Clinical Psychiatry News

DENVER – Psychedelics such as psilocybin “truly have the potential to transform how we treat a number of neuropsychiatric diseases, including headaches,” a neuropharmacologist told colleagues at the annual meeting of the American Headache Society.

However, Bryan Roth, MD, PhD, professor of pharmacology at the University of North Carolina at Chapel Hill, also offered a major cautionary note: There have been no randomized, phase 3 trials of psychedelics, and he bluntly said that “I do not recommend the use of psychedelics for any medical condition.”

The potential disease-altering powers of psychedelics have received a tremendous amount of research and media attention over the past several years. A landmark randomized, double-blind study released in 2016 triggered much of the interest, Dr. Roth said, when it suggested that high-dose psilocybin significantly lowered levels of depressed mood/anxiety in patients with life-threatening cancer. At 6 months, 80% of patients who took the dose reported moderate or greater improvement in well-being/life satisfaction.

“You have the potential – unprecedented in psychiatry – that a single dose of a therapeutic agent may induce a rapid, robust, and sustained antidepressant action,” he said. Also of note: The “vast majority” of subjects say their encounter with a psychedelic was “one of the most meaningful experiences of their lives.”

Dr. Roth said his own research suggests that psychedelics cause a “huge increase” in the asynchronous firing of neurons. “Noise is being injected into the system and is interpreted by the brain or the mind, which always likes to make a story about what’s going on. The story it makes up is idiosyncratic to every person and memorable for reasons that are not understood.”

Now, Dr. Roth said, he and colleagues are working to “create drugs that have this potential remarkable therapeutic efficacy in psychiatric and neurologic disorders without the psychedelic effects.” A $27 million grant from the Defense Advanced Research Projects Agency is providing support for their efforts, he said.

For the moment, he said, there’s no way to know if “the psychedelic experience is essential to the therapeutic action of these drugs. But it’s a testable hypothesis.”

As he noted, a tiny 2010 study of 2-bromo-lysergic acid diethylamide (LSD), which doesn’t cause hallucinations, showed promise as a treatment for cluster headaches.

For now, Dr. Roth said, his lab is synthesizing and testing new compounds that interact with the crucial 5-HT2A receptor.
 

Additional research

In another presentation at the AHS annual meeting, neurologist Emmanuelle A. D. Schindler, MD, PhD, of Yale School of Medicine, highlighted her 2021 study of an exploratory double-blind, placebo-controlled, cross-over study of psilocybin versus placebo for migraine headache. A single oral dose of the drug, the researchers found, reduced headache frequency and pain over 2 weeks. The study is small, with just 10 subjects, and multiple exclusion criteria.

She also revealed preliminary findings from an ongoing randomized, double-blind, placebo-controlled study of psilocybin versus placebo in cluster headaches. In 14 subjects, a psilocybin pulse was linked to fewer cluster attacks over 3 weeks, although the effect wasn’t statistically significant. However, there was a statistically significant reduction over 8 weeks in patients with chronic headache.

Dr. Schindler noted that “with these early studies, we only looked out to 2 weeks for migraine, and we only looked out to 2 months for cluster.” There are multiple other limitations, she acknowledged. “We have to do a lot more research and consider safety as well.”

However, “there is a really unique capacity for lasting effects after limited dosing,” she added, and the studies do show reductions in headache burden “that do not correlate with acute psychedelic effects.”

Moving forward, Dr. Roth cautioned that while U.S. states are allowing the use of psychedelics for medical purposes, “we don’t know if they ultimately are therapeutic. And we have strong reason to believe that microdosing or chronic dosing of these compounds is ultimately going to be deleterious to the health of our patients.”

Dr. Roth did not provide disclosure information. Dr. Schindler discloses research funding (Ceruvia Lifesciences, Wallace Research Foundation, Clusterbusters, Department of Veterans Affairs), serves on advisory boards (Ceruvia Lifesciences, Clusterbusters), and has a patent.

DENVER – Psychedelics such as psilocybin “truly have the potential to transform how we treat a number of neuropsychiatric diseases, including headaches,” a neuropharmacologist told colleagues at the annual meeting of the American Headache Society.

However, Bryan Roth, MD, PhD, professor of pharmacology at the University of North Carolina at Chapel Hill, also offered a major cautionary note: There have been no randomized, phase 3 trials of psychedelics, and he bluntly said that “I do not recommend the use of psychedelics for any medical condition.”

The potential disease-altering powers of psychedelics have received a tremendous amount of research and media attention over the past several years. A landmark randomized, double-blind study released in 2016 triggered much of the interest, Dr. Roth said, when it suggested that high-dose psilocybin significantly lowered levels of depressed mood/anxiety in patients with life-threatening cancer. At 6 months, 80% of patients who took the dose reported moderate or greater improvement in well-being/life satisfaction.

“You have the potential – unprecedented in psychiatry – that a single dose of a therapeutic agent may induce a rapid, robust, and sustained antidepressant action,” he said. Also of note: The “vast majority” of subjects say their encounter with a psychedelic was “one of the most meaningful experiences of their lives.”

Dr. Roth said his own research suggests that psychedelics cause a “huge increase” in the asynchronous firing of neurons. “Noise is being injected into the system and is interpreted by the brain or the mind, which always likes to make a story about what’s going on. The story it makes up is idiosyncratic to every person and memorable for reasons that are not understood.”

Now, Dr. Roth said, he and colleagues are working to “create drugs that have this potential remarkable therapeutic efficacy in psychiatric and neurologic disorders without the psychedelic effects.” A $27 million grant from the Defense Advanced Research Projects Agency is providing support for their efforts, he said.

For the moment, he said, there’s no way to know if “the psychedelic experience is essential to the therapeutic action of these drugs. But it’s a testable hypothesis.”

As he noted, a tiny 2010 study of 2-bromo-lysergic acid diethylamide (LSD), which doesn’t cause hallucinations, showed promise as a treatment for cluster headaches.

For now, Dr. Roth said, his lab is synthesizing and testing new compounds that interact with the crucial 5-HT2A receptor.
 

Additional research

In another presentation at the AHS annual meeting, neurologist Emmanuelle A. D. Schindler, MD, PhD, of Yale School of Medicine, highlighted her 2021 study of an exploratory double-blind, placebo-controlled, cross-over study of psilocybin versus placebo for migraine headache. A single oral dose of the drug, the researchers found, reduced headache frequency and pain over 2 weeks. The study is small, with just 10 subjects, and multiple exclusion criteria.

She also revealed preliminary findings from an ongoing randomized, double-blind, placebo-controlled study of psilocybin versus placebo in cluster headaches. In 14 subjects, a psilocybin pulse was linked to fewer cluster attacks over 3 weeks, although the effect wasn’t statistically significant. However, there was a statistically significant reduction over 8 weeks in patients with chronic headache.

Dr. Schindler noted that “with these early studies, we only looked out to 2 weeks for migraine, and we only looked out to 2 months for cluster.” There are multiple other limitations, she acknowledged. “We have to do a lot more research and consider safety as well.”

However, “there is a really unique capacity for lasting effects after limited dosing,” she added, and the studies do show reductions in headache burden “that do not correlate with acute psychedelic effects.”

Moving forward, Dr. Roth cautioned that while U.S. states are allowing the use of psychedelics for medical purposes, “we don’t know if they ultimately are therapeutic. And we have strong reason to believe that microdosing or chronic dosing of these compounds is ultimately going to be deleterious to the health of our patients.”

Dr. Roth did not provide disclosure information. Dr. Schindler discloses research funding (Ceruvia Lifesciences, Wallace Research Foundation, Clusterbusters, Department of Veterans Affairs), serves on advisory boards (Ceruvia Lifesciences, Clusterbusters), and has a patent.

DENVER – Psychedelics such as psilocybin “truly have the potential to transform how we treat a number of neuropsychiatric diseases, including headaches,” a neuropharmacologist told colleagues at the annual meeting of the American Headache Society.

However, Bryan Roth, MD, PhD, professor of pharmacology at the University of North Carolina at Chapel Hill, also offered a major cautionary note: There have been no randomized, phase 3 trials of psychedelics, and he bluntly said that “I do not recommend the use of psychedelics for any medical condition.”

The potential disease-altering powers of psychedelics have received a tremendous amount of research and media attention over the past several years. A landmark randomized, double-blind study released in 2016 triggered much of the interest, Dr. Roth said, when it suggested that high-dose psilocybin significantly lowered levels of depressed mood/anxiety in patients with life-threatening cancer. At 6 months, 80% of patients who took the dose reported moderate or greater improvement in well-being/life satisfaction.

“You have the potential – unprecedented in psychiatry – that a single dose of a therapeutic agent may induce a rapid, robust, and sustained antidepressant action,” he said. Also of note: The “vast majority” of subjects say their encounter with a psychedelic was “one of the most meaningful experiences of their lives.”

Dr. Roth said his own research suggests that psychedelics cause a “huge increase” in the asynchronous firing of neurons. “Noise is being injected into the system and is interpreted by the brain or the mind, which always likes to make a story about what’s going on. The story it makes up is idiosyncratic to every person and memorable for reasons that are not understood.”

Now, Dr. Roth said, he and colleagues are working to “create drugs that have this potential remarkable therapeutic efficacy in psychiatric and neurologic disorders without the psychedelic effects.” A $27 million grant from the Defense Advanced Research Projects Agency is providing support for their efforts, he said.

For the moment, he said, there’s no way to know if “the psychedelic experience is essential to the therapeutic action of these drugs. But it’s a testable hypothesis.”

As he noted, a tiny 2010 study of 2-bromo-lysergic acid diethylamide (LSD), which doesn’t cause hallucinations, showed promise as a treatment for cluster headaches.

For now, Dr. Roth said, his lab is synthesizing and testing new compounds that interact with the crucial 5-HT2A receptor.
 

Additional research

In another presentation at the AHS annual meeting, neurologist Emmanuelle A. D. Schindler, MD, PhD, of Yale School of Medicine, highlighted her 2021 study of an exploratory double-blind, placebo-controlled, cross-over study of psilocybin versus placebo for migraine headache. A single oral dose of the drug, the researchers found, reduced headache frequency and pain over 2 weeks. The study is small, with just 10 subjects, and multiple exclusion criteria.

She also revealed preliminary findings from an ongoing randomized, double-blind, placebo-controlled study of psilocybin versus placebo in cluster headaches. In 14 subjects, a psilocybin pulse was linked to fewer cluster attacks over 3 weeks, although the effect wasn’t statistically significant. However, there was a statistically significant reduction over 8 weeks in patients with chronic headache.

Dr. Schindler noted that “with these early studies, we only looked out to 2 weeks for migraine, and we only looked out to 2 months for cluster.” There are multiple other limitations, she acknowledged. “We have to do a lot more research and consider safety as well.”

However, “there is a really unique capacity for lasting effects after limited dosing,” she added, and the studies do show reductions in headache burden “that do not correlate with acute psychedelic effects.”

Moving forward, Dr. Roth cautioned that while U.S. states are allowing the use of psychedelics for medical purposes, “we don’t know if they ultimately are therapeutic. And we have strong reason to believe that microdosing or chronic dosing of these compounds is ultimately going to be deleterious to the health of our patients.”

Dr. Roth did not provide disclosure information. Dr. Schindler discloses research funding (Ceruvia Lifesciences, Wallace Research Foundation, Clusterbusters, Department of Veterans Affairs), serves on advisory boards (Ceruvia Lifesciences, Clusterbusters), and has a patent.

Crenezumab, an investigational medication designed to slow or prevent Alzheimer’s disease (AD), provides no cognitive benefit in patients at high genetic risk, new research suggests.

Top-line results for a phase 2 trial showed the novel drug, a monoclonal antibody designed to neutralize neurotoxic oligomers (a form of beta-amyloid), was not statistically superior to placebo in terms of cognitive ability or episodic memory function among cognitively unimpaired individuals with a genetic mutation for early-onset AD.

Genentech announced the negative results on June 16 together with Banner Alzheimer’s Institute, Phoenix.

During a press briefing, company representatives and researchers expressed disappointment with the initial results – but stressed numerous ongoing analyses have yet to be completed.

“This is the beginning of the story, but by no means the end of it,” Pierre N. Tariot, MD, director, Banner Alzheimer’s Institute, and one of the study leaders, said at the briefing.

API ADAD trial

The prospective, double-blind parallel-group Alzheimer’s Prevention Initiative (API) Autosomal Dominant Alzheimer’s Disease (ADAD) phase 2 trial enrolled 252 members of the world’s largest extended family with ADAD in Colombia. A total of 94% of the participants completed the study.

Two-thirds of participants carried the Presenilin 1 (PSEN1) E280A mutation, which virtually guarantees that carriers will develop AD at an average age of 44 years and dementia at an average age of 49 years.

Study participants were randomly assigned to receive crenezumab or placebo over a period of 5-8 years. The dose of crenezumab was increased at different time points during the trial as knowledge about potential treatment approaches for AD evolved.

Dr. Tariot noted the maximum dose was not provided for the entire treatment period. “The longest people received the highest dose was about 2 years,” he added.

Coprimary endpoints were rate of change in cognitive abilities, as measured by the API ADAD composite cognitive score, or episodic memory function, measured by the Free and Cued Selective Reminding Test Cueing Index.

Results showed these outcomes were not statistically significant for those receiving the active medication.

In addition to a range of cognitive measures, researchers also assessed amyloid PET and, later in the study, tau PET. MRI and cerebrospinal fluid (CSF) measures were also examined.

The investigators did find small numerical differences favoring crenezumab across the coprimary and multiple secondary and exploratory endpoints, but these were also not statistically significant.

Finally, no new safety issues were identified with crenezumab during the study.

Further analyses of data are ongoing and additional brain imaging and CSF biomarker results will be presented at the Alzheimer’s Association International Conference on Aug. 2.

While the study was not positive, it demonstrated that prevention trials are possible, even in less-than-ideal circumstances and generated a wealth of useful data, the investigators note.

“There were some differences between the treated and untreated patients, and we still need to understand which patients were most likely to experience those differences,” Rachelle Doody, MD, PhD, global head of neurodegeneration at Roche and Genentech, told briefing attendees.

“We need to understand the biomarkers involved and what [they’re] telling us about the disease and the timing of the intervention,” Dr. Doody said.

Prevention “needs to be one of our targeted therapeutic approaches but probably not our only one,” she added.

Beyond amyloid?

Commenting on the negative results, Howard Fillit, MD, cofounder and chief science officer of the Alzheimer’s Drug Discovery Foundation, said they demonstrate the need to focus beyond amyloid and more on the biology of aging.

“This broader approach coupled with advances in novel biomarkers is bringing us closer to the day when physicians will be able to zero in on the root causes of each patient’s Alzheimer’s – and tailor combinations of drug therapies to provide precision medicine,” Dr. Fillit, who was not involved with the research, said in statement.

Genentech is also evaluating the potential of gantenerumab for ADAD and for the prevention of sporadic AD and treatment of early Alzheimer’s in late-stage clinical trials. Results from the phase 3 GRADUATE studies of gantenerumab in early AD are expected by the end of the year.

The study was supported by the National Institute on Aging, contributions to Banner Alzheimer’s Foundation, and Genentech.

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

Crenezumab, an investigational medication designed to slow or prevent Alzheimer’s disease (AD), provides no cognitive benefit in patients at high genetic risk, new research suggests.

Top-line results for a phase 2 trial showed the novel drug, a monoclonal antibody designed to neutralize neurotoxic oligomers (a form of beta-amyloid), was not statistically superior to placebo in terms of cognitive ability or episodic memory function among cognitively unimpaired individuals with a genetic mutation for early-onset AD.

Genentech announced the negative results on June 16 together with Banner Alzheimer’s Institute, Phoenix.

During a press briefing, company representatives and researchers expressed disappointment with the initial results – but stressed numerous ongoing analyses have yet to be completed.

“This is the beginning of the story, but by no means the end of it,” Pierre N. Tariot, MD, director, Banner Alzheimer’s Institute, and one of the study leaders, said at the briefing.

API ADAD trial

The prospective, double-blind parallel-group Alzheimer’s Prevention Initiative (API) Autosomal Dominant Alzheimer’s Disease (ADAD) phase 2 trial enrolled 252 members of the world’s largest extended family with ADAD in Colombia. A total of 94% of the participants completed the study.

Two-thirds of participants carried the Presenilin 1 (PSEN1) E280A mutation, which virtually guarantees that carriers will develop AD at an average age of 44 years and dementia at an average age of 49 years.

Study participants were randomly assigned to receive crenezumab or placebo over a period of 5-8 years. The dose of crenezumab was increased at different time points during the trial as knowledge about potential treatment approaches for AD evolved.

Dr. Tariot noted the maximum dose was not provided for the entire treatment period. “The longest people received the highest dose was about 2 years,” he added.

Coprimary endpoints were rate of change in cognitive abilities, as measured by the API ADAD composite cognitive score, or episodic memory function, measured by the Free and Cued Selective Reminding Test Cueing Index.

Results showed these outcomes were not statistically significant for those receiving the active medication.

In addition to a range of cognitive measures, researchers also assessed amyloid PET and, later in the study, tau PET. MRI and cerebrospinal fluid (CSF) measures were also examined.

The investigators did find small numerical differences favoring crenezumab across the coprimary and multiple secondary and exploratory endpoints, but these were also not statistically significant.

Finally, no new safety issues were identified with crenezumab during the study.

Further analyses of data are ongoing and additional brain imaging and CSF biomarker results will be presented at the Alzheimer’s Association International Conference on Aug. 2.

While the study was not positive, it demonstrated that prevention trials are possible, even in less-than-ideal circumstances and generated a wealth of useful data, the investigators note.

“There were some differences between the treated and untreated patients, and we still need to understand which patients were most likely to experience those differences,” Rachelle Doody, MD, PhD, global head of neurodegeneration at Roche and Genentech, told briefing attendees.

“We need to understand the biomarkers involved and what [they’re] telling us about the disease and the timing of the intervention,” Dr. Doody said.

Prevention “needs to be one of our targeted therapeutic approaches but probably not our only one,” she added.

Beyond amyloid?

Commenting on the negative results, Howard Fillit, MD, cofounder and chief science officer of the Alzheimer’s Drug Discovery Foundation, said they demonstrate the need to focus beyond amyloid and more on the biology of aging.

“This broader approach coupled with advances in novel biomarkers is bringing us closer to the day when physicians will be able to zero in on the root causes of each patient’s Alzheimer’s – and tailor combinations of drug therapies to provide precision medicine,” Dr. Fillit, who was not involved with the research, said in statement.

Genentech is also evaluating the potential of gantenerumab for ADAD and for the prevention of sporadic AD and treatment of early Alzheimer’s in late-stage clinical trials. Results from the phase 3 GRADUATE studies of gantenerumab in early AD are expected by the end of the year.

The study was supported by the National Institute on Aging, contributions to Banner Alzheimer’s Foundation, and Genentech.

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

Crenezumab, an investigational medication designed to slow or prevent Alzheimer’s disease (AD), provides no cognitive benefit in patients at high genetic risk, new research suggests.

Top-line results for a phase 2 trial showed the novel drug, a monoclonal antibody designed to neutralize neurotoxic oligomers (a form of beta-amyloid), was not statistically superior to placebo in terms of cognitive ability or episodic memory function among cognitively unimpaired individuals with a genetic mutation for early-onset AD.

Genentech announced the negative results on June 16 together with Banner Alzheimer’s Institute, Phoenix.

During a press briefing, company representatives and researchers expressed disappointment with the initial results – but stressed numerous ongoing analyses have yet to be completed.

“This is the beginning of the story, but by no means the end of it,” Pierre N. Tariot, MD, director, Banner Alzheimer’s Institute, and one of the study leaders, said at the briefing.

API ADAD trial

The prospective, double-blind parallel-group Alzheimer’s Prevention Initiative (API) Autosomal Dominant Alzheimer’s Disease (ADAD) phase 2 trial enrolled 252 members of the world’s largest extended family with ADAD in Colombia. A total of 94% of the participants completed the study.

Two-thirds of participants carried the Presenilin 1 (PSEN1) E280A mutation, which virtually guarantees that carriers will develop AD at an average age of 44 years and dementia at an average age of 49 years.

Study participants were randomly assigned to receive crenezumab or placebo over a period of 5-8 years. The dose of crenezumab was increased at different time points during the trial as knowledge about potential treatment approaches for AD evolved.

Dr. Tariot noted the maximum dose was not provided for the entire treatment period. “The longest people received the highest dose was about 2 years,” he added.

Coprimary endpoints were rate of change in cognitive abilities, as measured by the API ADAD composite cognitive score, or episodic memory function, measured by the Free and Cued Selective Reminding Test Cueing Index.

Results showed these outcomes were not statistically significant for those receiving the active medication.

In addition to a range of cognitive measures, researchers also assessed amyloid PET and, later in the study, tau PET. MRI and cerebrospinal fluid (CSF) measures were also examined.

The investigators did find small numerical differences favoring crenezumab across the coprimary and multiple secondary and exploratory endpoints, but these were also not statistically significant.

Finally, no new safety issues were identified with crenezumab during the study.

Further analyses of data are ongoing and additional brain imaging and CSF biomarker results will be presented at the Alzheimer’s Association International Conference on Aug. 2.

While the study was not positive, it demonstrated that prevention trials are possible, even in less-than-ideal circumstances and generated a wealth of useful data, the investigators note.

“There were some differences between the treated and untreated patients, and we still need to understand which patients were most likely to experience those differences,” Rachelle Doody, MD, PhD, global head of neurodegeneration at Roche and Genentech, told briefing attendees.

“We need to understand the biomarkers involved and what [they’re] telling us about the disease and the timing of the intervention,” Dr. Doody said.

Prevention “needs to be one of our targeted therapeutic approaches but probably not our only one,” she added.

Beyond amyloid?

Commenting on the negative results, Howard Fillit, MD, cofounder and chief science officer of the Alzheimer’s Drug Discovery Foundation, said they demonstrate the need to focus beyond amyloid and more on the biology of aging.

“This broader approach coupled with advances in novel biomarkers is bringing us closer to the day when physicians will be able to zero in on the root causes of each patient’s Alzheimer’s – and tailor combinations of drug therapies to provide precision medicine,” Dr. Fillit, who was not involved with the research, said in statement.

Genentech is also evaluating the potential of gantenerumab for ADAD and for the prevention of sporadic AD and treatment of early Alzheimer’s in late-stage clinical trials. Results from the phase 3 GRADUATE studies of gantenerumab in early AD are expected by the end of the year.

The study was supported by the National Institute on Aging, contributions to Banner Alzheimer’s Foundation, and Genentech.

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

Menopause gets a bad rap in medical literature and throughout society, say authors of a new analysis. And they argue that the negativity undermines women’s health outlook in the years that should be a natural life transition.

Menopause has been medicalized over centuries and talked about as if it were a disease, they say, and that may increase women’s anxiety and apprehension about the midlife stage.

It’s time to change the narrative, says Martha Hickey, MD, with the department of obstetrics and gynaecology at the Royal Women’s Hospital in Victoria, Australia, and her coauthors. Their analysis was published online in the BMJ.

“The message that menopause signals decay and decline, which can potentially be delayed or reversed by hormonal treatments, persists and is reinforced by the media, medical literature, and information for women, often driven by marketing interests,” they write.

Such messages may chip away at women’s confidence. Dr. Hickey and colleagues cite surveys in the United States and Ireland that found that most women (65%-77%) feel unprepared for menopause.

“Together with limited public discussion and education and shame attached to ageing in women, this may contribute to embarrassment and negative expectations about menopause,” the authors write.
 

The ‘untold misery of oestrogen-starved women’

These messages have deep roots. Take for instance, gynecologist Robert Wilson’s words in his 1966 book “Feminine Forever.” The authors note he recommended estrogen for all menopausal women “to treat their ‘serious, painful and often crippling disease’ and avoid the ‘untold misery of alcoholism, drug addiction, divorce, and broken

homes caused by these unstable, oestrogen-starved women.’ ”

Women experience menopause in very different ways. Experience with menopause also differs by country, the authors explain. “Women’s experience of menopause is also strongly influenced by social values around reproduction and ageing, with positive or negative ramifications,” they write.

“For example, women tend to have worse experiences of menopause in countries where their value is predicated on youth and reproductive capacity and ageing is associated with decline.”

The authors argue that the medicalization of menopause has condensed the wide range of women’s experiences at a typical age into “a narrowly defined disease requiring treatment.”
 

Promoting exercise, stopping smoking among positive messages

An editorial by Haitham Hamoda, MD, and Sara Moger, with the British Menopause Society, notes that more than 75% of women experiencing menopause report symptoms, and more than 25% describe severe symptoms.

The editorialists point out that the National Institute of Health and Care Excellence and others recommend an individualized approach to addressing menopause that includes a comprehensive approach – advice on exercise, weight management, stopping smoking, and reducing alcohol as well as options such as hormone therapy (HT).

The literature says the main indication for HT is for severe symptoms and not as a preventive measure. “Evidence does not support use of HT to reduce the risk of dementia,” they point out.

While some women may benefit from HT, that should not be explored to the exclusion of other avenues of help, Dr. Hickey and colleagues write. Risks must also be considered.
 

Menopause blamed in a difficult time of life

Jennifer Howell, MD, an obstetrician/gynecologist and certified menopause provider at Duke University in Durham, N.C., told this news organization that menopause is often blamed in a time of life when women naturally are experiencing an array of stressful and emotional changes.

It often coincides with children heading to college, navigating midlife challenges in marriage, helping aging parents, managing demanding careers, and health issues.

People want a reason for changes women experience, and too often the finger gets pointed at menopause, Dr. Howell said.

The message women hear has always been, “It’s got to be your hormones. And people want to hear that there’s a hormonal solution.”

Making menopause the target also has led to nonevidence-based “snake-oil” type remedies sold in unregulated powders, creams, and pellets, Dr. Howell noted.

Dr. Howell has treated thousands of menopausal women in her clinic and she says she spends a good deal of time with them explaining a holistic view of the process, much like what the authors describe, with lifestyle changes and treatment options.

Sometimes HT is the solution, Dr. Howell says, but “it’s become a crutch. Hormones are not a panacea.”

She is frustrated with the amount of disinformation circulating online. Groups like the North American Menopause Society put out reliable evidence-based information, but they compete “with a lot of nonsense,” she says.

The message that women should hear, she says is that “[menopause] is a natural part of aging and there may or may not be symptoms that come along with it. If there are, there are things we can do,” she says.

Menopause gets a bad rap in medical literature and throughout society, say authors of a new analysis. And they argue that the negativity undermines women’s health outlook in the years that should be a natural life transition.

Menopause has been medicalized over centuries and talked about as if it were a disease, they say, and that may increase women’s anxiety and apprehension about the midlife stage.

It’s time to change the narrative, says Martha Hickey, MD, with the department of obstetrics and gynaecology at the Royal Women’s Hospital in Victoria, Australia, and her coauthors. Their analysis was published online in the BMJ.

“The message that menopause signals decay and decline, which can potentially be delayed or reversed by hormonal treatments, persists and is reinforced by the media, medical literature, and information for women, often driven by marketing interests,” they write.

Such messages may chip away at women’s confidence. Dr. Hickey and colleagues cite surveys in the United States and Ireland that found that most women (65%-77%) feel unprepared for menopause.

“Together with limited public discussion and education and shame attached to ageing in women, this may contribute to embarrassment and negative expectations about menopause,” the authors write.
 

The ‘untold misery of oestrogen-starved women’

These messages have deep roots. Take for instance, gynecologist Robert Wilson’s words in his 1966 book “Feminine Forever.” The authors note he recommended estrogen for all menopausal women “to treat their ‘serious, painful and often crippling disease’ and avoid the ‘untold misery of alcoholism, drug addiction, divorce, and broken

homes caused by these unstable, oestrogen-starved women.’ ”

Women experience menopause in very different ways. Experience with menopause also differs by country, the authors explain. “Women’s experience of menopause is also strongly influenced by social values around reproduction and ageing, with positive or negative ramifications,” they write.

“For example, women tend to have worse experiences of menopause in countries where their value is predicated on youth and reproductive capacity and ageing is associated with decline.”

The authors argue that the medicalization of menopause has condensed the wide range of women’s experiences at a typical age into “a narrowly defined disease requiring treatment.”
 

Promoting exercise, stopping smoking among positive messages

An editorial by Haitham Hamoda, MD, and Sara Moger, with the British Menopause Society, notes that more than 75% of women experiencing menopause report symptoms, and more than 25% describe severe symptoms.

The editorialists point out that the National Institute of Health and Care Excellence and others recommend an individualized approach to addressing menopause that includes a comprehensive approach – advice on exercise, weight management, stopping smoking, and reducing alcohol as well as options such as hormone therapy (HT).

The literature says the main indication for HT is for severe symptoms and not as a preventive measure. “Evidence does not support use of HT to reduce the risk of dementia,” they point out.

While some women may benefit from HT, that should not be explored to the exclusion of other avenues of help, Dr. Hickey and colleagues write. Risks must also be considered.
 

Menopause blamed in a difficult time of life

Jennifer Howell, MD, an obstetrician/gynecologist and certified menopause provider at Duke University in Durham, N.C., told this news organization that menopause is often blamed in a time of life when women naturally are experiencing an array of stressful and emotional changes.

It often coincides with children heading to college, navigating midlife challenges in marriage, helping aging parents, managing demanding careers, and health issues.

People want a reason for changes women experience, and too often the finger gets pointed at menopause, Dr. Howell said.

The message women hear has always been, “It’s got to be your hormones. And people want to hear that there’s a hormonal solution.”

Making menopause the target also has led to nonevidence-based “snake-oil” type remedies sold in unregulated powders, creams, and pellets, Dr. Howell noted.

Dr. Howell has treated thousands of menopausal women in her clinic and she says she spends a good deal of time with them explaining a holistic view of the process, much like what the authors describe, with lifestyle changes and treatment options.

Sometimes HT is the solution, Dr. Howell says, but “it’s become a crutch. Hormones are not a panacea.”

She is frustrated with the amount of disinformation circulating online. Groups like the North American Menopause Society put out reliable evidence-based information, but they compete “with a lot of nonsense,” she says.

The message that women should hear, she says is that “[menopause] is a natural part of aging and there may or may not be symptoms that come along with it. If there are, there are things we can do,” she says.

Menopause gets a bad rap in medical literature and throughout society, say authors of a new analysis. And they argue that the negativity undermines women’s health outlook in the years that should be a natural life transition.

Menopause has been medicalized over centuries and talked about as if it were a disease, they say, and that may increase women’s anxiety and apprehension about the midlife stage.

It’s time to change the narrative, says Martha Hickey, MD, with the department of obstetrics and gynaecology at the Royal Women’s Hospital in Victoria, Australia, and her coauthors. Their analysis was published online in the BMJ.

“The message that menopause signals decay and decline, which can potentially be delayed or reversed by hormonal treatments, persists and is reinforced by the media, medical literature, and information for women, often driven by marketing interests,” they write.

Such messages may chip away at women’s confidence. Dr. Hickey and colleagues cite surveys in the United States and Ireland that found that most women (65%-77%) feel unprepared for menopause.

“Together with limited public discussion and education and shame attached to ageing in women, this may contribute to embarrassment and negative expectations about menopause,” the authors write.
 

The ‘untold misery of oestrogen-starved women’

These messages have deep roots. Take for instance, gynecologist Robert Wilson’s words in his 1966 book “Feminine Forever.” The authors note he recommended estrogen for all menopausal women “to treat their ‘serious, painful and often crippling disease’ and avoid the ‘untold misery of alcoholism, drug addiction, divorce, and broken

homes caused by these unstable, oestrogen-starved women.’ ”

Women experience menopause in very different ways. Experience with menopause also differs by country, the authors explain. “Women’s experience of menopause is also strongly influenced by social values around reproduction and ageing, with positive or negative ramifications,” they write.

“For example, women tend to have worse experiences of menopause in countries where their value is predicated on youth and reproductive capacity and ageing is associated with decline.”

The authors argue that the medicalization of menopause has condensed the wide range of women’s experiences at a typical age into “a narrowly defined disease requiring treatment.”
 

Promoting exercise, stopping smoking among positive messages

An editorial by Haitham Hamoda, MD, and Sara Moger, with the British Menopause Society, notes that more than 75% of women experiencing menopause report symptoms, and more than 25% describe severe symptoms.

The editorialists point out that the National Institute of Health and Care Excellence and others recommend an individualized approach to addressing menopause that includes a comprehensive approach – advice on exercise, weight management, stopping smoking, and reducing alcohol as well as options such as hormone therapy (HT).

The literature says the main indication for HT is for severe symptoms and not as a preventive measure. “Evidence does not support use of HT to reduce the risk of dementia,” they point out.

While some women may benefit from HT, that should not be explored to the exclusion of other avenues of help, Dr. Hickey and colleagues write. Risks must also be considered.
 

Menopause blamed in a difficult time of life

Jennifer Howell, MD, an obstetrician/gynecologist and certified menopause provider at Duke University in Durham, N.C., told this news organization that menopause is often blamed in a time of life when women naturally are experiencing an array of stressful and emotional changes.

It often coincides with children heading to college, navigating midlife challenges in marriage, helping aging parents, managing demanding careers, and health issues.

People want a reason for changes women experience, and too often the finger gets pointed at menopause, Dr. Howell said.

The message women hear has always been, “It’s got to be your hormones. And people want to hear that there’s a hormonal solution.”

Making menopause the target also has led to nonevidence-based “snake-oil” type remedies sold in unregulated powders, creams, and pellets, Dr. Howell noted.

Dr. Howell has treated thousands of menopausal women in her clinic and she says she spends a good deal of time with them explaining a holistic view of the process, much like what the authors describe, with lifestyle changes and treatment options.

Sometimes HT is the solution, Dr. Howell says, but “it’s become a crutch. Hormones are not a panacea.”

She is frustrated with the amount of disinformation circulating online. Groups like the North American Menopause Society put out reliable evidence-based information, but they compete “with a lot of nonsense,” she says.

The message that women should hear, she says is that “[menopause] is a natural part of aging and there may or may not be symptoms that come along with it. If there are, there are things we can do,” she says.

President Joe Biden issued an executive order on June 15 banning conversion therapy and offering other LBGTQIA+ protections as part of White House efforts to advance equality during Pride Month.

“My order will use the full force of the federal government to end inhumane practices of conversion therapy,” President Biden said in a speech before signing the order. “This is the first time the federal government is making a coordinated effort against this dangerous and discredited practice.”

Conversion therapy is any emotional or physical therapy used to “cure” or “repair” a person’s attraction to the same sex, or their gender identity and expression. Providers claim these therapies can make someone heterosexual or “straight.” But there’s no evidence to support this.

Medical and mental health experts have rejected conversion therapy practices as dangerous and discriminatory for decades.

The executive order also addresses:

• The LGBTQIA+ youth mental health crisis, in part by expanding suicide prevention resources for that at-risk population.
• Discrimination within the foster care system against LGBTQIA+ children and parents.
• Discrimination, poverty and isolation challenges faced by LGBTQIA+ seniors.
• Efforts to strengthen federal data collection in this population to counter homelessness, housing insecurity and barriers to health care access.

Enforcement of executive order will rely on legal experts, including the Justice Department.

President Biden’s order comes at a time when multiple states are promoting or passing anti-LGBTQIA+ laws.

“I don’t have to tell you about the ultra-MAGA agenda attacking our freedoms. There are more than 300 discriminatory bills introduced in states across this country,” President Biden said. “In Texas, they are knocking on front doors to investigate parents who are raising transgender children, and in Florida they are going after Mickey Mouse for God’s sake.”

First Lady Jill Biden, PhD, said the order will not solve all problems. “Prejudice and discrimination still lurk. We will not let the progress we fought for slip away. Pride is a celebration of the courage it takes to stand up for what’s right.”

The American Psychiatric Association applauded President Biden’s action. This executive order will “protect the mental health of LGBTQ+ people, particularly children. APA has long condemned the practice of so-called ‘conversion therapy’ and we welcome the federal government’s efforts to raise public awareness about its harms, alongside other practices that will help to end it.”

The goal of the order is to “improve the health, wellbeing, and safety of countless families across the country,” senior White House administration officials said in a June 15 media call. “And they will send a powerful signal from the president of the United States to LGBTQIA+ kids across the country – who may be feeling scared and hopeless – that their president has their back.”

Biden also called on Congress to pass the Equality Act “to enshrine the long overdue civil rights to protect all Americans.”

The event was held in the East Room of the White House at a Pride event attended by Vice President Kamala Harris and her husband, the first lady, Transportation Secretary Pete Buttigieg, and hundreds of LGBTQIA+ leaders.
 

Guidance on starting transgender treatment

In other LGBTQIA+-related news, an international group focusing on transgender health lowered the minimum ages they recommend for starting hormone therapy or surgery for transgender youth.

The World Professional Association for Transgender Health said that hormones could be started at 14, 2 years earlier than the group’s previous advice. The association also said some surgeries can be performed at age 15 or 17, a year or so earlier than their previous recommendations.

The group acknowledged potential risks but said it is unethical and harmful to withhold early treatment, according to a report from The Associated Press.

Transgender treatment for teens has been a controversial issue, with experts disagreeing about whether teenagers can fully understand the ramifications of such life-altering decisions.

During the White House background media call, senior administration officials pointed to existing policy regarding transgender care. “We’ve already put out guidance through HHS about civil rights protections and making clear that the denial of medical care based on someone’s gender identity is discriminatory and have invited the members of the public to file complaints with the Office of Civil Rights.”

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

President Joe Biden issued an executive order on June 15 banning conversion therapy and offering other LBGTQIA+ protections as part of White House efforts to advance equality during Pride Month.

“My order will use the full force of the federal government to end inhumane practices of conversion therapy,” President Biden said in a speech before signing the order. “This is the first time the federal government is making a coordinated effort against this dangerous and discredited practice.”

Conversion therapy is any emotional or physical therapy used to “cure” or “repair” a person’s attraction to the same sex, or their gender identity and expression. Providers claim these therapies can make someone heterosexual or “straight.” But there’s no evidence to support this.

Medical and mental health experts have rejected conversion therapy practices as dangerous and discriminatory for decades.

The executive order also addresses:

• The LGBTQIA+ youth mental health crisis, in part by expanding suicide prevention resources for that at-risk population.
• Discrimination within the foster care system against LGBTQIA+ children and parents.
• Discrimination, poverty and isolation challenges faced by LGBTQIA+ seniors.
• Efforts to strengthen federal data collection in this population to counter homelessness, housing insecurity and barriers to health care access.

Enforcement of executive order will rely on legal experts, including the Justice Department.

President Biden’s order comes at a time when multiple states are promoting or passing anti-LGBTQIA+ laws.

“I don’t have to tell you about the ultra-MAGA agenda attacking our freedoms. There are more than 300 discriminatory bills introduced in states across this country,” President Biden said. “In Texas, they are knocking on front doors to investigate parents who are raising transgender children, and in Florida they are going after Mickey Mouse for God’s sake.”

First Lady Jill Biden, PhD, said the order will not solve all problems. “Prejudice and discrimination still lurk. We will not let the progress we fought for slip away. Pride is a celebration of the courage it takes to stand up for what’s right.”

The American Psychiatric Association applauded President Biden’s action. This executive order will “protect the mental health of LGBTQ+ people, particularly children. APA has long condemned the practice of so-called ‘conversion therapy’ and we welcome the federal government’s efforts to raise public awareness about its harms, alongside other practices that will help to end it.”

The goal of the order is to “improve the health, wellbeing, and safety of countless families across the country,” senior White House administration officials said in a June 15 media call. “And they will send a powerful signal from the president of the United States to LGBTQIA+ kids across the country – who may be feeling scared and hopeless – that their president has their back.”

Biden also called on Congress to pass the Equality Act “to enshrine the long overdue civil rights to protect all Americans.”

The event was held in the East Room of the White House at a Pride event attended by Vice President Kamala Harris and her husband, the first lady, Transportation Secretary Pete Buttigieg, and hundreds of LGBTQIA+ leaders.
 

Guidance on starting transgender treatment

In other LGBTQIA+-related news, an international group focusing on transgender health lowered the minimum ages they recommend for starting hormone therapy or surgery for transgender youth.

The World Professional Association for Transgender Health said that hormones could be started at 14, 2 years earlier than the group’s previous advice. The association also said some surgeries can be performed at age 15 or 17, a year or so earlier than their previous recommendations.

The group acknowledged potential risks but said it is unethical and harmful to withhold early treatment, according to a report from The Associated Press.

Transgender treatment for teens has been a controversial issue, with experts disagreeing about whether teenagers can fully understand the ramifications of such life-altering decisions.

During the White House background media call, senior administration officials pointed to existing policy regarding transgender care. “We’ve already put out guidance through HHS about civil rights protections and making clear that the denial of medical care based on someone’s gender identity is discriminatory and have invited the members of the public to file complaints with the Office of Civil Rights.”

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

President Joe Biden issued an executive order on June 15 banning conversion therapy and offering other LBGTQIA+ protections as part of White House efforts to advance equality during Pride Month.

“My order will use the full force of the federal government to end inhumane practices of conversion therapy,” President Biden said in a speech before signing the order. “This is the first time the federal government is making a coordinated effort against this dangerous and discredited practice.”

Conversion therapy is any emotional or physical therapy used to “cure” or “repair” a person’s attraction to the same sex, or their gender identity and expression. Providers claim these therapies can make someone heterosexual or “straight.” But there’s no evidence to support this.

Medical and mental health experts have rejected conversion therapy practices as dangerous and discriminatory for decades.

The executive order also addresses:

• The LGBTQIA+ youth mental health crisis, in part by expanding suicide prevention resources for that at-risk population.
• Discrimination within the foster care system against LGBTQIA+ children and parents.
• Discrimination, poverty and isolation challenges faced by LGBTQIA+ seniors.
• Efforts to strengthen federal data collection in this population to counter homelessness, housing insecurity and barriers to health care access.

Enforcement of executive order will rely on legal experts, including the Justice Department.

President Biden’s order comes at a time when multiple states are promoting or passing anti-LGBTQIA+ laws.

“I don’t have to tell you about the ultra-MAGA agenda attacking our freedoms. There are more than 300 discriminatory bills introduced in states across this country,” President Biden said. “In Texas, they are knocking on front doors to investigate parents who are raising transgender children, and in Florida they are going after Mickey Mouse for God’s sake.”

First Lady Jill Biden, PhD, said the order will not solve all problems. “Prejudice and discrimination still lurk. We will not let the progress we fought for slip away. Pride is a celebration of the courage it takes to stand up for what’s right.”

The American Psychiatric Association applauded President Biden’s action. This executive order will “protect the mental health of LGBTQ+ people, particularly children. APA has long condemned the practice of so-called ‘conversion therapy’ and we welcome the federal government’s efforts to raise public awareness about its harms, alongside other practices that will help to end it.”

The goal of the order is to “improve the health, wellbeing, and safety of countless families across the country,” senior White House administration officials said in a June 15 media call. “And they will send a powerful signal from the president of the United States to LGBTQIA+ kids across the country – who may be feeling scared and hopeless – that their president has their back.”

Biden also called on Congress to pass the Equality Act “to enshrine the long overdue civil rights to protect all Americans.”

The event was held in the East Room of the White House at a Pride event attended by Vice President Kamala Harris and her husband, the first lady, Transportation Secretary Pete Buttigieg, and hundreds of LGBTQIA+ leaders.
 

Guidance on starting transgender treatment

In other LGBTQIA+-related news, an international group focusing on transgender health lowered the minimum ages they recommend for starting hormone therapy or surgery for transgender youth.

The World Professional Association for Transgender Health said that hormones could be started at 14, 2 years earlier than the group’s previous advice. The association also said some surgeries can be performed at age 15 or 17, a year or so earlier than their previous recommendations.

The group acknowledged potential risks but said it is unethical and harmful to withhold early treatment, according to a report from The Associated Press.

Transgender treatment for teens has been a controversial issue, with experts disagreeing about whether teenagers can fully understand the ramifications of such life-altering decisions.

During the White House background media call, senior administration officials pointed to existing policy regarding transgender care. “We’ve already put out guidance through HHS about civil rights protections and making clear that the denial of medical care based on someone’s gender identity is discriminatory and have invited the members of the public to file complaints with the Office of Civil Rights.”

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

Illinois has a new law designed to boost the mental health care workforce at a time when it has been devastated by the COVID-19 pandemic, say state leaders.

Governor J.B. Pritzker (D) signed the legislation, which took effect on June 10.

The law seeks to attract psychologists, social workers, and counselors who have left the workforce within the past 5 years by temporarily ending relicensing requirements, including the need for continuing education credit completion, passing new exams, and fee payments. It also eases the process for those practicing in other states to become licensed in Illinois.

State legislators said there is currently a crushing need for mental health providers, estimating that there are only 14 behavioral health care professionals for every 10,000 Illinois residents. The preamble to the law noted that there will be 8,353 unfilled mental health care jobs in Illinois by 2026.

“We need a mental health care workforce that is robust enough to get people help when they need it – not after months on a waiting list,” Governor Pritzker said in news release. “This legislation invests in mental health infrastructure – and that infrastructure is people,” he added.
 

Grant pathway

“Being told you have to wait weeks – or months – for care is extremely discouraging,” State Senator Laura Fine (D), a lead sponsor of the legislation, noted in the release.

“We need to support people struggling with mental and behavioral health issues, as well as address difficulties our mental health providers are facing trying to see as many patients as possible,” said Senator Fine.

Marvin Lindsey, CEO of the Community Behavioral Healthcare Association, added that the law would “accelerate the process for out-of-state professionals to obtain their Illinois licensure and [increase] the pipeline and diversity of the behavioral health workforce by implementing a funding mechanism that supports new or existing licensure training of interns.”

The law sets up a grant pathway for community mental health centers, which often serve as training sites. The grants would provide funds to establish or enhance training and supervision of interns and behavioral health providers-in-training seeking to become licensed clinical social workers, licensed clinical professional counselors, or licensed marriage and family therapists.

The money for those grants still has to be appropriated.

The law will also allow patient visits at Specialized Mental Health Rehabilitation Facilities conducted by either a psychiatrist or an advanced practice registered mental health or psychiatric nurse.

Finally, it would establish tax credits for employers who hire individuals in recovery from a substance use disorder or a behavioral disorder. Beginning in January 2023, employers will be eligible for up to $2,000 in credits per employee hired.

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

Illinois has a new law designed to boost the mental health care workforce at a time when it has been devastated by the COVID-19 pandemic, say state leaders.

Governor J.B. Pritzker (D) signed the legislation, which took effect on June 10.

The law seeks to attract psychologists, social workers, and counselors who have left the workforce within the past 5 years by temporarily ending relicensing requirements, including the need for continuing education credit completion, passing new exams, and fee payments. It also eases the process for those practicing in other states to become licensed in Illinois.

State legislators said there is currently a crushing need for mental health providers, estimating that there are only 14 behavioral health care professionals for every 10,000 Illinois residents. The preamble to the law noted that there will be 8,353 unfilled mental health care jobs in Illinois by 2026.

“We need a mental health care workforce that is robust enough to get people help when they need it – not after months on a waiting list,” Governor Pritzker said in news release. “This legislation invests in mental health infrastructure – and that infrastructure is people,” he added.
 

Grant pathway

“Being told you have to wait weeks – or months – for care is extremely discouraging,” State Senator Laura Fine (D), a lead sponsor of the legislation, noted in the release.

“We need to support people struggling with mental and behavioral health issues, as well as address difficulties our mental health providers are facing trying to see as many patients as possible,” said Senator Fine.

Marvin Lindsey, CEO of the Community Behavioral Healthcare Association, added that the law would “accelerate the process for out-of-state professionals to obtain their Illinois licensure and [increase] the pipeline and diversity of the behavioral health workforce by implementing a funding mechanism that supports new or existing licensure training of interns.”

The law sets up a grant pathway for community mental health centers, which often serve as training sites. The grants would provide funds to establish or enhance training and supervision of interns and behavioral health providers-in-training seeking to become licensed clinical social workers, licensed clinical professional counselors, or licensed marriage and family therapists.

The money for those grants still has to be appropriated.

The law will also allow patient visits at Specialized Mental Health Rehabilitation Facilities conducted by either a psychiatrist or an advanced practice registered mental health or psychiatric nurse.

Finally, it would establish tax credits for employers who hire individuals in recovery from a substance use disorder or a behavioral disorder. Beginning in January 2023, employers will be eligible for up to $2,000 in credits per employee hired.

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

Illinois has a new law designed to boost the mental health care workforce at a time when it has been devastated by the COVID-19 pandemic, say state leaders.

Governor J.B. Pritzker (D) signed the legislation, which took effect on June 10.

The law seeks to attract psychologists, social workers, and counselors who have left the workforce within the past 5 years by temporarily ending relicensing requirements, including the need for continuing education credit completion, passing new exams, and fee payments. It also eases the process for those practicing in other states to become licensed in Illinois.

State legislators said there is currently a crushing need for mental health providers, estimating that there are only 14 behavioral health care professionals for every 10,000 Illinois residents. The preamble to the law noted that there will be 8,353 unfilled mental health care jobs in Illinois by 2026.

“We need a mental health care workforce that is robust enough to get people help when they need it – not after months on a waiting list,” Governor Pritzker said in news release. “This legislation invests in mental health infrastructure – and that infrastructure is people,” he added.
 

Grant pathway

“Being told you have to wait weeks – or months – for care is extremely discouraging,” State Senator Laura Fine (D), a lead sponsor of the legislation, noted in the release.

“We need to support people struggling with mental and behavioral health issues, as well as address difficulties our mental health providers are facing trying to see as many patients as possible,” said Senator Fine.

Marvin Lindsey, CEO of the Community Behavioral Healthcare Association, added that the law would “accelerate the process for out-of-state professionals to obtain their Illinois licensure and [increase] the pipeline and diversity of the behavioral health workforce by implementing a funding mechanism that supports new or existing licensure training of interns.”

The law sets up a grant pathway for community mental health centers, which often serve as training sites. The grants would provide funds to establish or enhance training and supervision of interns and behavioral health providers-in-training seeking to become licensed clinical social workers, licensed clinical professional counselors, or licensed marriage and family therapists.

The money for those grants still has to be appropriated.

The law will also allow patient visits at Specialized Mental Health Rehabilitation Facilities conducted by either a psychiatrist or an advanced practice registered mental health or psychiatric nurse.

Finally, it would establish tax credits for employers who hire individuals in recovery from a substance use disorder or a behavioral disorder. Beginning in January 2023, employers will be eligible for up to $2,000 in credits per employee hired.

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

It was wonderful to see long-term friends and colleagues again in New Orleans! Warmed me from the bottom of my COVID-scarred heart.

I had trepidation and anxiety about further COVID exposure, as I am sure many of you all did. I have carefully resumed traveling, although the rules on masking continue to change and confuse us all.

But I did it. I went to the American Psychiatric Association meeting in New Orleans and am so glad I did.

There was of course a lot of discussion about the pandemic, which separated us physically for 3 years – too many virtual meetings. And quiet discussions of grief and loss, both before and during the APA.

I just learned that Joe Napoli, MD, died. He was one of the hearts of the APA Disaster Psychiatry Committee. Others were lost as well, and I am processing those losses.

I do not want this column to be just a promotion for the APA, although it has been my home organization for decades. So, let me define further the cons and pros of going to the meeting. (Yes, I am deliberately reversing the order of these words.) I warn all the readers in advance that this is a soapbox.
 

Cons

The convention center in New Orleans is ridiculously long. Our convention was in Hall G down at end of its telescoping length. Only a couple of doors were open – clearly quite a challenge for folks with disabilities, or those aging into possible disability, like myself. I helped a psychiatrist with impaired vision down the endless hall and of course, felt good about it. (My motto: “Perform acts of kindness, and you will feel better yourself.”)

Another con: Too much going on at the same time. That’s a perpetual problem.

And the noise at the parties was way too loud. We could not hear each other.
 

Pros

Seeing people I have known for 40 years – with masks, without masks. Hugs or bows (on my part, I bow I do not yet hug in COVID times).

The receptions. Great networking. Mid-level psychiatrists who I had forgotten I had mentored. The “young ones” – the psychiatry residents. They seem to be a great and ambitious group.

I did several talks, including one on female veterans, and another on clinical management of the homeless population. The audiences were large and engaged. I am wondering how to make these topics an APA priority, especially engagement with strategies to take care of the unhoused/homeless folks.

Let me give you a brief synopsis of both of those talks, as they represent some of my passions. The first on female veterans. We tend to focus on PTSD and military sexual trauma. I am also concerned about reproductive and musculoskeletal concerns. Too many female service members get pregnant, then quit the military as they cannot manage being a Service member and a mother. They think they can make it (go to school, get a job) but they cannot manage it all.

Veterans services usually focus on single older men. There are not enough rooms and services for female veterans with children. In fairness to the Department of Veterans Affairs, they are trying to remedy this lack.

Transitioning to the homeless population in general, this is an incredible problem which is not easily solved. The VA has done an incredible job here, but the whole country should be mobilized.

My focus at the talk was the importance of assessing and treating medical problems. Again, homeless women are at high risk for barriers to contraception, sexual assault, pregnancy, and the corresponding difficulties of finding housing that will accept infants and small children.

Then there are the numerous medical issues in the unhoused population. Diabetes, hypertension, ulcers on the feet leading to cellulitis and amputation. I am advocating that we psychiatrists behave as medical doctors and think of the whole person, not just of the mind.

Another pro of the APA meeting: such desire to share what we know with the world. I found a few more potential authors for book chapters, specifically Dr. Anne Hansen to write a chapter in my capacity volume. And getting recruited myself, by Maria Llorente, MD, for one on centenarians (people who aged over 100.) Not sure if I know very much now, but I will try.

But another con: I am very tired of endless “scope of practice” discussions about what psychologists and nurse practitioners should do. They are all my comrades. We have plenty of business for all, in this never-ending anxiety tide of COVID.

Another con: I tested positive for COVID after my return, as did several of my friends.

I am sure our readers have many more takes on returning to the APA. These are a few of my thoughts.

Dr. Ritchie is chair of psychiatry at Medstar Washington (D.C.) Hospital Center. She is a member of the Clinical Psychiatry News editorial advisory board, and has no conflicts of interest.

It was wonderful to see long-term friends and colleagues again in New Orleans! Warmed me from the bottom of my COVID-scarred heart.

I had trepidation and anxiety about further COVID exposure, as I am sure many of you all did. I have carefully resumed traveling, although the rules on masking continue to change and confuse us all.

But I did it. I went to the American Psychiatric Association meeting in New Orleans and am so glad I did.

There was of course a lot of discussion about the pandemic, which separated us physically for 3 years – too many virtual meetings. And quiet discussions of grief and loss, both before and during the APA.

I just learned that Joe Napoli, MD, died. He was one of the hearts of the APA Disaster Psychiatry Committee. Others were lost as well, and I am processing those losses.

I do not want this column to be just a promotion for the APA, although it has been my home organization for decades. So, let me define further the cons and pros of going to the meeting. (Yes, I am deliberately reversing the order of these words.) I warn all the readers in advance that this is a soapbox.
 

Cons

The convention center in New Orleans is ridiculously long. Our convention was in Hall G down at end of its telescoping length. Only a couple of doors were open – clearly quite a challenge for folks with disabilities, or those aging into possible disability, like myself. I helped a psychiatrist with impaired vision down the endless hall and of course, felt good about it. (My motto: “Perform acts of kindness, and you will feel better yourself.”)

Another con: Too much going on at the same time. That’s a perpetual problem.

And the noise at the parties was way too loud. We could not hear each other.
 

Pros

Seeing people I have known for 40 years – with masks, without masks. Hugs or bows (on my part, I bow I do not yet hug in COVID times).

The receptions. Great networking. Mid-level psychiatrists who I had forgotten I had mentored. The “young ones” – the psychiatry residents. They seem to be a great and ambitious group.

I did several talks, including one on female veterans, and another on clinical management of the homeless population. The audiences were large and engaged. I am wondering how to make these topics an APA priority, especially engagement with strategies to take care of the unhoused/homeless folks.

Let me give you a brief synopsis of both of those talks, as they represent some of my passions. The first on female veterans. We tend to focus on PTSD and military sexual trauma. I am also concerned about reproductive and musculoskeletal concerns. Too many female service members get pregnant, then quit the military as they cannot manage being a Service member and a mother. They think they can make it (go to school, get a job) but they cannot manage it all.

Veterans services usually focus on single older men. There are not enough rooms and services for female veterans with children. In fairness to the Department of Veterans Affairs, they are trying to remedy this lack.

Transitioning to the homeless population in general, this is an incredible problem which is not easily solved. The VA has done an incredible job here, but the whole country should be mobilized.

My focus at the talk was the importance of assessing and treating medical problems. Again, homeless women are at high risk for barriers to contraception, sexual assault, pregnancy, and the corresponding difficulties of finding housing that will accept infants and small children.

Then there are the numerous medical issues in the unhoused population. Diabetes, hypertension, ulcers on the feet leading to cellulitis and amputation. I am advocating that we psychiatrists behave as medical doctors and think of the whole person, not just of the mind.

Another pro of the APA meeting: such desire to share what we know with the world. I found a few more potential authors for book chapters, specifically Dr. Anne Hansen to write a chapter in my capacity volume. And getting recruited myself, by Maria Llorente, MD, for one on centenarians (people who aged over 100.) Not sure if I know very much now, but I will try.

But another con: I am very tired of endless “scope of practice” discussions about what psychologists and nurse practitioners should do. They are all my comrades. We have plenty of business for all, in this never-ending anxiety tide of COVID.

Another con: I tested positive for COVID after my return, as did several of my friends.

I am sure our readers have many more takes on returning to the APA. These are a few of my thoughts.

Dr. Ritchie is chair of psychiatry at Medstar Washington (D.C.) Hospital Center. She is a member of the Clinical Psychiatry News editorial advisory board, and has no conflicts of interest.

It was wonderful to see long-term friends and colleagues again in New Orleans! Warmed me from the bottom of my COVID-scarred heart.

I had trepidation and anxiety about further COVID exposure, as I am sure many of you all did. I have carefully resumed traveling, although the rules on masking continue to change and confuse us all.

But I did it. I went to the American Psychiatric Association meeting in New Orleans and am so glad I did.

There was of course a lot of discussion about the pandemic, which separated us physically for 3 years – too many virtual meetings. And quiet discussions of grief and loss, both before and during the APA.

I just learned that Joe Napoli, MD, died. He was one of the hearts of the APA Disaster Psychiatry Committee. Others were lost as well, and I am processing those losses.

I do not want this column to be just a promotion for the APA, although it has been my home organization for decades. So, let me define further the cons and pros of going to the meeting. (Yes, I am deliberately reversing the order of these words.) I warn all the readers in advance that this is a soapbox.
 

Cons

The convention center in New Orleans is ridiculously long. Our convention was in Hall G down at end of its telescoping length. Only a couple of doors were open – clearly quite a challenge for folks with disabilities, or those aging into possible disability, like myself. I helped a psychiatrist with impaired vision down the endless hall and of course, felt good about it. (My motto: “Perform acts of kindness, and you will feel better yourself.”)

Another con: Too much going on at the same time. That’s a perpetual problem.

And the noise at the parties was way too loud. We could not hear each other.
 

Pros

Seeing people I have known for 40 years – with masks, without masks. Hugs or bows (on my part, I bow I do not yet hug in COVID times).

The receptions. Great networking. Mid-level psychiatrists who I had forgotten I had mentored. The “young ones” – the psychiatry residents. They seem to be a great and ambitious group.

I did several talks, including one on female veterans, and another on clinical management of the homeless population. The audiences were large and engaged. I am wondering how to make these topics an APA priority, especially engagement with strategies to take care of the unhoused/homeless folks.

Let me give you a brief synopsis of both of those talks, as they represent some of my passions. The first on female veterans. We tend to focus on PTSD and military sexual trauma. I am also concerned about reproductive and musculoskeletal concerns. Too many female service members get pregnant, then quit the military as they cannot manage being a Service member and a mother. They think they can make it (go to school, get a job) but they cannot manage it all.

Veterans services usually focus on single older men. There are not enough rooms and services for female veterans with children. In fairness to the Department of Veterans Affairs, they are trying to remedy this lack.

Transitioning to the homeless population in general, this is an incredible problem which is not easily solved. The VA has done an incredible job here, but the whole country should be mobilized.

My focus at the talk was the importance of assessing and treating medical problems. Again, homeless women are at high risk for barriers to contraception, sexual assault, pregnancy, and the corresponding difficulties of finding housing that will accept infants and small children.

Then there are the numerous medical issues in the unhoused population. Diabetes, hypertension, ulcers on the feet leading to cellulitis and amputation. I am advocating that we psychiatrists behave as medical doctors and think of the whole person, not just of the mind.

Another pro of the APA meeting: such desire to share what we know with the world. I found a few more potential authors for book chapters, specifically Dr. Anne Hansen to write a chapter in my capacity volume. And getting recruited myself, by Maria Llorente, MD, for one on centenarians (people who aged over 100.) Not sure if I know very much now, but I will try.

But another con: I am very tired of endless “scope of practice” discussions about what psychologists and nurse practitioners should do. They are all my comrades. We have plenty of business for all, in this never-ending anxiety tide of COVID.

Another con: I tested positive for COVID after my return, as did several of my friends.

I am sure our readers have many more takes on returning to the APA. These are a few of my thoughts.

Dr. Ritchie is chair of psychiatry at Medstar Washington (D.C.) Hospital Center. She is a member of the Clinical Psychiatry News editorial advisory board, and has no conflicts of interest.

Your gut microbiome will thank you later

A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?

In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.

Beer? Yes. Beer.

Engin Akyurt/Pixabay

We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?

In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.

So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
 

We’ve lost our minds, but at least we know how fast they’re going

The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”

Massimiliano De Deo, LNGS-INFN

When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.

To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.

That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.

The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
 

Missing links: A real fish story

Dear LOTME:

Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?

Restless in Roswell

Dear Restless:

The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.

IVPP

For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?

The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.

“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.

In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.

So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
 

Can you lend me an ear?

If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?

850977/Pixabay

Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?

“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.

And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”

The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!

Your gut microbiome will thank you later

A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?

In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.

Beer? Yes. Beer.

Engin Akyurt/Pixabay

We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?

In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.

So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
 

We’ve lost our minds, but at least we know how fast they’re going

The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”

Massimiliano De Deo, LNGS-INFN

When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.

To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.

That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.

The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
 

Missing links: A real fish story

Dear LOTME:

Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?

Restless in Roswell

Dear Restless:

The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.

IVPP

For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?

The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.

“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.

In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.

So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
 

Can you lend me an ear?

If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?

850977/Pixabay

Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?

“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.

And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”

The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!

Your gut microbiome will thank you later

A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?

In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.

Beer? Yes. Beer.

Engin Akyurt/Pixabay

We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?

In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.

So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
 

We’ve lost our minds, but at least we know how fast they’re going

The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”

Massimiliano De Deo, LNGS-INFN

When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.

To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.

That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.

The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
 

Missing links: A real fish story

Dear LOTME:

Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?

Restless in Roswell

Dear Restless:

The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.

IVPP

For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?

The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.

“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.

In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.

So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
 

Can you lend me an ear?

If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?

850977/Pixabay

Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?

“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.

And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”

The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!

Sleep time may be a modifiable risk factor for cancer, according to a recent study from Japan.

The findings reveal that sleeping 10-plus hours may increase a woman’s risk of getting cancer and both men and women’s risk of dying from cancer. 

The researchers say their findings may help refine sleep recommendations in Japan, which currently advise working, middle-aged adults to sleep “as long as they can.”

Based on the new findings, a sleep duration of 6-8 hours for men and 6-9 hours for women “may be the safest” regarding cancer incidence and mortality risk among Japanese adults, the authors conclude.

The findings were published online in the International Journal of Cancer. 

The literature on sleep time and cancer risk is mixed. A trio of meta-analyses conducted between 2016 and 2019 found that long sleep duration, but not short, was associated with a slightly elevated risk of all cancer mortality in Asians.

A separate meta-analysis conducted in 2018 found that both short and long sleep durations were not related to cancer incidence. But in the stratified analysis, shorter sleep time was associated with 36% increased cancer risk among Asians.

To investigate further, the researchers pooled data from six population-based cohorts that included 271,694 adults – 126,930 men and 144,764 women – with 40,751 total incident cancer cases and 18,323 total cancer deaths during a follow-up lasting about 5.9 million person-years.

In the multivariable analysis, longer sleep duration was not associated with total cancer incidence in men. In women, however, sleeping 10 or more hours vs. 7 was associated with a 19% increased risk of cancer.

In addition, sleeping 10 or more hours was associated with an increased risk of dying from cancer in women (hazard ratio, 1.44) and men (HR, 1.18).

Sleeping for 5 hours or fewer, compared with 7, was not associated with cancer incidence and mortality. However, among postmenopausal women, shorter sleep durations did increase the risk of dying from cancer (HR, 1.15).

The authors highlight several strengths of the analysis, including a large sample size as well as stratification of the results by body mass index and menopause status, which has rarely been done in previous studies.

Limitations include self-reported sleep durations and lack of data on sleep quality. The researchers note that the mechanism by which sleep time may influence cancer incidence and mortality is unclear but likely to be complex and cancer site specific.

It’s also possible that reverse causation could explain associations between sleep duration and cancer occurrence and mortality – with pain from cancer, for instance, impairing sleep duration and quality. However, the sensitivity analysis found no evidence of reverse causality or other confounding factors.

Based on these findings, the researchers say sleep duration “may be an important variable to include in cancer incidence and mortality risk prediction models.”

The study had no specific funding. The authors declared no relevant conflicts of interest.

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

Sleep time may be a modifiable risk factor for cancer, according to a recent study from Japan.

The findings reveal that sleeping 10-plus hours may increase a woman’s risk of getting cancer and both men and women’s risk of dying from cancer. 

The researchers say their findings may help refine sleep recommendations in Japan, which currently advise working, middle-aged adults to sleep “as long as they can.”

Based on the new findings, a sleep duration of 6-8 hours for men and 6-9 hours for women “may be the safest” regarding cancer incidence and mortality risk among Japanese adults, the authors conclude.

The findings were published online in the International Journal of Cancer. 

The literature on sleep time and cancer risk is mixed. A trio of meta-analyses conducted between 2016 and 2019 found that long sleep duration, but not short, was associated with a slightly elevated risk of all cancer mortality in Asians.

A separate meta-analysis conducted in 2018 found that both short and long sleep durations were not related to cancer incidence. But in the stratified analysis, shorter sleep time was associated with 36% increased cancer risk among Asians.

To investigate further, the researchers pooled data from six population-based cohorts that included 271,694 adults – 126,930 men and 144,764 women – with 40,751 total incident cancer cases and 18,323 total cancer deaths during a follow-up lasting about 5.9 million person-years.

In the multivariable analysis, longer sleep duration was not associated with total cancer incidence in men. In women, however, sleeping 10 or more hours vs. 7 was associated with a 19% increased risk of cancer.

In addition, sleeping 10 or more hours was associated with an increased risk of dying from cancer in women (hazard ratio, 1.44) and men (HR, 1.18).

Sleeping for 5 hours or fewer, compared with 7, was not associated with cancer incidence and mortality. However, among postmenopausal women, shorter sleep durations did increase the risk of dying from cancer (HR, 1.15).

The authors highlight several strengths of the analysis, including a large sample size as well as stratification of the results by body mass index and menopause status, which has rarely been done in previous studies.

Limitations include self-reported sleep durations and lack of data on sleep quality. The researchers note that the mechanism by which sleep time may influence cancer incidence and mortality is unclear but likely to be complex and cancer site specific.

It’s also possible that reverse causation could explain associations between sleep duration and cancer occurrence and mortality – with pain from cancer, for instance, impairing sleep duration and quality. However, the sensitivity analysis found no evidence of reverse causality or other confounding factors.

Based on these findings, the researchers say sleep duration “may be an important variable to include in cancer incidence and mortality risk prediction models.”

The study had no specific funding. The authors declared no relevant conflicts of interest.

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

Sleep time may be a modifiable risk factor for cancer, according to a recent study from Japan.

The findings reveal that sleeping 10-plus hours may increase a woman’s risk of getting cancer and both men and women’s risk of dying from cancer. 

The researchers say their findings may help refine sleep recommendations in Japan, which currently advise working, middle-aged adults to sleep “as long as they can.”

Based on the new findings, a sleep duration of 6-8 hours for men and 6-9 hours for women “may be the safest” regarding cancer incidence and mortality risk among Japanese adults, the authors conclude.

The findings were published online in the International Journal of Cancer. 

The literature on sleep time and cancer risk is mixed. A trio of meta-analyses conducted between 2016 and 2019 found that long sleep duration, but not short, was associated with a slightly elevated risk of all cancer mortality in Asians.

A separate meta-analysis conducted in 2018 found that both short and long sleep durations were not related to cancer incidence. But in the stratified analysis, shorter sleep time was associated with 36% increased cancer risk among Asians.

To investigate further, the researchers pooled data from six population-based cohorts that included 271,694 adults – 126,930 men and 144,764 women – with 40,751 total incident cancer cases and 18,323 total cancer deaths during a follow-up lasting about 5.9 million person-years.

In the multivariable analysis, longer sleep duration was not associated with total cancer incidence in men. In women, however, sleeping 10 or more hours vs. 7 was associated with a 19% increased risk of cancer.

In addition, sleeping 10 or more hours was associated with an increased risk of dying from cancer in women (hazard ratio, 1.44) and men (HR, 1.18).

Sleeping for 5 hours or fewer, compared with 7, was not associated with cancer incidence and mortality. However, among postmenopausal women, shorter sleep durations did increase the risk of dying from cancer (HR, 1.15).

The authors highlight several strengths of the analysis, including a large sample size as well as stratification of the results by body mass index and menopause status, which has rarely been done in previous studies.

Limitations include self-reported sleep durations and lack of data on sleep quality. The researchers note that the mechanism by which sleep time may influence cancer incidence and mortality is unclear but likely to be complex and cancer site specific.

It’s also possible that reverse causation could explain associations between sleep duration and cancer occurrence and mortality – with pain from cancer, for instance, impairing sleep duration and quality. However, the sensitivity analysis found no evidence of reverse causality or other confounding factors.

Based on these findings, the researchers say sleep duration “may be an important variable to include in cancer incidence and mortality risk prediction models.”

The study had no specific funding. The authors declared no relevant conflicts of interest.

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

CHARLOTTE, N.C. – What may be the largest case-based study of patients with migraine and sleep-disordered breathing to date has found that, counter to prevailing thought, they may not be at higher risk of having obstructive sleep apnea (OSA) than nonmigraine patients, although further prospective studies are needed to validate that finding.

“This in no way for me changes the fact that, for patients that complain of headaches, sleep apnea remains to be something that should be considered as possible cause of their headaches,” neurologist and Cleveland Clinic postdoctoral fellow Eric Gruenthal, MD, said in an interview after he presented his results at the annual meeting of the Associated Professional Sleep Societies.

The study suggested that patients with migraine may have an OSA risk that “may be a little lower” than their nonmigraine counterparts, Dr. Gruenthal said. “But we have really yet to determine whether that’s true or not.”
 

Large case-based study

The retrospective case study included 4,783 migraine cases from the Cleveland Clinic electronic health record database who were case matched on a 1:3 basis with 14,287 controls. Patients with migraine had an average age of 47.5 years (±13.3) and body mass index of 33.7 kg/m² (±8.6), and 76.4% were White. All patients had polysomnography (PSG) at a Cleveland Clinic facility from 1998 to 2021.

The analysis evaluated the collected data in two domains: sleep architecture, consisting of arousal index (AI), total sleep time (TST) and percentage of sleep stage time; and sleep-disordered breathing, including apnea hypopnea index (AHI) and mean oxygen saturation. The key findings of the migraine patients versus controls include:

• Lower AI, 19.6 (95% confidence interval, 12.8-30.9) versus 22.6 (95% CI, 14.7-34.9; P < .001).
• Shorter TST, 359 (95% CI, 307-421) versus 363 (95% CI, 306-432.5) minutes (P = .01).
• With regard to sleep stage, the percentage of N2 sleep was higher, 67.8% (95% CI, 59.6%-75.6%) versus 67% (95% CI, 58.4%-74.8%; P < .001); but the percentage of REM was lower at 16.7% (95% CI, 10%-22%) versus 17% (95% CI, 11.1%-22.2%; P = .012).
• Lower AHI, 7.4 (95% CI, 2.6-17) versus 9.5 (95% CI, 3.7-22.1, P < .001).
• Higher mean oxygen saturation, 93.7 (±2.4) versus 93.3% (±2.6; P < .001).

“Also,” Dr. Gruenthal added, “we found that the percentage of sleep time with oxygen saturation below 90% was lower among patients with migraine, at 1.3% versus 2.4%” (P < .001).
 

A unique profile?

The goal of the study was to determine whether migraine patients would have a unique PSG profile, Dr. Gruenthal said. “We were trying to overcome some of the limitations of previous studies, most notably those that use small sample sizes, and in some cases a lack of controls.”

The findings that migraine patients would have higher AI and elevated AHI ran counter to the study’s hypotheses, but fell in line with the expectation that they would have reduced TST, Dr. Gruenthal said.

Patients with migraine “may, in fact, exhibit a lower burden of sleep-disordered breathing, and that’s based on our findings such as the lower AHI and decreased burden of hypoxemia,” he said. “We theorized that this may be related to patients with migraine having a unique CGRP [calcitonin gene-related peptide] and serotonin physiology.” He noted that previously published research has shown that sleep CGRP and serotonin have a central role in causing arousal in response to rising CO₂ levels during sleep, which can occur during apneas and hypopneas.

Dr. Gruenthal noted that the researchers are still analyzing the findings. “We theorized that possible indication bias may be present in our study,” he said. “It may be the case that patients with migraine are more likely to get their PSG done because of their headache and not for things like snoring and witnessed apneas, which may be more predictive of significant sleep apnea.” They’re also evaluating the “question of medicine confounding.”

Dr. Gruenthal added that “the big unanswered question out there is, if you have a patient with migraine who also has sleep apnea, by treating the sleep apnea will that improve their migraine?”
 

More questions than answers

Commenting on the study, Donald Bliwise, PhD, professor of neurology at Emory Sleep Center, Atlanta, said the study findings shouldn’t change how clinicians approach migraine in relation to sleep.

“It’s a case series, it’s retrospective,” said Dr. Bliwise, who was not involved in the study. “It’s the largest study that I know of that has ever looked at the diagnosis of migraine in relation to polysomnographic measures of sleep, but it’s imprecise to the extent that migraine is a clinical diagnosis, so not everyone that carries the diagnosis of migraine has the diagnosis made by a neurologist.”

The study raises more questions than it answers, he said, “but that’s not necessarily a bad thing. I think we need more prospective studies.” Those studies should be more granular in how they analyze sleep in migraine patients “Since migraine is an intermittent event, and sleep quality and length, and percentage of REM sleep and even sleep apnea can vary from night to night, it would be fascinating to look at headaches over a month in relation to sleep over a month.”

Dr. Gruenthal and Dr. Bliwise have no disclosures. The Association of Migraine Disorders provided funding for the study.

CHARLOTTE, N.C. – What may be the largest case-based study of patients with migraine and sleep-disordered breathing to date has found that, counter to prevailing thought, they may not be at higher risk of having obstructive sleep apnea (OSA) than nonmigraine patients, although further prospective studies are needed to validate that finding.

“This in no way for me changes the fact that, for patients that complain of headaches, sleep apnea remains to be something that should be considered as possible cause of their headaches,” neurologist and Cleveland Clinic postdoctoral fellow Eric Gruenthal, MD, said in an interview after he presented his results at the annual meeting of the Associated Professional Sleep Societies.

The study suggested that patients with migraine may have an OSA risk that “may be a little lower” than their nonmigraine counterparts, Dr. Gruenthal said. “But we have really yet to determine whether that’s true or not.”
 

Large case-based study

The retrospective case study included 4,783 migraine cases from the Cleveland Clinic electronic health record database who were case matched on a 1:3 basis with 14,287 controls. Patients with migraine had an average age of 47.5 years (±13.3) and body mass index of 33.7 kg/m² (±8.6), and 76.4% were White. All patients had polysomnography (PSG) at a Cleveland Clinic facility from 1998 to 2021.

The analysis evaluated the collected data in two domains: sleep architecture, consisting of arousal index (AI), total sleep time (TST) and percentage of sleep stage time; and sleep-disordered breathing, including apnea hypopnea index (AHI) and mean oxygen saturation. The key findings of the migraine patients versus controls include:

• Lower AI, 19.6 (95% confidence interval, 12.8-30.9) versus 22.6 (95% CI, 14.7-34.9; P < .001).
• Shorter TST, 359 (95% CI, 307-421) versus 363 (95% CI, 306-432.5) minutes (P = .01).
• With regard to sleep stage, the percentage of N2 sleep was higher, 67.8% (95% CI, 59.6%-75.6%) versus 67% (95% CI, 58.4%-74.8%; P < .001); but the percentage of REM was lower at 16.7% (95% CI, 10%-22%) versus 17% (95% CI, 11.1%-22.2%; P = .012).
• Lower AHI, 7.4 (95% CI, 2.6-17) versus 9.5 (95% CI, 3.7-22.1, P < .001).
• Higher mean oxygen saturation, 93.7 (±2.4) versus 93.3% (±2.6; P < .001).

“Also,” Dr. Gruenthal added, “we found that the percentage of sleep time with oxygen saturation below 90% was lower among patients with migraine, at 1.3% versus 2.4%” (P < .001).
 

A unique profile?

The goal of the study was to determine whether migraine patients would have a unique PSG profile, Dr. Gruenthal said. “We were trying to overcome some of the limitations of previous studies, most notably those that use small sample sizes, and in some cases a lack of controls.”

The findings that migraine patients would have higher AI and elevated AHI ran counter to the study’s hypotheses, but fell in line with the expectation that they would have reduced TST, Dr. Gruenthal said.

Patients with migraine “may, in fact, exhibit a lower burden of sleep-disordered breathing, and that’s based on our findings such as the lower AHI and decreased burden of hypoxemia,” he said. “We theorized that this may be related to patients with migraine having a unique CGRP [calcitonin gene-related peptide] and serotonin physiology.” He noted that previously published research has shown that sleep CGRP and serotonin have a central role in causing arousal in response to rising CO₂ levels during sleep, which can occur during apneas and hypopneas.

Dr. Gruenthal noted that the researchers are still analyzing the findings. “We theorized that possible indication bias may be present in our study,” he said. “It may be the case that patients with migraine are more likely to get their PSG done because of their headache and not for things like snoring and witnessed apneas, which may be more predictive of significant sleep apnea.” They’re also evaluating the “question of medicine confounding.”

Dr. Gruenthal added that “the big unanswered question out there is, if you have a patient with migraine who also has sleep apnea, by treating the sleep apnea will that improve their migraine?”
 

More questions than answers

Commenting on the study, Donald Bliwise, PhD, professor of neurology at Emory Sleep Center, Atlanta, said the study findings shouldn’t change how clinicians approach migraine in relation to sleep.

“It’s a case series, it’s retrospective,” said Dr. Bliwise, who was not involved in the study. “It’s the largest study that I know of that has ever looked at the diagnosis of migraine in relation to polysomnographic measures of sleep, but it’s imprecise to the extent that migraine is a clinical diagnosis, so not everyone that carries the diagnosis of migraine has the diagnosis made by a neurologist.”

The study raises more questions than it answers, he said, “but that’s not necessarily a bad thing. I think we need more prospective studies.” Those studies should be more granular in how they analyze sleep in migraine patients “Since migraine is an intermittent event, and sleep quality and length, and percentage of REM sleep and even sleep apnea can vary from night to night, it would be fascinating to look at headaches over a month in relation to sleep over a month.”

Dr. Gruenthal and Dr. Bliwise have no disclosures. The Association of Migraine Disorders provided funding for the study.

CHARLOTTE, N.C. – What may be the largest case-based study of patients with migraine and sleep-disordered breathing to date has found that, counter to prevailing thought, they may not be at higher risk of having obstructive sleep apnea (OSA) than nonmigraine patients, although further prospective studies are needed to validate that finding.

“This in no way for me changes the fact that, for patients that complain of headaches, sleep apnea remains to be something that should be considered as possible cause of their headaches,” neurologist and Cleveland Clinic postdoctoral fellow Eric Gruenthal, MD, said in an interview after he presented his results at the annual meeting of the Associated Professional Sleep Societies.

The study suggested that patients with migraine may have an OSA risk that “may be a little lower” than their nonmigraine counterparts, Dr. Gruenthal said. “But we have really yet to determine whether that’s true or not.”
 

Large case-based study

The retrospective case study included 4,783 migraine cases from the Cleveland Clinic electronic health record database who were case matched on a 1:3 basis with 14,287 controls. Patients with migraine had an average age of 47.5 years (±13.3) and body mass index of 33.7 kg/m² (±8.6), and 76.4% were White. All patients had polysomnography (PSG) at a Cleveland Clinic facility from 1998 to 2021.

The analysis evaluated the collected data in two domains: sleep architecture, consisting of arousal index (AI), total sleep time (TST) and percentage of sleep stage time; and sleep-disordered breathing, including apnea hypopnea index (AHI) and mean oxygen saturation. The key findings of the migraine patients versus controls include:

• Lower AI, 19.6 (95% confidence interval, 12.8-30.9) versus 22.6 (95% CI, 14.7-34.9; P < .001).
• Shorter TST, 359 (95% CI, 307-421) versus 363 (95% CI, 306-432.5) minutes (P = .01).
• With regard to sleep stage, the percentage of N2 sleep was higher, 67.8% (95% CI, 59.6%-75.6%) versus 67% (95% CI, 58.4%-74.8%; P < .001); but the percentage of REM was lower at 16.7% (95% CI, 10%-22%) versus 17% (95% CI, 11.1%-22.2%; P = .012).
• Lower AHI, 7.4 (95% CI, 2.6-17) versus 9.5 (95% CI, 3.7-22.1, P < .001).
• Higher mean oxygen saturation, 93.7 (±2.4) versus 93.3% (±2.6; P < .001).

“Also,” Dr. Gruenthal added, “we found that the percentage of sleep time with oxygen saturation below 90% was lower among patients with migraine, at 1.3% versus 2.4%” (P < .001).
 

A unique profile?

The goal of the study was to determine whether migraine patients would have a unique PSG profile, Dr. Gruenthal said. “We were trying to overcome some of the limitations of previous studies, most notably those that use small sample sizes, and in some cases a lack of controls.”

The findings that migraine patients would have higher AI and elevated AHI ran counter to the study’s hypotheses, but fell in line with the expectation that they would have reduced TST, Dr. Gruenthal said.

Patients with migraine “may, in fact, exhibit a lower burden of sleep-disordered breathing, and that’s based on our findings such as the lower AHI and decreased burden of hypoxemia,” he said. “We theorized that this may be related to patients with migraine having a unique CGRP [calcitonin gene-related peptide] and serotonin physiology.” He noted that previously published research has shown that sleep CGRP and serotonin have a central role in causing arousal in response to rising CO₂ levels during sleep, which can occur during apneas and hypopneas.

Dr. Gruenthal noted that the researchers are still analyzing the findings. “We theorized that possible indication bias may be present in our study,” he said. “It may be the case that patients with migraine are more likely to get their PSG done because of their headache and not for things like snoring and witnessed apneas, which may be more predictive of significant sleep apnea.” They’re also evaluating the “question of medicine confounding.”

Dr. Gruenthal added that “the big unanswered question out there is, if you have a patient with migraine who also has sleep apnea, by treating the sleep apnea will that improve their migraine?”
 

More questions than answers

Commenting on the study, Donald Bliwise, PhD, professor of neurology at Emory Sleep Center, Atlanta, said the study findings shouldn’t change how clinicians approach migraine in relation to sleep.

“It’s a case series, it’s retrospective,” said Dr. Bliwise, who was not involved in the study. “It’s the largest study that I know of that has ever looked at the diagnosis of migraine in relation to polysomnographic measures of sleep, but it’s imprecise to the extent that migraine is a clinical diagnosis, so not everyone that carries the diagnosis of migraine has the diagnosis made by a neurologist.”

The study raises more questions than it answers, he said, “but that’s not necessarily a bad thing. I think we need more prospective studies.” Those studies should be more granular in how they analyze sleep in migraine patients “Since migraine is an intermittent event, and sleep quality and length, and percentage of REM sleep and even sleep apnea can vary from night to night, it would be fascinating to look at headaches over a month in relation to sleep over a month.”

Dr. Gruenthal and Dr. Bliwise have no disclosures. The Association of Migraine Disorders provided funding for the study.

CHARLOTTE, N.C. – Erratic sleep patterns over years or even decades, along with a patient’s age and history of depression, may be harbingers of cognitive impairment later in life, an analysis of decades of data from a large sleep study has found.

“What we were a little surprised to find in this model was that sleep duration, whether short, long or average, was not significant, but the sleep variability – the change in sleep across those time measurements—was significantly impacting the incidence of cognitive impairment,” Samantha Keil, PhD, a postdoctoral fellow at the University of Washington, Seattle, reported at the at the annual meeting of the Associated Professional Sleep Societies.

The researchers analyzed sleep and cognition data collected over decades on 1,104 adults who participated in the Seattle Longitudinal Study. Study participants ranged from age 55 to over 100, with almost 80% of the study cohort aged 65 and older.

The Seattle Longitudinal Study first started gathering data in the 1950s. Participants in the study cohort underwent an extensive cognitive battery, which was added to the study in 1984 and gathered every 5-7 years, and completed a health behavioral questionnaire (HBQ), which was added in 1993 and administered every 3-5 years, Dr. Keil said. The HBQ included a question on average nightly sleep duration.

The study used a multivariable Cox proportional hazard regression model to evaluate the overall effect of average sleep duration and changes in sleep duration over time on cognitive impairment. Covariates used in the model included apolipoprotein E4 (APOE4) genotype, gender, years of education, ethnicity, and depression.

Dr. Keil said the model found, as expected, that the  demographic variables of education, APOE status, and depression were significantly associated with cognitive impairment (hazard ratios of 1.11; 95% confidence interval [CI], 1.02-1.21; P = .01; and 2.08; 95% CI, 1.31-3.31; P < .005; and 1.08; 95% CI, 1.04-1.13; P < .005, respectively). Importantly, when evaluating the duration, change and variability of sleep, the researchers found that increased sleep variability was significantly associated with cognitive impairment (HR, 3.15; 95% CI, 1.69-5.87; P < .005).  

Under this analysis, “sleep variability over time and not median sleep duration was associated with cognitive impairment,” she said. When sleep variability was added into the model, it improved the concordance score – a value that reflects the ability of a model to predict an outcome better than random chance – from .63 to .73 (a value of .5 indicates the model is no better at predicting an outcome than a random chance model; a value of .7 or greater indicates a good model).

Identification of sleep variability as a sleep pattern of interest in longitudinal studies is important, Dr. Keil said, because simply evaluating mean or median sleep duration across time might not account for a subject’s variable sleep phenotype. Most importantly, further evaluation of sleep variability with a linear regression prediction analysis (F statistic 8.796, P < .0001, adjusted R-squared .235) found that increased age, depression, and sleep variability significantly predicted cognitive impairment 10 years downstream. “Longitudinal sleep variability is perhaps for the first time being reported as significantly associated with the development of downstream cognitive impairment,” Dr. Keil said.

What makes this study unique, Dr. Keil said in an interview, is that it used self-reported longitudinal data gathered at 3- to 5-year intervals for up to 25 years, allowing for the assessment of variation of sleep duration across this entire time frame. “If you could use that shift in sleep duration as a point of therapeutic intervention, that would be really exciting,” she said.

Future research will evaluate how sleep variability and cognitive function are impacted by other variables gathered in the Seattle Longitudinal Study over the years, including factors such as diabetes and hypertension status, diet, alcohol and tobacco use, and marital and family status. Follow-up studies will be investigating the impact of sleep variability on neuropathologic disease progression and lymphatic system impairment, Dr. Keil said.
 

A newer approach

By linking sleep variability and daytime functioning, the study employs a “newer approach,” said Joseph M. Dzierzewski, PhD, director of behavioral medicine concentration in the department of psychology at Virginia Commonwealth University in Richmond. “While some previous work has examined night-to-night fluctuation in various sleep characteristics and cognitive functioning, what differentiates the present study from these previous works is the duration of the investigation,” he said. The “richness of data” in the Seattle Longitudinal Study and how it tracks sleep and cognition over years make it “quite unique and novel.”

Future studies, he said, should be deliberate in how they evaluate sleep and neurocognitive function across years. “Disentangling short-term moment-to-moment and day-to-day fluctuation, which may be more reversible in nature, from long-term, enduring month-to-month or year-to-year fluctuation, which may be more permanent, will be important for continuing to advance our understanding of these complex phenomena,” Dr. Dzierzewski said. “An additional important area of future investigation would be to continue the hunt for a common biological factor underpinning both sleep variability and Alzheimer’s disease.” That, he said, may help identify potential intervention targets.

Dr. Keil and Dr. Dzierzewski have no relevant disclosures.

CHARLOTTE, N.C. – Erratic sleep patterns over years or even decades, along with a patient’s age and history of depression, may be harbingers of cognitive impairment later in life, an analysis of decades of data from a large sleep study has found.

“What we were a little surprised to find in this model was that sleep duration, whether short, long or average, was not significant, but the sleep variability – the change in sleep across those time measurements—was significantly impacting the incidence of cognitive impairment,” Samantha Keil, PhD, a postdoctoral fellow at the University of Washington, Seattle, reported at the at the annual meeting of the Associated Professional Sleep Societies.

The researchers analyzed sleep and cognition data collected over decades on 1,104 adults who participated in the Seattle Longitudinal Study. Study participants ranged from age 55 to over 100, with almost 80% of the study cohort aged 65 and older.

The Seattle Longitudinal Study first started gathering data in the 1950s. Participants in the study cohort underwent an extensive cognitive battery, which was added to the study in 1984 and gathered every 5-7 years, and completed a health behavioral questionnaire (HBQ), which was added in 1993 and administered every 3-5 years, Dr. Keil said. The HBQ included a question on average nightly sleep duration.

The study used a multivariable Cox proportional hazard regression model to evaluate the overall effect of average sleep duration and changes in sleep duration over time on cognitive impairment. Covariates used in the model included apolipoprotein E4 (APOE4) genotype, gender, years of education, ethnicity, and depression.

Dr. Keil said the model found, as expected, that the  demographic variables of education, APOE status, and depression were significantly associated with cognitive impairment (hazard ratios of 1.11; 95% confidence interval [CI], 1.02-1.21; P = .01; and 2.08; 95% CI, 1.31-3.31; P < .005; and 1.08; 95% CI, 1.04-1.13; P < .005, respectively). Importantly, when evaluating the duration, change and variability of sleep, the researchers found that increased sleep variability was significantly associated with cognitive impairment (HR, 3.15; 95% CI, 1.69-5.87; P < .005).  

Under this analysis, “sleep variability over time and not median sleep duration was associated with cognitive impairment,” she said. When sleep variability was added into the model, it improved the concordance score – a value that reflects the ability of a model to predict an outcome better than random chance – from .63 to .73 (a value of .5 indicates the model is no better at predicting an outcome than a random chance model; a value of .7 or greater indicates a good model).

Identification of sleep variability as a sleep pattern of interest in longitudinal studies is important, Dr. Keil said, because simply evaluating mean or median sleep duration across time might not account for a subject’s variable sleep phenotype. Most importantly, further evaluation of sleep variability with a linear regression prediction analysis (F statistic 8.796, P < .0001, adjusted R-squared .235) found that increased age, depression, and sleep variability significantly predicted cognitive impairment 10 years downstream. “Longitudinal sleep variability is perhaps for the first time being reported as significantly associated with the development of downstream cognitive impairment,” Dr. Keil said.

What makes this study unique, Dr. Keil said in an interview, is that it used self-reported longitudinal data gathered at 3- to 5-year intervals for up to 25 years, allowing for the assessment of variation of sleep duration across this entire time frame. “If you could use that shift in sleep duration as a point of therapeutic intervention, that would be really exciting,” she said.

Future research will evaluate how sleep variability and cognitive function are impacted by other variables gathered in the Seattle Longitudinal Study over the years, including factors such as diabetes and hypertension status, diet, alcohol and tobacco use, and marital and family status. Follow-up studies will be investigating the impact of sleep variability on neuropathologic disease progression and lymphatic system impairment, Dr. Keil said.
 

A newer approach

By linking sleep variability and daytime functioning, the study employs a “newer approach,” said Joseph M. Dzierzewski, PhD, director of behavioral medicine concentration in the department of psychology at Virginia Commonwealth University in Richmond. “While some previous work has examined night-to-night fluctuation in various sleep characteristics and cognitive functioning, what differentiates the present study from these previous works is the duration of the investigation,” he said. The “richness of data” in the Seattle Longitudinal Study and how it tracks sleep and cognition over years make it “quite unique and novel.”

Future studies, he said, should be deliberate in how they evaluate sleep and neurocognitive function across years. “Disentangling short-term moment-to-moment and day-to-day fluctuation, which may be more reversible in nature, from long-term, enduring month-to-month or year-to-year fluctuation, which may be more permanent, will be important for continuing to advance our understanding of these complex phenomena,” Dr. Dzierzewski said. “An additional important area of future investigation would be to continue the hunt for a common biological factor underpinning both sleep variability and Alzheimer’s disease.” That, he said, may help identify potential intervention targets.

Dr. Keil and Dr. Dzierzewski have no relevant disclosures.

CHARLOTTE, N.C. – Erratic sleep patterns over years or even decades, along with a patient’s age and history of depression, may be harbingers of cognitive impairment later in life, an analysis of decades of data from a large sleep study has found.

“What we were a little surprised to find in this model was that sleep duration, whether short, long or average, was not significant, but the sleep variability – the change in sleep across those time measurements—was significantly impacting the incidence of cognitive impairment,” Samantha Keil, PhD, a postdoctoral fellow at the University of Washington, Seattle, reported at the at the annual meeting of the Associated Professional Sleep Societies.

The researchers analyzed sleep and cognition data collected over decades on 1,104 adults who participated in the Seattle Longitudinal Study. Study participants ranged from age 55 to over 100, with almost 80% of the study cohort aged 65 and older.

The Seattle Longitudinal Study first started gathering data in the 1950s. Participants in the study cohort underwent an extensive cognitive battery, which was added to the study in 1984 and gathered every 5-7 years, and completed a health behavioral questionnaire (HBQ), which was added in 1993 and administered every 3-5 years, Dr. Keil said. The HBQ included a question on average nightly sleep duration.

The study used a multivariable Cox proportional hazard regression model to evaluate the overall effect of average sleep duration and changes in sleep duration over time on cognitive impairment. Covariates used in the model included apolipoprotein E4 (APOE4) genotype, gender, years of education, ethnicity, and depression.

Dr. Keil said the model found, as expected, that the  demographic variables of education, APOE status, and depression were significantly associated with cognitive impairment (hazard ratios of 1.11; 95% confidence interval [CI], 1.02-1.21; P = .01; and 2.08; 95% CI, 1.31-3.31; P < .005; and 1.08; 95% CI, 1.04-1.13; P < .005, respectively). Importantly, when evaluating the duration, change and variability of sleep, the researchers found that increased sleep variability was significantly associated with cognitive impairment (HR, 3.15; 95% CI, 1.69-5.87; P < .005).  

Under this analysis, “sleep variability over time and not median sleep duration was associated with cognitive impairment,” she said. When sleep variability was added into the model, it improved the concordance score – a value that reflects the ability of a model to predict an outcome better than random chance – from .63 to .73 (a value of .5 indicates the model is no better at predicting an outcome than a random chance model; a value of .7 or greater indicates a good model).

Identification of sleep variability as a sleep pattern of interest in longitudinal studies is important, Dr. Keil said, because simply evaluating mean or median sleep duration across time might not account for a subject’s variable sleep phenotype. Most importantly, further evaluation of sleep variability with a linear regression prediction analysis (F statistic 8.796, P < .0001, adjusted R-squared .235) found that increased age, depression, and sleep variability significantly predicted cognitive impairment 10 years downstream. “Longitudinal sleep variability is perhaps for the first time being reported as significantly associated with the development of downstream cognitive impairment,” Dr. Keil said.

What makes this study unique, Dr. Keil said in an interview, is that it used self-reported longitudinal data gathered at 3- to 5-year intervals for up to 25 years, allowing for the assessment of variation of sleep duration across this entire time frame. “If you could use that shift in sleep duration as a point of therapeutic intervention, that would be really exciting,” she said.

Future research will evaluate how sleep variability and cognitive function are impacted by other variables gathered in the Seattle Longitudinal Study over the years, including factors such as diabetes and hypertension status, diet, alcohol and tobacco use, and marital and family status. Follow-up studies will be investigating the impact of sleep variability on neuropathologic disease progression and lymphatic system impairment, Dr. Keil said.
 

A newer approach

By linking sleep variability and daytime functioning, the study employs a “newer approach,” said Joseph M. Dzierzewski, PhD, director of behavioral medicine concentration in the department of psychology at Virginia Commonwealth University in Richmond. “While some previous work has examined night-to-night fluctuation in various sleep characteristics and cognitive functioning, what differentiates the present study from these previous works is the duration of the investigation,” he said. The “richness of data” in the Seattle Longitudinal Study and how it tracks sleep and cognition over years make it “quite unique and novel.”

Future studies, he said, should be deliberate in how they evaluate sleep and neurocognitive function across years. “Disentangling short-term moment-to-moment and day-to-day fluctuation, which may be more reversible in nature, from long-term, enduring month-to-month or year-to-year fluctuation, which may be more permanent, will be important for continuing to advance our understanding of these complex phenomena,” Dr. Dzierzewski said. “An additional important area of future investigation would be to continue the hunt for a common biological factor underpinning both sleep variability and Alzheimer’s disease.” That, he said, may help identify potential intervention targets.

Dr. Keil and Dr. Dzierzewski have no relevant disclosures.