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Parkinson’s Risk in Women and History of Migraine: New Data

Article Type
Changed
Wed, 09/11/2024 - 11:49

 

TOPLINE:

A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.

METHODOLOGY:

  • Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
  • At baseline, 7321 women (18.6%) had migraine.
  • The mean follow-up duration was 22 years.
  • The primary outcome was a self-reported, physician-confirmed diagnosis of PD.

TAKEAWAY:

  • During the study period, 685 women self-reported a diagnosis of PD.
  • Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
  • No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
  • Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.

IN PRACTICE:

“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.

SOURCE:

The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.

LIMITATIONS:

The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.

DISCLOSURES:

The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE:

A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.

METHODOLOGY:

  • Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
  • At baseline, 7321 women (18.6%) had migraine.
  • The mean follow-up duration was 22 years.
  • The primary outcome was a self-reported, physician-confirmed diagnosis of PD.

TAKEAWAY:

  • During the study period, 685 women self-reported a diagnosis of PD.
  • Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
  • No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
  • Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.

IN PRACTICE:

“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.

SOURCE:

The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.

LIMITATIONS:

The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.

DISCLOSURES:

The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE:

A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.

METHODOLOGY:

  • Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
  • At baseline, 7321 women (18.6%) had migraine.
  • The mean follow-up duration was 22 years.
  • The primary outcome was a self-reported, physician-confirmed diagnosis of PD.

TAKEAWAY:

  • During the study period, 685 women self-reported a diagnosis of PD.
  • Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
  • No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
  • Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.

IN PRACTICE:

“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.

SOURCE:

The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.

LIMITATIONS:

The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.

DISCLOSURES:

The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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Can Antihistamines Trigger Seizures in Young Kids?

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Changed
Tue, 09/10/2024 - 14:59

 

TOPLINE:

First-generation antihistamines are linked to a 22% higher risk for seizures in children, new research shows. The risk appears to be most pronounced in children aged 6-24 months.

METHODOLOGY:

  • Researchers in Korea used a self-controlled case-crossover design to assess the risk for seizures associated with prescriptions of first-generation antihistamines.
  • They analyzed data from 11,729 children who had a seizure event (an emergency department visit with a diagnosis of epilepsy, status epilepticus, or convulsion) and had previously received a prescription for a first-generation antihistamine, including chlorpheniramine maleate, mequitazine, oxatomide, piprinhydrinate, or hydroxyzine hydrochloride.
  • Prescriptions during the 15 days before a seizure were considered to have been received during a hazard period, whereas earlier prescriptions were considered to have been received during a control period.
  • The researchers excluded patients with febrile seizures.

TAKEAWAY:

  • In an adjusted analysis, a prescription for an antihistamine during the hazard period was associated with a 22% higher risk for seizures in children (adjusted odds ratio, 1.22; 95% CI, 1.13-1.31).
  • The seizure risk was significant in children aged 6-24 months, with an adjusted odds ratio of 1.49 (95% CI, 1.31-1.70).
  • For older children, the risk was not statistically significant.

IN PRACTICE:

“The study underscores a substantial increase in seizure risk associated with antihistamine prescription among children aged 6-24 months,” the authors of the study wrote. “We are not aware of any other studies that have pointed out the increased risk of seizures with first-generation antihistamines in this particular age group. ... The benefits and risks of antihistamine use should always be carefully considered, especially when prescribing H1 antihistamines to vulnerable infants.”

The findings raise a host of questions for clinicians, including how a “relatively small risk” should translate into practice, and whether the risk may be attenuated with newer antihistamines, wrote Frank Max Charles Besag, MB, ChB, with East London NHS Foundation Trust in England, in an editorial accompanying the study. “It would be reasonable to inform families that at least one study has suggested a relatively small increase in the risk of seizures with first-generation antihistamines, adding that there are still too few data to draw any firm conclusions and also providing families with the information on what to do if the child were to have a seizure.” 
 

SOURCE:

Seonkyeong Rhie, MD, and Man Yong Han, MD, both with the Department of Pediatrics at CHA University School of Medicine, in Seongnam, South Korea, were the corresponding authors on the study. The research was published online in JAMA Network Open.

LIMITATIONS:

The researchers did not have details about seizure symptoms, did not include children seen in outpatient clinics, and were unable to verify the actual intake of the prescribed antihistamines. Although second-generation antihistamines may be less likely to cross the blood-brain barrier, one newer medication, desloratadine, has been associated with seizures.

DISCLOSURES:

The study was supported by grants from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, the Ministry of Health and Welfare, Republic of Korea.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE:

First-generation antihistamines are linked to a 22% higher risk for seizures in children, new research shows. The risk appears to be most pronounced in children aged 6-24 months.

METHODOLOGY:

  • Researchers in Korea used a self-controlled case-crossover design to assess the risk for seizures associated with prescriptions of first-generation antihistamines.
  • They analyzed data from 11,729 children who had a seizure event (an emergency department visit with a diagnosis of epilepsy, status epilepticus, or convulsion) and had previously received a prescription for a first-generation antihistamine, including chlorpheniramine maleate, mequitazine, oxatomide, piprinhydrinate, or hydroxyzine hydrochloride.
  • Prescriptions during the 15 days before a seizure were considered to have been received during a hazard period, whereas earlier prescriptions were considered to have been received during a control period.
  • The researchers excluded patients with febrile seizures.

TAKEAWAY:

  • In an adjusted analysis, a prescription for an antihistamine during the hazard period was associated with a 22% higher risk for seizures in children (adjusted odds ratio, 1.22; 95% CI, 1.13-1.31).
  • The seizure risk was significant in children aged 6-24 months, with an adjusted odds ratio of 1.49 (95% CI, 1.31-1.70).
  • For older children, the risk was not statistically significant.

IN PRACTICE:

“The study underscores a substantial increase in seizure risk associated with antihistamine prescription among children aged 6-24 months,” the authors of the study wrote. “We are not aware of any other studies that have pointed out the increased risk of seizures with first-generation antihistamines in this particular age group. ... The benefits and risks of antihistamine use should always be carefully considered, especially when prescribing H1 antihistamines to vulnerable infants.”

The findings raise a host of questions for clinicians, including how a “relatively small risk” should translate into practice, and whether the risk may be attenuated with newer antihistamines, wrote Frank Max Charles Besag, MB, ChB, with East London NHS Foundation Trust in England, in an editorial accompanying the study. “It would be reasonable to inform families that at least one study has suggested a relatively small increase in the risk of seizures with first-generation antihistamines, adding that there are still too few data to draw any firm conclusions and also providing families with the information on what to do if the child were to have a seizure.” 
 

SOURCE:

Seonkyeong Rhie, MD, and Man Yong Han, MD, both with the Department of Pediatrics at CHA University School of Medicine, in Seongnam, South Korea, were the corresponding authors on the study. The research was published online in JAMA Network Open.

LIMITATIONS:

The researchers did not have details about seizure symptoms, did not include children seen in outpatient clinics, and were unable to verify the actual intake of the prescribed antihistamines. Although second-generation antihistamines may be less likely to cross the blood-brain barrier, one newer medication, desloratadine, has been associated with seizures.

DISCLOSURES:

The study was supported by grants from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, the Ministry of Health and Welfare, Republic of Korea.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE:

First-generation antihistamines are linked to a 22% higher risk for seizures in children, new research shows. The risk appears to be most pronounced in children aged 6-24 months.

METHODOLOGY:

  • Researchers in Korea used a self-controlled case-crossover design to assess the risk for seizures associated with prescriptions of first-generation antihistamines.
  • They analyzed data from 11,729 children who had a seizure event (an emergency department visit with a diagnosis of epilepsy, status epilepticus, or convulsion) and had previously received a prescription for a first-generation antihistamine, including chlorpheniramine maleate, mequitazine, oxatomide, piprinhydrinate, or hydroxyzine hydrochloride.
  • Prescriptions during the 15 days before a seizure were considered to have been received during a hazard period, whereas earlier prescriptions were considered to have been received during a control period.
  • The researchers excluded patients with febrile seizures.

TAKEAWAY:

  • In an adjusted analysis, a prescription for an antihistamine during the hazard period was associated with a 22% higher risk for seizures in children (adjusted odds ratio, 1.22; 95% CI, 1.13-1.31).
  • The seizure risk was significant in children aged 6-24 months, with an adjusted odds ratio of 1.49 (95% CI, 1.31-1.70).
  • For older children, the risk was not statistically significant.

IN PRACTICE:

“The study underscores a substantial increase in seizure risk associated with antihistamine prescription among children aged 6-24 months,” the authors of the study wrote. “We are not aware of any other studies that have pointed out the increased risk of seizures with first-generation antihistamines in this particular age group. ... The benefits and risks of antihistamine use should always be carefully considered, especially when prescribing H1 antihistamines to vulnerable infants.”

The findings raise a host of questions for clinicians, including how a “relatively small risk” should translate into practice, and whether the risk may be attenuated with newer antihistamines, wrote Frank Max Charles Besag, MB, ChB, with East London NHS Foundation Trust in England, in an editorial accompanying the study. “It would be reasonable to inform families that at least one study has suggested a relatively small increase in the risk of seizures with first-generation antihistamines, adding that there are still too few data to draw any firm conclusions and also providing families with the information on what to do if the child were to have a seizure.” 
 

SOURCE:

Seonkyeong Rhie, MD, and Man Yong Han, MD, both with the Department of Pediatrics at CHA University School of Medicine, in Seongnam, South Korea, were the corresponding authors on the study. The research was published online in JAMA Network Open.

LIMITATIONS:

The researchers did not have details about seizure symptoms, did not include children seen in outpatient clinics, and were unable to verify the actual intake of the prescribed antihistamines. Although second-generation antihistamines may be less likely to cross the blood-brain barrier, one newer medication, desloratadine, has been associated with seizures.

DISCLOSURES:

The study was supported by grants from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, the Ministry of Health and Welfare, Republic of Korea.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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The Link Between Vision Impairment and Dementia in Older Adults

Article Type
Changed
Tue, 09/17/2024 - 10:48

 

TOPLINE:

Addressing vision impairments could help with dementia prevention, as vision impairment is linked to 19% of dementia cases in older adults.
 

METHODOLOGY:

  • Researchers conducted a cross-sectional analysis using data from the National Health and Aging Trends Study (NHATS).
  • The analysis included 2767 US adults aged 71 years or older (54.7% female and 45.3% male).
  • Vision impairments were defined using 2019 World Health Organization criteria. Near and distance vision impairments were defined as greater than 0.30 logMAR, and contrast sensitivity impairment was identified by scores below 1.55 logCS.
  • Dementia was classified using a standardized algorithm developed in NHATS, which incorporated a series of tests measuring cognition, memory and orientation, reports of Alzheimer’s disease, or a dementia diagnosis from the patient or a proxy, and an informant questionnaire (Ascertain Dementia-8 Dementia Screening Interview).
  • The study analyzed data from 2021, with the primary outcome being the population attributable fraction (PAF) of dementia from vision impairment.

TAKEAWAY:

  • The PAF of dementia associated with at least one vision impairment was 19% (95% CI, 8.2-29.7).
  • Impairment in contrast sensitivity had the highest PAF among all other vision issues, at 15% (95% CI, 6.6-23.6). This figure was higher than that for impairment of near acuity, at 9.7% (95% CI, 2.6-17.0), or distance acuity, at 4.9% (95% CI, 0.1-9.9).
  • The highest PAFs for dementia due to vision impairment was among participants aged 71-79 years (24.3%; 95% CI, 6.6-41.8), women (26.8%; 95% CI, 12.2-39.9), and non-Hispanic White participants (22.3%; 95% CI, 9.6-34.5).

IN PRACTICE:

“While not proving a cause-and-effect relationship, these findings support inclusion of multiple objective measures of vision impairments, including contrast sensitivity and visual acuity, to capture the total potential impact of addressing vision impairment on dementia,” study authors wrote.

SOURCE:

This study was led by Jason R. Smith, ScM, of the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore. It was published online in JAMA Ophthalmology.

LIMITATIONS:

The limited sample sizes for American Indian, Alaska Native, Asian, and Hispanic groups prevented researchers from calculating PAFs for these populations. The cross-sectional design prevented the researchers from examining the timing of vision impairment in relation to a diagnosis of dementia. The study did not explore links between other measures of vision and dementia. Those with early cognitive impairment may not have updated glasses, affecting visual performance. The findings from the study may not apply to institutionalized older adults.

DISCLOSURES:

Jennifer A. Deal, PhD, MHS, reported receiving personal fees from Frontiers in Epidemiology, Velux Stiftung, and Medical Education Speakers Network outside the submitted work. Nicholas S. Reed, AuD, PhD, reported receiving stock options from Neosensory outside the submitted work. No other disclosures were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.A version of this article appeared on Medscape.com.

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TOPLINE:

Addressing vision impairments could help with dementia prevention, as vision impairment is linked to 19% of dementia cases in older adults.
 

METHODOLOGY:

  • Researchers conducted a cross-sectional analysis using data from the National Health and Aging Trends Study (NHATS).
  • The analysis included 2767 US adults aged 71 years or older (54.7% female and 45.3% male).
  • Vision impairments were defined using 2019 World Health Organization criteria. Near and distance vision impairments were defined as greater than 0.30 logMAR, and contrast sensitivity impairment was identified by scores below 1.55 logCS.
  • Dementia was classified using a standardized algorithm developed in NHATS, which incorporated a series of tests measuring cognition, memory and orientation, reports of Alzheimer’s disease, or a dementia diagnosis from the patient or a proxy, and an informant questionnaire (Ascertain Dementia-8 Dementia Screening Interview).
  • The study analyzed data from 2021, with the primary outcome being the population attributable fraction (PAF) of dementia from vision impairment.

TAKEAWAY:

  • The PAF of dementia associated with at least one vision impairment was 19% (95% CI, 8.2-29.7).
  • Impairment in contrast sensitivity had the highest PAF among all other vision issues, at 15% (95% CI, 6.6-23.6). This figure was higher than that for impairment of near acuity, at 9.7% (95% CI, 2.6-17.0), or distance acuity, at 4.9% (95% CI, 0.1-9.9).
  • The highest PAFs for dementia due to vision impairment was among participants aged 71-79 years (24.3%; 95% CI, 6.6-41.8), women (26.8%; 95% CI, 12.2-39.9), and non-Hispanic White participants (22.3%; 95% CI, 9.6-34.5).

IN PRACTICE:

“While not proving a cause-and-effect relationship, these findings support inclusion of multiple objective measures of vision impairments, including contrast sensitivity and visual acuity, to capture the total potential impact of addressing vision impairment on dementia,” study authors wrote.

SOURCE:

This study was led by Jason R. Smith, ScM, of the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore. It was published online in JAMA Ophthalmology.

LIMITATIONS:

The limited sample sizes for American Indian, Alaska Native, Asian, and Hispanic groups prevented researchers from calculating PAFs for these populations. The cross-sectional design prevented the researchers from examining the timing of vision impairment in relation to a diagnosis of dementia. The study did not explore links between other measures of vision and dementia. Those with early cognitive impairment may not have updated glasses, affecting visual performance. The findings from the study may not apply to institutionalized older adults.

DISCLOSURES:

Jennifer A. Deal, PhD, MHS, reported receiving personal fees from Frontiers in Epidemiology, Velux Stiftung, and Medical Education Speakers Network outside the submitted work. Nicholas S. Reed, AuD, PhD, reported receiving stock options from Neosensory outside the submitted work. No other disclosures were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.A version of this article appeared on Medscape.com.

 

TOPLINE:

Addressing vision impairments could help with dementia prevention, as vision impairment is linked to 19% of dementia cases in older adults.
 

METHODOLOGY:

  • Researchers conducted a cross-sectional analysis using data from the National Health and Aging Trends Study (NHATS).
  • The analysis included 2767 US adults aged 71 years or older (54.7% female and 45.3% male).
  • Vision impairments were defined using 2019 World Health Organization criteria. Near and distance vision impairments were defined as greater than 0.30 logMAR, and contrast sensitivity impairment was identified by scores below 1.55 logCS.
  • Dementia was classified using a standardized algorithm developed in NHATS, which incorporated a series of tests measuring cognition, memory and orientation, reports of Alzheimer’s disease, or a dementia diagnosis from the patient or a proxy, and an informant questionnaire (Ascertain Dementia-8 Dementia Screening Interview).
  • The study analyzed data from 2021, with the primary outcome being the population attributable fraction (PAF) of dementia from vision impairment.

TAKEAWAY:

  • The PAF of dementia associated with at least one vision impairment was 19% (95% CI, 8.2-29.7).
  • Impairment in contrast sensitivity had the highest PAF among all other vision issues, at 15% (95% CI, 6.6-23.6). This figure was higher than that for impairment of near acuity, at 9.7% (95% CI, 2.6-17.0), or distance acuity, at 4.9% (95% CI, 0.1-9.9).
  • The highest PAFs for dementia due to vision impairment was among participants aged 71-79 years (24.3%; 95% CI, 6.6-41.8), women (26.8%; 95% CI, 12.2-39.9), and non-Hispanic White participants (22.3%; 95% CI, 9.6-34.5).

IN PRACTICE:

“While not proving a cause-and-effect relationship, these findings support inclusion of multiple objective measures of vision impairments, including contrast sensitivity and visual acuity, to capture the total potential impact of addressing vision impairment on dementia,” study authors wrote.

SOURCE:

This study was led by Jason R. Smith, ScM, of the Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health in Baltimore. It was published online in JAMA Ophthalmology.

LIMITATIONS:

The limited sample sizes for American Indian, Alaska Native, Asian, and Hispanic groups prevented researchers from calculating PAFs for these populations. The cross-sectional design prevented the researchers from examining the timing of vision impairment in relation to a diagnosis of dementia. The study did not explore links between other measures of vision and dementia. Those with early cognitive impairment may not have updated glasses, affecting visual performance. The findings from the study may not apply to institutionalized older adults.

DISCLOSURES:

Jennifer A. Deal, PhD, MHS, reported receiving personal fees from Frontiers in Epidemiology, Velux Stiftung, and Medical Education Speakers Network outside the submitted work. Nicholas S. Reed, AuD, PhD, reported receiving stock options from Neosensory outside the submitted work. No other disclosures were reported.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.A version of this article appeared on Medscape.com.

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Not Kidding: Yellow Dye 5 May Lead to Invisibility

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Tue, 09/10/2024 - 12:16

 

The same dye that gives Twinkies their yellowish hue could be the key to invisibility. 

Applying the dye to lab mice made their skin temporarily transparent, allowing Stanford University researchers to observe the rodents’ digestive system, muscle fibers, and blood vessels, according to a study published in Science.

“It’s a stunning result,” said senior author Guosong Hong, PhD, who is assistant professor of materials science and engineering at Stanford University in California. “If the same technique could be applied to humans, it could offer a variety of benefits in biology, diagnostics, and even cosmetics.” 

The work drew upon optical concepts first described in the early 20th century to form a surprising theory: Applying a light-absorbing substance could render skin transparent by reducing the chaotic scattering of light as it strikes proteins, fats, and water in tissue. 

A search for a suitable light absorber led to FD&C Yellow 5, also called tartrazine, a synthetic color additive certified by the Food and Drug Administration (FDA) for use in foods, cosmetics, and medications. 

Rubbed on live mice (after areas of fur were removed using a drugstore depilatory cream), tartrazine rendered skin on their bellies, hind legs, and heads transparent within 5 minutes. With the naked eye, the researchers watched a mouse’s intestines, bladder, and liver at work. Using a microscope, they observed muscle fibers and saw blood vessels in a living mouse’s brain — all without making incisions. Transparency faded quickly when the dye was washed off.

Someday, the concept could be used in doctors’ offices and hospitals, Dr. Hong said. 

“Instead of relying on invasive biopsies, doctors might be able to diagnose deep-seated tumors by simply examining a person’s tissue without the need for invasive surgical removal,” he said. “This technique could potentially make blood draws less painful by helping phlebotomists easily locate veins under the skin. It could also enhance procedures like laser tattoo removal by allowing more precise targeting of the pigment beneath the skin.”
 

From Cake Frosting to Groundbreaking Research

Yellow 5 food dye can be found in everything from cereal, soda, spices, and cake frosting to lipstick, mouthwash, shampoo, dietary supplements, and house paint. Although it’s in some topical medications, more research is needed before it could be used in human diagnostics, said Christopher J. Rowlands, PhD, a senior lecturer in the Department of Bioengineering at Imperial College London, England, where he studies biophotonic instrumentation — ways to image structures inside the body more quickly and clearly. 

But the finding could prove useful in research. In a commentary published in Science, Dr. Rowlands and his colleague Jon Gorecki, PhD, an experimental optical physicist also at Imperial College London, noted that the dye could be an alternative to other optical clearing agents currently used in lab studies, such as glycerol, fructose, or acetic acid. Advantages are the effect is reversible and works at lower concentrations with fewer side effects. This could broaden the types of studies possible in lab animals, so researchers don’t have to rely on naturally transparent creatures like nematodes and zebrafish. 

The dye could also be paired with imaging techniques such as MRI or electron microscopy. 

“Imaging techniques all have pros and cons,” Dr. Rowlands said. “MRI can see all the way through the body albeit with limited resolution and contrast. Electron microscopy has excellent resolution but limited compatibility with live tissue and penetration depth. Optical microscopy has subcellular resolution, the ability to label things, excellent biocompatibility but less than 1 millimeter of penetration depth. This clearing method will give a substantial boost to optical imaging for medicine and biology.”

The discovery could improve the depth imaging equipment can achieve by tenfold, according to the commentary. 

Brain research especially stands to benefit. “Neurobiology in particular will have great use for combinations of multiphoton, optogenetics, and tissue clearing to record and control neural activity over (potentially) the whole mouse brain,” he said.
 

Refraction, Absorption, and The Invisible Man

The dye discovery has distant echoes in H.G. Wells’ 1897 novel The Invisible Man, Dr. Rowlands noted. In the book, a serum makes the main character invisible by changing the light scattering — or refractive index (RI) — of his cells to match the air around him.

The Stanford engineers looked to the past for inspiration, but not to fiction. They turned to a concept first described in the 1920s called the Kramers-Kronig relations, a mathematical principle that can be applied to relationships between the way light is refracted and absorbed in different materials. They also read up on Lorentz oscillation, which describes how electrons and atoms inside molecules react to light. 

They reasoned that light-absorbing compounds could equalize the differences between the light-scattering properties of proteins, lipids, and water that make skin opaque. 

With that, the search was on. The study’s first author, postdoctoral researcher Zihao Ou, PhD, began testing strong dyes to find a candidate. Tartrazine was a front-runner. 

“We found that dye molecules are more efficient in raising the refractive index of water than conventional RI-matching agents, thus resulting in transparency at a much lower concentration,” Dr. Hong said. “The underlying physics, explained by the Lorentz oscillator model and Kramers-Kronig relations, reveals that conventional RI matching agents like fructose are not as efficient because they are not ‘colored’ enough.”
 

What’s Next

Though the dye is already in products that people consume and apply to their skin, medical use is years away. In some people, tartrazine can cause skin or respiratory reactions. 

The National Science Foundation (NSF), which helped fund the research, posted a home or classroom activity related to the work on its website. It involves painting a tartrazine solution on a thin slice of raw chicken breast, making it transparent. The experiment should only be done while wearing a mask, eye protection, lab coat, and lab-quality nitrile gloves for protection, according to the NSF.

Meanwhile, Dr. Hong said his lab is looking for new compounds that will improve visibility through transparent skin, removing a red tone seen in the current experiments. And they’re looking for ways to induce cells to make their own “see-through” compounds. 

“We are exploring methods for cells to express intensely absorbing molecules endogenously, enabling genetically encoded tissue transparency in live animals,” he said.

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

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The same dye that gives Twinkies their yellowish hue could be the key to invisibility. 

Applying the dye to lab mice made their skin temporarily transparent, allowing Stanford University researchers to observe the rodents’ digestive system, muscle fibers, and blood vessels, according to a study published in Science.

“It’s a stunning result,” said senior author Guosong Hong, PhD, who is assistant professor of materials science and engineering at Stanford University in California. “If the same technique could be applied to humans, it could offer a variety of benefits in biology, diagnostics, and even cosmetics.” 

The work drew upon optical concepts first described in the early 20th century to form a surprising theory: Applying a light-absorbing substance could render skin transparent by reducing the chaotic scattering of light as it strikes proteins, fats, and water in tissue. 

A search for a suitable light absorber led to FD&C Yellow 5, also called tartrazine, a synthetic color additive certified by the Food and Drug Administration (FDA) for use in foods, cosmetics, and medications. 

Rubbed on live mice (after areas of fur were removed using a drugstore depilatory cream), tartrazine rendered skin on their bellies, hind legs, and heads transparent within 5 minutes. With the naked eye, the researchers watched a mouse’s intestines, bladder, and liver at work. Using a microscope, they observed muscle fibers and saw blood vessels in a living mouse’s brain — all without making incisions. Transparency faded quickly when the dye was washed off.

Someday, the concept could be used in doctors’ offices and hospitals, Dr. Hong said. 

“Instead of relying on invasive biopsies, doctors might be able to diagnose deep-seated tumors by simply examining a person’s tissue without the need for invasive surgical removal,” he said. “This technique could potentially make blood draws less painful by helping phlebotomists easily locate veins under the skin. It could also enhance procedures like laser tattoo removal by allowing more precise targeting of the pigment beneath the skin.”
 

From Cake Frosting to Groundbreaking Research

Yellow 5 food dye can be found in everything from cereal, soda, spices, and cake frosting to lipstick, mouthwash, shampoo, dietary supplements, and house paint. Although it’s in some topical medications, more research is needed before it could be used in human diagnostics, said Christopher J. Rowlands, PhD, a senior lecturer in the Department of Bioengineering at Imperial College London, England, where he studies biophotonic instrumentation — ways to image structures inside the body more quickly and clearly. 

But the finding could prove useful in research. In a commentary published in Science, Dr. Rowlands and his colleague Jon Gorecki, PhD, an experimental optical physicist also at Imperial College London, noted that the dye could be an alternative to other optical clearing agents currently used in lab studies, such as glycerol, fructose, or acetic acid. Advantages are the effect is reversible and works at lower concentrations with fewer side effects. This could broaden the types of studies possible in lab animals, so researchers don’t have to rely on naturally transparent creatures like nematodes and zebrafish. 

The dye could also be paired with imaging techniques such as MRI or electron microscopy. 

“Imaging techniques all have pros and cons,” Dr. Rowlands said. “MRI can see all the way through the body albeit with limited resolution and contrast. Electron microscopy has excellent resolution but limited compatibility with live tissue and penetration depth. Optical microscopy has subcellular resolution, the ability to label things, excellent biocompatibility but less than 1 millimeter of penetration depth. This clearing method will give a substantial boost to optical imaging for medicine and biology.”

The discovery could improve the depth imaging equipment can achieve by tenfold, according to the commentary. 

Brain research especially stands to benefit. “Neurobiology in particular will have great use for combinations of multiphoton, optogenetics, and tissue clearing to record and control neural activity over (potentially) the whole mouse brain,” he said.
 

Refraction, Absorption, and The Invisible Man

The dye discovery has distant echoes in H.G. Wells’ 1897 novel The Invisible Man, Dr. Rowlands noted. In the book, a serum makes the main character invisible by changing the light scattering — or refractive index (RI) — of his cells to match the air around him.

The Stanford engineers looked to the past for inspiration, but not to fiction. They turned to a concept first described in the 1920s called the Kramers-Kronig relations, a mathematical principle that can be applied to relationships between the way light is refracted and absorbed in different materials. They also read up on Lorentz oscillation, which describes how electrons and atoms inside molecules react to light. 

They reasoned that light-absorbing compounds could equalize the differences between the light-scattering properties of proteins, lipids, and water that make skin opaque. 

With that, the search was on. The study’s first author, postdoctoral researcher Zihao Ou, PhD, began testing strong dyes to find a candidate. Tartrazine was a front-runner. 

“We found that dye molecules are more efficient in raising the refractive index of water than conventional RI-matching agents, thus resulting in transparency at a much lower concentration,” Dr. Hong said. “The underlying physics, explained by the Lorentz oscillator model and Kramers-Kronig relations, reveals that conventional RI matching agents like fructose are not as efficient because they are not ‘colored’ enough.”
 

What’s Next

Though the dye is already in products that people consume and apply to their skin, medical use is years away. In some people, tartrazine can cause skin or respiratory reactions. 

The National Science Foundation (NSF), which helped fund the research, posted a home or classroom activity related to the work on its website. It involves painting a tartrazine solution on a thin slice of raw chicken breast, making it transparent. The experiment should only be done while wearing a mask, eye protection, lab coat, and lab-quality nitrile gloves for protection, according to the NSF.

Meanwhile, Dr. Hong said his lab is looking for new compounds that will improve visibility through transparent skin, removing a red tone seen in the current experiments. And they’re looking for ways to induce cells to make their own “see-through” compounds. 

“We are exploring methods for cells to express intensely absorbing molecules endogenously, enabling genetically encoded tissue transparency in live animals,” he said.

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

 

The same dye that gives Twinkies their yellowish hue could be the key to invisibility. 

Applying the dye to lab mice made their skin temporarily transparent, allowing Stanford University researchers to observe the rodents’ digestive system, muscle fibers, and blood vessels, according to a study published in Science.

“It’s a stunning result,” said senior author Guosong Hong, PhD, who is assistant professor of materials science and engineering at Stanford University in California. “If the same technique could be applied to humans, it could offer a variety of benefits in biology, diagnostics, and even cosmetics.” 

The work drew upon optical concepts first described in the early 20th century to form a surprising theory: Applying a light-absorbing substance could render skin transparent by reducing the chaotic scattering of light as it strikes proteins, fats, and water in tissue. 

A search for a suitable light absorber led to FD&C Yellow 5, also called tartrazine, a synthetic color additive certified by the Food and Drug Administration (FDA) for use in foods, cosmetics, and medications. 

Rubbed on live mice (after areas of fur were removed using a drugstore depilatory cream), tartrazine rendered skin on their bellies, hind legs, and heads transparent within 5 minutes. With the naked eye, the researchers watched a mouse’s intestines, bladder, and liver at work. Using a microscope, they observed muscle fibers and saw blood vessels in a living mouse’s brain — all without making incisions. Transparency faded quickly when the dye was washed off.

Someday, the concept could be used in doctors’ offices and hospitals, Dr. Hong said. 

“Instead of relying on invasive biopsies, doctors might be able to diagnose deep-seated tumors by simply examining a person’s tissue without the need for invasive surgical removal,” he said. “This technique could potentially make blood draws less painful by helping phlebotomists easily locate veins under the skin. It could also enhance procedures like laser tattoo removal by allowing more precise targeting of the pigment beneath the skin.”
 

From Cake Frosting to Groundbreaking Research

Yellow 5 food dye can be found in everything from cereal, soda, spices, and cake frosting to lipstick, mouthwash, shampoo, dietary supplements, and house paint. Although it’s in some topical medications, more research is needed before it could be used in human diagnostics, said Christopher J. Rowlands, PhD, a senior lecturer in the Department of Bioengineering at Imperial College London, England, where he studies biophotonic instrumentation — ways to image structures inside the body more quickly and clearly. 

But the finding could prove useful in research. In a commentary published in Science, Dr. Rowlands and his colleague Jon Gorecki, PhD, an experimental optical physicist also at Imperial College London, noted that the dye could be an alternative to other optical clearing agents currently used in lab studies, such as glycerol, fructose, or acetic acid. Advantages are the effect is reversible and works at lower concentrations with fewer side effects. This could broaden the types of studies possible in lab animals, so researchers don’t have to rely on naturally transparent creatures like nematodes and zebrafish. 

The dye could also be paired with imaging techniques such as MRI or electron microscopy. 

“Imaging techniques all have pros and cons,” Dr. Rowlands said. “MRI can see all the way through the body albeit with limited resolution and contrast. Electron microscopy has excellent resolution but limited compatibility with live tissue and penetration depth. Optical microscopy has subcellular resolution, the ability to label things, excellent biocompatibility but less than 1 millimeter of penetration depth. This clearing method will give a substantial boost to optical imaging for medicine and biology.”

The discovery could improve the depth imaging equipment can achieve by tenfold, according to the commentary. 

Brain research especially stands to benefit. “Neurobiology in particular will have great use for combinations of multiphoton, optogenetics, and tissue clearing to record and control neural activity over (potentially) the whole mouse brain,” he said.
 

Refraction, Absorption, and The Invisible Man

The dye discovery has distant echoes in H.G. Wells’ 1897 novel The Invisible Man, Dr. Rowlands noted. In the book, a serum makes the main character invisible by changing the light scattering — or refractive index (RI) — of his cells to match the air around him.

The Stanford engineers looked to the past for inspiration, but not to fiction. They turned to a concept first described in the 1920s called the Kramers-Kronig relations, a mathematical principle that can be applied to relationships between the way light is refracted and absorbed in different materials. They also read up on Lorentz oscillation, which describes how electrons and atoms inside molecules react to light. 

They reasoned that light-absorbing compounds could equalize the differences between the light-scattering properties of proteins, lipids, and water that make skin opaque. 

With that, the search was on. The study’s first author, postdoctoral researcher Zihao Ou, PhD, began testing strong dyes to find a candidate. Tartrazine was a front-runner. 

“We found that dye molecules are more efficient in raising the refractive index of water than conventional RI-matching agents, thus resulting in transparency at a much lower concentration,” Dr. Hong said. “The underlying physics, explained by the Lorentz oscillator model and Kramers-Kronig relations, reveals that conventional RI matching agents like fructose are not as efficient because they are not ‘colored’ enough.”
 

What’s Next

Though the dye is already in products that people consume and apply to their skin, medical use is years away. In some people, tartrazine can cause skin or respiratory reactions. 

The National Science Foundation (NSF), which helped fund the research, posted a home or classroom activity related to the work on its website. It involves painting a tartrazine solution on a thin slice of raw chicken breast, making it transparent. The experiment should only be done while wearing a mask, eye protection, lab coat, and lab-quality nitrile gloves for protection, according to the NSF.

Meanwhile, Dr. Hong said his lab is looking for new compounds that will improve visibility through transparent skin, removing a red tone seen in the current experiments. And they’re looking for ways to induce cells to make their own “see-through” compounds. 

“We are exploring methods for cells to express intensely absorbing molecules endogenously, enabling genetically encoded tissue transparency in live animals,” he said.

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

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Why More Doctors Are Joining Unions

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Tue, 09/10/2024 - 12:16

 

With huge shifts over the past decade in the way doctors are employed — half of all doctors now work for a health system or large medical group — the idea of unionizing is not only being explored but gaining traction within the profession. In fact, 8% of the physician workforce (or 70,000 physicians) belong to a union, according to statistics gathered in 2022.

Exact numbers are hard to come by, and, interestingly, although the American Medical Association (AMA) “ supports the right of physicians to engage in collective bargaining,” the organization doesn’t track union membership among physicians, according to an AMA spokesperson. 
 

Forming a Union

One challenge is that forming a union is not only time-consuming but also difficult, owing to several barriers. For starters, the laws dictating unionization differ by state, and the rules governing unionization vary if a hospital is public or private. If there’s enough momentum from doctors leading unionization efforts, approval from hospital leaders is required before an official election can be requested from the National Labor Relations Board.

That said, for doctors who are in a union — the two most popular are the Union of American Physicians and Dentists and the Doctors Council branch of the Service Employees International Union (SEIU)—the benefits are immense, especially because union members can focus on what matters, such as providing the best patient care possible.

For a profession that historically has not been unionized, this year alone, nine medical residency programs at hospitals such as Stanford Health, Montefiore Medical Center, and the University of Pennsylvania, formed unions, reported WBUR in Boston.
 

Belonging Matters 

“When you build a relationship with your patients, it’s special, and that connection isn’t replaceable,” said Nicholas VenOsdel, MD, a pediatrician at Allina Health Primary Care in Hastings, Minnesota, and a union member of the Doctors Council. “However, a lot of us have felt like that hasn’t been respected as the climate of healthcare has changed so fast.”

In fact, autonomy over how much time doctors spend with patients is driving a lot of interest in unionization.

“We don’t necessarily have that autonomy now,” said Amber Higgins, MD, an emergency physician and an obstetrician at ChristianaCare, a hospital network in Newark, Delaware, and a member of the Doctors Council. “There are so many other demands, whether it’s billing, patient documentation, or other demands from the employer, and all of that takes time away from patient care.”

Another primary driver of physician unionization is the physician burnout epidemic. Physicians collectively complain that they spend more time on electronic health record documentation and bureaucratic administration. Yet if unions can improve these working conditions, the benefit to physicians and their patients would be a welcome change.

Union members are bullish and believe that having a cohesive voice will make a difference.

“We need to use our collective voices to get back to focusing on patient care instead of staring at a computer screen for 80% of the day,” Dr. Higgins told this news organization. “So much of medicine involves getting to the correct diagnosis, listening to patients, observing them, and building a relationship with them. We need time to build that.”

With corporate consolidation and a profit-driven mandate by healthcare systems, doctors are increasingly frustrated and feel that their voices haven’t been heard enough when it comes to issues like workplace safety, working hours, and benefits, said Stuart Bussey, MD, JD, a family practice physician and president of the Union of American Physicians and Dentists in Sacramento, California. 

However, he adds that urging doctors to join together to fight for a better working environment hasn’t been easy.

“Doctors are individualists, and they don’t know how to work in packs like hospital administrators do,” said Dr. Bussey. “They’re hard to organize, but I want them to understand that unless they join hands, sign petitions, and speak as one voice, they’re going to lose out on an amazing opportunity.”
 

 

 

Overcoming Misperceptions About Unions

One barrier to doctors getting involved is the sentiment that unions might do the opposite of what’s intended — that is, they might further reduce a doctor’s autonomy and work flexibility. Or there may be a perception that the drive to join a union is predicated on making more money. 

Though he’s now in a union, Dr. VenOsdel, who has been in a hospital-based practice for 7 years, admits that he initially felt very differently about unions than he does today.

“Even though I have family members in healthcare unions, I had a neutral to even slightly negative view of unions,” said Dr. VenOsdel. “It took me working directly with the Minnesota Nurses Association and the Doctors Council to learn the other side of the story.”

Armed with more information, he began lobbying for stricter rules about how his state’s large healthcare systems were closing hospitals and ending much-needed community services.

“I remember standing at the Capitol in Minnesota and telling one of the members that I once felt negatively about unions,” he added. “I realized then that I only knew what employers were telling me via such things as emails about strikes — that information was all being shared from the employers’ perspective.”

The other misperception is that unions only exist to argue against management, including against colleagues who are also part of the management structure, said Dr. Higgins.

“Some doctors perceive being in a union as ‘how can those same leaders also be in a union,’” she said. She feels that they currently don’t have leadership representing them that can help with such things as restructuring their support teams or getting them help with certain tasks. “That’s another way unions can help.” 
 

Social Justice Plays a Role

For Dr. VenOsdel, being part of a union has helped him return to what he calls the “art” of medicine.

“Philosophically, the union gave me an option for change in what felt like a hopeless situation,” he said. “It wasn’t just that I was tossing the keys to someone else and saying, ‘I can’t fix this.’ Instead, we’re taking the reins back and fixing things ourselves.”

Bussey argues that as the uneven balance between administrators and providers in many healthcare organizations grows, the time to consider forming a union is now.

“We’re in a $4 trillion medical industrial revolution,” he said. “Administrators and bureaucrats are multiplying 30-fold times vs providers, and most of that $4 trillion supports things that don’t contribute to the doctor-patient relationship.”

Furthermore, union proponents say that where a one-on-one relationship between doctor and patient once existed, that has now been “triangulated” to include administrators.

“We’ve lost power in every way,” Dr. Bussey said. “We have the degrees, the liability, and the knowledge — we should have more power to make our workplaces safer and better.”

Ultimately, for some unionized doctors, the very holding of a union card is rooted in supporting social justice issues.

“When doctors realize how powerful a tool a union can be for social justice and change, this will alter perceptions of unions within our profession,” Dr. VenOsdel said. “Our union helps give us a voice to stand up for other staff who aren’t unionized and, most importantly, to stand up for the patients who need us.”
 

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

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With huge shifts over the past decade in the way doctors are employed — half of all doctors now work for a health system or large medical group — the idea of unionizing is not only being explored but gaining traction within the profession. In fact, 8% of the physician workforce (or 70,000 physicians) belong to a union, according to statistics gathered in 2022.

Exact numbers are hard to come by, and, interestingly, although the American Medical Association (AMA) “ supports the right of physicians to engage in collective bargaining,” the organization doesn’t track union membership among physicians, according to an AMA spokesperson. 
 

Forming a Union

One challenge is that forming a union is not only time-consuming but also difficult, owing to several barriers. For starters, the laws dictating unionization differ by state, and the rules governing unionization vary if a hospital is public or private. If there’s enough momentum from doctors leading unionization efforts, approval from hospital leaders is required before an official election can be requested from the National Labor Relations Board.

That said, for doctors who are in a union — the two most popular are the Union of American Physicians and Dentists and the Doctors Council branch of the Service Employees International Union (SEIU)—the benefits are immense, especially because union members can focus on what matters, such as providing the best patient care possible.

For a profession that historically has not been unionized, this year alone, nine medical residency programs at hospitals such as Stanford Health, Montefiore Medical Center, and the University of Pennsylvania, formed unions, reported WBUR in Boston.
 

Belonging Matters 

“When you build a relationship with your patients, it’s special, and that connection isn’t replaceable,” said Nicholas VenOsdel, MD, a pediatrician at Allina Health Primary Care in Hastings, Minnesota, and a union member of the Doctors Council. “However, a lot of us have felt like that hasn’t been respected as the climate of healthcare has changed so fast.”

In fact, autonomy over how much time doctors spend with patients is driving a lot of interest in unionization.

“We don’t necessarily have that autonomy now,” said Amber Higgins, MD, an emergency physician and an obstetrician at ChristianaCare, a hospital network in Newark, Delaware, and a member of the Doctors Council. “There are so many other demands, whether it’s billing, patient documentation, or other demands from the employer, and all of that takes time away from patient care.”

Another primary driver of physician unionization is the physician burnout epidemic. Physicians collectively complain that they spend more time on electronic health record documentation and bureaucratic administration. Yet if unions can improve these working conditions, the benefit to physicians and their patients would be a welcome change.

Union members are bullish and believe that having a cohesive voice will make a difference.

“We need to use our collective voices to get back to focusing on patient care instead of staring at a computer screen for 80% of the day,” Dr. Higgins told this news organization. “So much of medicine involves getting to the correct diagnosis, listening to patients, observing them, and building a relationship with them. We need time to build that.”

With corporate consolidation and a profit-driven mandate by healthcare systems, doctors are increasingly frustrated and feel that their voices haven’t been heard enough when it comes to issues like workplace safety, working hours, and benefits, said Stuart Bussey, MD, JD, a family practice physician and president of the Union of American Physicians and Dentists in Sacramento, California. 

However, he adds that urging doctors to join together to fight for a better working environment hasn’t been easy.

“Doctors are individualists, and they don’t know how to work in packs like hospital administrators do,” said Dr. Bussey. “They’re hard to organize, but I want them to understand that unless they join hands, sign petitions, and speak as one voice, they’re going to lose out on an amazing opportunity.”
 

 

 

Overcoming Misperceptions About Unions

One barrier to doctors getting involved is the sentiment that unions might do the opposite of what’s intended — that is, they might further reduce a doctor’s autonomy and work flexibility. Or there may be a perception that the drive to join a union is predicated on making more money. 

Though he’s now in a union, Dr. VenOsdel, who has been in a hospital-based practice for 7 years, admits that he initially felt very differently about unions than he does today.

“Even though I have family members in healthcare unions, I had a neutral to even slightly negative view of unions,” said Dr. VenOsdel. “It took me working directly with the Minnesota Nurses Association and the Doctors Council to learn the other side of the story.”

Armed with more information, he began lobbying for stricter rules about how his state’s large healthcare systems were closing hospitals and ending much-needed community services.

“I remember standing at the Capitol in Minnesota and telling one of the members that I once felt negatively about unions,” he added. “I realized then that I only knew what employers were telling me via such things as emails about strikes — that information was all being shared from the employers’ perspective.”

The other misperception is that unions only exist to argue against management, including against colleagues who are also part of the management structure, said Dr. Higgins.

“Some doctors perceive being in a union as ‘how can those same leaders also be in a union,’” she said. She feels that they currently don’t have leadership representing them that can help with such things as restructuring their support teams or getting them help with certain tasks. “That’s another way unions can help.” 
 

Social Justice Plays a Role

For Dr. VenOsdel, being part of a union has helped him return to what he calls the “art” of medicine.

“Philosophically, the union gave me an option for change in what felt like a hopeless situation,” he said. “It wasn’t just that I was tossing the keys to someone else and saying, ‘I can’t fix this.’ Instead, we’re taking the reins back and fixing things ourselves.”

Bussey argues that as the uneven balance between administrators and providers in many healthcare organizations grows, the time to consider forming a union is now.

“We’re in a $4 trillion medical industrial revolution,” he said. “Administrators and bureaucrats are multiplying 30-fold times vs providers, and most of that $4 trillion supports things that don’t contribute to the doctor-patient relationship.”

Furthermore, union proponents say that where a one-on-one relationship between doctor and patient once existed, that has now been “triangulated” to include administrators.

“We’ve lost power in every way,” Dr. Bussey said. “We have the degrees, the liability, and the knowledge — we should have more power to make our workplaces safer and better.”

Ultimately, for some unionized doctors, the very holding of a union card is rooted in supporting social justice issues.

“When doctors realize how powerful a tool a union can be for social justice and change, this will alter perceptions of unions within our profession,” Dr. VenOsdel said. “Our union helps give us a voice to stand up for other staff who aren’t unionized and, most importantly, to stand up for the patients who need us.”
 

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

 

With huge shifts over the past decade in the way doctors are employed — half of all doctors now work for a health system or large medical group — the idea of unionizing is not only being explored but gaining traction within the profession. In fact, 8% of the physician workforce (or 70,000 physicians) belong to a union, according to statistics gathered in 2022.

Exact numbers are hard to come by, and, interestingly, although the American Medical Association (AMA) “ supports the right of physicians to engage in collective bargaining,” the organization doesn’t track union membership among physicians, according to an AMA spokesperson. 
 

Forming a Union

One challenge is that forming a union is not only time-consuming but also difficult, owing to several barriers. For starters, the laws dictating unionization differ by state, and the rules governing unionization vary if a hospital is public or private. If there’s enough momentum from doctors leading unionization efforts, approval from hospital leaders is required before an official election can be requested from the National Labor Relations Board.

That said, for doctors who are in a union — the two most popular are the Union of American Physicians and Dentists and the Doctors Council branch of the Service Employees International Union (SEIU)—the benefits are immense, especially because union members can focus on what matters, such as providing the best patient care possible.

For a profession that historically has not been unionized, this year alone, nine medical residency programs at hospitals such as Stanford Health, Montefiore Medical Center, and the University of Pennsylvania, formed unions, reported WBUR in Boston.
 

Belonging Matters 

“When you build a relationship with your patients, it’s special, and that connection isn’t replaceable,” said Nicholas VenOsdel, MD, a pediatrician at Allina Health Primary Care in Hastings, Minnesota, and a union member of the Doctors Council. “However, a lot of us have felt like that hasn’t been respected as the climate of healthcare has changed so fast.”

In fact, autonomy over how much time doctors spend with patients is driving a lot of interest in unionization.

“We don’t necessarily have that autonomy now,” said Amber Higgins, MD, an emergency physician and an obstetrician at ChristianaCare, a hospital network in Newark, Delaware, and a member of the Doctors Council. “There are so many other demands, whether it’s billing, patient documentation, or other demands from the employer, and all of that takes time away from patient care.”

Another primary driver of physician unionization is the physician burnout epidemic. Physicians collectively complain that they spend more time on electronic health record documentation and bureaucratic administration. Yet if unions can improve these working conditions, the benefit to physicians and their patients would be a welcome change.

Union members are bullish and believe that having a cohesive voice will make a difference.

“We need to use our collective voices to get back to focusing on patient care instead of staring at a computer screen for 80% of the day,” Dr. Higgins told this news organization. “So much of medicine involves getting to the correct diagnosis, listening to patients, observing them, and building a relationship with them. We need time to build that.”

With corporate consolidation and a profit-driven mandate by healthcare systems, doctors are increasingly frustrated and feel that their voices haven’t been heard enough when it comes to issues like workplace safety, working hours, and benefits, said Stuart Bussey, MD, JD, a family practice physician and president of the Union of American Physicians and Dentists in Sacramento, California. 

However, he adds that urging doctors to join together to fight for a better working environment hasn’t been easy.

“Doctors are individualists, and they don’t know how to work in packs like hospital administrators do,” said Dr. Bussey. “They’re hard to organize, but I want them to understand that unless they join hands, sign petitions, and speak as one voice, they’re going to lose out on an amazing opportunity.”
 

 

 

Overcoming Misperceptions About Unions

One barrier to doctors getting involved is the sentiment that unions might do the opposite of what’s intended — that is, they might further reduce a doctor’s autonomy and work flexibility. Or there may be a perception that the drive to join a union is predicated on making more money. 

Though he’s now in a union, Dr. VenOsdel, who has been in a hospital-based practice for 7 years, admits that he initially felt very differently about unions than he does today.

“Even though I have family members in healthcare unions, I had a neutral to even slightly negative view of unions,” said Dr. VenOsdel. “It took me working directly with the Minnesota Nurses Association and the Doctors Council to learn the other side of the story.”

Armed with more information, he began lobbying for stricter rules about how his state’s large healthcare systems were closing hospitals and ending much-needed community services.

“I remember standing at the Capitol in Minnesota and telling one of the members that I once felt negatively about unions,” he added. “I realized then that I only knew what employers were telling me via such things as emails about strikes — that information was all being shared from the employers’ perspective.”

The other misperception is that unions only exist to argue against management, including against colleagues who are also part of the management structure, said Dr. Higgins.

“Some doctors perceive being in a union as ‘how can those same leaders also be in a union,’” she said. She feels that they currently don’t have leadership representing them that can help with such things as restructuring their support teams or getting them help with certain tasks. “That’s another way unions can help.” 
 

Social Justice Plays a Role

For Dr. VenOsdel, being part of a union has helped him return to what he calls the “art” of medicine.

“Philosophically, the union gave me an option for change in what felt like a hopeless situation,” he said. “It wasn’t just that I was tossing the keys to someone else and saying, ‘I can’t fix this.’ Instead, we’re taking the reins back and fixing things ourselves.”

Bussey argues that as the uneven balance between administrators and providers in many healthcare organizations grows, the time to consider forming a union is now.

“We’re in a $4 trillion medical industrial revolution,” he said. “Administrators and bureaucrats are multiplying 30-fold times vs providers, and most of that $4 trillion supports things that don’t contribute to the doctor-patient relationship.”

Furthermore, union proponents say that where a one-on-one relationship between doctor and patient once existed, that has now been “triangulated” to include administrators.

“We’ve lost power in every way,” Dr. Bussey said. “We have the degrees, the liability, and the knowledge — we should have more power to make our workplaces safer and better.”

Ultimately, for some unionized doctors, the very holding of a union card is rooted in supporting social justice issues.

“When doctors realize how powerful a tool a union can be for social justice and change, this will alter perceptions of unions within our profession,” Dr. VenOsdel said. “Our union helps give us a voice to stand up for other staff who aren’t unionized and, most importantly, to stand up for the patients who need us.”
 

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

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The Small Business of Medicine

Article Type
Changed
Mon, 09/09/2024 - 12:08

 

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Dr. Allan M. Block, a neurologist in Scottsdale, Arizona.
Dr. Allan M. Block

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

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

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Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Dr. Allan M. Block, a neurologist in Scottsdale, Arizona.
Dr. Allan M. Block

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

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

 

Black Friday is coming up. Although it seems (fortunately) to have lost some of its insanity since the pandemic, it’s still a huge shopping day for those who want to spend their day off in hand-to-hand combat at a Walmart. For me it’s a good day not to leave my house at all.

Following Black Friday we have Cyber Monday, where people go online to start buying stuff, presumably using business WiFi when they’re back at work. In spite of the apparent contradiction of having an online shopping day when people are at their jobs, it’s shamelessly promoted by the online retail giants.

Dr. Allan M. Block, a neurologist in Scottsdale, Arizona.
Dr. Allan M. Block

Sandwiched between them is the quieter Small Business Saturday, started in 2010 by American Express and since gradually taking hold here and across the pond. The idea is to support the smaller local, perhaps family-owned, stores of varying kinds. Politicians love to talk about small businesses, calling them the backbone of the economy, promising to support them, etc.

I have no issue with that. I agree with it. I try to support my smaller, local places whenever I can. I’m glad AMEX started it, and that it’s taken off.

So why don’t we have a campaign to support small medical practices? Aren’t we small businesses, too? I’m the only doctor at my place, that’s about as small as you can get.

Like other small businesses, I don’t have the resources to advertise, aside from a simple website. At the same time I can’t drive too far without seeing a billboard, or hearing a radio ad, for one of the large local healthcare systems promising better convenience and care than that of their competitors.

I’m certainly not in a position to offer extended or weekend hours — I mean, I could, but I also have my own sanity to keep. But at the same time small practices may know their patients better than Huge Medicine Inc. We don’t have as many patients, and the staff turnover at small places is usually lower.

No one, though, is going to stand up for us, AMEX included (outside of cosmetic services, doctor visit charges are probably a tiny fraction of credit card company charges). Even our own organizations, like the AMA and others, won’t (at least not too much). They might pay lip service to us, but the reality is that most of their members work for large healthcare systems. Those groups probably make some big donations to them, too. So the last thing they want to do is tick them off.

I’m not against large groups. They have capabilities I don’t, like the ability to run research trials and have subspecialists. Even the best of us in solo practice needs someone better to refer to, such as an epileptologist, Parkinsonologist, neuromuscular disease-ologist, When I can’t help a patient any further those are the doctors I turn to, and, believe me, I appreciate them.

But it sometimes seems odd that, in a world where financial companies and public figures often stress their support for small business, those of us in the small medical practice are forgotten.
 

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

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Does MS Protect Against Alzheimer’s Disease?

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Changed
Mon, 09/09/2024 - 10:09

 

In a recent study, patients with multiple sclerosis (MS) had half the rate of amyloid beta pathology versus matched controls without MS, supporting authors’ suspicion that MS may protect against Alzheimer’s disease. Understanding how MS does this may drive new treatment strategies, said the authors of the study, which was published online in Annals of Neurology. Regarding current treatments, they added, the availability of new disease-modifying Alzheimer’s disease therapies increases the importance of early diagnosis in cognitively impaired people including those with MS.

Confirmatory Studies Needed

“Replication and confirmation of these findings, including in studies representative of the real-world Alzheimer’s population in race/ethnicity and sex/gender, are needed before any clinical implications can be drawn,” said Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach. She was not involved with the study but was asked to comment.

The study’s most important immediate implication, said Dr. Sexton, is that it “opens the door to questions about why MS may be associated with Alzheimer’s risk.”

Alzheimer's Association
Dr. Claire Sexton

 

Anecdotal Observation

Although life expectancy for people with MS is increasing, the authors, led by Matthew R. Brier, MD, PhD, an assistant professor at Washington University in St. Louis, Missouri, said they have seen no concomitant rise in Alzheimer’s disease dementia among their patients with MS. This anecdotal observation fueled their hypothesis that Alzheimer’s disease pathology occurs less frequently in this population.

To test their hypothesis, the investigators sequentially enrolled 100 patients with MS (age 60 years or older), along with 300 non-MS controls matched for age, sex, apolipoprotein E (apoE) proteotype, and cognitive status. All participants underwent the Mini-Mental State Examination (MMSE) and PrecivityAD2 (C2N Diagnostics) blood testing.

Washngton University
Dr. Matthew R. Brier


Overall, patients with MS had lower p-tau217 (t = 3.76, P = .00019) and amyloid probability score 2 (APS2; t = 3.83, P = .00015) ratios than did those without MS. APS2 combines p-tau217 ratio with Abeta42/40 ratio. In addition, APS2 and p-tau217 ratios were lower in patients with MS and ApoE3/apoE3 or apoE3/apoE4 proteotype. MMSE scores were also slightly lower in the MS cohort: 27.6 versus 28.44 for controls. Of 11 patients with MS who underwent Pittsburgh Compound B (PiB) positron emission tomography (PET), nine had congruent PiB PET and plasma results.

When the investigators applied clinical cutoffs, 7.1% of patients with MS were APS2-positive, versus 15.3% of controls (P = .0043). The corresponding figures for p-tau217 ratio positivity were 9% and 18.3%, respectively (P = .0024). Mean Abeta42/40 scores showed no difference between groups.

Patients with MS and positive amyloid biomarkers often had atypical MS features at diagnosis. Compared with biomarker-negative patients with MS, odds ratios for having at least two atypical MS features at diagnosis among APS2-positive and p-tau217 ratio-positive patients with MS were 23.3 and 11.38, respectively.

Data regarding the actual incidence of Alzheimer’s disease among people with MS are scarce and conflicting. An autopsy study published in Annals of Neurology in 2008 revealed the expected rate of amyloid pathology in MS brain tissue, along with extensive microglia activation. In a PET study published in Annals of Neurology in 2020, however, researchers found less amyloid pathology among patients with MS than those without, but little difference in tau pathology.

Because MS and Alzheimer’s disease can each cause cognitive impairment, the rate of co-occurrence of MS and Alzheimer’s disease has been difficult to ascertain without accurate biomarkers. But, the authors said, the advent of disease-modifying therapies makes identifying early Alzheimer’s dementia in MS patients relevant.
 

 

 

Possible Explanations

The authors hypothesized that the lower rate of amyloid pathology observed in their patients with MS may stem from the following possibly overlapping mechanisms:

  • MS components, such as persistent perilesional immune activity, may inhibit amyloid beta deposition or facilitate its clearance.
  • Exposure to MS drugs may impact Alzheimer’s disease pathology. Most study patients with MS were exposed to beta interferons or glatiramer acetate, the authors noted, and 39 had switched to high-efficacy medications such as B-cell depleting therapies and natalizumab.
  • MS’s genetic signature may protect against AD.

“Investigating these ideas would advance our understanding of the relationship between MS and Alzheimer’s, and potentially inform avenues for treatment,” said Dr. Sexton. In this regard, the Alzheimer’s Association has funded an ongoing study examining a drug currently used to promote myelin formation in individuals with MS in genetically engineered Alzheimer’s-like mice. Additional Association-funded studies that examine inflammation also may improve understanding of the mechanisms that may link these diseases, said Dr. Sexton. 

The study authors added that unusual cases, such as a study patient who had high amyloid burden by PET but negative APS2 and tau PET, also may shed light on interactions between MS, amyloid pathology, and tau pathology.

Limitations of the present study include the fact that plasma Alzheimer’s disease biomarkers are potentially affected by other conditions as well, according to a study published in Nature Medicine. Additional shortcomings include the MS cohort’s relatively small size and lack of diagnostic confirmation by cerebrospinal fluid. Although MMSE scores among patients with MS were slightly lower, the authors added, this disparity would lead one to expect more, not less, amyloid pathology among these patients if their cognitive impairment resulted from Alzheimer’s disease.

Dr. Sexton reported no relevant financial interests.

The study was supported by the Hope Center for Neurological Disorders at Washington University in St. Louis and by C2N Diagnostics. Washington University in St. Louis holds equity in C2N Diagnostics and may receive royalties resulting from use of PrecivityAD2.

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In a recent study, patients with multiple sclerosis (MS) had half the rate of amyloid beta pathology versus matched controls without MS, supporting authors’ suspicion that MS may protect against Alzheimer’s disease. Understanding how MS does this may drive new treatment strategies, said the authors of the study, which was published online in Annals of Neurology. Regarding current treatments, they added, the availability of new disease-modifying Alzheimer’s disease therapies increases the importance of early diagnosis in cognitively impaired people including those with MS.

Confirmatory Studies Needed

“Replication and confirmation of these findings, including in studies representative of the real-world Alzheimer’s population in race/ethnicity and sex/gender, are needed before any clinical implications can be drawn,” said Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach. She was not involved with the study but was asked to comment.

The study’s most important immediate implication, said Dr. Sexton, is that it “opens the door to questions about why MS may be associated with Alzheimer’s risk.”

Alzheimer's Association
Dr. Claire Sexton

 

Anecdotal Observation

Although life expectancy for people with MS is increasing, the authors, led by Matthew R. Brier, MD, PhD, an assistant professor at Washington University in St. Louis, Missouri, said they have seen no concomitant rise in Alzheimer’s disease dementia among their patients with MS. This anecdotal observation fueled their hypothesis that Alzheimer’s disease pathology occurs less frequently in this population.

To test their hypothesis, the investigators sequentially enrolled 100 patients with MS (age 60 years or older), along with 300 non-MS controls matched for age, sex, apolipoprotein E (apoE) proteotype, and cognitive status. All participants underwent the Mini-Mental State Examination (MMSE) and PrecivityAD2 (C2N Diagnostics) blood testing.

Washngton University
Dr. Matthew R. Brier


Overall, patients with MS had lower p-tau217 (t = 3.76, P = .00019) and amyloid probability score 2 (APS2; t = 3.83, P = .00015) ratios than did those without MS. APS2 combines p-tau217 ratio with Abeta42/40 ratio. In addition, APS2 and p-tau217 ratios were lower in patients with MS and ApoE3/apoE3 or apoE3/apoE4 proteotype. MMSE scores were also slightly lower in the MS cohort: 27.6 versus 28.44 for controls. Of 11 patients with MS who underwent Pittsburgh Compound B (PiB) positron emission tomography (PET), nine had congruent PiB PET and plasma results.

When the investigators applied clinical cutoffs, 7.1% of patients with MS were APS2-positive, versus 15.3% of controls (P = .0043). The corresponding figures for p-tau217 ratio positivity were 9% and 18.3%, respectively (P = .0024). Mean Abeta42/40 scores showed no difference between groups.

Patients with MS and positive amyloid biomarkers often had atypical MS features at diagnosis. Compared with biomarker-negative patients with MS, odds ratios for having at least two atypical MS features at diagnosis among APS2-positive and p-tau217 ratio-positive patients with MS were 23.3 and 11.38, respectively.

Data regarding the actual incidence of Alzheimer’s disease among people with MS are scarce and conflicting. An autopsy study published in Annals of Neurology in 2008 revealed the expected rate of amyloid pathology in MS brain tissue, along with extensive microglia activation. In a PET study published in Annals of Neurology in 2020, however, researchers found less amyloid pathology among patients with MS than those without, but little difference in tau pathology.

Because MS and Alzheimer’s disease can each cause cognitive impairment, the rate of co-occurrence of MS and Alzheimer’s disease has been difficult to ascertain without accurate biomarkers. But, the authors said, the advent of disease-modifying therapies makes identifying early Alzheimer’s dementia in MS patients relevant.
 

 

 

Possible Explanations

The authors hypothesized that the lower rate of amyloid pathology observed in their patients with MS may stem from the following possibly overlapping mechanisms:

  • MS components, such as persistent perilesional immune activity, may inhibit amyloid beta deposition or facilitate its clearance.
  • Exposure to MS drugs may impact Alzheimer’s disease pathology. Most study patients with MS were exposed to beta interferons or glatiramer acetate, the authors noted, and 39 had switched to high-efficacy medications such as B-cell depleting therapies and natalizumab.
  • MS’s genetic signature may protect against AD.

“Investigating these ideas would advance our understanding of the relationship between MS and Alzheimer’s, and potentially inform avenues for treatment,” said Dr. Sexton. In this regard, the Alzheimer’s Association has funded an ongoing study examining a drug currently used to promote myelin formation in individuals with MS in genetically engineered Alzheimer’s-like mice. Additional Association-funded studies that examine inflammation also may improve understanding of the mechanisms that may link these diseases, said Dr. Sexton. 

The study authors added that unusual cases, such as a study patient who had high amyloid burden by PET but negative APS2 and tau PET, also may shed light on interactions between MS, amyloid pathology, and tau pathology.

Limitations of the present study include the fact that plasma Alzheimer’s disease biomarkers are potentially affected by other conditions as well, according to a study published in Nature Medicine. Additional shortcomings include the MS cohort’s relatively small size and lack of diagnostic confirmation by cerebrospinal fluid. Although MMSE scores among patients with MS were slightly lower, the authors added, this disparity would lead one to expect more, not less, amyloid pathology among these patients if their cognitive impairment resulted from Alzheimer’s disease.

Dr. Sexton reported no relevant financial interests.

The study was supported by the Hope Center for Neurological Disorders at Washington University in St. Louis and by C2N Diagnostics. Washington University in St. Louis holds equity in C2N Diagnostics and may receive royalties resulting from use of PrecivityAD2.

 

In a recent study, patients with multiple sclerosis (MS) had half the rate of amyloid beta pathology versus matched controls without MS, supporting authors’ suspicion that MS may protect against Alzheimer’s disease. Understanding how MS does this may drive new treatment strategies, said the authors of the study, which was published online in Annals of Neurology. Regarding current treatments, they added, the availability of new disease-modifying Alzheimer’s disease therapies increases the importance of early diagnosis in cognitively impaired people including those with MS.

Confirmatory Studies Needed

“Replication and confirmation of these findings, including in studies representative of the real-world Alzheimer’s population in race/ethnicity and sex/gender, are needed before any clinical implications can be drawn,” said Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach. She was not involved with the study but was asked to comment.

The study’s most important immediate implication, said Dr. Sexton, is that it “opens the door to questions about why MS may be associated with Alzheimer’s risk.”

Alzheimer's Association
Dr. Claire Sexton

 

Anecdotal Observation

Although life expectancy for people with MS is increasing, the authors, led by Matthew R. Brier, MD, PhD, an assistant professor at Washington University in St. Louis, Missouri, said they have seen no concomitant rise in Alzheimer’s disease dementia among their patients with MS. This anecdotal observation fueled their hypothesis that Alzheimer’s disease pathology occurs less frequently in this population.

To test their hypothesis, the investigators sequentially enrolled 100 patients with MS (age 60 years or older), along with 300 non-MS controls matched for age, sex, apolipoprotein E (apoE) proteotype, and cognitive status. All participants underwent the Mini-Mental State Examination (MMSE) and PrecivityAD2 (C2N Diagnostics) blood testing.

Washngton University
Dr. Matthew R. Brier


Overall, patients with MS had lower p-tau217 (t = 3.76, P = .00019) and amyloid probability score 2 (APS2; t = 3.83, P = .00015) ratios than did those without MS. APS2 combines p-tau217 ratio with Abeta42/40 ratio. In addition, APS2 and p-tau217 ratios were lower in patients with MS and ApoE3/apoE3 or apoE3/apoE4 proteotype. MMSE scores were also slightly lower in the MS cohort: 27.6 versus 28.44 for controls. Of 11 patients with MS who underwent Pittsburgh Compound B (PiB) positron emission tomography (PET), nine had congruent PiB PET and plasma results.

When the investigators applied clinical cutoffs, 7.1% of patients with MS were APS2-positive, versus 15.3% of controls (P = .0043). The corresponding figures for p-tau217 ratio positivity were 9% and 18.3%, respectively (P = .0024). Mean Abeta42/40 scores showed no difference between groups.

Patients with MS and positive amyloid biomarkers often had atypical MS features at diagnosis. Compared with biomarker-negative patients with MS, odds ratios for having at least two atypical MS features at diagnosis among APS2-positive and p-tau217 ratio-positive patients with MS were 23.3 and 11.38, respectively.

Data regarding the actual incidence of Alzheimer’s disease among people with MS are scarce and conflicting. An autopsy study published in Annals of Neurology in 2008 revealed the expected rate of amyloid pathology in MS brain tissue, along with extensive microglia activation. In a PET study published in Annals of Neurology in 2020, however, researchers found less amyloid pathology among patients with MS than those without, but little difference in tau pathology.

Because MS and Alzheimer’s disease can each cause cognitive impairment, the rate of co-occurrence of MS and Alzheimer’s disease has been difficult to ascertain without accurate biomarkers. But, the authors said, the advent of disease-modifying therapies makes identifying early Alzheimer’s dementia in MS patients relevant.
 

 

 

Possible Explanations

The authors hypothesized that the lower rate of amyloid pathology observed in their patients with MS may stem from the following possibly overlapping mechanisms:

  • MS components, such as persistent perilesional immune activity, may inhibit amyloid beta deposition or facilitate its clearance.
  • Exposure to MS drugs may impact Alzheimer’s disease pathology. Most study patients with MS were exposed to beta interferons or glatiramer acetate, the authors noted, and 39 had switched to high-efficacy medications such as B-cell depleting therapies and natalizumab.
  • MS’s genetic signature may protect against AD.

“Investigating these ideas would advance our understanding of the relationship between MS and Alzheimer’s, and potentially inform avenues for treatment,” said Dr. Sexton. In this regard, the Alzheimer’s Association has funded an ongoing study examining a drug currently used to promote myelin formation in individuals with MS in genetically engineered Alzheimer’s-like mice. Additional Association-funded studies that examine inflammation also may improve understanding of the mechanisms that may link these diseases, said Dr. Sexton. 

The study authors added that unusual cases, such as a study patient who had high amyloid burden by PET but negative APS2 and tau PET, also may shed light on interactions between MS, amyloid pathology, and tau pathology.

Limitations of the present study include the fact that plasma Alzheimer’s disease biomarkers are potentially affected by other conditions as well, according to a study published in Nature Medicine. Additional shortcomings include the MS cohort’s relatively small size and lack of diagnostic confirmation by cerebrospinal fluid. Although MMSE scores among patients with MS were slightly lower, the authors added, this disparity would lead one to expect more, not less, amyloid pathology among these patients if their cognitive impairment resulted from Alzheimer’s disease.

Dr. Sexton reported no relevant financial interests.

The study was supported by the Hope Center for Neurological Disorders at Washington University in St. Louis and by C2N Diagnostics. Washington University in St. Louis holds equity in C2N Diagnostics and may receive royalties resulting from use of PrecivityAD2.

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Brain Network Significantly Larger in People With Depression, Even in Childhood

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Changed
Fri, 09/06/2024 - 13:35

Researchers have discovered that a brain network involved in reward processing and attention to stimuli is markedly bigger in people with depression, remains stable over time, is unaffected by mood changes, and can be detected in children before onset of depression symptoms.

Using a novel brain-mapping technique, researchers found that the frontostriatal salience network was expanded nearly twofold in the brains of most individuals studied with depression compared with controls.

“This expansion in cortex was trait-like, meaning it was stable over time and did not change as symptoms changed over time,” said lead author Charles Lynch, PhD, assistant professor of neuroscience, Department of Psychiatry, Weill Cornell Medicine in New York.

It could also be detected in children who later developed depression, suggesting it may serve as a biomarker of depression risk. Investigators said the findings could aid in prevention and early detection of depression, as well as the development of more personalized treatment.

The study was published online in Nature.
 

Prewired for Depression?

Precision functional mapping is a relatively new approach to brain mapping in individuals that uses large amounts of fMRI data from hours of scans per person. The technique has been used to show differences in brain networks between and in healthy individuals but had not been used to study brain networks in people with depression.

“We leveraged our large longitudinal datasets — with many hours of functional MRI scanning per subject — to construct individual-specific maps of functional brain networks in each patient using precision functional mapping, instead of relying on group average,” Dr. Lynch said.

In the primary analysis of 141 adults with major depression and 37 healthy controls, the frontostriatal salience network — which is involved in reward processing and attention to internal and external stimuli — was markedly larger in these individuals with depression.

“This is one of the first times these kinds of personalized maps have been created in individuals with depression, and this is how we first observed of the salience network being larger in individuals with depression,” Dr. Lynch said.

In four of the six individuals, the salience network was expanded more than twofold, outside the range observed in all 37 healthy controls. On average, the salience network occupied 73% more of the cortical surface relative to the average in healthy controls.

The findings were replicated using independent samples of repeatedly sampled individuals with depression and in large-scale group average data.

The expansion of the salience network did not change over time and was unaffected by changes in mood state.

“These observations led us to propose that instead of driving changes in depressive symptoms over time, salience network expansion may be a stable marker of risk for developing depression,” the study team wrote.

An analysis of brain scans from 57 children who went on to develop depressive symptoms during adolescence and an equal number of children who did not develop depressive symptoms supports this theory.

On average, the salience network occupied roughly 36% more of cortex in the children with no current or previous symptoms of depression at the time of their fMRI scans but who subsequently developed clinically significant symptoms of depression, relative to children with no depressive symptoms at any study time point, the researchers found.
 

 

 

Immediate Clinical Impact?

Reached for comment, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, said this research “exemplifies the promising intersection of neurology and digital health, where advanced neuroimaging and data-driven approaches can transform mental health care into a more precise and individualized practice,” Dr. Lakhan said. “By identifying this brain network expansion, we’re unlocking new possibilities for precision medicine in mental health.”

Dr. Lakhan, who wasn’t involved in this research, said identifying the expansion of the frontostriatal salience network in individuals with depression opens new avenues for developing novel therapeutics.

“By targeting this network through neuromodulation techniques like deep brain stimulation, transcranial magnetic stimulation, and prescription digital therapeutics, treatments can be more precisely tailored to individual neurobiological profiles,” Dr. Lakhan said. “Additionally, this network expansion could serve as a biomarker for early detection, allowing for preventive strategies or personalized treatment plans, particularly for those at risk of developing depression.”

In addition, a greater understanding of the mechanisms driving salience network expansion offers potential for discovering new pharmacological targets, Dr. Lakhan noted.

“Drugs that modulate synaptic plasticity or network connectivity might be developed to reverse or mitigate these neural changes. The findings also support the use of longitudinal monitoring to predict and preempt symptom emergence, improving outcomes through timely intervention. This research paves the way for more personalized, precise, and proactive approaches in treating depression,” Dr. Lakhan concluded.

Also weighing in, Teddy Akiki, MD, with the Department of Psychiatry and Behavioral Sciences at Stanford Medicine in California, noted that the effect size of the frontostriatal salience network difference in depression is “remarkably larger than typically seen in neuroimaging studies of depression, which often describe subtle differences. The consistency across multiple datasets and across time at the individual level adds significant weight to these findings, suggesting that it is a trait marker rather than a state-dependent marker.”

“The observation that this expansion is present even before the onset of depressive symptoms in adolescence suggests its potential as a biomarker for depression risk,” Dr. Akiki said. “This approach could lead to earlier identification of at-risk individuals and potentially inform the development of targeted preventive interventions.”

He cautioned that it remains to be seen whether interventions targeting the salience network can effectively prevent or treat depression.

This research was supported in part by the National Institute of Mental Health, the National Institute on Drug Addiction, the Hope for Depression Research Foundation, and the Foundation for OCD Research. Dr. Lynch and a coauthor are listed as inventors for Cornell University patent applications on neuroimaging biomarkers for depression which are pending or in preparation. Dr. Liston has served as a scientific advisor or consultant to Compass Pathways PLC, Delix Therapeutics, and Brainify.AI. Dr. Lakhan and Dr. Akiki had no relevant disclosures.

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

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Researchers have discovered that a brain network involved in reward processing and attention to stimuli is markedly bigger in people with depression, remains stable over time, is unaffected by mood changes, and can be detected in children before onset of depression symptoms.

Using a novel brain-mapping technique, researchers found that the frontostriatal salience network was expanded nearly twofold in the brains of most individuals studied with depression compared with controls.

“This expansion in cortex was trait-like, meaning it was stable over time and did not change as symptoms changed over time,” said lead author Charles Lynch, PhD, assistant professor of neuroscience, Department of Psychiatry, Weill Cornell Medicine in New York.

It could also be detected in children who later developed depression, suggesting it may serve as a biomarker of depression risk. Investigators said the findings could aid in prevention and early detection of depression, as well as the development of more personalized treatment.

The study was published online in Nature.
 

Prewired for Depression?

Precision functional mapping is a relatively new approach to brain mapping in individuals that uses large amounts of fMRI data from hours of scans per person. The technique has been used to show differences in brain networks between and in healthy individuals but had not been used to study brain networks in people with depression.

“We leveraged our large longitudinal datasets — with many hours of functional MRI scanning per subject — to construct individual-specific maps of functional brain networks in each patient using precision functional mapping, instead of relying on group average,” Dr. Lynch said.

In the primary analysis of 141 adults with major depression and 37 healthy controls, the frontostriatal salience network — which is involved in reward processing and attention to internal and external stimuli — was markedly larger in these individuals with depression.

“This is one of the first times these kinds of personalized maps have been created in individuals with depression, and this is how we first observed of the salience network being larger in individuals with depression,” Dr. Lynch said.

In four of the six individuals, the salience network was expanded more than twofold, outside the range observed in all 37 healthy controls. On average, the salience network occupied 73% more of the cortical surface relative to the average in healthy controls.

The findings were replicated using independent samples of repeatedly sampled individuals with depression and in large-scale group average data.

The expansion of the salience network did not change over time and was unaffected by changes in mood state.

“These observations led us to propose that instead of driving changes in depressive symptoms over time, salience network expansion may be a stable marker of risk for developing depression,” the study team wrote.

An analysis of brain scans from 57 children who went on to develop depressive symptoms during adolescence and an equal number of children who did not develop depressive symptoms supports this theory.

On average, the salience network occupied roughly 36% more of cortex in the children with no current or previous symptoms of depression at the time of their fMRI scans but who subsequently developed clinically significant symptoms of depression, relative to children with no depressive symptoms at any study time point, the researchers found.
 

 

 

Immediate Clinical Impact?

Reached for comment, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, said this research “exemplifies the promising intersection of neurology and digital health, where advanced neuroimaging and data-driven approaches can transform mental health care into a more precise and individualized practice,” Dr. Lakhan said. “By identifying this brain network expansion, we’re unlocking new possibilities for precision medicine in mental health.”

Dr. Lakhan, who wasn’t involved in this research, said identifying the expansion of the frontostriatal salience network in individuals with depression opens new avenues for developing novel therapeutics.

“By targeting this network through neuromodulation techniques like deep brain stimulation, transcranial magnetic stimulation, and prescription digital therapeutics, treatments can be more precisely tailored to individual neurobiological profiles,” Dr. Lakhan said. “Additionally, this network expansion could serve as a biomarker for early detection, allowing for preventive strategies or personalized treatment plans, particularly for those at risk of developing depression.”

In addition, a greater understanding of the mechanisms driving salience network expansion offers potential for discovering new pharmacological targets, Dr. Lakhan noted.

“Drugs that modulate synaptic plasticity or network connectivity might be developed to reverse or mitigate these neural changes. The findings also support the use of longitudinal monitoring to predict and preempt symptom emergence, improving outcomes through timely intervention. This research paves the way for more personalized, precise, and proactive approaches in treating depression,” Dr. Lakhan concluded.

Also weighing in, Teddy Akiki, MD, with the Department of Psychiatry and Behavioral Sciences at Stanford Medicine in California, noted that the effect size of the frontostriatal salience network difference in depression is “remarkably larger than typically seen in neuroimaging studies of depression, which often describe subtle differences. The consistency across multiple datasets and across time at the individual level adds significant weight to these findings, suggesting that it is a trait marker rather than a state-dependent marker.”

“The observation that this expansion is present even before the onset of depressive symptoms in adolescence suggests its potential as a biomarker for depression risk,” Dr. Akiki said. “This approach could lead to earlier identification of at-risk individuals and potentially inform the development of targeted preventive interventions.”

He cautioned that it remains to be seen whether interventions targeting the salience network can effectively prevent or treat depression.

This research was supported in part by the National Institute of Mental Health, the National Institute on Drug Addiction, the Hope for Depression Research Foundation, and the Foundation for OCD Research. Dr. Lynch and a coauthor are listed as inventors for Cornell University patent applications on neuroimaging biomarkers for depression which are pending or in preparation. Dr. Liston has served as a scientific advisor or consultant to Compass Pathways PLC, Delix Therapeutics, and Brainify.AI. Dr. Lakhan and Dr. Akiki had no relevant disclosures.

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

Researchers have discovered that a brain network involved in reward processing and attention to stimuli is markedly bigger in people with depression, remains stable over time, is unaffected by mood changes, and can be detected in children before onset of depression symptoms.

Using a novel brain-mapping technique, researchers found that the frontostriatal salience network was expanded nearly twofold in the brains of most individuals studied with depression compared with controls.

“This expansion in cortex was trait-like, meaning it was stable over time and did not change as symptoms changed over time,” said lead author Charles Lynch, PhD, assistant professor of neuroscience, Department of Psychiatry, Weill Cornell Medicine in New York.

It could also be detected in children who later developed depression, suggesting it may serve as a biomarker of depression risk. Investigators said the findings could aid in prevention and early detection of depression, as well as the development of more personalized treatment.

The study was published online in Nature.
 

Prewired for Depression?

Precision functional mapping is a relatively new approach to brain mapping in individuals that uses large amounts of fMRI data from hours of scans per person. The technique has been used to show differences in brain networks between and in healthy individuals but had not been used to study brain networks in people with depression.

“We leveraged our large longitudinal datasets — with many hours of functional MRI scanning per subject — to construct individual-specific maps of functional brain networks in each patient using precision functional mapping, instead of relying on group average,” Dr. Lynch said.

In the primary analysis of 141 adults with major depression and 37 healthy controls, the frontostriatal salience network — which is involved in reward processing and attention to internal and external stimuli — was markedly larger in these individuals with depression.

“This is one of the first times these kinds of personalized maps have been created in individuals with depression, and this is how we first observed of the salience network being larger in individuals with depression,” Dr. Lynch said.

In four of the six individuals, the salience network was expanded more than twofold, outside the range observed in all 37 healthy controls. On average, the salience network occupied 73% more of the cortical surface relative to the average in healthy controls.

The findings were replicated using independent samples of repeatedly sampled individuals with depression and in large-scale group average data.

The expansion of the salience network did not change over time and was unaffected by changes in mood state.

“These observations led us to propose that instead of driving changes in depressive symptoms over time, salience network expansion may be a stable marker of risk for developing depression,” the study team wrote.

An analysis of brain scans from 57 children who went on to develop depressive symptoms during adolescence and an equal number of children who did not develop depressive symptoms supports this theory.

On average, the salience network occupied roughly 36% more of cortex in the children with no current or previous symptoms of depression at the time of their fMRI scans but who subsequently developed clinically significant symptoms of depression, relative to children with no depressive symptoms at any study time point, the researchers found.
 

 

 

Immediate Clinical Impact?

Reached for comment, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, said this research “exemplifies the promising intersection of neurology and digital health, where advanced neuroimaging and data-driven approaches can transform mental health care into a more precise and individualized practice,” Dr. Lakhan said. “By identifying this brain network expansion, we’re unlocking new possibilities for precision medicine in mental health.”

Dr. Lakhan, who wasn’t involved in this research, said identifying the expansion of the frontostriatal salience network in individuals with depression opens new avenues for developing novel therapeutics.

“By targeting this network through neuromodulation techniques like deep brain stimulation, transcranial magnetic stimulation, and prescription digital therapeutics, treatments can be more precisely tailored to individual neurobiological profiles,” Dr. Lakhan said. “Additionally, this network expansion could serve as a biomarker for early detection, allowing for preventive strategies or personalized treatment plans, particularly for those at risk of developing depression.”

In addition, a greater understanding of the mechanisms driving salience network expansion offers potential for discovering new pharmacological targets, Dr. Lakhan noted.

“Drugs that modulate synaptic plasticity or network connectivity might be developed to reverse or mitigate these neural changes. The findings also support the use of longitudinal monitoring to predict and preempt symptom emergence, improving outcomes through timely intervention. This research paves the way for more personalized, precise, and proactive approaches in treating depression,” Dr. Lakhan concluded.

Also weighing in, Teddy Akiki, MD, with the Department of Psychiatry and Behavioral Sciences at Stanford Medicine in California, noted that the effect size of the frontostriatal salience network difference in depression is “remarkably larger than typically seen in neuroimaging studies of depression, which often describe subtle differences. The consistency across multiple datasets and across time at the individual level adds significant weight to these findings, suggesting that it is a trait marker rather than a state-dependent marker.”

“The observation that this expansion is present even before the onset of depressive symptoms in adolescence suggests its potential as a biomarker for depression risk,” Dr. Akiki said. “This approach could lead to earlier identification of at-risk individuals and potentially inform the development of targeted preventive interventions.”

He cautioned that it remains to be seen whether interventions targeting the salience network can effectively prevent or treat depression.

This research was supported in part by the National Institute of Mental Health, the National Institute on Drug Addiction, the Hope for Depression Research Foundation, and the Foundation for OCD Research. Dr. Lynch and a coauthor are listed as inventors for Cornell University patent applications on neuroimaging biomarkers for depression which are pending or in preparation. Dr. Liston has served as a scientific advisor or consultant to Compass Pathways PLC, Delix Therapeutics, and Brainify.AI. Dr. Lakhan and Dr. Akiki had no relevant disclosures.

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

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Nighttime Outdoor Light Pollution Linked to Alzheimer’s Risk

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Fri, 09/06/2024 - 12:54

Living in areas saturated with artificial outdoor light at night is associated with an increased risk for Alzheimer’s disease, a new national study suggested.

Analyses of state and county light pollution data and Medicare claims showed that areas with higher average nighttime light intensity had a greater prevalence of Alzheimer’s disease.

Among people aged 65 years or older, Alzheimer’s disease prevalence was more strongly associated with nightly light pollution exposure than with alcohol misuse, chronic kidney disease, depression, or obesity.

In those younger than 65 years, greater nighttime light intensity had a stronger association with Alzheimer’s disease prevalence than any other risk factor included in the study.

“The results are pretty striking when you do these comparisons and it’s true for people of all ages,” said Robin Voigt-Zuwala, PhD, lead author and director, Circadian Rhythm Research Laboratory, Rush University, Chicago, Illinois.

The study was published online in Frontiers of Neuroscience.
 

Shining a Light

Exposure to artificial outdoor light at night has been associated with adverse health effects such as sleep disruption, obesity, atherosclerosis, and cancer, but this is the first study to look specifically at Alzheimer’s disease, investigators noted.

Two recent studies reported higher risks for mild cognitive impairment among Chinese veterans and late-onset dementia among Italian residents living in areas with brighter outdoor light at night.

For this study, Dr. Voigt-Zuwala and colleagues examined the relationship between Alzheimer’s disease prevalence and average nighttime light intensity in the lower 48 states using data from Medicare Part A and B, the Centers for Disease Control and Prevention, and NASA satellite–acquired radiance data.

The data were averaged for the years 2012-2018 and states divided into five groups based on average nighttime light intensity.

The darkest states were Montana, Wyoming, South Dakota, Idaho, Maine, New Mexico, Vermont, Oregon, Utah, and Nevada. The brightest states were Indiana, Illinois, Florida, Ohio, Massachusetts, Connecticut, Maryland, Delaware, Rhode Island, and New Jersey.

Analysis of variance revealed a significant difference in Alzheimer’s disease prevalence between state groups (P < .0001). Multiple comparisons testing also showed that states with the lowest average nighttime light had significantly different Alzheimer’s disease prevalence than those with higher intensity.

The same positive relationship was observed when each year was assessed individually and at the county level, using data from 45 counties and the District of Columbia.
 

Strong Association

The investigators also found that state average nighttime light intensity is significantly associated with Alzheimer’s disease prevalence (P = .006). This effect was seen across all ages, sexes, and races except Asian Pacific Island, the latter possibly related to statistical power, the authors said.

When known or proposed risk factors for Alzheimer’s disease were added to the model, atrial fibrillation, diabetes, hyperlipidemia, hypertension, and stroke had a stronger association with Alzheimer’s disease than average nighttime light intensity.

Nighttime light intensity, however, was more strongly associated with Alzheimer’s disease prevalence than alcohol abuse, chronic kidney disease, depression, heart failure, and obesity.

Moreover, in people younger than 65 years, nighttime light pollution had a stronger association with Alzheimer’s disease prevalence than all other risk factors (P = .007).

The mechanism behind this increased vulnerability is unclear, but there may be an interplay between genetic susceptibility of an individual and how they respond to light, Dr. Voigt-Zuwala suggested.

APOE4 is the genotype most highly associated with Alzheimer’s disease risk, and maybe the people who have that genotype are just more sensitive to the effects of light exposure at night, more sensitive to circadian rhythm disruption,” she said.

The authors noted that additional research is needed but suggested light pollution may also influence Alzheimer’s disease through sleep disruption, which can promote inflammation, activate microglia and astrocytes, and negatively alter the clearance of amyloid beta, and by decreasing the levels of brain-derived neurotrophic factor.
 

 

 

Are We Measuring the Right Light?

“It’s a good article and it’s got a good message, but I have some caveats to that,” said George C. Brainard, PhD, director, Light Research Program, Thomas Jefferson University in Philadelphia, Pennsylvania, and a pioneer in the study of how light affects biology including breast cancer in night-shift workers.

The biggest caveat, and one acknowledged by the authors, is that the study didn’t measure indoor light exposure and relied instead on satellite imaging.

“They’re very striking images, but they may not be particularly relevant. And here’s why: People don’t live outdoors all night,” Dr. Brainard said.

Instead, people spend much of their time at night indoors where they’re exposed to lighting in the home and from smartphones, laptops, and television screens.

“It doesn’t invalidate their work. It’s an important advancement, an important observation,” Dr. Brainard said. “But the important thing really is to find out what is the population exposed to that triggers this response, and it’s probably indoor lighting related to the amount and physical characteristics of indoor lighting. It doesn’t mean outdoor lighting can’t play a role. It certainly can.”

Reached for comment, Erik Musiek, MD, PhD, a professor of neurology whose lab at Washington University School of Medicine in St. Louis, Missouri, has extensively studied circadian clock disruption and Alzheimer’s disease pathology in the brain, said the study provides a 10,000-foot view of the issue.

For example, the study was not designed to detect whether people living in high light pollution areas are actually experiencing more outdoor light at night and if risk factors such as air pollution and low socioeconomic status may correlate with these areas.

“Most of what we worry about is do people have lights on in the house, do they have their TV on, their screens up to their face late at night? This can’t tell us about that,” Dr. Musiek said. “But on the other hand, this kind of light exposure is something that public policy can affect.”

“It’s hard to control people’s personal habits nor should we probably, but we can control what types of bulbs you put into streetlights, how bright they are, and where you put lighting in a public place,” he added. “So I do think there’s value there.”

At least 19 states, the District of Columbia, and Puerto Rico have laws in place to reduce light pollution, with the majority doing so to promote energy conservation, public safety, aesthetic interests, or astronomical research, according to the National Conference of State Legislatures.

To respond to some of the limitations in this study, Dr. Voigt-Zuwala is writing a grant application for a new project to look at both indoor and outdoor light exposure on an individual level.

“This is what I’ve been wanting to study for a long time, and this study is just sort of the stepping stone, the proof of concept that this is something we need to be investigating,” she said.

Dr. Voigt-Zuwala reported RO1 and R24 grants from the National Institutes of Health (NIH), one coauthor reported an NIH R24 grant; another reported having no conflicts of interest. Dr. Brainard reported having no relevant conflicts of interest. Dr. Musiek reported research funding from Eisai Pharmaceuticals.

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

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Living in areas saturated with artificial outdoor light at night is associated with an increased risk for Alzheimer’s disease, a new national study suggested.

Analyses of state and county light pollution data and Medicare claims showed that areas with higher average nighttime light intensity had a greater prevalence of Alzheimer’s disease.

Among people aged 65 years or older, Alzheimer’s disease prevalence was more strongly associated with nightly light pollution exposure than with alcohol misuse, chronic kidney disease, depression, or obesity.

In those younger than 65 years, greater nighttime light intensity had a stronger association with Alzheimer’s disease prevalence than any other risk factor included in the study.

“The results are pretty striking when you do these comparisons and it’s true for people of all ages,” said Robin Voigt-Zuwala, PhD, lead author and director, Circadian Rhythm Research Laboratory, Rush University, Chicago, Illinois.

The study was published online in Frontiers of Neuroscience.
 

Shining a Light

Exposure to artificial outdoor light at night has been associated with adverse health effects such as sleep disruption, obesity, atherosclerosis, and cancer, but this is the first study to look specifically at Alzheimer’s disease, investigators noted.

Two recent studies reported higher risks for mild cognitive impairment among Chinese veterans and late-onset dementia among Italian residents living in areas with brighter outdoor light at night.

For this study, Dr. Voigt-Zuwala and colleagues examined the relationship between Alzheimer’s disease prevalence and average nighttime light intensity in the lower 48 states using data from Medicare Part A and B, the Centers for Disease Control and Prevention, and NASA satellite–acquired radiance data.

The data were averaged for the years 2012-2018 and states divided into five groups based on average nighttime light intensity.

The darkest states were Montana, Wyoming, South Dakota, Idaho, Maine, New Mexico, Vermont, Oregon, Utah, and Nevada. The brightest states were Indiana, Illinois, Florida, Ohio, Massachusetts, Connecticut, Maryland, Delaware, Rhode Island, and New Jersey.

Analysis of variance revealed a significant difference in Alzheimer’s disease prevalence between state groups (P < .0001). Multiple comparisons testing also showed that states with the lowest average nighttime light had significantly different Alzheimer’s disease prevalence than those with higher intensity.

The same positive relationship was observed when each year was assessed individually and at the county level, using data from 45 counties and the District of Columbia.
 

Strong Association

The investigators also found that state average nighttime light intensity is significantly associated with Alzheimer’s disease prevalence (P = .006). This effect was seen across all ages, sexes, and races except Asian Pacific Island, the latter possibly related to statistical power, the authors said.

When known or proposed risk factors for Alzheimer’s disease were added to the model, atrial fibrillation, diabetes, hyperlipidemia, hypertension, and stroke had a stronger association with Alzheimer’s disease than average nighttime light intensity.

Nighttime light intensity, however, was more strongly associated with Alzheimer’s disease prevalence than alcohol abuse, chronic kidney disease, depression, heart failure, and obesity.

Moreover, in people younger than 65 years, nighttime light pollution had a stronger association with Alzheimer’s disease prevalence than all other risk factors (P = .007).

The mechanism behind this increased vulnerability is unclear, but there may be an interplay between genetic susceptibility of an individual and how they respond to light, Dr. Voigt-Zuwala suggested.

APOE4 is the genotype most highly associated with Alzheimer’s disease risk, and maybe the people who have that genotype are just more sensitive to the effects of light exposure at night, more sensitive to circadian rhythm disruption,” she said.

The authors noted that additional research is needed but suggested light pollution may also influence Alzheimer’s disease through sleep disruption, which can promote inflammation, activate microglia and astrocytes, and negatively alter the clearance of amyloid beta, and by decreasing the levels of brain-derived neurotrophic factor.
 

 

 

Are We Measuring the Right Light?

“It’s a good article and it’s got a good message, but I have some caveats to that,” said George C. Brainard, PhD, director, Light Research Program, Thomas Jefferson University in Philadelphia, Pennsylvania, and a pioneer in the study of how light affects biology including breast cancer in night-shift workers.

The biggest caveat, and one acknowledged by the authors, is that the study didn’t measure indoor light exposure and relied instead on satellite imaging.

“They’re very striking images, but they may not be particularly relevant. And here’s why: People don’t live outdoors all night,” Dr. Brainard said.

Instead, people spend much of their time at night indoors where they’re exposed to lighting in the home and from smartphones, laptops, and television screens.

“It doesn’t invalidate their work. It’s an important advancement, an important observation,” Dr. Brainard said. “But the important thing really is to find out what is the population exposed to that triggers this response, and it’s probably indoor lighting related to the amount and physical characteristics of indoor lighting. It doesn’t mean outdoor lighting can’t play a role. It certainly can.”

Reached for comment, Erik Musiek, MD, PhD, a professor of neurology whose lab at Washington University School of Medicine in St. Louis, Missouri, has extensively studied circadian clock disruption and Alzheimer’s disease pathology in the brain, said the study provides a 10,000-foot view of the issue.

For example, the study was not designed to detect whether people living in high light pollution areas are actually experiencing more outdoor light at night and if risk factors such as air pollution and low socioeconomic status may correlate with these areas.

“Most of what we worry about is do people have lights on in the house, do they have their TV on, their screens up to their face late at night? This can’t tell us about that,” Dr. Musiek said. “But on the other hand, this kind of light exposure is something that public policy can affect.”

“It’s hard to control people’s personal habits nor should we probably, but we can control what types of bulbs you put into streetlights, how bright they are, and where you put lighting in a public place,” he added. “So I do think there’s value there.”

At least 19 states, the District of Columbia, and Puerto Rico have laws in place to reduce light pollution, with the majority doing so to promote energy conservation, public safety, aesthetic interests, or astronomical research, according to the National Conference of State Legislatures.

To respond to some of the limitations in this study, Dr. Voigt-Zuwala is writing a grant application for a new project to look at both indoor and outdoor light exposure on an individual level.

“This is what I’ve been wanting to study for a long time, and this study is just sort of the stepping stone, the proof of concept that this is something we need to be investigating,” she said.

Dr. Voigt-Zuwala reported RO1 and R24 grants from the National Institutes of Health (NIH), one coauthor reported an NIH R24 grant; another reported having no conflicts of interest. Dr. Brainard reported having no relevant conflicts of interest. Dr. Musiek reported research funding from Eisai Pharmaceuticals.

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

Living in areas saturated with artificial outdoor light at night is associated with an increased risk for Alzheimer’s disease, a new national study suggested.

Analyses of state and county light pollution data and Medicare claims showed that areas with higher average nighttime light intensity had a greater prevalence of Alzheimer’s disease.

Among people aged 65 years or older, Alzheimer’s disease prevalence was more strongly associated with nightly light pollution exposure than with alcohol misuse, chronic kidney disease, depression, or obesity.

In those younger than 65 years, greater nighttime light intensity had a stronger association with Alzheimer’s disease prevalence than any other risk factor included in the study.

“The results are pretty striking when you do these comparisons and it’s true for people of all ages,” said Robin Voigt-Zuwala, PhD, lead author and director, Circadian Rhythm Research Laboratory, Rush University, Chicago, Illinois.

The study was published online in Frontiers of Neuroscience.
 

Shining a Light

Exposure to artificial outdoor light at night has been associated with adverse health effects such as sleep disruption, obesity, atherosclerosis, and cancer, but this is the first study to look specifically at Alzheimer’s disease, investigators noted.

Two recent studies reported higher risks for mild cognitive impairment among Chinese veterans and late-onset dementia among Italian residents living in areas with brighter outdoor light at night.

For this study, Dr. Voigt-Zuwala and colleagues examined the relationship between Alzheimer’s disease prevalence and average nighttime light intensity in the lower 48 states using data from Medicare Part A and B, the Centers for Disease Control and Prevention, and NASA satellite–acquired radiance data.

The data were averaged for the years 2012-2018 and states divided into five groups based on average nighttime light intensity.

The darkest states were Montana, Wyoming, South Dakota, Idaho, Maine, New Mexico, Vermont, Oregon, Utah, and Nevada. The brightest states were Indiana, Illinois, Florida, Ohio, Massachusetts, Connecticut, Maryland, Delaware, Rhode Island, and New Jersey.

Analysis of variance revealed a significant difference in Alzheimer’s disease prevalence between state groups (P < .0001). Multiple comparisons testing also showed that states with the lowest average nighttime light had significantly different Alzheimer’s disease prevalence than those with higher intensity.

The same positive relationship was observed when each year was assessed individually and at the county level, using data from 45 counties and the District of Columbia.
 

Strong Association

The investigators also found that state average nighttime light intensity is significantly associated with Alzheimer’s disease prevalence (P = .006). This effect was seen across all ages, sexes, and races except Asian Pacific Island, the latter possibly related to statistical power, the authors said.

When known or proposed risk factors for Alzheimer’s disease were added to the model, atrial fibrillation, diabetes, hyperlipidemia, hypertension, and stroke had a stronger association with Alzheimer’s disease than average nighttime light intensity.

Nighttime light intensity, however, was more strongly associated with Alzheimer’s disease prevalence than alcohol abuse, chronic kidney disease, depression, heart failure, and obesity.

Moreover, in people younger than 65 years, nighttime light pollution had a stronger association with Alzheimer’s disease prevalence than all other risk factors (P = .007).

The mechanism behind this increased vulnerability is unclear, but there may be an interplay between genetic susceptibility of an individual and how they respond to light, Dr. Voigt-Zuwala suggested.

APOE4 is the genotype most highly associated with Alzheimer’s disease risk, and maybe the people who have that genotype are just more sensitive to the effects of light exposure at night, more sensitive to circadian rhythm disruption,” she said.

The authors noted that additional research is needed but suggested light pollution may also influence Alzheimer’s disease through sleep disruption, which can promote inflammation, activate microglia and astrocytes, and negatively alter the clearance of amyloid beta, and by decreasing the levels of brain-derived neurotrophic factor.
 

 

 

Are We Measuring the Right Light?

“It’s a good article and it’s got a good message, but I have some caveats to that,” said George C. Brainard, PhD, director, Light Research Program, Thomas Jefferson University in Philadelphia, Pennsylvania, and a pioneer in the study of how light affects biology including breast cancer in night-shift workers.

The biggest caveat, and one acknowledged by the authors, is that the study didn’t measure indoor light exposure and relied instead on satellite imaging.

“They’re very striking images, but they may not be particularly relevant. And here’s why: People don’t live outdoors all night,” Dr. Brainard said.

Instead, people spend much of their time at night indoors where they’re exposed to lighting in the home and from smartphones, laptops, and television screens.

“It doesn’t invalidate their work. It’s an important advancement, an important observation,” Dr. Brainard said. “But the important thing really is to find out what is the population exposed to that triggers this response, and it’s probably indoor lighting related to the amount and physical characteristics of indoor lighting. It doesn’t mean outdoor lighting can’t play a role. It certainly can.”

Reached for comment, Erik Musiek, MD, PhD, a professor of neurology whose lab at Washington University School of Medicine in St. Louis, Missouri, has extensively studied circadian clock disruption and Alzheimer’s disease pathology in the brain, said the study provides a 10,000-foot view of the issue.

For example, the study was not designed to detect whether people living in high light pollution areas are actually experiencing more outdoor light at night and if risk factors such as air pollution and low socioeconomic status may correlate with these areas.

“Most of what we worry about is do people have lights on in the house, do they have their TV on, their screens up to their face late at night? This can’t tell us about that,” Dr. Musiek said. “But on the other hand, this kind of light exposure is something that public policy can affect.”

“It’s hard to control people’s personal habits nor should we probably, but we can control what types of bulbs you put into streetlights, how bright they are, and where you put lighting in a public place,” he added. “So I do think there’s value there.”

At least 19 states, the District of Columbia, and Puerto Rico have laws in place to reduce light pollution, with the majority doing so to promote energy conservation, public safety, aesthetic interests, or astronomical research, according to the National Conference of State Legislatures.

To respond to some of the limitations in this study, Dr. Voigt-Zuwala is writing a grant application for a new project to look at both indoor and outdoor light exposure on an individual level.

“This is what I’ve been wanting to study for a long time, and this study is just sort of the stepping stone, the proof of concept that this is something we need to be investigating,” she said.

Dr. Voigt-Zuwala reported RO1 and R24 grants from the National Institutes of Health (NIH), one coauthor reported an NIH R24 grant; another reported having no conflicts of interest. Dr. Brainard reported having no relevant conflicts of interest. Dr. Musiek reported research funding from Eisai Pharmaceuticals.

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

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Stroke Risk from Atrial Fibrillation Rises in Presence of Rheumatoid Arthritis

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Tue, 09/10/2024 - 02:15

 

TOPLINE: 

Patients with both rheumatoid arthritis (RA) and atrial fibrillation (AF) have a higher risk for ischemic stroke than those with only AF. They are also less likely to receive oral anticoagulant treatment, which may contribute to this increased stroke risk.

METHODOLOGY:

  • Researchers conducted a registry-based retrospective cohort study using the Norwegian Cardio-Rheuma Register to evaluate the risk for ischemic stroke following the diagnosis of AF in patients with or without RA.
  • They included 163,595 patients with newly diagnosed AF between 2010 and 2017, of whom 2750 had RA. Patients had to be diagnosed with RA before the diagnosis of AF.
  • They also assessed whether patients with RA were less likely to receive oral anticoagulants for stroke prevention within 3 months of AF diagnosis than those without RA.
  • The median follow-up time was 2.5 years for patients with RA and 3.0 years for those without RA.
  • The primary endpoint was ischemic stroke, which was identified through hospital admissions and visits.

TAKEAWAY:

  • At 5 years, patients with both RA and AF showed a higher cumulative incidence of ischemic stroke than those with only AF (7.3% vs 5.0%).
  • Among patients with AF, the risk of having a stroke was 25% higher in those with RA than in those without RA (adjusted hazard ratio, 1.25; 95% CI, 1.05-1.50).
  • Patients with RA were also less likely to receive treatment with oral anticoagulants than those without RA, driven by concerns over potential interactions with RA medications, bleeding risk, or other factors (adjusted odds ratio, 0.88; 95% CI, 0.80-0.97). 

IN PRACTICE:

“Our study prompts preventive measures such as meticulous cardiovascular risk factor control among patients with RA and AF and raises the question whether the presence of RA should be taken into account when considering OAC [oral anticoagulant] treatment for AF patients,” the authors wrote.

SOURCE:

This study was led by Anne M. Kerola, MD, PhD, Helsinki University Hospital and University of Helsinki in Finland. It was published online in Rheumatology.

LIMITATIONS: 

This study lacked data on smoking, blood pressure measurements, alcohol use, and obesity, which may have affected the comprehensiveness of the findings. The study population was limited to Norway and may not be generalizable to other populations.

DISCLOSURES:

This study was supported by the Olav Thon Foundation, the Research Council of Norway, and the Foundation for Research in Rheumatology. Some authors received speaker fees, participated in advisory boards, served as consultants, or had other ties with some pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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TOPLINE: 

Patients with both rheumatoid arthritis (RA) and atrial fibrillation (AF) have a higher risk for ischemic stroke than those with only AF. They are also less likely to receive oral anticoagulant treatment, which may contribute to this increased stroke risk.

METHODOLOGY:

  • Researchers conducted a registry-based retrospective cohort study using the Norwegian Cardio-Rheuma Register to evaluate the risk for ischemic stroke following the diagnosis of AF in patients with or without RA.
  • They included 163,595 patients with newly diagnosed AF between 2010 and 2017, of whom 2750 had RA. Patients had to be diagnosed with RA before the diagnosis of AF.
  • They also assessed whether patients with RA were less likely to receive oral anticoagulants for stroke prevention within 3 months of AF diagnosis than those without RA.
  • The median follow-up time was 2.5 years for patients with RA and 3.0 years for those without RA.
  • The primary endpoint was ischemic stroke, which was identified through hospital admissions and visits.

TAKEAWAY:

  • At 5 years, patients with both RA and AF showed a higher cumulative incidence of ischemic stroke than those with only AF (7.3% vs 5.0%).
  • Among patients with AF, the risk of having a stroke was 25% higher in those with RA than in those without RA (adjusted hazard ratio, 1.25; 95% CI, 1.05-1.50).
  • Patients with RA were also less likely to receive treatment with oral anticoagulants than those without RA, driven by concerns over potential interactions with RA medications, bleeding risk, or other factors (adjusted odds ratio, 0.88; 95% CI, 0.80-0.97). 

IN PRACTICE:

“Our study prompts preventive measures such as meticulous cardiovascular risk factor control among patients with RA and AF and raises the question whether the presence of RA should be taken into account when considering OAC [oral anticoagulant] treatment for AF patients,” the authors wrote.

SOURCE:

This study was led by Anne M. Kerola, MD, PhD, Helsinki University Hospital and University of Helsinki in Finland. It was published online in Rheumatology.

LIMITATIONS: 

This study lacked data on smoking, blood pressure measurements, alcohol use, and obesity, which may have affected the comprehensiveness of the findings. The study population was limited to Norway and may not be generalizable to other populations.

DISCLOSURES:

This study was supported by the Olav Thon Foundation, the Research Council of Norway, and the Foundation for Research in Rheumatology. Some authors received speaker fees, participated in advisory boards, served as consultants, or had other ties with some pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

 

TOPLINE: 

Patients with both rheumatoid arthritis (RA) and atrial fibrillation (AF) have a higher risk for ischemic stroke than those with only AF. They are also less likely to receive oral anticoagulant treatment, which may contribute to this increased stroke risk.

METHODOLOGY:

  • Researchers conducted a registry-based retrospective cohort study using the Norwegian Cardio-Rheuma Register to evaluate the risk for ischemic stroke following the diagnosis of AF in patients with or without RA.
  • They included 163,595 patients with newly diagnosed AF between 2010 and 2017, of whom 2750 had RA. Patients had to be diagnosed with RA before the diagnosis of AF.
  • They also assessed whether patients with RA were less likely to receive oral anticoagulants for stroke prevention within 3 months of AF diagnosis than those without RA.
  • The median follow-up time was 2.5 years for patients with RA and 3.0 years for those without RA.
  • The primary endpoint was ischemic stroke, which was identified through hospital admissions and visits.

TAKEAWAY:

  • At 5 years, patients with both RA and AF showed a higher cumulative incidence of ischemic stroke than those with only AF (7.3% vs 5.0%).
  • Among patients with AF, the risk of having a stroke was 25% higher in those with RA than in those without RA (adjusted hazard ratio, 1.25; 95% CI, 1.05-1.50).
  • Patients with RA were also less likely to receive treatment with oral anticoagulants than those without RA, driven by concerns over potential interactions with RA medications, bleeding risk, or other factors (adjusted odds ratio, 0.88; 95% CI, 0.80-0.97). 

IN PRACTICE:

“Our study prompts preventive measures such as meticulous cardiovascular risk factor control among patients with RA and AF and raises the question whether the presence of RA should be taken into account when considering OAC [oral anticoagulant] treatment for AF patients,” the authors wrote.

SOURCE:

This study was led by Anne M. Kerola, MD, PhD, Helsinki University Hospital and University of Helsinki in Finland. It was published online in Rheumatology.

LIMITATIONS: 

This study lacked data on smoking, blood pressure measurements, alcohol use, and obesity, which may have affected the comprehensiveness of the findings. The study population was limited to Norway and may not be generalizable to other populations.

DISCLOSURES:

This study was supported by the Olav Thon Foundation, the Research Council of Norway, and the Foundation for Research in Rheumatology. Some authors received speaker fees, participated in advisory boards, served as consultants, or had other ties with some pharmaceutical companies and institutions.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

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