwick, MD, summarizes a series of topics to be addressed at the AVAHO 2022 annual meeting, including provider well-being, patient experience, multidisciplinary reflective care, and precision oncology.

In addition to the exciting presentations and sessions, Dr Burwick invokes the more informal aspects of AVAHO 2022, such as meeting colleagues and friends and taking the time to appreciate the host city of San Diego. Above all, Dr Burwick underscores this year’s theme of self-care and resilience in the cancer care setting.

The 3 “Rs” of multiple sclerosis (MS)—repair, remyelinate, and restore—spell out the goals of patients and physicians alike. MS is an incurable, immune-mediated, neurodegenerative disease of the central nervous system (CNS), and is thought to develop from unexplained autoimmune attacks directed at myelin (the covering on neurons) and glial cells, or “oligodendrocytes.” Neurodegeneration is evident early in the disease process and is characterized by mitochondrial dysfunction, energy failure, and neuronal and glial death.

While most new and investigational therapies aim to address immune dysfunction, a new idea—

one not involving immune dysregulation—is being explored in various studies: Are there agents, outside of traditional MS therapies, able to help with remyelination?

Mitochondria, oxidative stress, and MS

Neurons, oligodendrocytes, and oligodendrocyte precursor cells (OPCs) are particularly sensitive to oxidative stress. In MS, chronic inflammation and autoimmunity are key drivers of oxidative stress and secondary mitochondrial dysfunction. 

Mitochondrial dysfunction is particularly relevant for neurodegeneration in MS. The observed dysfunction includes mitochondrial DNA damage, deficiency in mitochondrial DNA repair, reduced levels of antioxidants, and increased free radicals. Furthermore, the structure and number of mitochondria temporarily increase to accommodate the increased energy needs. Despite the attempted adaptation, energy failure ultimately occurs, resulting in a mismatch between energy needs or consumption and energy production. Neuroinflammation and the imbalance between energy consumption and generation create a vicious, continuous cycle that is characteristic in progressive MS. The energy failure is then associated with neuronal death, Wallerian degeneration, and subsequent accumulation of neurologic disability. 

Current therapeutic landscape

While the therapeutic landscape for MS continues to evolve, the approved 20-plus therapies are primarily directed at the immune system. The overall goal is to modulate immune dysregulation  and decrease inflammation. Current therapies  may be able to control this macroscopic inflammatory activity. 

However, current treatments only show modest effects on disease progression, and do not help to repair neurons, remyelinate axons, or restore function that was impaired due to disease progression. Some US Food and Drug Administration (FDA)–approved therapies are thought to modulate mitochondrial functions. For example, the class of fumarates (eg, dimethyl fumarate, diroximel fumarate, monomethyl fumarate) activates the nuclear factor erythroid 2 -related factor 2 (Nrf2) pathway in treated MS patients. However, it is unclear whether activation of the Nrf2 pathway is involved in the therapeutic effects of fumarates. A recent study challenged the importance of the Nrf2 pathway as a therapeutic target for fumarates. It showed that in an MS animal model, the effects of fumarates on disease control were similar between Nrf2 knock-out mice and the wild type, suggesting that fumarates' therapeutic effects are independent of the Nrf2 pathway. Furthermore, fumarates failed to show benefits in progressive forms of MS both clinically and on a biomarker level. 

Metformin, the mitochondria, and neurodegeneration

Metformin (1,1-dimethylbiguanide) is an oral medication used primarily as first-line treatment for type 2 diabetes. However, due to its pharmacologic properties, mitochondrial effects, and the ability to cross the blood-brain barrier, scientists have shown recent interest in studying metformin in neurodegenerative diseases, including MS. Some of the potential benefits of metformin in neurodegenerative diseases include reduction of oxidative stress and countering mitochondrial dysfunction. It is known that metformin inhibits mitochondrial complex 1. Also, several studies have shown a positive effect of metformin on the reduction of oxidative stress and mitochondrial DNA regulation. Therefore, could metformin help combat mitochondrial dysfunction in MS or rejuvenate certain elements within the CNS in people with neurodegenerative diseases, including MS?

Oligodendrocytes and remyelination

Oligodendrocytes are cells responsible for myelinating axons within the CNS. Those cells originate from progenitors called OPCs. Interestingly, in humans, OPCs can mature into oligodendrocytes throughout their lifecycle, although to a much lesser extent in adults compared with children. However, therapeutic efforts to facilitate OPC maturation in vivo in MS lesions have failed thus far. Examples include high-dose biotin, the anti-LINGO-1 opicinumab, and the anticancer, retinoid-analog drug bexarotene.

So, what is behind these unfortunate failures? Some molecules (eg, biotin, opicinumab) failed to meet their clinical endpoints in randomized clinical trials, while others had severe toxicity that halted further clinical testing (eg, bexarotene). On the other hand, some molecules (eg,      clemastine fumarate), showed a modest yet promising effect on biomarkers in small clinical trials. 

A discussion on molecule failures

What could explain the failure of molecules with such promising preclinical findings? One could argue that clinical trial designs may have been insufficient to detect small remyelinating effects. One could also argue that the maturation of OPCs into oligodendrocytes is too complex to facilitate using 1 molecule that may be an inhibitor of maturation or to activate/augment a facilitator of the maturation process. There are too many natural inhibitors and facilitators of OPC maturation, and an approach with combination therapy might have a better chance at achieving a favorable therapeutic effect. 

Another piece of the complexity of OPC maturation is the recent discovery that, in humans, nonhuman primates, and other mammals, aged OPCs do not have the same capacity to mature into oligodendrocytes as young OPCs. There might be some clinical support here, as children with MS have more ability to recover from MS attacks than their adult counterparts. Also, the older the individual with MS is, the less likely they are to recover from MS attacks and the more likely they are to show signs of disease progression compared with their younger counterparts. 

Theoretically, age-related recovery from clinical attacks may be partially explained by complications due to OPC aging. To this point, can we rejuvenate OPCs and restore their ability to mature into oligodendrocytes? Can metformin be the medicine that does so? 

Interestingly, scientists could restore the ability of older OPCs to mature into oligodendrocytes, at least in the rodent model, through calorie restriction (eg, intermittent fasting) or by mimicking this state using metformin. 

Metformin and the 3 “Rs”

One idea is to use metformin to create a biochemical state that allows OPCs to regain their ability to mature into oligodendrocytes in adult or aging individuals with MS. If that is achieved, other molecules may augment OPC' maturation or inhibit OPC maturation-inhibitors and become successful in promoting remyelination. A phase 2 clinical trial in the United Kingdom that is currently recruiting participants intends to investigate a combination of metformin and clemastine fumarate in 50 patients with relapsing-remitting MS. The goal is to learn whether metformin plus clemastine allows for therapeutic remyelination. In addition, a Canadian study is investigating metformin in children with MS. Two other studies are currently recruiting to study metformin in relapsing MS (Egypt) and progressive MS (United States). 

Although testing metformin as a treatment for MS is still in the early stages, the scientific rationale is valid and supported by compelling preclinical evidence. Ongoing clinical trials will likely provide preliminary results on whether metformin will advance in clinical testing and provide clinically meaningful improvements for people living with MS.

If metformin is, in fact, a conditioning agent for use in remyelinating therapies, future clinical trials could be designed to administer metformin to rejuvenate OPCs before the administration of any molecule combination designed to facilitate OPC maturation. However, these trials will need to address an important issue: dosage. In type 2 diabetes, the typical daily dose is between 500 and 3000 mg per day. But in tests on rodents – which weigh about 10 grams – to rejuvenate OPCs, the doses of metformin were very high: 200 to 300 mg/kg. Given the body weight of humans and to avoid drug toxicity, the resulting smaller doses of metformin will take time to exert their potential therapeutic effect.
 

Should future research be successful in developing combination molecular therapies with diverse and synergistic therapeutic targets, then the 3 “Rs” in MS will allow for a fourth “R” to effectively succeed: repair, remyelinate, restore, and rehabilitate.

The 3 “Rs” of multiple sclerosis (MS)—repair, remyelinate, and restore—spell out the goals of patients and physicians alike. MS is an incurable, immune-mediated, neurodegenerative disease of the central nervous system (CNS), and is thought to develop from unexplained autoimmune attacks directed at myelin (the covering on neurons) and glial cells, or “oligodendrocytes.” Neurodegeneration is evident early in the disease process and is characterized by mitochondrial dysfunction, energy failure, and neuronal and glial death.

While most new and investigational therapies aim to address immune dysfunction, a new idea—

one not involving immune dysregulation—is being explored in various studies: Are there agents, outside of traditional MS therapies, able to help with remyelination?

Mitochondria, oxidative stress, and MS

Neurons, oligodendrocytes, and oligodendrocyte precursor cells (OPCs) are particularly sensitive to oxidative stress. In MS, chronic inflammation and autoimmunity are key drivers of oxidative stress and secondary mitochondrial dysfunction. 

Mitochondrial dysfunction is particularly relevant for neurodegeneration in MS. The observed dysfunction includes mitochondrial DNA damage, deficiency in mitochondrial DNA repair, reduced levels of antioxidants, and increased free radicals. Furthermore, the structure and number of mitochondria temporarily increase to accommodate the increased energy needs. Despite the attempted adaptation, energy failure ultimately occurs, resulting in a mismatch between energy needs or consumption and energy production. Neuroinflammation and the imbalance between energy consumption and generation create a vicious, continuous cycle that is characteristic in progressive MS. The energy failure is then associated with neuronal death, Wallerian degeneration, and subsequent accumulation of neurologic disability. 

Current therapeutic landscape

While the therapeutic landscape for MS continues to evolve, the approved 20-plus therapies are primarily directed at the immune system. The overall goal is to modulate immune dysregulation  and decrease inflammation. Current therapies  may be able to control this macroscopic inflammatory activity. 

However, current treatments only show modest effects on disease progression, and do not help to repair neurons, remyelinate axons, or restore function that was impaired due to disease progression. Some US Food and Drug Administration (FDA)–approved therapies are thought to modulate mitochondrial functions. For example, the class of fumarates (eg, dimethyl fumarate, diroximel fumarate, monomethyl fumarate) activates the nuclear factor erythroid 2 -related factor 2 (Nrf2) pathway in treated MS patients. However, it is unclear whether activation of the Nrf2 pathway is involved in the therapeutic effects of fumarates. A recent study challenged the importance of the Nrf2 pathway as a therapeutic target for fumarates. It showed that in an MS animal model, the effects of fumarates on disease control were similar between Nrf2 knock-out mice and the wild type, suggesting that fumarates' therapeutic effects are independent of the Nrf2 pathway. Furthermore, fumarates failed to show benefits in progressive forms of MS both clinically and on a biomarker level. 

Metformin, the mitochondria, and neurodegeneration

Metformin (1,1-dimethylbiguanide) is an oral medication used primarily as first-line treatment for type 2 diabetes. However, due to its pharmacologic properties, mitochondrial effects, and the ability to cross the blood-brain barrier, scientists have shown recent interest in studying metformin in neurodegenerative diseases, including MS. Some of the potential benefits of metformin in neurodegenerative diseases include reduction of oxidative stress and countering mitochondrial dysfunction. It is known that metformin inhibits mitochondrial complex 1. Also, several studies have shown a positive effect of metformin on the reduction of oxidative stress and mitochondrial DNA regulation. Therefore, could metformin help combat mitochondrial dysfunction in MS or rejuvenate certain elements within the CNS in people with neurodegenerative diseases, including MS?

Oligodendrocytes and remyelination

Oligodendrocytes are cells responsible for myelinating axons within the CNS. Those cells originate from progenitors called OPCs. Interestingly, in humans, OPCs can mature into oligodendrocytes throughout their lifecycle, although to a much lesser extent in adults compared with children. However, therapeutic efforts to facilitate OPC maturation in vivo in MS lesions have failed thus far. Examples include high-dose biotin, the anti-LINGO-1 opicinumab, and the anticancer, retinoid-analog drug bexarotene.

So, what is behind these unfortunate failures? Some molecules (eg, biotin, opicinumab) failed to meet their clinical endpoints in randomized clinical trials, while others had severe toxicity that halted further clinical testing (eg, bexarotene). On the other hand, some molecules (eg,      clemastine fumarate), showed a modest yet promising effect on biomarkers in small clinical trials. 

A discussion on molecule failures

What could explain the failure of molecules with such promising preclinical findings? One could argue that clinical trial designs may have been insufficient to detect small remyelinating effects. One could also argue that the maturation of OPCs into oligodendrocytes is too complex to facilitate using 1 molecule that may be an inhibitor of maturation or to activate/augment a facilitator of the maturation process. There are too many natural inhibitors and facilitators of OPC maturation, and an approach with combination therapy might have a better chance at achieving a favorable therapeutic effect. 

Another piece of the complexity of OPC maturation is the recent discovery that, in humans, nonhuman primates, and other mammals, aged OPCs do not have the same capacity to mature into oligodendrocytes as young OPCs. There might be some clinical support here, as children with MS have more ability to recover from MS attacks than their adult counterparts. Also, the older the individual with MS is, the less likely they are to recover from MS attacks and the more likely they are to show signs of disease progression compared with their younger counterparts. 

Theoretically, age-related recovery from clinical attacks may be partially explained by complications due to OPC aging. To this point, can we rejuvenate OPCs and restore their ability to mature into oligodendrocytes? Can metformin be the medicine that does so? 

Interestingly, scientists could restore the ability of older OPCs to mature into oligodendrocytes, at least in the rodent model, through calorie restriction (eg, intermittent fasting) or by mimicking this state using metformin. 

Metformin and the 3 “Rs”

One idea is to use metformin to create a biochemical state that allows OPCs to regain their ability to mature into oligodendrocytes in adult or aging individuals with MS. If that is achieved, other molecules may augment OPC' maturation or inhibit OPC maturation-inhibitors and become successful in promoting remyelination. A phase 2 clinical trial in the United Kingdom that is currently recruiting participants intends to investigate a combination of metformin and clemastine fumarate in 50 patients with relapsing-remitting MS. The goal is to learn whether metformin plus clemastine allows for therapeutic remyelination. In addition, a Canadian study is investigating metformin in children with MS. Two other studies are currently recruiting to study metformin in relapsing MS (Egypt) and progressive MS (United States). 

Although testing metformin as a treatment for MS is still in the early stages, the scientific rationale is valid and supported by compelling preclinical evidence. Ongoing clinical trials will likely provide preliminary results on whether metformin will advance in clinical testing and provide clinically meaningful improvements for people living with MS.

If metformin is, in fact, a conditioning agent for use in remyelinating therapies, future clinical trials could be designed to administer metformin to rejuvenate OPCs before the administration of any molecule combination designed to facilitate OPC maturation. However, these trials will need to address an important issue: dosage. In type 2 diabetes, the typical daily dose is between 500 and 3000 mg per day. But in tests on rodents – which weigh about 10 grams – to rejuvenate OPCs, the doses of metformin were very high: 200 to 300 mg/kg. Given the body weight of humans and to avoid drug toxicity, the resulting smaller doses of metformin will take time to exert their potential therapeutic effect.
 

Should future research be successful in developing combination molecular therapies with diverse and synergistic therapeutic targets, then the 3 “Rs” in MS will allow for a fourth “R” to effectively succeed: repair, remyelinate, restore, and rehabilitate.

The 3 “Rs” of multiple sclerosis (MS)—repair, remyelinate, and restore—spell out the goals of patients and physicians alike. MS is an incurable, immune-mediated, neurodegenerative disease of the central nervous system (CNS), and is thought to develop from unexplained autoimmune attacks directed at myelin (the covering on neurons) and glial cells, or “oligodendrocytes.” Neurodegeneration is evident early in the disease process and is characterized by mitochondrial dysfunction, energy failure, and neuronal and glial death.

While most new and investigational therapies aim to address immune dysfunction, a new idea—

one not involving immune dysregulation—is being explored in various studies: Are there agents, outside of traditional MS therapies, able to help with remyelination?

Mitochondria, oxidative stress, and MS

Neurons, oligodendrocytes, and oligodendrocyte precursor cells (OPCs) are particularly sensitive to oxidative stress. In MS, chronic inflammation and autoimmunity are key drivers of oxidative stress and secondary mitochondrial dysfunction. 

Mitochondrial dysfunction is particularly relevant for neurodegeneration in MS. The observed dysfunction includes mitochondrial DNA damage, deficiency in mitochondrial DNA repair, reduced levels of antioxidants, and increased free radicals. Furthermore, the structure and number of mitochondria temporarily increase to accommodate the increased energy needs. Despite the attempted adaptation, energy failure ultimately occurs, resulting in a mismatch between energy needs or consumption and energy production. Neuroinflammation and the imbalance between energy consumption and generation create a vicious, continuous cycle that is characteristic in progressive MS. The energy failure is then associated with neuronal death, Wallerian degeneration, and subsequent accumulation of neurologic disability. 

Current therapeutic landscape

While the therapeutic landscape for MS continues to evolve, the approved 20-plus therapies are primarily directed at the immune system. The overall goal is to modulate immune dysregulation  and decrease inflammation. Current therapies  may be able to control this macroscopic inflammatory activity. 

However, current treatments only show modest effects on disease progression, and do not help to repair neurons, remyelinate axons, or restore function that was impaired due to disease progression. Some US Food and Drug Administration (FDA)–approved therapies are thought to modulate mitochondrial functions. For example, the class of fumarates (eg, dimethyl fumarate, diroximel fumarate, monomethyl fumarate) activates the nuclear factor erythroid 2 -related factor 2 (Nrf2) pathway in treated MS patients. However, it is unclear whether activation of the Nrf2 pathway is involved in the therapeutic effects of fumarates. A recent study challenged the importance of the Nrf2 pathway as a therapeutic target for fumarates. It showed that in an MS animal model, the effects of fumarates on disease control were similar between Nrf2 knock-out mice and the wild type, suggesting that fumarates' therapeutic effects are independent of the Nrf2 pathway. Furthermore, fumarates failed to show benefits in progressive forms of MS both clinically and on a biomarker level. 

Metformin, the mitochondria, and neurodegeneration

Metformin (1,1-dimethylbiguanide) is an oral medication used primarily as first-line treatment for type 2 diabetes. However, due to its pharmacologic properties, mitochondrial effects, and the ability to cross the blood-brain barrier, scientists have shown recent interest in studying metformin in neurodegenerative diseases, including MS. Some of the potential benefits of metformin in neurodegenerative diseases include reduction of oxidative stress and countering mitochondrial dysfunction. It is known that metformin inhibits mitochondrial complex 1. Also, several studies have shown a positive effect of metformin on the reduction of oxidative stress and mitochondrial DNA regulation. Therefore, could metformin help combat mitochondrial dysfunction in MS or rejuvenate certain elements within the CNS in people with neurodegenerative diseases, including MS?

Oligodendrocytes and remyelination

Oligodendrocytes are cells responsible for myelinating axons within the CNS. Those cells originate from progenitors called OPCs. Interestingly, in humans, OPCs can mature into oligodendrocytes throughout their lifecycle, although to a much lesser extent in adults compared with children. However, therapeutic efforts to facilitate OPC maturation in vivo in MS lesions have failed thus far. Examples include high-dose biotin, the anti-LINGO-1 opicinumab, and the anticancer, retinoid-analog drug bexarotene.

So, what is behind these unfortunate failures? Some molecules (eg, biotin, opicinumab) failed to meet their clinical endpoints in randomized clinical trials, while others had severe toxicity that halted further clinical testing (eg, bexarotene). On the other hand, some molecules (eg,      clemastine fumarate), showed a modest yet promising effect on biomarkers in small clinical trials. 

A discussion on molecule failures

What could explain the failure of molecules with such promising preclinical findings? One could argue that clinical trial designs may have been insufficient to detect small remyelinating effects. One could also argue that the maturation of OPCs into oligodendrocytes is too complex to facilitate using 1 molecule that may be an inhibitor of maturation or to activate/augment a facilitator of the maturation process. There are too many natural inhibitors and facilitators of OPC maturation, and an approach with combination therapy might have a better chance at achieving a favorable therapeutic effect. 

Another piece of the complexity of OPC maturation is the recent discovery that, in humans, nonhuman primates, and other mammals, aged OPCs do not have the same capacity to mature into oligodendrocytes as young OPCs. There might be some clinical support here, as children with MS have more ability to recover from MS attacks than their adult counterparts. Also, the older the individual with MS is, the less likely they are to recover from MS attacks and the more likely they are to show signs of disease progression compared with their younger counterparts. 

Theoretically, age-related recovery from clinical attacks may be partially explained by complications due to OPC aging. To this point, can we rejuvenate OPCs and restore their ability to mature into oligodendrocytes? Can metformin be the medicine that does so? 

Interestingly, scientists could restore the ability of older OPCs to mature into oligodendrocytes, at least in the rodent model, through calorie restriction (eg, intermittent fasting) or by mimicking this state using metformin. 

Metformin and the 3 “Rs”

One idea is to use metformin to create a biochemical state that allows OPCs to regain their ability to mature into oligodendrocytes in adult or aging individuals with MS. If that is achieved, other molecules may augment OPC' maturation or inhibit OPC maturation-inhibitors and become successful in promoting remyelination. A phase 2 clinical trial in the United Kingdom that is currently recruiting participants intends to investigate a combination of metformin and clemastine fumarate in 50 patients with relapsing-remitting MS. The goal is to learn whether metformin plus clemastine allows for therapeutic remyelination. In addition, a Canadian study is investigating metformin in children with MS. Two other studies are currently recruiting to study metformin in relapsing MS (Egypt) and progressive MS (United States). 

Although testing metformin as a treatment for MS is still in the early stages, the scientific rationale is valid and supported by compelling preclinical evidence. Ongoing clinical trials will likely provide preliminary results on whether metformin will advance in clinical testing and provide clinically meaningful improvements for people living with MS.

If metformin is, in fact, a conditioning agent for use in remyelinating therapies, future clinical trials could be designed to administer metformin to rejuvenate OPCs before the administration of any molecule combination designed to facilitate OPC maturation. However, these trials will need to address an important issue: dosage. In type 2 diabetes, the typical daily dose is between 500 and 3000 mg per day. But in tests on rodents – which weigh about 10 grams – to rejuvenate OPCs, the doses of metformin were very high: 200 to 300 mg/kg. Given the body weight of humans and to avoid drug toxicity, the resulting smaller doses of metformin will take time to exert their potential therapeutic effect.
 

Should future research be successful in developing combination molecular therapies with diverse and synergistic therapeutic targets, then the 3 “Rs” in MS will allow for a fourth “R” to effectively succeed: repair, remyelinate, restore, and rehabilitate.

Approximately 30% of U.S. adults experience troublesome reflux symptoms of heartburn, regurgitation and noncardiac chest pain. Because the mechanisms driving symptoms vary across patients, phenotyping patients via a step-wise diagnostic framework effectively guides personalized management in GERD.

For instance, PPI trials are appropriate when esophageal symptoms are present, whereas up-front reflux monitoring rather than empiric PPI trials are recommended for evaluation of isolated extra-esophageal symptoms. All patients undergoing evaluation for GERD should receive counseling on weight management and lifestyle modifications as well as the brain-gut axis relationship. In the common scenario of inadequate symptom response to PPIs, upper GI endoscopy is recommended to assess for erosive reflux disease (which confirms a diagnosis of GERD) as well as the anti-reflux barrier integrity. For instance, the presence of a large hiatal hernia and/or grade III/IV gastro-esophageal flap valve may point to mechanical gastro-esophageal reflux as a driver of symptoms and lower the threshold for surgical referral. In the absence of erosive reflux disease the next recommended step is ambulatory reflux monitoring off PPI therapy, either as prolonged wireless telemetry (which can be done concurrently with index endoscopy as long as PPI was discontinued > 7 days) or 24-hour transnasal pH-impedance catheter-based testing. Studies suggest that 96-hour monitoring is optimal for diagnostic accuracy and to guide therapeutic strategies.

Patients without evidence of GERD on endoscopy or ambulatory reflux monitoring likely have a functional esophageal disorder for which therapy hinges on pharmacologic neuromodulation or behavioral interventions as well as PPI cessation.

Alternatively, management for GERD (erosive or nonerosive) aims to optimize lifestyle, PPI therapy and the individualized use of adjunctive therapy, which include H2-receptor antagonists, alginate antacids, GABA agonists, neuromodulation and/or behavioral interventions. Surgical or endoscopic antireflux interventions are also an option for refractory GERD. Prior to intervention, achalasia must be excluded (typically with esophageal manometry), and confirmation of PPI refractory GERD on pH-impedance monitoring on PPI is of value, particularly when the phenotype is unclear. Again, the choice of antireflux intervention (e.g., laparoscopic fundoplication, magnetic sphincter augmentation, transoral incisionless fundoplication, Roux-en-Y gastric bypass) should be individualized to the patient’s anatomy, physiology, and clinical profile.

A multitude of treatment options are available to manage GERD, including behavioral interventions, lifestyle modifications, pharmacotherapy, and endoscopic/surgical interventions. However, not every treatment strategy is appropriate for every patient. Data gathered from the step-down diagnostic approach, which starts with clinical presentation, then endoscopy, then reflux monitoring, then esophageal physiologic testing, helps determine the GERD phenotype and effectively guide therapy.
 

Dr. Yadlapati is associate professor of clinical medicine, and medical director, UCSD Center for Esophageal Diseases; director, GI Motility Lab, division of gastroenterology, University of California San Diego, La Jolla, Calif. She disclosed ties with Medtronic, Phathom Pharmaceuticals, StatLinkMD, Medscape, Ironwood Pharmaceuticals, and RJS Mediagnostix. These remarks were made during one of the AGA Postgraduate Course sessions held at DDW 2022.

Approximately 30% of U.S. adults experience troublesome reflux symptoms of heartburn, regurgitation and noncardiac chest pain. Because the mechanisms driving symptoms vary across patients, phenotyping patients via a step-wise diagnostic framework effectively guides personalized management in GERD.

For instance, PPI trials are appropriate when esophageal symptoms are present, whereas up-front reflux monitoring rather than empiric PPI trials are recommended for evaluation of isolated extra-esophageal symptoms. All patients undergoing evaluation for GERD should receive counseling on weight management and lifestyle modifications as well as the brain-gut axis relationship. In the common scenario of inadequate symptom response to PPIs, upper GI endoscopy is recommended to assess for erosive reflux disease (which confirms a diagnosis of GERD) as well as the anti-reflux barrier integrity. For instance, the presence of a large hiatal hernia and/or grade III/IV gastro-esophageal flap valve may point to mechanical gastro-esophageal reflux as a driver of symptoms and lower the threshold for surgical referral. In the absence of erosive reflux disease the next recommended step is ambulatory reflux monitoring off PPI therapy, either as prolonged wireless telemetry (which can be done concurrently with index endoscopy as long as PPI was discontinued > 7 days) or 24-hour transnasal pH-impedance catheter-based testing. Studies suggest that 96-hour monitoring is optimal for diagnostic accuracy and to guide therapeutic strategies.

Patients without evidence of GERD on endoscopy or ambulatory reflux monitoring likely have a functional esophageal disorder for which therapy hinges on pharmacologic neuromodulation or behavioral interventions as well as PPI cessation.

Alternatively, management for GERD (erosive or nonerosive) aims to optimize lifestyle, PPI therapy and the individualized use of adjunctive therapy, which include H2-receptor antagonists, alginate antacids, GABA agonists, neuromodulation and/or behavioral interventions. Surgical or endoscopic antireflux interventions are also an option for refractory GERD. Prior to intervention, achalasia must be excluded (typically with esophageal manometry), and confirmation of PPI refractory GERD on pH-impedance monitoring on PPI is of value, particularly when the phenotype is unclear. Again, the choice of antireflux intervention (e.g., laparoscopic fundoplication, magnetic sphincter augmentation, transoral incisionless fundoplication, Roux-en-Y gastric bypass) should be individualized to the patient’s anatomy, physiology, and clinical profile.

A multitude of treatment options are available to manage GERD, including behavioral interventions, lifestyle modifications, pharmacotherapy, and endoscopic/surgical interventions. However, not every treatment strategy is appropriate for every patient. Data gathered from the step-down diagnostic approach, which starts with clinical presentation, then endoscopy, then reflux monitoring, then esophageal physiologic testing, helps determine the GERD phenotype and effectively guide therapy.
 

Dr. Yadlapati is associate professor of clinical medicine, and medical director, UCSD Center for Esophageal Diseases; director, GI Motility Lab, division of gastroenterology, University of California San Diego, La Jolla, Calif. She disclosed ties with Medtronic, Phathom Pharmaceuticals, StatLinkMD, Medscape, Ironwood Pharmaceuticals, and RJS Mediagnostix. These remarks were made during one of the AGA Postgraduate Course sessions held at DDW 2022.

Approximately 30% of U.S. adults experience troublesome reflux symptoms of heartburn, regurgitation and noncardiac chest pain. Because the mechanisms driving symptoms vary across patients, phenotyping patients via a step-wise diagnostic framework effectively guides personalized management in GERD.

For instance, PPI trials are appropriate when esophageal symptoms are present, whereas up-front reflux monitoring rather than empiric PPI trials are recommended for evaluation of isolated extra-esophageal symptoms. All patients undergoing evaluation for GERD should receive counseling on weight management and lifestyle modifications as well as the brain-gut axis relationship. In the common scenario of inadequate symptom response to PPIs, upper GI endoscopy is recommended to assess for erosive reflux disease (which confirms a diagnosis of GERD) as well as the anti-reflux barrier integrity. For instance, the presence of a large hiatal hernia and/or grade III/IV gastro-esophageal flap valve may point to mechanical gastro-esophageal reflux as a driver of symptoms and lower the threshold for surgical referral. In the absence of erosive reflux disease the next recommended step is ambulatory reflux monitoring off PPI therapy, either as prolonged wireless telemetry (which can be done concurrently with index endoscopy as long as PPI was discontinued > 7 days) or 24-hour transnasal pH-impedance catheter-based testing. Studies suggest that 96-hour monitoring is optimal for diagnostic accuracy and to guide therapeutic strategies.

Patients without evidence of GERD on endoscopy or ambulatory reflux monitoring likely have a functional esophageal disorder for which therapy hinges on pharmacologic neuromodulation or behavioral interventions as well as PPI cessation.

Alternatively, management for GERD (erosive or nonerosive) aims to optimize lifestyle, PPI therapy and the individualized use of adjunctive therapy, which include H2-receptor antagonists, alginate antacids, GABA agonists, neuromodulation and/or behavioral interventions. Surgical or endoscopic antireflux interventions are also an option for refractory GERD. Prior to intervention, achalasia must be excluded (typically with esophageal manometry), and confirmation of PPI refractory GERD on pH-impedance monitoring on PPI is of value, particularly when the phenotype is unclear. Again, the choice of antireflux intervention (e.g., laparoscopic fundoplication, magnetic sphincter augmentation, transoral incisionless fundoplication, Roux-en-Y gastric bypass) should be individualized to the patient’s anatomy, physiology, and clinical profile.

A multitude of treatment options are available to manage GERD, including behavioral interventions, lifestyle modifications, pharmacotherapy, and endoscopic/surgical interventions. However, not every treatment strategy is appropriate for every patient. Data gathered from the step-down diagnostic approach, which starts with clinical presentation, then endoscopy, then reflux monitoring, then esophageal physiologic testing, helps determine the GERD phenotype and effectively guide therapy.
 

Dr. Yadlapati is associate professor of clinical medicine, and medical director, UCSD Center for Esophageal Diseases; director, GI Motility Lab, division of gastroenterology, University of California San Diego, La Jolla, Calif. She disclosed ties with Medtronic, Phathom Pharmaceuticals, StatLinkMD, Medscape, Ironwood Pharmaceuticals, and RJS Mediagnostix. These remarks were made during one of the AGA Postgraduate Course sessions held at DDW 2022.