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Coffee’s brain-boosting effect goes beyond caffeine
“There is a widespread anticipation that coffee boosts alertness and psychomotor performance. By gaining a deeper understanding of the mechanisms underlying this biological phenomenon, we pave the way for investigating the factors that can influence it and even exploring the potential advantages of those mechanisms,” study investigator Nuno Sousa, MD, PhD, with the University of Minho, Braga, Portugal, said in a statement.
The study was published online in Frontiers in Behavioral Neuroscience.
Caffeine can’t take all the credit
Certain compounds in coffee, including caffeine and chlorogenic acids, have well-documented psychoactive effects, but the psychological impact of coffee/caffeine consumption as a whole remains a matter of debate.
The researchers investigated the neurobiological impact of coffee drinking on brain connectivity using resting-state functional MRI (fMRI).
They recruited 47 generally healthy adults (mean age, 30 years; 31 women) who regularly drank a minimum of one cup of coffee per day. Participants refrained from eating or drinking caffeinated beverages for at least 3 hours prior to undergoing fMRI.
To tease out the specific impact of caffeinated coffee intake, 30 habitual coffee drinkers (mean age, 32 years; 27 women) were given hot water containing the same amount of caffeine, but they were not given coffee.
The investigators conducted two fMRI scans – one before, and one 30 minutes after drinking coffee or caffeine-infused water.
Both drinking coffee and drinking plain caffeine in water led to a decrease in functional connectivity of the brain’s default mode network, which is typically active during self-reflection in resting states.
This finding suggests that consuming either coffee or caffeine heightened individuals’ readiness to transition from a state of rest to engaging in task-related activities, the researchers noted.
However, drinking a cup of coffee also boosted connectivity in the higher visual network and the right executive control network, which are linked to working memory, cognitive control, and goal-directed behavior – something that did not occur from drinking caffeinated water.
“Put simply, individuals exhibited a heightened state of preparedness, being more responsive and attentive to external stimuli after drinking coffee,” said first author Maria Picó-Pérez, PhD, with the University of Minho.
Given that some of the effects of coffee also occurred with caffeine alone, it’s “plausible to assume that other caffeinated beverages may share similar effects,” she added.
Still, certain effects were specific to coffee drinking, “likely influenced by factors such as the distinct aroma and taste of coffee or the psychological expectations associated with consuming this particular beverage,” the researcher wrote.
The investigators report that the observations could provide a scientific foundation for the common belief that coffee increases alertness and cognitive functioning. Further research is needed to differentiate the effects of caffeine from the overall experience of drinking coffee.
A limitation of the study is the absence of a nondrinker control sample (to rule out the withdrawal effect) or an alternative group that consumed decaffeinated coffee (to rule out the placebo effect of coffee intake) – something that should be considered in future studies, the researchers noted.
The study was funded by the Institute for the Scientific Information on Coffee. The authors declared no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
“There is a widespread anticipation that coffee boosts alertness and psychomotor performance. By gaining a deeper understanding of the mechanisms underlying this biological phenomenon, we pave the way for investigating the factors that can influence it and even exploring the potential advantages of those mechanisms,” study investigator Nuno Sousa, MD, PhD, with the University of Minho, Braga, Portugal, said in a statement.
The study was published online in Frontiers in Behavioral Neuroscience.
Caffeine can’t take all the credit
Certain compounds in coffee, including caffeine and chlorogenic acids, have well-documented psychoactive effects, but the psychological impact of coffee/caffeine consumption as a whole remains a matter of debate.
The researchers investigated the neurobiological impact of coffee drinking on brain connectivity using resting-state functional MRI (fMRI).
They recruited 47 generally healthy adults (mean age, 30 years; 31 women) who regularly drank a minimum of one cup of coffee per day. Participants refrained from eating or drinking caffeinated beverages for at least 3 hours prior to undergoing fMRI.
To tease out the specific impact of caffeinated coffee intake, 30 habitual coffee drinkers (mean age, 32 years; 27 women) were given hot water containing the same amount of caffeine, but they were not given coffee.
The investigators conducted two fMRI scans – one before, and one 30 minutes after drinking coffee or caffeine-infused water.
Both drinking coffee and drinking plain caffeine in water led to a decrease in functional connectivity of the brain’s default mode network, which is typically active during self-reflection in resting states.
This finding suggests that consuming either coffee or caffeine heightened individuals’ readiness to transition from a state of rest to engaging in task-related activities, the researchers noted.
However, drinking a cup of coffee also boosted connectivity in the higher visual network and the right executive control network, which are linked to working memory, cognitive control, and goal-directed behavior – something that did not occur from drinking caffeinated water.
“Put simply, individuals exhibited a heightened state of preparedness, being more responsive and attentive to external stimuli after drinking coffee,” said first author Maria Picó-Pérez, PhD, with the University of Minho.
Given that some of the effects of coffee also occurred with caffeine alone, it’s “plausible to assume that other caffeinated beverages may share similar effects,” she added.
Still, certain effects were specific to coffee drinking, “likely influenced by factors such as the distinct aroma and taste of coffee or the psychological expectations associated with consuming this particular beverage,” the researcher wrote.
The investigators report that the observations could provide a scientific foundation for the common belief that coffee increases alertness and cognitive functioning. Further research is needed to differentiate the effects of caffeine from the overall experience of drinking coffee.
A limitation of the study is the absence of a nondrinker control sample (to rule out the withdrawal effect) or an alternative group that consumed decaffeinated coffee (to rule out the placebo effect of coffee intake) – something that should be considered in future studies, the researchers noted.
The study was funded by the Institute for the Scientific Information on Coffee. The authors declared no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
“There is a widespread anticipation that coffee boosts alertness and psychomotor performance. By gaining a deeper understanding of the mechanisms underlying this biological phenomenon, we pave the way for investigating the factors that can influence it and even exploring the potential advantages of those mechanisms,” study investigator Nuno Sousa, MD, PhD, with the University of Minho, Braga, Portugal, said in a statement.
The study was published online in Frontiers in Behavioral Neuroscience.
Caffeine can’t take all the credit
Certain compounds in coffee, including caffeine and chlorogenic acids, have well-documented psychoactive effects, but the psychological impact of coffee/caffeine consumption as a whole remains a matter of debate.
The researchers investigated the neurobiological impact of coffee drinking on brain connectivity using resting-state functional MRI (fMRI).
They recruited 47 generally healthy adults (mean age, 30 years; 31 women) who regularly drank a minimum of one cup of coffee per day. Participants refrained from eating or drinking caffeinated beverages for at least 3 hours prior to undergoing fMRI.
To tease out the specific impact of caffeinated coffee intake, 30 habitual coffee drinkers (mean age, 32 years; 27 women) were given hot water containing the same amount of caffeine, but they were not given coffee.
The investigators conducted two fMRI scans – one before, and one 30 minutes after drinking coffee or caffeine-infused water.
Both drinking coffee and drinking plain caffeine in water led to a decrease in functional connectivity of the brain’s default mode network, which is typically active during self-reflection in resting states.
This finding suggests that consuming either coffee or caffeine heightened individuals’ readiness to transition from a state of rest to engaging in task-related activities, the researchers noted.
However, drinking a cup of coffee also boosted connectivity in the higher visual network and the right executive control network, which are linked to working memory, cognitive control, and goal-directed behavior – something that did not occur from drinking caffeinated water.
“Put simply, individuals exhibited a heightened state of preparedness, being more responsive and attentive to external stimuli after drinking coffee,” said first author Maria Picó-Pérez, PhD, with the University of Minho.
Given that some of the effects of coffee also occurred with caffeine alone, it’s “plausible to assume that other caffeinated beverages may share similar effects,” she added.
Still, certain effects were specific to coffee drinking, “likely influenced by factors such as the distinct aroma and taste of coffee or the psychological expectations associated with consuming this particular beverage,” the researcher wrote.
The investigators report that the observations could provide a scientific foundation for the common belief that coffee increases alertness and cognitive functioning. Further research is needed to differentiate the effects of caffeine from the overall experience of drinking coffee.
A limitation of the study is the absence of a nondrinker control sample (to rule out the withdrawal effect) or an alternative group that consumed decaffeinated coffee (to rule out the placebo effect of coffee intake) – something that should be considered in future studies, the researchers noted.
The study was funded by the Institute for the Scientific Information on Coffee. The authors declared no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
FROM FRONTIERS IN BEHAVIORAL NEUROSCIENCE
Treating obesity: Will new drugs end the crisis?
This is the second in a three-part series on the obesity crisis. Part one tackles a complicated question – why does the obesity rate keep rising despite our efforts to stop it? – and can be found here. Part three shows how doctors and patients can make treatment better and can be found here.
In the mid-1980s, Louis J. Aronne, MD, strolled into a lab at Rockefeller University in New York where a colleague was breeding mice. “I will never forget what he showed me,” said Dr. Aronne, now the director of obesity research and treatment at Weill Cornell Medicine in New York. “He had a cage with 10 mice, one severely obese and the others normal weight. He took blood from one of the thin mice and gave it to the fat mouse.”
When Dr. Aronne returned 3 days later, that obese mouse had turned thin.
It was proof of something Dr. Aronne already suspected: Obesity had biological causes and wasn’t just a failure of willpower.
Years later, in 1994, that research led to the discovery of leptin, a hormone released from fat cells that’s involved in the regulation of body weight. It was a watershed moment in obesity research.
Since then, Dr. Aronne and others have worked to build the clinical field of obesity medicine, attempting to shift the public and medical view of obesity from a purely behavioral issue to a disease worthy of medical treatment.
All the while, the U.S. obesity rate soared.
Now, another watershed moment: We finally have highly effective obesity drugs. The hype is real, and so are the weight loss results.
“I’ve been saying for 30 years that when we find treatments that really work, people aren’t going to believe the results,” Dr. Aronne said. “It took longer than I expected, but it’s gratifying now to see.”
The big question
The emerging class of obesity medications known as GLP-1 agonists is indeed a game changer. The weight loss drug semaglutide (Ozempic, Wegovy) showed groundbreaking results, and studies suggest a parade of even more impressive drugs is on the way.
Yes, the drugs offer new hope to millions with obesity complications. But to truly turn the tide on our 42% obesity rate, much more work remains to be done, researchers said, including answering a big question:
How do these weight loss drugs work?
“We have new blockbuster drugs, and we don’t even know why they reduce body weight,” said Samuel Klein, MD, professor of medicine and nutritional science at Washington University in St. Louis. “It was by accident that this was discovered.”
Oops, we created a weight loss drug
Developed to treat diabetes, the GLP-1 drugs’ weight loss effects were a surprise. Now that those effects are confirmed, pharmaceutical companies and researchers are racing to figure out how these drugs work.
In the 1960s, scientists discovered the incretin effect – when you eat glucose (sugar), your body makes more insulin than it does if glucose is given intravenously. Glucose passes through the GI tract and the gut releases hormones that stimulate insulin secretion. It’s “essentially a feed-forward signal to your pancreas to tell it, ‘By the way, you need to be ready because there’s a bunch of glucose coming,’ ” said Randy Seeley, MD, director of the Michigan Nutrition Obesity Research Center, funded by the National Institutes of Health.
One of these hormones – or “incretins” – is GLP-1. In experiments, people with type 2 diabetes who were hooked up to GLP-1 saw their blood sugar go down.
“That led to the idea that if we could take this native hormone and make it last longer, we’d have a therapy for type 2 diabetes,” said Dr. Seeley. Thanks to a GLP-1-like compound in the saliva of the Gila monster, that idea became reality in the 2000s.
Along the way, a surprising side finding came to light: In early trials, diabetes patients on these drugs dropped weight.
Both Ozempic and Wegovy – brand names for semaglutide – are once-weekly injections (pill forms to treat obesity are on the way), but the latter is a higher dose.
“That dose results in about 40% of patients in the clinical trials achieving a 20% weight loss. We’ve just had nothing like that in terms of efficacy before,” said Dr. Seeley, who has worked with some of the drug companies (including Novo Nordisk, the maker of Ozempic and Wegovy, and Eli Lilly, maker of Mounjaro) that market the GLP-1s.
By contrast, semaglutide’s once-a-day predecessor liraglutide (Saxenda, made by Novo Nordisk) can lead to about 10% weight loss.
“And one of the ironies is, we don’t really know why,” Dr. Seeley said. “We don’t know why semaglutide is a better molecule for weight loss than liraglutide.”
Initially, scientists believed that the drugs, in addition to telling the pancreas to secrete more insulin, were also signaling the brain that you’re full. “Turns out that’s not really the way it works,” Dr. Seeley said. “GLP-1 made from your gut probably doesn’t get into your brain very much. But you make GLP-1 in your brain as well.”
For weight loss, it’s the brain’s GLP-1 system, not the gut’s, that the drugs are thought to hijack. But exactly which parts of the brain they affect and how is unknown. “That’s something lots of people are working on, including our own lab,” Dr. Seeley said. (Another surprise: The drugs may have potential as an anti-addiction treatment.)
The diabetes medication tirzepatide (Mounjaro), expected to be approved for weight loss as early as this year, is also a weekly injection, but it has a unique feature: It starts a response not just for GLP-1 but also for another incretin called GIP. Turns out, two is better than one: Trial participants on tirzepatide lost up to 22.5% of their body weight.
More of these hybrid drugs are on the way, Dr. Seeley said. In mid-stage clinical trials, the drug retatrutide, which targets three hormones, led to 24% weight loss. “The idea is the more bullets we can load into the gun, the more we can push the biology into a place where it’s easier to lose weight.”
Shifting from prevention to damage control
Less invasive and more scalable than surgery (only 1% of the eligible population gets bariatric surgery), the drugs offer doctors a safe, effective way to treat many patients with obesity. That’s cause for excitement, but concerns remain because they are expensive, costing about $800 to $1,300 per month out of pocket. Many health insurers, including Medicare, do not cover them for weight loss.
“You have this significant advance in obesity treatment, but very few will be able to access it,” said Gary Foster, PhD, adjunct professor of psychology in psychiatry at the University of Pennsylvania, Philadelphia, and chief scientific officer at WW (formerly Weight Watchers).
There is a push, including a proposed bill, to get Medicare to cover obesity medication. But given the expense of the drugs, the health economics do not support that move, according to an editorial in the New England Journal of Medicine. If Medicare were to cover obesity meds, the budget impact would likely be huge, potentially driving up premiums. If other payers followed suit, the impact could be felt across the U.S. health care system.
Other drawbacks include side effects – including nausea, diarrhea, stomach pain, and vomiting – that can be so bad that some patients can’t tolerate them.
And critically, the drugs do not deal with the root cause of the problem, said Robert Lustig, MD, an endocrinologist and pediatrician at the University of California, San Francisco, who has suggested that excess insulin is driving obesity. “No one has the disease that these drugs are treating. No one has GLP-1 deficiency. They’re bypassing the problem. They’re band-aiding the problem.”
Because the drugs work by mimicking starvation – they appear to curb hunger, so you eat less – people on them lose not just fat but also healthy lean mass, Dr. Lustig said.
Concerns about pancreatitis did not really bear out in postmarketing reports. (The drugs are still not recommended in people with pancreatitis or multiple endocrine neoplasia.) But predicting longer-term outcomes can be difficult, noted Dr. Lustig.
Then there are philosophical questions, said James Hill, PhD, director of the Nutrition Obesity Research Center at the University of Alabama at Birmingham.. “If you’re continuing to not exercise and eat not healthy foods and take a medication, is that success? Have we won when people are at a lower weight but not doing a healthy behavior?”
‘We can’t treat our way out of this’
The fact is, ending the obesity epidemic is a tall order, even for drugs as impressive as these.
“We can’t treat our way out of this,” said Jamy Ard, MD, codirector of Wake Forest Baptist Health Weight Management Center in Winston-Salem, N.C. “The treatments we have now are great, and there will be more coming. But we do need to figure out the prevention side of things.”
Dr. Seeley agreed but added that we can’t diet-and-exercise our way out either.
“There’s no switch to be flipped,” Dr. Seeley said. “If you told me we shouldn’t spend all this money on these drugs, we should spend it on prevention – great! What would we do?”
And prevention efforts won’t help the millions already living with health problems from obesity, Dr. Aronne said.
“Getting people to stop smoking prevents lung cancer. But stopping smoking doesn’t treat lung cancer,” Dr. Aronne said. “Once the physical changes occur in the lung that cause a tumor to grow, it’s too late. You have to think of obesity the same way.”
Dr. Seeley pointed out that “fearmongering” around the drugs highlights our lingering bias that obesity is a lifestyle issue that should not be medically treated.
“People say, ‘When you stop taking it, you’re going to gain the weight back,’ ” Dr. Seeley said. “There’s truth to that, but when you stop taking your hypertension medication, your blood pressure goes up. We don’t think of that as a [reason] for why you shouldn’t take your blood pressure medication. But that gets trumpeted into all these conversations about whether people [with obesity] should be treated at all.”
Like obesity, blood pressure was once thought to be a behavioral problem, Dr. Aronne said. But blood pressure meds prevent heart attacks and strokes. And it’s likely obesity meds will do the same.
One 55-year-old patient on the road to kidney failure lost weight on obesity medications, including semaglutide, Dr. Aronne said. Now, 6 years later, his kidney function is back to normal. “Normally, we think of kidney disease as irreversible,” Dr. Aronne said.
In that respect, these drugs should save money in the long run by virtue of heading off those health care costs, said Dr. Seeley, who imagines a future where obesity is not gone but better managed, like high blood pressure is now.
In the end, the drugs are another step toward what Dr. Aronne and many others have always pushed for: Treating obesity as a disease.
A version of this article originally appeared on WebMD.com.
This is the second in a three-part series on the obesity crisis. Part one tackles a complicated question – why does the obesity rate keep rising despite our efforts to stop it? – and can be found here. Part three shows how doctors and patients can make treatment better and can be found here.
In the mid-1980s, Louis J. Aronne, MD, strolled into a lab at Rockefeller University in New York where a colleague was breeding mice. “I will never forget what he showed me,” said Dr. Aronne, now the director of obesity research and treatment at Weill Cornell Medicine in New York. “He had a cage with 10 mice, one severely obese and the others normal weight. He took blood from one of the thin mice and gave it to the fat mouse.”
When Dr. Aronne returned 3 days later, that obese mouse had turned thin.
It was proof of something Dr. Aronne already suspected: Obesity had biological causes and wasn’t just a failure of willpower.
Years later, in 1994, that research led to the discovery of leptin, a hormone released from fat cells that’s involved in the regulation of body weight. It was a watershed moment in obesity research.
Since then, Dr. Aronne and others have worked to build the clinical field of obesity medicine, attempting to shift the public and medical view of obesity from a purely behavioral issue to a disease worthy of medical treatment.
All the while, the U.S. obesity rate soared.
Now, another watershed moment: We finally have highly effective obesity drugs. The hype is real, and so are the weight loss results.
“I’ve been saying for 30 years that when we find treatments that really work, people aren’t going to believe the results,” Dr. Aronne said. “It took longer than I expected, but it’s gratifying now to see.”
The big question
The emerging class of obesity medications known as GLP-1 agonists is indeed a game changer. The weight loss drug semaglutide (Ozempic, Wegovy) showed groundbreaking results, and studies suggest a parade of even more impressive drugs is on the way.
Yes, the drugs offer new hope to millions with obesity complications. But to truly turn the tide on our 42% obesity rate, much more work remains to be done, researchers said, including answering a big question:
How do these weight loss drugs work?
“We have new blockbuster drugs, and we don’t even know why they reduce body weight,” said Samuel Klein, MD, professor of medicine and nutritional science at Washington University in St. Louis. “It was by accident that this was discovered.”
Oops, we created a weight loss drug
Developed to treat diabetes, the GLP-1 drugs’ weight loss effects were a surprise. Now that those effects are confirmed, pharmaceutical companies and researchers are racing to figure out how these drugs work.
In the 1960s, scientists discovered the incretin effect – when you eat glucose (sugar), your body makes more insulin than it does if glucose is given intravenously. Glucose passes through the GI tract and the gut releases hormones that stimulate insulin secretion. It’s “essentially a feed-forward signal to your pancreas to tell it, ‘By the way, you need to be ready because there’s a bunch of glucose coming,’ ” said Randy Seeley, MD, director of the Michigan Nutrition Obesity Research Center, funded by the National Institutes of Health.
One of these hormones – or “incretins” – is GLP-1. In experiments, people with type 2 diabetes who were hooked up to GLP-1 saw their blood sugar go down.
“That led to the idea that if we could take this native hormone and make it last longer, we’d have a therapy for type 2 diabetes,” said Dr. Seeley. Thanks to a GLP-1-like compound in the saliva of the Gila monster, that idea became reality in the 2000s.
Along the way, a surprising side finding came to light: In early trials, diabetes patients on these drugs dropped weight.
Both Ozempic and Wegovy – brand names for semaglutide – are once-weekly injections (pill forms to treat obesity are on the way), but the latter is a higher dose.
“That dose results in about 40% of patients in the clinical trials achieving a 20% weight loss. We’ve just had nothing like that in terms of efficacy before,” said Dr. Seeley, who has worked with some of the drug companies (including Novo Nordisk, the maker of Ozempic and Wegovy, and Eli Lilly, maker of Mounjaro) that market the GLP-1s.
By contrast, semaglutide’s once-a-day predecessor liraglutide (Saxenda, made by Novo Nordisk) can lead to about 10% weight loss.
“And one of the ironies is, we don’t really know why,” Dr. Seeley said. “We don’t know why semaglutide is a better molecule for weight loss than liraglutide.”
Initially, scientists believed that the drugs, in addition to telling the pancreas to secrete more insulin, were also signaling the brain that you’re full. “Turns out that’s not really the way it works,” Dr. Seeley said. “GLP-1 made from your gut probably doesn’t get into your brain very much. But you make GLP-1 in your brain as well.”
For weight loss, it’s the brain’s GLP-1 system, not the gut’s, that the drugs are thought to hijack. But exactly which parts of the brain they affect and how is unknown. “That’s something lots of people are working on, including our own lab,” Dr. Seeley said. (Another surprise: The drugs may have potential as an anti-addiction treatment.)
The diabetes medication tirzepatide (Mounjaro), expected to be approved for weight loss as early as this year, is also a weekly injection, but it has a unique feature: It starts a response not just for GLP-1 but also for another incretin called GIP. Turns out, two is better than one: Trial participants on tirzepatide lost up to 22.5% of their body weight.
More of these hybrid drugs are on the way, Dr. Seeley said. In mid-stage clinical trials, the drug retatrutide, which targets three hormones, led to 24% weight loss. “The idea is the more bullets we can load into the gun, the more we can push the biology into a place where it’s easier to lose weight.”
Shifting from prevention to damage control
Less invasive and more scalable than surgery (only 1% of the eligible population gets bariatric surgery), the drugs offer doctors a safe, effective way to treat many patients with obesity. That’s cause for excitement, but concerns remain because they are expensive, costing about $800 to $1,300 per month out of pocket. Many health insurers, including Medicare, do not cover them for weight loss.
“You have this significant advance in obesity treatment, but very few will be able to access it,” said Gary Foster, PhD, adjunct professor of psychology in psychiatry at the University of Pennsylvania, Philadelphia, and chief scientific officer at WW (formerly Weight Watchers).
There is a push, including a proposed bill, to get Medicare to cover obesity medication. But given the expense of the drugs, the health economics do not support that move, according to an editorial in the New England Journal of Medicine. If Medicare were to cover obesity meds, the budget impact would likely be huge, potentially driving up premiums. If other payers followed suit, the impact could be felt across the U.S. health care system.
Other drawbacks include side effects – including nausea, diarrhea, stomach pain, and vomiting – that can be so bad that some patients can’t tolerate them.
And critically, the drugs do not deal with the root cause of the problem, said Robert Lustig, MD, an endocrinologist and pediatrician at the University of California, San Francisco, who has suggested that excess insulin is driving obesity. “No one has the disease that these drugs are treating. No one has GLP-1 deficiency. They’re bypassing the problem. They’re band-aiding the problem.”
Because the drugs work by mimicking starvation – they appear to curb hunger, so you eat less – people on them lose not just fat but also healthy lean mass, Dr. Lustig said.
Concerns about pancreatitis did not really bear out in postmarketing reports. (The drugs are still not recommended in people with pancreatitis or multiple endocrine neoplasia.) But predicting longer-term outcomes can be difficult, noted Dr. Lustig.
Then there are philosophical questions, said James Hill, PhD, director of the Nutrition Obesity Research Center at the University of Alabama at Birmingham.. “If you’re continuing to not exercise and eat not healthy foods and take a medication, is that success? Have we won when people are at a lower weight but not doing a healthy behavior?”
‘We can’t treat our way out of this’
The fact is, ending the obesity epidemic is a tall order, even for drugs as impressive as these.
“We can’t treat our way out of this,” said Jamy Ard, MD, codirector of Wake Forest Baptist Health Weight Management Center in Winston-Salem, N.C. “The treatments we have now are great, and there will be more coming. But we do need to figure out the prevention side of things.”
Dr. Seeley agreed but added that we can’t diet-and-exercise our way out either.
“There’s no switch to be flipped,” Dr. Seeley said. “If you told me we shouldn’t spend all this money on these drugs, we should spend it on prevention – great! What would we do?”
And prevention efforts won’t help the millions already living with health problems from obesity, Dr. Aronne said.
“Getting people to stop smoking prevents lung cancer. But stopping smoking doesn’t treat lung cancer,” Dr. Aronne said. “Once the physical changes occur in the lung that cause a tumor to grow, it’s too late. You have to think of obesity the same way.”
Dr. Seeley pointed out that “fearmongering” around the drugs highlights our lingering bias that obesity is a lifestyle issue that should not be medically treated.
“People say, ‘When you stop taking it, you’re going to gain the weight back,’ ” Dr. Seeley said. “There’s truth to that, but when you stop taking your hypertension medication, your blood pressure goes up. We don’t think of that as a [reason] for why you shouldn’t take your blood pressure medication. But that gets trumpeted into all these conversations about whether people [with obesity] should be treated at all.”
Like obesity, blood pressure was once thought to be a behavioral problem, Dr. Aronne said. But blood pressure meds prevent heart attacks and strokes. And it’s likely obesity meds will do the same.
One 55-year-old patient on the road to kidney failure lost weight on obesity medications, including semaglutide, Dr. Aronne said. Now, 6 years later, his kidney function is back to normal. “Normally, we think of kidney disease as irreversible,” Dr. Aronne said.
In that respect, these drugs should save money in the long run by virtue of heading off those health care costs, said Dr. Seeley, who imagines a future where obesity is not gone but better managed, like high blood pressure is now.
In the end, the drugs are another step toward what Dr. Aronne and many others have always pushed for: Treating obesity as a disease.
A version of this article originally appeared on WebMD.com.
This is the second in a three-part series on the obesity crisis. Part one tackles a complicated question – why does the obesity rate keep rising despite our efforts to stop it? – and can be found here. Part three shows how doctors and patients can make treatment better and can be found here.
In the mid-1980s, Louis J. Aronne, MD, strolled into a lab at Rockefeller University in New York where a colleague was breeding mice. “I will never forget what he showed me,” said Dr. Aronne, now the director of obesity research and treatment at Weill Cornell Medicine in New York. “He had a cage with 10 mice, one severely obese and the others normal weight. He took blood from one of the thin mice and gave it to the fat mouse.”
When Dr. Aronne returned 3 days later, that obese mouse had turned thin.
It was proof of something Dr. Aronne already suspected: Obesity had biological causes and wasn’t just a failure of willpower.
Years later, in 1994, that research led to the discovery of leptin, a hormone released from fat cells that’s involved in the regulation of body weight. It was a watershed moment in obesity research.
Since then, Dr. Aronne and others have worked to build the clinical field of obesity medicine, attempting to shift the public and medical view of obesity from a purely behavioral issue to a disease worthy of medical treatment.
All the while, the U.S. obesity rate soared.
Now, another watershed moment: We finally have highly effective obesity drugs. The hype is real, and so are the weight loss results.
“I’ve been saying for 30 years that when we find treatments that really work, people aren’t going to believe the results,” Dr. Aronne said. “It took longer than I expected, but it’s gratifying now to see.”
The big question
The emerging class of obesity medications known as GLP-1 agonists is indeed a game changer. The weight loss drug semaglutide (Ozempic, Wegovy) showed groundbreaking results, and studies suggest a parade of even more impressive drugs is on the way.
Yes, the drugs offer new hope to millions with obesity complications. But to truly turn the tide on our 42% obesity rate, much more work remains to be done, researchers said, including answering a big question:
How do these weight loss drugs work?
“We have new blockbuster drugs, and we don’t even know why they reduce body weight,” said Samuel Klein, MD, professor of medicine and nutritional science at Washington University in St. Louis. “It was by accident that this was discovered.”
Oops, we created a weight loss drug
Developed to treat diabetes, the GLP-1 drugs’ weight loss effects were a surprise. Now that those effects are confirmed, pharmaceutical companies and researchers are racing to figure out how these drugs work.
In the 1960s, scientists discovered the incretin effect – when you eat glucose (sugar), your body makes more insulin than it does if glucose is given intravenously. Glucose passes through the GI tract and the gut releases hormones that stimulate insulin secretion. It’s “essentially a feed-forward signal to your pancreas to tell it, ‘By the way, you need to be ready because there’s a bunch of glucose coming,’ ” said Randy Seeley, MD, director of the Michigan Nutrition Obesity Research Center, funded by the National Institutes of Health.
One of these hormones – or “incretins” – is GLP-1. In experiments, people with type 2 diabetes who were hooked up to GLP-1 saw their blood sugar go down.
“That led to the idea that if we could take this native hormone and make it last longer, we’d have a therapy for type 2 diabetes,” said Dr. Seeley. Thanks to a GLP-1-like compound in the saliva of the Gila monster, that idea became reality in the 2000s.
Along the way, a surprising side finding came to light: In early trials, diabetes patients on these drugs dropped weight.
Both Ozempic and Wegovy – brand names for semaglutide – are once-weekly injections (pill forms to treat obesity are on the way), but the latter is a higher dose.
“That dose results in about 40% of patients in the clinical trials achieving a 20% weight loss. We’ve just had nothing like that in terms of efficacy before,” said Dr. Seeley, who has worked with some of the drug companies (including Novo Nordisk, the maker of Ozempic and Wegovy, and Eli Lilly, maker of Mounjaro) that market the GLP-1s.
By contrast, semaglutide’s once-a-day predecessor liraglutide (Saxenda, made by Novo Nordisk) can lead to about 10% weight loss.
“And one of the ironies is, we don’t really know why,” Dr. Seeley said. “We don’t know why semaglutide is a better molecule for weight loss than liraglutide.”
Initially, scientists believed that the drugs, in addition to telling the pancreas to secrete more insulin, were also signaling the brain that you’re full. “Turns out that’s not really the way it works,” Dr. Seeley said. “GLP-1 made from your gut probably doesn’t get into your brain very much. But you make GLP-1 in your brain as well.”
For weight loss, it’s the brain’s GLP-1 system, not the gut’s, that the drugs are thought to hijack. But exactly which parts of the brain they affect and how is unknown. “That’s something lots of people are working on, including our own lab,” Dr. Seeley said. (Another surprise: The drugs may have potential as an anti-addiction treatment.)
The diabetes medication tirzepatide (Mounjaro), expected to be approved for weight loss as early as this year, is also a weekly injection, but it has a unique feature: It starts a response not just for GLP-1 but also for another incretin called GIP. Turns out, two is better than one: Trial participants on tirzepatide lost up to 22.5% of their body weight.
More of these hybrid drugs are on the way, Dr. Seeley said. In mid-stage clinical trials, the drug retatrutide, which targets three hormones, led to 24% weight loss. “The idea is the more bullets we can load into the gun, the more we can push the biology into a place where it’s easier to lose weight.”
Shifting from prevention to damage control
Less invasive and more scalable than surgery (only 1% of the eligible population gets bariatric surgery), the drugs offer doctors a safe, effective way to treat many patients with obesity. That’s cause for excitement, but concerns remain because they are expensive, costing about $800 to $1,300 per month out of pocket. Many health insurers, including Medicare, do not cover them for weight loss.
“You have this significant advance in obesity treatment, but very few will be able to access it,” said Gary Foster, PhD, adjunct professor of psychology in psychiatry at the University of Pennsylvania, Philadelphia, and chief scientific officer at WW (formerly Weight Watchers).
There is a push, including a proposed bill, to get Medicare to cover obesity medication. But given the expense of the drugs, the health economics do not support that move, according to an editorial in the New England Journal of Medicine. If Medicare were to cover obesity meds, the budget impact would likely be huge, potentially driving up premiums. If other payers followed suit, the impact could be felt across the U.S. health care system.
Other drawbacks include side effects – including nausea, diarrhea, stomach pain, and vomiting – that can be so bad that some patients can’t tolerate them.
And critically, the drugs do not deal with the root cause of the problem, said Robert Lustig, MD, an endocrinologist and pediatrician at the University of California, San Francisco, who has suggested that excess insulin is driving obesity. “No one has the disease that these drugs are treating. No one has GLP-1 deficiency. They’re bypassing the problem. They’re band-aiding the problem.”
Because the drugs work by mimicking starvation – they appear to curb hunger, so you eat less – people on them lose not just fat but also healthy lean mass, Dr. Lustig said.
Concerns about pancreatitis did not really bear out in postmarketing reports. (The drugs are still not recommended in people with pancreatitis or multiple endocrine neoplasia.) But predicting longer-term outcomes can be difficult, noted Dr. Lustig.
Then there are philosophical questions, said James Hill, PhD, director of the Nutrition Obesity Research Center at the University of Alabama at Birmingham.. “If you’re continuing to not exercise and eat not healthy foods and take a medication, is that success? Have we won when people are at a lower weight but not doing a healthy behavior?”
‘We can’t treat our way out of this’
The fact is, ending the obesity epidemic is a tall order, even for drugs as impressive as these.
“We can’t treat our way out of this,” said Jamy Ard, MD, codirector of Wake Forest Baptist Health Weight Management Center in Winston-Salem, N.C. “The treatments we have now are great, and there will be more coming. But we do need to figure out the prevention side of things.”
Dr. Seeley agreed but added that we can’t diet-and-exercise our way out either.
“There’s no switch to be flipped,” Dr. Seeley said. “If you told me we shouldn’t spend all this money on these drugs, we should spend it on prevention – great! What would we do?”
And prevention efforts won’t help the millions already living with health problems from obesity, Dr. Aronne said.
“Getting people to stop smoking prevents lung cancer. But stopping smoking doesn’t treat lung cancer,” Dr. Aronne said. “Once the physical changes occur in the lung that cause a tumor to grow, it’s too late. You have to think of obesity the same way.”
Dr. Seeley pointed out that “fearmongering” around the drugs highlights our lingering bias that obesity is a lifestyle issue that should not be medically treated.
“People say, ‘When you stop taking it, you’re going to gain the weight back,’ ” Dr. Seeley said. “There’s truth to that, but when you stop taking your hypertension medication, your blood pressure goes up. We don’t think of that as a [reason] for why you shouldn’t take your blood pressure medication. But that gets trumpeted into all these conversations about whether people [with obesity] should be treated at all.”
Like obesity, blood pressure was once thought to be a behavioral problem, Dr. Aronne said. But blood pressure meds prevent heart attacks and strokes. And it’s likely obesity meds will do the same.
One 55-year-old patient on the road to kidney failure lost weight on obesity medications, including semaglutide, Dr. Aronne said. Now, 6 years later, his kidney function is back to normal. “Normally, we think of kidney disease as irreversible,” Dr. Aronne said.
In that respect, these drugs should save money in the long run by virtue of heading off those health care costs, said Dr. Seeley, who imagines a future where obesity is not gone but better managed, like high blood pressure is now.
In the end, the drugs are another step toward what Dr. Aronne and many others have always pushed for: Treating obesity as a disease.
A version of this article originally appeared on WebMD.com.
Higher alcohol consumption linked to early-onset CRC
TOPLINE:
Higher levels of alcohol consumption appear to increase an individual’s risk of early-onset colorectal cancer (CRC), particularly distal colon and rectal cancers, according to a population-based study from South Korea.
METHODOLOGY:
- The investigators retrospectively compared average daily alcohol consumption with early-onset CRC risk among nearly 5.7 million adults younger than 50 years, using data from the Korean National Health Insurance Service.
- Alcohol consumption levels were defined as nondrinker, light (< 10 g/day or < 0.7 U.S. drinks/day), moderate (10-30 g/day for men, 10-20 g/day for women), and heavy (≥ 30 g/day or ≥ 2.1 drinks/day for men, ≥ 20 g/day or ≥ 1.4 drinks/day for women).
- The primary outcome was incidence of early-onset CRC diagnosed before age 50. Models were adjusted for age, sex, smoking status, exercise, and income, as well as for comorbidities.
TAKEAWAY:
- Overall, 8,314 incident early-onset CRC cases occurred during the mean follow-up period of 7.4 years.
- Compared with light drinking, moderate and heavy drinking were associated with a significantly elevated risk of early-onset CRC (adjusted hazard ratio, 1.09 and 1.20, respectively); by sex, significant associations were found only among men.
- Among men, heavy drinking vs. light drinking was associated with a 26% increased risk of distal colon cancer, a 17% higher risk of rectal cancer, and a 29% higher risk of unspecified colon cancer (but not proximal colon cancer).
- Among women, moderate drinking was associated with a 47% increased risk of distal colon cancer. Among nondrinkers, there was a 14% reduced risk of rectal cancer, compared with light drinkers.
IN PRACTICE:
“This population-based study provides evidence that higher levels of alcohol consumption may increase the risk of early-onset CRC,” the investigators concluded. “[E]ffective interventions are required to discourage alcohol consumption among young people and to tailor CRC screening approaches for high-risk individuals.”
SOURCE:
The study was led by researchers at Seoul National University, South Korea. It was published online in the Journal of Clinical Oncology.
LIMITATIONS:
Study limitations include self-reported alcohol consumption. Data were missing for a higher number of male participants and younger participants, and there was a potential problem related to multiple comparisons and confounders. Only Korean individuals were included in the study, so larger studies involving various races are needed.
DISCLOSURES:
Funding was provided by grants from the Korea Health Technology R&D Project and the Ministry of Health and Welfare, Republic of Korea. No potential conflicts of interest were reported.
A version of this article first appeared on Medscape.com.
TOPLINE:
Higher levels of alcohol consumption appear to increase an individual’s risk of early-onset colorectal cancer (CRC), particularly distal colon and rectal cancers, according to a population-based study from South Korea.
METHODOLOGY:
- The investigators retrospectively compared average daily alcohol consumption with early-onset CRC risk among nearly 5.7 million adults younger than 50 years, using data from the Korean National Health Insurance Service.
- Alcohol consumption levels were defined as nondrinker, light (< 10 g/day or < 0.7 U.S. drinks/day), moderate (10-30 g/day for men, 10-20 g/day for women), and heavy (≥ 30 g/day or ≥ 2.1 drinks/day for men, ≥ 20 g/day or ≥ 1.4 drinks/day for women).
- The primary outcome was incidence of early-onset CRC diagnosed before age 50. Models were adjusted for age, sex, smoking status, exercise, and income, as well as for comorbidities.
TAKEAWAY:
- Overall, 8,314 incident early-onset CRC cases occurred during the mean follow-up period of 7.4 years.
- Compared with light drinking, moderate and heavy drinking were associated with a significantly elevated risk of early-onset CRC (adjusted hazard ratio, 1.09 and 1.20, respectively); by sex, significant associations were found only among men.
- Among men, heavy drinking vs. light drinking was associated with a 26% increased risk of distal colon cancer, a 17% higher risk of rectal cancer, and a 29% higher risk of unspecified colon cancer (but not proximal colon cancer).
- Among women, moderate drinking was associated with a 47% increased risk of distal colon cancer. Among nondrinkers, there was a 14% reduced risk of rectal cancer, compared with light drinkers.
IN PRACTICE:
“This population-based study provides evidence that higher levels of alcohol consumption may increase the risk of early-onset CRC,” the investigators concluded. “[E]ffective interventions are required to discourage alcohol consumption among young people and to tailor CRC screening approaches for high-risk individuals.”
SOURCE:
The study was led by researchers at Seoul National University, South Korea. It was published online in the Journal of Clinical Oncology.
LIMITATIONS:
Study limitations include self-reported alcohol consumption. Data were missing for a higher number of male participants and younger participants, and there was a potential problem related to multiple comparisons and confounders. Only Korean individuals were included in the study, so larger studies involving various races are needed.
DISCLOSURES:
Funding was provided by grants from the Korea Health Technology R&D Project and the Ministry of Health and Welfare, Republic of Korea. No potential conflicts of interest were reported.
A version of this article first appeared on Medscape.com.
TOPLINE:
Higher levels of alcohol consumption appear to increase an individual’s risk of early-onset colorectal cancer (CRC), particularly distal colon and rectal cancers, according to a population-based study from South Korea.
METHODOLOGY:
- The investigators retrospectively compared average daily alcohol consumption with early-onset CRC risk among nearly 5.7 million adults younger than 50 years, using data from the Korean National Health Insurance Service.
- Alcohol consumption levels were defined as nondrinker, light (< 10 g/day or < 0.7 U.S. drinks/day), moderate (10-30 g/day for men, 10-20 g/day for women), and heavy (≥ 30 g/day or ≥ 2.1 drinks/day for men, ≥ 20 g/day or ≥ 1.4 drinks/day for women).
- The primary outcome was incidence of early-onset CRC diagnosed before age 50. Models were adjusted for age, sex, smoking status, exercise, and income, as well as for comorbidities.
TAKEAWAY:
- Overall, 8,314 incident early-onset CRC cases occurred during the mean follow-up period of 7.4 years.
- Compared with light drinking, moderate and heavy drinking were associated with a significantly elevated risk of early-onset CRC (adjusted hazard ratio, 1.09 and 1.20, respectively); by sex, significant associations were found only among men.
- Among men, heavy drinking vs. light drinking was associated with a 26% increased risk of distal colon cancer, a 17% higher risk of rectal cancer, and a 29% higher risk of unspecified colon cancer (but not proximal colon cancer).
- Among women, moderate drinking was associated with a 47% increased risk of distal colon cancer. Among nondrinkers, there was a 14% reduced risk of rectal cancer, compared with light drinkers.
IN PRACTICE:
“This population-based study provides evidence that higher levels of alcohol consumption may increase the risk of early-onset CRC,” the investigators concluded. “[E]ffective interventions are required to discourage alcohol consumption among young people and to tailor CRC screening approaches for high-risk individuals.”
SOURCE:
The study was led by researchers at Seoul National University, South Korea. It was published online in the Journal of Clinical Oncology.
LIMITATIONS:
Study limitations include self-reported alcohol consumption. Data were missing for a higher number of male participants and younger participants, and there was a potential problem related to multiple comparisons and confounders. Only Korean individuals were included in the study, so larger studies involving various races are needed.
DISCLOSURES:
Funding was provided by grants from the Korea Health Technology R&D Project and the Ministry of Health and Welfare, Republic of Korea. No potential conflicts of interest were reported.
A version of this article first appeared on Medscape.com.
Novel tool accurately predicts suicide after self-harm
Investigators have developed and validated a new risk calculator to help predict death by suicide in the 6-12 months after an episode of nonfatal self-harm, new research shows.
A study led by Seena Fazel, MBChB, MD, University of Oxford, England, suggests the Oxford Suicide Assessment Tool for Self-harm (OxSATS) may help guide treatment decisions and target resources to those most in need, the researchers note.
“Many tools use only simple high/low categories, whereas OxSATS includes probability scores, which align more closely with risk calculators in cardiovascular medicine, such as the Framingham Risk Score, and prognostic models in cancer medicine, which provide 5-year survival probabilities. This potentially allows OxSATS to inform clinical decision-making more directly,” Dr. Fazel told this news organization.
The findings were published online in BMJ Mental Health.
Targeted tool
Self-harm is associated with a 1-year risk of suicide that is 20 times higher than that of the general population. Given that about 16 million people self-harm annually, the impact at a population level is potentially quite large, the researchers note.
Current structured approaches to gauge suicide risk among those who have engaged in self-harm are based on tools developed for other purposes and symptom checklists. “Their poor to moderate performance is therefore not unexpected,” Dr. Fazel told this news organization.
In contrast, OxSATS was specifically developed to predict suicide mortality after self-harm.
Dr. Fazel’s group evaluated data on 53,172 Swedish individuals aged 10 years and older who sought emergency medical care after episodes of self-harm.
The development cohort included 37,523 individuals. Of these, 391 died by suicide within 12 months. The validation cohort included 15,649 individuals; of these people, 178 died by suicide within 12 months.
The final OxSATS model includes 11 predictors related to age and sex, as well as variables related to substance misuse, mental health, and treatment and history of self-harm.
“The performance of the model in external validation was good, with c-index at 6 and 12 months of 0.77,” the researchers note.
Using a cutoff threshold of 1%, the OxSATS correctly identified 68% of those who died by suicide within 6 months, while 71% of those who didn’t die were correctly classified as being at low risk. The figures for risk prediction at 12 months were 82% and 54%, respectively.
The OxSATS has been made into a simple online tool with probability scores for suicide at 6 and 12 months after an episode of self-harm, but without linkage to interventions. A tool on its own is unlikely to improve outcomes, said Dr. Fazel.
“However,” he added, “it can improve consistency in the assessment process, especially in busy clinical settings where people from different professional backgrounds and experience undertake such assessments. It can also highlight the role of modifiable risk factors and provide an opportunity to transparently discuss risk with patients and their carers.”
Valuable work
Reached for comment, Igor Galynker, MD, PhD, professor of psychiatry at the Icahn School of Medicine at Mount Sinai, New York, said that this is a “very solid study with a very large sample size and solid statistical analysis.”
Another strength of the research is the outcome of suicide death versus suicide attempt or suicidal ideation. “In that respect, it is a valuable paper,” Dr. Galynker, who directs the Mount Sinai Beth Israel Suicide Research Laboratory, told this news organization.
He noted that there are no new risk factors in the model. Rather, the model contains the typical risk factors for suicide, which include male sex, substance misuse, past suicide attempt, and psychiatric diagnosis.
“The strongest risk factor in the model is self-harm by hanging, strangulation, or suffocation, which has been shown before and is therefore unsurprising,” said Dr. Galynker.
In general, the risk factors included in the model are often part of administrative tools for suicide risk assessment, said Dr. Galynker, but the OxSATS “seems easier to use because it has 11 items only.”
Broadly speaking, individuals with mental illness and past suicide attempt, past self-harm, alcohol use, and other risk factors “should be treated proactively with suicide prevention measures,” he told this news organization.
As previously reported, Dr. Galynker and colleagues have developed the Abbreviated Suicide Crisis Syndrome Checklist (A-SCS-C), a novel tool to help identify which suicidal patients who present to the emergency department should be admitted to hospital and which patients can be safely discharged.
Funding for the study was provided by Wellcome Trust and the Swedish Research Council. Dr. Fazel and Dr. Galynker have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Investigators have developed and validated a new risk calculator to help predict death by suicide in the 6-12 months after an episode of nonfatal self-harm, new research shows.
A study led by Seena Fazel, MBChB, MD, University of Oxford, England, suggests the Oxford Suicide Assessment Tool for Self-harm (OxSATS) may help guide treatment decisions and target resources to those most in need, the researchers note.
“Many tools use only simple high/low categories, whereas OxSATS includes probability scores, which align more closely with risk calculators in cardiovascular medicine, such as the Framingham Risk Score, and prognostic models in cancer medicine, which provide 5-year survival probabilities. This potentially allows OxSATS to inform clinical decision-making more directly,” Dr. Fazel told this news organization.
The findings were published online in BMJ Mental Health.
Targeted tool
Self-harm is associated with a 1-year risk of suicide that is 20 times higher than that of the general population. Given that about 16 million people self-harm annually, the impact at a population level is potentially quite large, the researchers note.
Current structured approaches to gauge suicide risk among those who have engaged in self-harm are based on tools developed for other purposes and symptom checklists. “Their poor to moderate performance is therefore not unexpected,” Dr. Fazel told this news organization.
In contrast, OxSATS was specifically developed to predict suicide mortality after self-harm.
Dr. Fazel’s group evaluated data on 53,172 Swedish individuals aged 10 years and older who sought emergency medical care after episodes of self-harm.
The development cohort included 37,523 individuals. Of these, 391 died by suicide within 12 months. The validation cohort included 15,649 individuals; of these people, 178 died by suicide within 12 months.
The final OxSATS model includes 11 predictors related to age and sex, as well as variables related to substance misuse, mental health, and treatment and history of self-harm.
“The performance of the model in external validation was good, with c-index at 6 and 12 months of 0.77,” the researchers note.
Using a cutoff threshold of 1%, the OxSATS correctly identified 68% of those who died by suicide within 6 months, while 71% of those who didn’t die were correctly classified as being at low risk. The figures for risk prediction at 12 months were 82% and 54%, respectively.
The OxSATS has been made into a simple online tool with probability scores for suicide at 6 and 12 months after an episode of self-harm, but without linkage to interventions. A tool on its own is unlikely to improve outcomes, said Dr. Fazel.
“However,” he added, “it can improve consistency in the assessment process, especially in busy clinical settings where people from different professional backgrounds and experience undertake such assessments. It can also highlight the role of modifiable risk factors and provide an opportunity to transparently discuss risk with patients and their carers.”
Valuable work
Reached for comment, Igor Galynker, MD, PhD, professor of psychiatry at the Icahn School of Medicine at Mount Sinai, New York, said that this is a “very solid study with a very large sample size and solid statistical analysis.”
Another strength of the research is the outcome of suicide death versus suicide attempt or suicidal ideation. “In that respect, it is a valuable paper,” Dr. Galynker, who directs the Mount Sinai Beth Israel Suicide Research Laboratory, told this news organization.
He noted that there are no new risk factors in the model. Rather, the model contains the typical risk factors for suicide, which include male sex, substance misuse, past suicide attempt, and psychiatric diagnosis.
“The strongest risk factor in the model is self-harm by hanging, strangulation, or suffocation, which has been shown before and is therefore unsurprising,” said Dr. Galynker.
In general, the risk factors included in the model are often part of administrative tools for suicide risk assessment, said Dr. Galynker, but the OxSATS “seems easier to use because it has 11 items only.”
Broadly speaking, individuals with mental illness and past suicide attempt, past self-harm, alcohol use, and other risk factors “should be treated proactively with suicide prevention measures,” he told this news organization.
As previously reported, Dr. Galynker and colleagues have developed the Abbreviated Suicide Crisis Syndrome Checklist (A-SCS-C), a novel tool to help identify which suicidal patients who present to the emergency department should be admitted to hospital and which patients can be safely discharged.
Funding for the study was provided by Wellcome Trust and the Swedish Research Council. Dr. Fazel and Dr. Galynker have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Investigators have developed and validated a new risk calculator to help predict death by suicide in the 6-12 months after an episode of nonfatal self-harm, new research shows.
A study led by Seena Fazel, MBChB, MD, University of Oxford, England, suggests the Oxford Suicide Assessment Tool for Self-harm (OxSATS) may help guide treatment decisions and target resources to those most in need, the researchers note.
“Many tools use only simple high/low categories, whereas OxSATS includes probability scores, which align more closely with risk calculators in cardiovascular medicine, such as the Framingham Risk Score, and prognostic models in cancer medicine, which provide 5-year survival probabilities. This potentially allows OxSATS to inform clinical decision-making more directly,” Dr. Fazel told this news organization.
The findings were published online in BMJ Mental Health.
Targeted tool
Self-harm is associated with a 1-year risk of suicide that is 20 times higher than that of the general population. Given that about 16 million people self-harm annually, the impact at a population level is potentially quite large, the researchers note.
Current structured approaches to gauge suicide risk among those who have engaged in self-harm are based on tools developed for other purposes and symptom checklists. “Their poor to moderate performance is therefore not unexpected,” Dr. Fazel told this news organization.
In contrast, OxSATS was specifically developed to predict suicide mortality after self-harm.
Dr. Fazel’s group evaluated data on 53,172 Swedish individuals aged 10 years and older who sought emergency medical care after episodes of self-harm.
The development cohort included 37,523 individuals. Of these, 391 died by suicide within 12 months. The validation cohort included 15,649 individuals; of these people, 178 died by suicide within 12 months.
The final OxSATS model includes 11 predictors related to age and sex, as well as variables related to substance misuse, mental health, and treatment and history of self-harm.
“The performance of the model in external validation was good, with c-index at 6 and 12 months of 0.77,” the researchers note.
Using a cutoff threshold of 1%, the OxSATS correctly identified 68% of those who died by suicide within 6 months, while 71% of those who didn’t die were correctly classified as being at low risk. The figures for risk prediction at 12 months were 82% and 54%, respectively.
The OxSATS has been made into a simple online tool with probability scores for suicide at 6 and 12 months after an episode of self-harm, but without linkage to interventions. A tool on its own is unlikely to improve outcomes, said Dr. Fazel.
“However,” he added, “it can improve consistency in the assessment process, especially in busy clinical settings where people from different professional backgrounds and experience undertake such assessments. It can also highlight the role of modifiable risk factors and provide an opportunity to transparently discuss risk with patients and their carers.”
Valuable work
Reached for comment, Igor Galynker, MD, PhD, professor of psychiatry at the Icahn School of Medicine at Mount Sinai, New York, said that this is a “very solid study with a very large sample size and solid statistical analysis.”
Another strength of the research is the outcome of suicide death versus suicide attempt or suicidal ideation. “In that respect, it is a valuable paper,” Dr. Galynker, who directs the Mount Sinai Beth Israel Suicide Research Laboratory, told this news organization.
He noted that there are no new risk factors in the model. Rather, the model contains the typical risk factors for suicide, which include male sex, substance misuse, past suicide attempt, and psychiatric diagnosis.
“The strongest risk factor in the model is self-harm by hanging, strangulation, or suffocation, which has been shown before and is therefore unsurprising,” said Dr. Galynker.
In general, the risk factors included in the model are often part of administrative tools for suicide risk assessment, said Dr. Galynker, but the OxSATS “seems easier to use because it has 11 items only.”
Broadly speaking, individuals with mental illness and past suicide attempt, past self-harm, alcohol use, and other risk factors “should be treated proactively with suicide prevention measures,” he told this news organization.
As previously reported, Dr. Galynker and colleagues have developed the Abbreviated Suicide Crisis Syndrome Checklist (A-SCS-C), a novel tool to help identify which suicidal patients who present to the emergency department should be admitted to hospital and which patients can be safely discharged.
Funding for the study was provided by Wellcome Trust and the Swedish Research Council. Dr. Fazel and Dr. Galynker have no relevant disclosures.
A version of this article first appeared on Medscape.com.
Patient aggression against receptionists demands protocols
“I’ve been hit in the head by a walking stick,” a primary care receptionist reported.
“A mother came in and was screaming and swearing at me because she couldn’t get an appointment for her daughters,” another receptionist reported.
“I’ve had people throw a bag of syringes at me because we don’t accept syringes,” said another.
Reports such as these are part of the literature supporting a review that finds patient aggression against receptionists is a serious safety concern for primary care offices and affects delivery of health care.
The review was published online in the BMJ’s Family Medicine and Community Health journal.
“Receptionists in general practice deserve evidence-based measures to improve their working conditions and well-being,” say the authors, led by Fiona Willer, PhD, of the Centre for Community Health and Wellbeing at the University of Queensland, Brisbane, Australia.
Though the study looked primarily at European and Australian practices, physicians in the United States say the incidences are familiar.
Cause often lack of access
Dr. Willer and colleagues point out that the root cause of patient regression is typically related to operational factors, such as inefficient scheduling or lack of access to the medical providers.
“However, reception staff are placed in the unenviable position of having to deal with the aftermath of the poor function of these systems without having the status or autonomy to overhaul them,” the authors note.
Authors analyzed 20 studies on aggression against receptionists.
Among the findings:
- All studies reported that patient hostility and verbal abuse of receptionists “was a frequent, routine, and relatively unavoidable occurrence in general practice.”
- Nine studies reported acts of physical violence toward receptionists, with all reporting that physical abuse occurred much less frequently than verbal abuse.
- Some acts were very severe, including being hit, shaken, held at gunpoint, stalked, and threatened with a razorblade.
The studies also discussed ways to prevent potential aggression or react to it, including:
- Regular staff training for managing patient aggression.
- Designing clinics with “safe rooms” and “cool down” spaces.
- Providing clear acrylic shields between receptionists and patients.
- Developing formal policy/procedure/protocol/action guides relating to management of patients.
Behavior can interrupt health care delivery
Carrie Janiski, DO, regional medical director at Golden Valley Health Centers in California, who was not part of the review, said she has seen the aggressive behavior the authors document in her practice’s lobby, “including yelling, name-calling, and threatening language or physical behavior.”
The instances disrupt health care delivery to the patient, who is often in crisis, and all patients and staff in the clinic, she said.
“The patient needs help and the aggressive way they are seeking it could cause harm to others or prevent them from receiving all the help they need,” she said.
She says in practices she has worked in, some effective mitigation strategies have included open-access scheduling, increased walk-in availability for appointments, de-escalation training for front-line staff, and office and exam room layout designed for safety.
She added that incident review is important and should include a process for patient dismissal from the practice.
Dustin Arnold, DO, an internal medicine specialist and chief medical officer at UnityPoint Health-St. Luke’s Hospital, Cedar Rapids, IA, said he agrees with the authors on the urgency for action.
“This is an urgent concern for practices across the country. Your receptionist is the face of your practice, and you should invest in them,” said Dr. Arnold, who was not part of the review.
He said he has seen “verbal abuse and generalized incivility” from patients against receptionists in practices where he has worked.
He said the measure the authors list that he thinks is most effective is staff de-escalation training.
“However, the best preventative measure is for the physician to be on time and minimize cancellation of appointments,” he said. “These are the two primary triggers of a patient becoming disruptive.”
He said his practice has installed a panic button at the front desk and built an alert into the electronic health record indicating that a patient has shown disruptive behavior in the past.
The authors conclude: “Staff training and protocols to manage patient aggression and ongoing structured staff support should be considered essential in general practice. Evidence-based strategies to prevent, manage, and mitigate the harms of patient aggression towards general practice reception staff are urgently needed.”
The authors and Dr. Janiski and Dr. Arnold declared no relevant financial relationships.
“I’ve been hit in the head by a walking stick,” a primary care receptionist reported.
“A mother came in and was screaming and swearing at me because she couldn’t get an appointment for her daughters,” another receptionist reported.
“I’ve had people throw a bag of syringes at me because we don’t accept syringes,” said another.
Reports such as these are part of the literature supporting a review that finds patient aggression against receptionists is a serious safety concern for primary care offices and affects delivery of health care.
The review was published online in the BMJ’s Family Medicine and Community Health journal.
“Receptionists in general practice deserve evidence-based measures to improve their working conditions and well-being,” say the authors, led by Fiona Willer, PhD, of the Centre for Community Health and Wellbeing at the University of Queensland, Brisbane, Australia.
Though the study looked primarily at European and Australian practices, physicians in the United States say the incidences are familiar.
Cause often lack of access
Dr. Willer and colleagues point out that the root cause of patient regression is typically related to operational factors, such as inefficient scheduling or lack of access to the medical providers.
“However, reception staff are placed in the unenviable position of having to deal with the aftermath of the poor function of these systems without having the status or autonomy to overhaul them,” the authors note.
Authors analyzed 20 studies on aggression against receptionists.
Among the findings:
- All studies reported that patient hostility and verbal abuse of receptionists “was a frequent, routine, and relatively unavoidable occurrence in general practice.”
- Nine studies reported acts of physical violence toward receptionists, with all reporting that physical abuse occurred much less frequently than verbal abuse.
- Some acts were very severe, including being hit, shaken, held at gunpoint, stalked, and threatened with a razorblade.
The studies also discussed ways to prevent potential aggression or react to it, including:
- Regular staff training for managing patient aggression.
- Designing clinics with “safe rooms” and “cool down” spaces.
- Providing clear acrylic shields between receptionists and patients.
- Developing formal policy/procedure/protocol/action guides relating to management of patients.
Behavior can interrupt health care delivery
Carrie Janiski, DO, regional medical director at Golden Valley Health Centers in California, who was not part of the review, said she has seen the aggressive behavior the authors document in her practice’s lobby, “including yelling, name-calling, and threatening language or physical behavior.”
The instances disrupt health care delivery to the patient, who is often in crisis, and all patients and staff in the clinic, she said.
“The patient needs help and the aggressive way they are seeking it could cause harm to others or prevent them from receiving all the help they need,” she said.
She says in practices she has worked in, some effective mitigation strategies have included open-access scheduling, increased walk-in availability for appointments, de-escalation training for front-line staff, and office and exam room layout designed for safety.
She added that incident review is important and should include a process for patient dismissal from the practice.
Dustin Arnold, DO, an internal medicine specialist and chief medical officer at UnityPoint Health-St. Luke’s Hospital, Cedar Rapids, IA, said he agrees with the authors on the urgency for action.
“This is an urgent concern for practices across the country. Your receptionist is the face of your practice, and you should invest in them,” said Dr. Arnold, who was not part of the review.
He said he has seen “verbal abuse and generalized incivility” from patients against receptionists in practices where he has worked.
He said the measure the authors list that he thinks is most effective is staff de-escalation training.
“However, the best preventative measure is for the physician to be on time and minimize cancellation of appointments,” he said. “These are the two primary triggers of a patient becoming disruptive.”
He said his practice has installed a panic button at the front desk and built an alert into the electronic health record indicating that a patient has shown disruptive behavior in the past.
The authors conclude: “Staff training and protocols to manage patient aggression and ongoing structured staff support should be considered essential in general practice. Evidence-based strategies to prevent, manage, and mitigate the harms of patient aggression towards general practice reception staff are urgently needed.”
The authors and Dr. Janiski and Dr. Arnold declared no relevant financial relationships.
“I’ve been hit in the head by a walking stick,” a primary care receptionist reported.
“A mother came in and was screaming and swearing at me because she couldn’t get an appointment for her daughters,” another receptionist reported.
“I’ve had people throw a bag of syringes at me because we don’t accept syringes,” said another.
Reports such as these are part of the literature supporting a review that finds patient aggression against receptionists is a serious safety concern for primary care offices and affects delivery of health care.
The review was published online in the BMJ’s Family Medicine and Community Health journal.
“Receptionists in general practice deserve evidence-based measures to improve their working conditions and well-being,” say the authors, led by Fiona Willer, PhD, of the Centre for Community Health and Wellbeing at the University of Queensland, Brisbane, Australia.
Though the study looked primarily at European and Australian practices, physicians in the United States say the incidences are familiar.
Cause often lack of access
Dr. Willer and colleagues point out that the root cause of patient regression is typically related to operational factors, such as inefficient scheduling or lack of access to the medical providers.
“However, reception staff are placed in the unenviable position of having to deal with the aftermath of the poor function of these systems without having the status or autonomy to overhaul them,” the authors note.
Authors analyzed 20 studies on aggression against receptionists.
Among the findings:
- All studies reported that patient hostility and verbal abuse of receptionists “was a frequent, routine, and relatively unavoidable occurrence in general practice.”
- Nine studies reported acts of physical violence toward receptionists, with all reporting that physical abuse occurred much less frequently than verbal abuse.
- Some acts were very severe, including being hit, shaken, held at gunpoint, stalked, and threatened with a razorblade.
The studies also discussed ways to prevent potential aggression or react to it, including:
- Regular staff training for managing patient aggression.
- Designing clinics with “safe rooms” and “cool down” spaces.
- Providing clear acrylic shields between receptionists and patients.
- Developing formal policy/procedure/protocol/action guides relating to management of patients.
Behavior can interrupt health care delivery
Carrie Janiski, DO, regional medical director at Golden Valley Health Centers in California, who was not part of the review, said she has seen the aggressive behavior the authors document in her practice’s lobby, “including yelling, name-calling, and threatening language or physical behavior.”
The instances disrupt health care delivery to the patient, who is often in crisis, and all patients and staff in the clinic, she said.
“The patient needs help and the aggressive way they are seeking it could cause harm to others or prevent them from receiving all the help they need,” she said.
She says in practices she has worked in, some effective mitigation strategies have included open-access scheduling, increased walk-in availability for appointments, de-escalation training for front-line staff, and office and exam room layout designed for safety.
She added that incident review is important and should include a process for patient dismissal from the practice.
Dustin Arnold, DO, an internal medicine specialist and chief medical officer at UnityPoint Health-St. Luke’s Hospital, Cedar Rapids, IA, said he agrees with the authors on the urgency for action.
“This is an urgent concern for practices across the country. Your receptionist is the face of your practice, and you should invest in them,” said Dr. Arnold, who was not part of the review.
He said he has seen “verbal abuse and generalized incivility” from patients against receptionists in practices where he has worked.
He said the measure the authors list that he thinks is most effective is staff de-escalation training.
“However, the best preventative measure is for the physician to be on time and minimize cancellation of appointments,” he said. “These are the two primary triggers of a patient becoming disruptive.”
He said his practice has installed a panic button at the front desk and built an alert into the electronic health record indicating that a patient has shown disruptive behavior in the past.
The authors conclude: “Staff training and protocols to manage patient aggression and ongoing structured staff support should be considered essential in general practice. Evidence-based strategies to prevent, manage, and mitigate the harms of patient aggression towards general practice reception staff are urgently needed.”
The authors and Dr. Janiski and Dr. Arnold declared no relevant financial relationships.
FROM FAMILY MEDICINE AND COMMUNITY HEALTH
Cardiorespiratory fitness linked to cancer risk, mortality?
TOPLINE:
a large Swedish cohort study suggests.
METHODOLOGY:
- A prospective cohort study included 177,709 Swedish men (mean age, 42; mean body mass index, 26 kg/m2) who completed an occupational health profile assessment and were followed for a mean of 9.6 years.
- CRF was assessed by determining maximal oxygen consumption during an aerobic fitness test, known as a submaximal Åstrand cycle ergometer test.
- Participants reported physical activity habits, lifestyle, and perceived health.
- Data on prostate, colon, and lung cancer incidence and mortality were derived from national registers.
- Outcomes from three higher CRF groups (low, > 25-35; moderate, > 35-45; high, > 45 mL/min per kg) were compared with those from the very low CRF group (25 mL/min per kg or less). Models were adjusted for various factors, including age, BMI, education, dietary habits, comorbidity, and smoking.
TAKEAWAY:
- During follow-up, investigators identified 1,918 prostate, 499 colon, and 283 lung cancer cases as well as 141 prostate, 207 lung, and 152 colon cancer deaths.
- In the fully adjusted model, higher CRF levels were associated with a significantly lower risk for colon cancer (hazard ratio, 0.72 for moderate; HR, 0.63 for high).
- In this model, higher CRF was also associated with a lower risk of death from prostate cancer (HR, 0.67 for low; HR, 0.57 for moderate; HR, 0.29 for high).
- For lung cancer mortality, only high CRF was associated with a significantly lower risk of death (HR, 0.41).
- An association between CRF and lung cancer incidence (HR, 0.99) and death (HR, 0.99) was only evident among adults aged 60 and older.
IN PRACTICE:
“The clinical implications of these findings further emphasize the importance of CRF for possibly reducing cancer incidence and mortality,” the authors concluded. “It is important for the general public to understand that higher-intensity [physical activity] has greater effects on CRF and is likely to be more protective against the risk of developing and dying from certain cancers.”
SOURCE:
The study was led by Elin Ekblom-Bak, PhD, from the Swedish School of Sport and Health Sciences, Stockholm. It was published online in JAMA Network Open.
LIMITATIONS:
The study was limited by voluntary participation, inclusion of only employed individuals, and estimations of CRF via submaximal tests. Data on smoking status were not optimal and there was a small number of cancer cases and deaths.
DISCLOSURES:
Funding was provided by the Swedish Cancer Society. The authors have reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
TOPLINE:
a large Swedish cohort study suggests.
METHODOLOGY:
- A prospective cohort study included 177,709 Swedish men (mean age, 42; mean body mass index, 26 kg/m2) who completed an occupational health profile assessment and were followed for a mean of 9.6 years.
- CRF was assessed by determining maximal oxygen consumption during an aerobic fitness test, known as a submaximal Åstrand cycle ergometer test.
- Participants reported physical activity habits, lifestyle, and perceived health.
- Data on prostate, colon, and lung cancer incidence and mortality were derived from national registers.
- Outcomes from three higher CRF groups (low, > 25-35; moderate, > 35-45; high, > 45 mL/min per kg) were compared with those from the very low CRF group (25 mL/min per kg or less). Models were adjusted for various factors, including age, BMI, education, dietary habits, comorbidity, and smoking.
TAKEAWAY:
- During follow-up, investigators identified 1,918 prostate, 499 colon, and 283 lung cancer cases as well as 141 prostate, 207 lung, and 152 colon cancer deaths.
- In the fully adjusted model, higher CRF levels were associated with a significantly lower risk for colon cancer (hazard ratio, 0.72 for moderate; HR, 0.63 for high).
- In this model, higher CRF was also associated with a lower risk of death from prostate cancer (HR, 0.67 for low; HR, 0.57 for moderate; HR, 0.29 for high).
- For lung cancer mortality, only high CRF was associated with a significantly lower risk of death (HR, 0.41).
- An association between CRF and lung cancer incidence (HR, 0.99) and death (HR, 0.99) was only evident among adults aged 60 and older.
IN PRACTICE:
“The clinical implications of these findings further emphasize the importance of CRF for possibly reducing cancer incidence and mortality,” the authors concluded. “It is important for the general public to understand that higher-intensity [physical activity] has greater effects on CRF and is likely to be more protective against the risk of developing and dying from certain cancers.”
SOURCE:
The study was led by Elin Ekblom-Bak, PhD, from the Swedish School of Sport and Health Sciences, Stockholm. It was published online in JAMA Network Open.
LIMITATIONS:
The study was limited by voluntary participation, inclusion of only employed individuals, and estimations of CRF via submaximal tests. Data on smoking status were not optimal and there was a small number of cancer cases and deaths.
DISCLOSURES:
Funding was provided by the Swedish Cancer Society. The authors have reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
TOPLINE:
a large Swedish cohort study suggests.
METHODOLOGY:
- A prospective cohort study included 177,709 Swedish men (mean age, 42; mean body mass index, 26 kg/m2) who completed an occupational health profile assessment and were followed for a mean of 9.6 years.
- CRF was assessed by determining maximal oxygen consumption during an aerobic fitness test, known as a submaximal Åstrand cycle ergometer test.
- Participants reported physical activity habits, lifestyle, and perceived health.
- Data on prostate, colon, and lung cancer incidence and mortality were derived from national registers.
- Outcomes from three higher CRF groups (low, > 25-35; moderate, > 35-45; high, > 45 mL/min per kg) were compared with those from the very low CRF group (25 mL/min per kg or less). Models were adjusted for various factors, including age, BMI, education, dietary habits, comorbidity, and smoking.
TAKEAWAY:
- During follow-up, investigators identified 1,918 prostate, 499 colon, and 283 lung cancer cases as well as 141 prostate, 207 lung, and 152 colon cancer deaths.
- In the fully adjusted model, higher CRF levels were associated with a significantly lower risk for colon cancer (hazard ratio, 0.72 for moderate; HR, 0.63 for high).
- In this model, higher CRF was also associated with a lower risk of death from prostate cancer (HR, 0.67 for low; HR, 0.57 for moderate; HR, 0.29 for high).
- For lung cancer mortality, only high CRF was associated with a significantly lower risk of death (HR, 0.41).
- An association between CRF and lung cancer incidence (HR, 0.99) and death (HR, 0.99) was only evident among adults aged 60 and older.
IN PRACTICE:
“The clinical implications of these findings further emphasize the importance of CRF for possibly reducing cancer incidence and mortality,” the authors concluded. “It is important for the general public to understand that higher-intensity [physical activity] has greater effects on CRF and is likely to be more protective against the risk of developing and dying from certain cancers.”
SOURCE:
The study was led by Elin Ekblom-Bak, PhD, from the Swedish School of Sport and Health Sciences, Stockholm. It was published online in JAMA Network Open.
LIMITATIONS:
The study was limited by voluntary participation, inclusion of only employed individuals, and estimations of CRF via submaximal tests. Data on smoking status were not optimal and there was a small number of cancer cases and deaths.
DISCLOSURES:
Funding was provided by the Swedish Cancer Society. The authors have reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Long COVID ‘brain fog’ confounds doctors, but new research offers hope
Kate Whitley was petrified of COVID-19 from the beginning of the pandemic because she has Hashimoto disease, an autoimmune disorder that she knew put her at high risk for complications.
She was right to be worried. Two months after contracting the infection in September 2022, the 42-year-old Nashville resident was diagnosed with long COVID. For Ms. Whitley, the resulting brain fog has been the most challenging factor. She is the owner of a successful paper goods store, and she can’t remember basic aspects of her job. She can’t tolerate loud noises and gets so distracted that she has trouble remembering what she was doing.
Ms. Whitley doesn’t like the term “brain fog” because it doesn’t begin to describe the dramatic disruption to her life over the past 7 months.
Brain fog is among the most common symptoms of long COVID, and also one of the most poorly understood. A reported 46% of those diagnosed with long COVID complain of brain fog or a loss of memory. Many clinicians agree that the term is vague and often doesn’t truly represent the condition. That, in turn, makes it harder for doctors to diagnose and treat it. There are no standard tests for it, nor are there guidelines for symptom management or treatment.
“There’s a lot of imprecision in the term because it might mean different things to different patients,” said James C. Jackson, PsyD, a neuropsychiatrist at Vanderbilt University, Nashville, Tenn., and author of a new book, “Clearing the Fog: From Surviving to Thriving With Long COVID – A Practical Guide.”
Dr. Jackson, who began treating Ms. Whitley in February 2023, said that it makes more sense to call brain fog a brain impairment or an acquired brain injury (ABI) because it doesn’t occur gradually. COVID damages the brain and causes injury. For those with long COVID who were previously in the intensive care unit and may have undergone ventilation, hypoxic brain injury may result from the lack of oxygen to the brain.
Even among those with milder cases of acute COVID, there’s some evidence that persistent neuroinflammation in the brain caused by an activated immune system may also cause damage.
In both cases, the results can be debilitating. Ms. Whitley also has dysautonomia – a disorder of the autonomic nervous system that can cause dizziness, sweating, and headaches along with fatigue and heart palpitations.
She said that she’s so forgetful that when she sees people socially, she’s nervous of what she’ll say. “I feel like I’m constantly sticking my foot in my mouth because I can’t remember details of other people’s lives,” she said.
Although brain disorders such as Alzheimer’s disease and other forms of dementia are marked by a slow decline, ABI occurs more suddenly and may include a loss of executive function and attention.
“With a brain injury, you’re doing fine, and then some event happens (in this case COVID), and immediately after that, your cognitive function is different,” said Dr. Jackson.
Additionally, ABI is an actual diagnosis, whereas brain fog is not.
“With a brain injury, there’s a treatment pathway for cognitive rehabilitation,” said Dr. Jackson.
Treatments may include speech, cognitive, and occupational therapy as well as meeting with a neuropsychiatrist for treatment of the mental and behavioral disorders that may result. Dr. Jackson said that while many patients aren’t functioning cognitively or physically at 100%, they can make enough strides that they don’t have to give up things such as driving and, in some cases, their jobs.
Other experts agree that long COVID may damage the brain. An April 2022 study published in the journal Nature found strong evidence that SARS-CoV-2 infection may cause brain-related abnormalities, for example, a reduction in gray matter in certain parts of the brain, including the prefrontal cortex, hypothalamus, and amygdala.
Additionally, white matter, which is found deeper in the brain and is responsible for the exchange of information between different parts of the brain, may also be at risk of damage as a result of the virus, according to a November 2022 study published in the journal SN Comprehensive Clinical Medicine.
Calling it a “fog” makes it easier for clinicians and the general public to dismiss its severity, said Tyler Reed Bell, PhD, a researcher who specializes in viruses that cause brain injury. He is a fellow in the department of psychiatry at the University of California, San Diego. Brain fog can make driving and returning to work especially dangerous. Because of difficulty focusing, patients are much more likely to make mistakes that cause accidents.
“The COVID virus is very invasive to the brain,” Dr. Bell said.
Others contend this may be a rush to judgment. Karla L. Thompson, PhD, lead neuropsychologist at the University of North Carolina at Chapel Hill’s COVID Recovery Clinic, agrees that in more serious cases of COVID that cause a lack of oxygen to the brain, it’s reasonable to call it a brain injury. But brain fog can also be associated with other long COVID symptoms, not just damage to the brain.
Chronic fatigue and poor sleep are both commonly reported symptoms of long COVID that negatively affect brain function, she said. Sleep disturbances, cardiac problems, dysautonomia, and emotional distress could also affect the way the brain functions post COVID. Finding the right treatment requires identifying all the factors contributing to cognitive impairment.
Part of the problem in treating long COVID brain fog is that diagnostic technology is not sensitive enough to detect inflammation that could be causing damage.
Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, said her team is working on identifying biomarkers that could detect brain inflammation in a way similar to the manner researchers have identified biomarkers to help diagnose chronic fatigue syndrome. Additionally, a new study published last month in JAMA for the first time clearly defined 12 symptoms of long COVID, and brain fog was listed among them. All of this contributes to the development of clear diagnostic criteria.
“It will make a big difference once we have some consistency among clinicians in diagnosing the condition,” said Dr. McComsey.
Ms. Whitley is thankful for the treatment that she’s received thus far. She’s seeing a cognitive rehabilitation therapist, who assesses her memory, cognition, and attention span and gives her tools to break up simple tasks, such as driving, so that they don’t feel overwhelming. She’s back behind the wheel and back to work.
But perhaps most importantly, Ms. Whitley joined a support group, led by Dr. Jackson, that includes other people experiencing the same symptoms she is. When she was at her darkest, they understood.
“Talking to other survivors has been the only solace in all this,” Ms. Whitley said. “Together, we grieve all that’s been lost.”
A version of this article first appeared on Medscape.com.
Kate Whitley was petrified of COVID-19 from the beginning of the pandemic because she has Hashimoto disease, an autoimmune disorder that she knew put her at high risk for complications.
She was right to be worried. Two months after contracting the infection in September 2022, the 42-year-old Nashville resident was diagnosed with long COVID. For Ms. Whitley, the resulting brain fog has been the most challenging factor. She is the owner of a successful paper goods store, and she can’t remember basic aspects of her job. She can’t tolerate loud noises and gets so distracted that she has trouble remembering what she was doing.
Ms. Whitley doesn’t like the term “brain fog” because it doesn’t begin to describe the dramatic disruption to her life over the past 7 months.
Brain fog is among the most common symptoms of long COVID, and also one of the most poorly understood. A reported 46% of those diagnosed with long COVID complain of brain fog or a loss of memory. Many clinicians agree that the term is vague and often doesn’t truly represent the condition. That, in turn, makes it harder for doctors to diagnose and treat it. There are no standard tests for it, nor are there guidelines for symptom management or treatment.
“There’s a lot of imprecision in the term because it might mean different things to different patients,” said James C. Jackson, PsyD, a neuropsychiatrist at Vanderbilt University, Nashville, Tenn., and author of a new book, “Clearing the Fog: From Surviving to Thriving With Long COVID – A Practical Guide.”
Dr. Jackson, who began treating Ms. Whitley in February 2023, said that it makes more sense to call brain fog a brain impairment or an acquired brain injury (ABI) because it doesn’t occur gradually. COVID damages the brain and causes injury. For those with long COVID who were previously in the intensive care unit and may have undergone ventilation, hypoxic brain injury may result from the lack of oxygen to the brain.
Even among those with milder cases of acute COVID, there’s some evidence that persistent neuroinflammation in the brain caused by an activated immune system may also cause damage.
In both cases, the results can be debilitating. Ms. Whitley also has dysautonomia – a disorder of the autonomic nervous system that can cause dizziness, sweating, and headaches along with fatigue and heart palpitations.
She said that she’s so forgetful that when she sees people socially, she’s nervous of what she’ll say. “I feel like I’m constantly sticking my foot in my mouth because I can’t remember details of other people’s lives,” she said.
Although brain disorders such as Alzheimer’s disease and other forms of dementia are marked by a slow decline, ABI occurs more suddenly and may include a loss of executive function and attention.
“With a brain injury, you’re doing fine, and then some event happens (in this case COVID), and immediately after that, your cognitive function is different,” said Dr. Jackson.
Additionally, ABI is an actual diagnosis, whereas brain fog is not.
“With a brain injury, there’s a treatment pathway for cognitive rehabilitation,” said Dr. Jackson.
Treatments may include speech, cognitive, and occupational therapy as well as meeting with a neuropsychiatrist for treatment of the mental and behavioral disorders that may result. Dr. Jackson said that while many patients aren’t functioning cognitively or physically at 100%, they can make enough strides that they don’t have to give up things such as driving and, in some cases, their jobs.
Other experts agree that long COVID may damage the brain. An April 2022 study published in the journal Nature found strong evidence that SARS-CoV-2 infection may cause brain-related abnormalities, for example, a reduction in gray matter in certain parts of the brain, including the prefrontal cortex, hypothalamus, and amygdala.
Additionally, white matter, which is found deeper in the brain and is responsible for the exchange of information between different parts of the brain, may also be at risk of damage as a result of the virus, according to a November 2022 study published in the journal SN Comprehensive Clinical Medicine.
Calling it a “fog” makes it easier for clinicians and the general public to dismiss its severity, said Tyler Reed Bell, PhD, a researcher who specializes in viruses that cause brain injury. He is a fellow in the department of psychiatry at the University of California, San Diego. Brain fog can make driving and returning to work especially dangerous. Because of difficulty focusing, patients are much more likely to make mistakes that cause accidents.
“The COVID virus is very invasive to the brain,” Dr. Bell said.
Others contend this may be a rush to judgment. Karla L. Thompson, PhD, lead neuropsychologist at the University of North Carolina at Chapel Hill’s COVID Recovery Clinic, agrees that in more serious cases of COVID that cause a lack of oxygen to the brain, it’s reasonable to call it a brain injury. But brain fog can also be associated with other long COVID symptoms, not just damage to the brain.
Chronic fatigue and poor sleep are both commonly reported symptoms of long COVID that negatively affect brain function, she said. Sleep disturbances, cardiac problems, dysautonomia, and emotional distress could also affect the way the brain functions post COVID. Finding the right treatment requires identifying all the factors contributing to cognitive impairment.
Part of the problem in treating long COVID brain fog is that diagnostic technology is not sensitive enough to detect inflammation that could be causing damage.
Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, said her team is working on identifying biomarkers that could detect brain inflammation in a way similar to the manner researchers have identified biomarkers to help diagnose chronic fatigue syndrome. Additionally, a new study published last month in JAMA for the first time clearly defined 12 symptoms of long COVID, and brain fog was listed among them. All of this contributes to the development of clear diagnostic criteria.
“It will make a big difference once we have some consistency among clinicians in diagnosing the condition,” said Dr. McComsey.
Ms. Whitley is thankful for the treatment that she’s received thus far. She’s seeing a cognitive rehabilitation therapist, who assesses her memory, cognition, and attention span and gives her tools to break up simple tasks, such as driving, so that they don’t feel overwhelming. She’s back behind the wheel and back to work.
But perhaps most importantly, Ms. Whitley joined a support group, led by Dr. Jackson, that includes other people experiencing the same symptoms she is. When she was at her darkest, they understood.
“Talking to other survivors has been the only solace in all this,” Ms. Whitley said. “Together, we grieve all that’s been lost.”
A version of this article first appeared on Medscape.com.
Kate Whitley was petrified of COVID-19 from the beginning of the pandemic because she has Hashimoto disease, an autoimmune disorder that she knew put her at high risk for complications.
She was right to be worried. Two months after contracting the infection in September 2022, the 42-year-old Nashville resident was diagnosed with long COVID. For Ms. Whitley, the resulting brain fog has been the most challenging factor. She is the owner of a successful paper goods store, and she can’t remember basic aspects of her job. She can’t tolerate loud noises and gets so distracted that she has trouble remembering what she was doing.
Ms. Whitley doesn’t like the term “brain fog” because it doesn’t begin to describe the dramatic disruption to her life over the past 7 months.
Brain fog is among the most common symptoms of long COVID, and also one of the most poorly understood. A reported 46% of those diagnosed with long COVID complain of brain fog or a loss of memory. Many clinicians agree that the term is vague and often doesn’t truly represent the condition. That, in turn, makes it harder for doctors to diagnose and treat it. There are no standard tests for it, nor are there guidelines for symptom management or treatment.
“There’s a lot of imprecision in the term because it might mean different things to different patients,” said James C. Jackson, PsyD, a neuropsychiatrist at Vanderbilt University, Nashville, Tenn., and author of a new book, “Clearing the Fog: From Surviving to Thriving With Long COVID – A Practical Guide.”
Dr. Jackson, who began treating Ms. Whitley in February 2023, said that it makes more sense to call brain fog a brain impairment or an acquired brain injury (ABI) because it doesn’t occur gradually. COVID damages the brain and causes injury. For those with long COVID who were previously in the intensive care unit and may have undergone ventilation, hypoxic brain injury may result from the lack of oxygen to the brain.
Even among those with milder cases of acute COVID, there’s some evidence that persistent neuroinflammation in the brain caused by an activated immune system may also cause damage.
In both cases, the results can be debilitating. Ms. Whitley also has dysautonomia – a disorder of the autonomic nervous system that can cause dizziness, sweating, and headaches along with fatigue and heart palpitations.
She said that she’s so forgetful that when she sees people socially, she’s nervous of what she’ll say. “I feel like I’m constantly sticking my foot in my mouth because I can’t remember details of other people’s lives,” she said.
Although brain disorders such as Alzheimer’s disease and other forms of dementia are marked by a slow decline, ABI occurs more suddenly and may include a loss of executive function and attention.
“With a brain injury, you’re doing fine, and then some event happens (in this case COVID), and immediately after that, your cognitive function is different,” said Dr. Jackson.
Additionally, ABI is an actual diagnosis, whereas brain fog is not.
“With a brain injury, there’s a treatment pathway for cognitive rehabilitation,” said Dr. Jackson.
Treatments may include speech, cognitive, and occupational therapy as well as meeting with a neuropsychiatrist for treatment of the mental and behavioral disorders that may result. Dr. Jackson said that while many patients aren’t functioning cognitively or physically at 100%, they can make enough strides that they don’t have to give up things such as driving and, in some cases, their jobs.
Other experts agree that long COVID may damage the brain. An April 2022 study published in the journal Nature found strong evidence that SARS-CoV-2 infection may cause brain-related abnormalities, for example, a reduction in gray matter in certain parts of the brain, including the prefrontal cortex, hypothalamus, and amygdala.
Additionally, white matter, which is found deeper in the brain and is responsible for the exchange of information between different parts of the brain, may also be at risk of damage as a result of the virus, according to a November 2022 study published in the journal SN Comprehensive Clinical Medicine.
Calling it a “fog” makes it easier for clinicians and the general public to dismiss its severity, said Tyler Reed Bell, PhD, a researcher who specializes in viruses that cause brain injury. He is a fellow in the department of psychiatry at the University of California, San Diego. Brain fog can make driving and returning to work especially dangerous. Because of difficulty focusing, patients are much more likely to make mistakes that cause accidents.
“The COVID virus is very invasive to the brain,” Dr. Bell said.
Others contend this may be a rush to judgment. Karla L. Thompson, PhD, lead neuropsychologist at the University of North Carolina at Chapel Hill’s COVID Recovery Clinic, agrees that in more serious cases of COVID that cause a lack of oxygen to the brain, it’s reasonable to call it a brain injury. But brain fog can also be associated with other long COVID symptoms, not just damage to the brain.
Chronic fatigue and poor sleep are both commonly reported symptoms of long COVID that negatively affect brain function, she said. Sleep disturbances, cardiac problems, dysautonomia, and emotional distress could also affect the way the brain functions post COVID. Finding the right treatment requires identifying all the factors contributing to cognitive impairment.
Part of the problem in treating long COVID brain fog is that diagnostic technology is not sensitive enough to detect inflammation that could be causing damage.
Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, said her team is working on identifying biomarkers that could detect brain inflammation in a way similar to the manner researchers have identified biomarkers to help diagnose chronic fatigue syndrome. Additionally, a new study published last month in JAMA for the first time clearly defined 12 symptoms of long COVID, and brain fog was listed among them. All of this contributes to the development of clear diagnostic criteria.
“It will make a big difference once we have some consistency among clinicians in diagnosing the condition,” said Dr. McComsey.
Ms. Whitley is thankful for the treatment that she’s received thus far. She’s seeing a cognitive rehabilitation therapist, who assesses her memory, cognition, and attention span and gives her tools to break up simple tasks, such as driving, so that they don’t feel overwhelming. She’s back behind the wheel and back to work.
But perhaps most importantly, Ms. Whitley joined a support group, led by Dr. Jackson, that includes other people experiencing the same symptoms she is. When she was at her darkest, they understood.
“Talking to other survivors has been the only solace in all this,” Ms. Whitley said. “Together, we grieve all that’s been lost.”
A version of this article first appeared on Medscape.com.
Postacute effects of COVID on par with those of sepsis, flu
A large observational study examined population-wide data for 13 postacute conditions in patients who had been hospitalized with a COVID-19 infection and found that all but one of these conditions, venous thromboembolism, occurred at comparable rates in those hospitalized for sepsis and influenza.
“For us, the main takeaway was that patients hospitalized for severe illness in general really require ongoing treatment and support after they’re discharged. That type of care is often very challenging to coordinate for people in a sometimes siloed and fragmented health care system,” study author Kieran Quinn, MD, PhD, a clinician at Sinai Health in Toronto, and assistant professor at the University of Toronto, said in an interview.
The study was published in JAMA Internal Medicine.
Postacute effects
The investigators compared clinical and health administrative data from 26,499 Ontarians hospitalized with COVID-19 with data from three additional cohorts who had been hospitalized with influenza (17,516 patients) and sepsis. The sepsis cohort was divided into two groups, those hospitalized during the COVID-19 pandemic (52,878 patients) and a historical control population (282,473 patients).
These comparators allowed the researchers to compare COVID-19 with other severe infectious illnesses and control for any changes in health care delivery that may have occurred during the pandemic. The addition of sepsis cohorts was needed for the latter purpose, since influenza rates dropped significantly after the onset of the pandemic.
The study outcomes (including cardiovascular, neurological, and mental health conditions and rheumatoid arthritis) were selected based on previous associations with COVID-19 infections, as well as their availability in the data, according to Dr. Quinn. The investigators used diagnostic codes recorded in Ontario’s Institute for Clinical Evaluative Sciences database. The investigators observed some of the studied conditions in their own patients. “Many of us on the research team are practicing clinicians who care for people living with long COVID,” said Dr. Quinn.
Compared with cohorts with other serious infections, those hospitalized with COVID-19 were not at increased risk for selected cardiovascular or neurological disorders, rheumatoid arthritis, or mental health conditions within 1 year following hospitalization. Incident venous thromboembolic disease, however, was more common after hospitalization for COVID-19 than after hospitalization for influenza (adjusted hazard ratio, 1.77).
The study results corroborate previous findings that influenza and sepsis can have serious long-term health effects, such as heart failure, dementia, and depression, and found that the same was true for COVID-19 infections. For all three infections, patients at high risk require additional support after their initial discharge.
Defining long COVID
Although there was no increased risk with COVID-19 for most conditions, these results do not mean that the postacute effects of the infection, often called “long COVID,” are not significant, Dr. Quinn emphasized. The researcher believes that it’s important to listen to the many patients reporting symptoms and validate their experiences.
There needs to be greater consensus among the global health community on what constitutes long COVID. While the research led by Dr. Quinn focuses on postacute health conditions, some definitions of long COVID, such as that of the World Health Organization, refer only to ongoing symptoms of the original infection.
While there is now a diagnostic code for treating long COVID in Ontario, the data available to the researchers did not include information on some common symptoms of post-COVID condition, like chronic fatigue. In the data used, there was not an accurate way to identify patients who had developed conditions like myalgic encephalomyelitis/chronic fatigue syndrome and postural orthostatic tachycardia syndrome, said Dr. Quinn.
In addition to creating clear definitions and determining the best treatments, prevention is essential, said Dr. Quinn. Prior studies have shown that vaccination helps prevent ICU admission for COVID-19.
‘Important questions remain’
Commenting on the finding, Aravind Ganesh, MD, DPhil, a neurologist at the University of Calgary (Alta.), said that by including control populations, the study addressed an important limitation of previous research. Dr. Ganesh, who was not involved in the study, said that the controls help to determine the cause of associations found in other studies, including his own research on long-term symptoms following outpatient care for COVID-19.
“I think what this tells us is that maybe a lot of the issues that we’ve been seeing as complications attributable to COVID are, in fact, complications attributable to serious illness,” said Dr. Ganesh. He also found the association with venous thromboembolism interesting because the condition is recognized as a key risk factor for COVID-19 outcomes.
Compared with smaller randomized control trials, the population-level data provided a much larger sample size for the study. However, this design comes with limitations as well, Dr. Ganesh noted. The study relies on the administrative data of diagnostic codes and misses symptoms that aren’t associated with a diagnosis. In addition, because the cohorts were not assigned randomly, it may not account for preexisting risk factors.
While the study demonstrates associations with physical and mental health conditions, the cause of postacute effects from COVID-19, influenza, and sepsis is still unclear. “Important questions remain,” said Dr. Ganesh. “Why is it that these patients are experiencing these symptoms?”
The study was supported by ICES and the Canadian Institutes of Health Research. Dr. Quinn reported part-time employment at Public Health Ontario and stock in Pfizer and BioNTech. Dr. Ganesh reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A large observational study examined population-wide data for 13 postacute conditions in patients who had been hospitalized with a COVID-19 infection and found that all but one of these conditions, venous thromboembolism, occurred at comparable rates in those hospitalized for sepsis and influenza.
“For us, the main takeaway was that patients hospitalized for severe illness in general really require ongoing treatment and support after they’re discharged. That type of care is often very challenging to coordinate for people in a sometimes siloed and fragmented health care system,” study author Kieran Quinn, MD, PhD, a clinician at Sinai Health in Toronto, and assistant professor at the University of Toronto, said in an interview.
The study was published in JAMA Internal Medicine.
Postacute effects
The investigators compared clinical and health administrative data from 26,499 Ontarians hospitalized with COVID-19 with data from three additional cohorts who had been hospitalized with influenza (17,516 patients) and sepsis. The sepsis cohort was divided into two groups, those hospitalized during the COVID-19 pandemic (52,878 patients) and a historical control population (282,473 patients).
These comparators allowed the researchers to compare COVID-19 with other severe infectious illnesses and control for any changes in health care delivery that may have occurred during the pandemic. The addition of sepsis cohorts was needed for the latter purpose, since influenza rates dropped significantly after the onset of the pandemic.
The study outcomes (including cardiovascular, neurological, and mental health conditions and rheumatoid arthritis) were selected based on previous associations with COVID-19 infections, as well as their availability in the data, according to Dr. Quinn. The investigators used diagnostic codes recorded in Ontario’s Institute for Clinical Evaluative Sciences database. The investigators observed some of the studied conditions in their own patients. “Many of us on the research team are practicing clinicians who care for people living with long COVID,” said Dr. Quinn.
Compared with cohorts with other serious infections, those hospitalized with COVID-19 were not at increased risk for selected cardiovascular or neurological disorders, rheumatoid arthritis, or mental health conditions within 1 year following hospitalization. Incident venous thromboembolic disease, however, was more common after hospitalization for COVID-19 than after hospitalization for influenza (adjusted hazard ratio, 1.77).
The study results corroborate previous findings that influenza and sepsis can have serious long-term health effects, such as heart failure, dementia, and depression, and found that the same was true for COVID-19 infections. For all three infections, patients at high risk require additional support after their initial discharge.
Defining long COVID
Although there was no increased risk with COVID-19 for most conditions, these results do not mean that the postacute effects of the infection, often called “long COVID,” are not significant, Dr. Quinn emphasized. The researcher believes that it’s important to listen to the many patients reporting symptoms and validate their experiences.
There needs to be greater consensus among the global health community on what constitutes long COVID. While the research led by Dr. Quinn focuses on postacute health conditions, some definitions of long COVID, such as that of the World Health Organization, refer only to ongoing symptoms of the original infection.
While there is now a diagnostic code for treating long COVID in Ontario, the data available to the researchers did not include information on some common symptoms of post-COVID condition, like chronic fatigue. In the data used, there was not an accurate way to identify patients who had developed conditions like myalgic encephalomyelitis/chronic fatigue syndrome and postural orthostatic tachycardia syndrome, said Dr. Quinn.
In addition to creating clear definitions and determining the best treatments, prevention is essential, said Dr. Quinn. Prior studies have shown that vaccination helps prevent ICU admission for COVID-19.
‘Important questions remain’
Commenting on the finding, Aravind Ganesh, MD, DPhil, a neurologist at the University of Calgary (Alta.), said that by including control populations, the study addressed an important limitation of previous research. Dr. Ganesh, who was not involved in the study, said that the controls help to determine the cause of associations found in other studies, including his own research on long-term symptoms following outpatient care for COVID-19.
“I think what this tells us is that maybe a lot of the issues that we’ve been seeing as complications attributable to COVID are, in fact, complications attributable to serious illness,” said Dr. Ganesh. He also found the association with venous thromboembolism interesting because the condition is recognized as a key risk factor for COVID-19 outcomes.
Compared with smaller randomized control trials, the population-level data provided a much larger sample size for the study. However, this design comes with limitations as well, Dr. Ganesh noted. The study relies on the administrative data of diagnostic codes and misses symptoms that aren’t associated with a diagnosis. In addition, because the cohorts were not assigned randomly, it may not account for preexisting risk factors.
While the study demonstrates associations with physical and mental health conditions, the cause of postacute effects from COVID-19, influenza, and sepsis is still unclear. “Important questions remain,” said Dr. Ganesh. “Why is it that these patients are experiencing these symptoms?”
The study was supported by ICES and the Canadian Institutes of Health Research. Dr. Quinn reported part-time employment at Public Health Ontario and stock in Pfizer and BioNTech. Dr. Ganesh reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A large observational study examined population-wide data for 13 postacute conditions in patients who had been hospitalized with a COVID-19 infection and found that all but one of these conditions, venous thromboembolism, occurred at comparable rates in those hospitalized for sepsis and influenza.
“For us, the main takeaway was that patients hospitalized for severe illness in general really require ongoing treatment and support after they’re discharged. That type of care is often very challenging to coordinate for people in a sometimes siloed and fragmented health care system,” study author Kieran Quinn, MD, PhD, a clinician at Sinai Health in Toronto, and assistant professor at the University of Toronto, said in an interview.
The study was published in JAMA Internal Medicine.
Postacute effects
The investigators compared clinical and health administrative data from 26,499 Ontarians hospitalized with COVID-19 with data from three additional cohorts who had been hospitalized with influenza (17,516 patients) and sepsis. The sepsis cohort was divided into two groups, those hospitalized during the COVID-19 pandemic (52,878 patients) and a historical control population (282,473 patients).
These comparators allowed the researchers to compare COVID-19 with other severe infectious illnesses and control for any changes in health care delivery that may have occurred during the pandemic. The addition of sepsis cohorts was needed for the latter purpose, since influenza rates dropped significantly after the onset of the pandemic.
The study outcomes (including cardiovascular, neurological, and mental health conditions and rheumatoid arthritis) were selected based on previous associations with COVID-19 infections, as well as their availability in the data, according to Dr. Quinn. The investigators used diagnostic codes recorded in Ontario’s Institute for Clinical Evaluative Sciences database. The investigators observed some of the studied conditions in their own patients. “Many of us on the research team are practicing clinicians who care for people living with long COVID,” said Dr. Quinn.
Compared with cohorts with other serious infections, those hospitalized with COVID-19 were not at increased risk for selected cardiovascular or neurological disorders, rheumatoid arthritis, or mental health conditions within 1 year following hospitalization. Incident venous thromboembolic disease, however, was more common after hospitalization for COVID-19 than after hospitalization for influenza (adjusted hazard ratio, 1.77).
The study results corroborate previous findings that influenza and sepsis can have serious long-term health effects, such as heart failure, dementia, and depression, and found that the same was true for COVID-19 infections. For all three infections, patients at high risk require additional support after their initial discharge.
Defining long COVID
Although there was no increased risk with COVID-19 for most conditions, these results do not mean that the postacute effects of the infection, often called “long COVID,” are not significant, Dr. Quinn emphasized. The researcher believes that it’s important to listen to the many patients reporting symptoms and validate their experiences.
There needs to be greater consensus among the global health community on what constitutes long COVID. While the research led by Dr. Quinn focuses on postacute health conditions, some definitions of long COVID, such as that of the World Health Organization, refer only to ongoing symptoms of the original infection.
While there is now a diagnostic code for treating long COVID in Ontario, the data available to the researchers did not include information on some common symptoms of post-COVID condition, like chronic fatigue. In the data used, there was not an accurate way to identify patients who had developed conditions like myalgic encephalomyelitis/chronic fatigue syndrome and postural orthostatic tachycardia syndrome, said Dr. Quinn.
In addition to creating clear definitions and determining the best treatments, prevention is essential, said Dr. Quinn. Prior studies have shown that vaccination helps prevent ICU admission for COVID-19.
‘Important questions remain’
Commenting on the finding, Aravind Ganesh, MD, DPhil, a neurologist at the University of Calgary (Alta.), said that by including control populations, the study addressed an important limitation of previous research. Dr. Ganesh, who was not involved in the study, said that the controls help to determine the cause of associations found in other studies, including his own research on long-term symptoms following outpatient care for COVID-19.
“I think what this tells us is that maybe a lot of the issues that we’ve been seeing as complications attributable to COVID are, in fact, complications attributable to serious illness,” said Dr. Ganesh. He also found the association with venous thromboembolism interesting because the condition is recognized as a key risk factor for COVID-19 outcomes.
Compared with smaller randomized control trials, the population-level data provided a much larger sample size for the study. However, this design comes with limitations as well, Dr. Ganesh noted. The study relies on the administrative data of diagnostic codes and misses symptoms that aren’t associated with a diagnosis. In addition, because the cohorts were not assigned randomly, it may not account for preexisting risk factors.
While the study demonstrates associations with physical and mental health conditions, the cause of postacute effects from COVID-19, influenza, and sepsis is still unclear. “Important questions remain,” said Dr. Ganesh. “Why is it that these patients are experiencing these symptoms?”
The study was supported by ICES and the Canadian Institutes of Health Research. Dr. Quinn reported part-time employment at Public Health Ontario and stock in Pfizer and BioNTech. Dr. Ganesh reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA INTERNAL MEDICINE
Diabetes may short circuit pembrolizumab benefits in NSCLC
TOPLINE:
METHODOLOGY:
- Investigators reviewed the medical records of 203 consecutive patients with metastatic NSCLC who received first-line pembrolizumab either alone or in combination with chemotherapy at a single tertiary center in Israel.
- Overall, 1 in 4 patients (n = 51) had diabetes mellitus; most (n = 42) were being treated with oral hypoglycemic agents, frequently metformin, and 7 were taking insulin.
- Rates of tumors with PD‐L1 expression above 50% were not significantly different among patients with diabetes and those without.
TAKEAWAY:
- Overall, among patients with diabetes, median progression-free survival (PFS) was significantly shorter than among patients without diabetes (5.9 vs. 7.1 months), as was overall survival (12 vs. 21 months).
- Shorter overall survival was more pronounced among those with diabetes who received pembrolizumab alone (12 vs. 27 months) in comparison with patients who received pembrolizumab plus chemotherapy (14.3 vs. 19.4 months).
- After adjusting for potential confounders, multivariate analysis confirmed that diabetes was an independent risk factor for shorter PFS (hazard ratio, 1.67) and shorter overall survival (HR, 1.73) for patients with NSCLC.
- In a validation cohort of 452 patients with metastatic NSCLC, only 19.6% of those with diabetes continued to take pembrolizumab at 12 months versus 31.7% of those without diabetes.
IN PRACTICE:
“As NSCLC patients with [diabetes] constitute a significant subgroup, there is an urgent need to validate our findings and explore whether outcomes in these patients can be improved by better glycemic control,” the authors said, adding that “chemotherapy may offset some of the deleterious effects” of diabetes.
SOURCE:
The study was led by Yasmin Leshem, MD, PhD, of the Tel Aviv Sourasky Medical Center, and was published in Cancer.
LIMITATIONS:
- Without access to blood test results outside the hospital, the researchers could not determine whether better glycemic control might have improved outcomes.
- The incidence of type 1 or 2 diabetes was not well documented.
DISCLOSURES:
- No funding source was reported.
- Two investigators reported receiving consulting and/or other fees from Bristol-Myers Squibb, Roche, Merck, Novartis, and Merck Sharp and Dohme.
A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Investigators reviewed the medical records of 203 consecutive patients with metastatic NSCLC who received first-line pembrolizumab either alone or in combination with chemotherapy at a single tertiary center in Israel.
- Overall, 1 in 4 patients (n = 51) had diabetes mellitus; most (n = 42) were being treated with oral hypoglycemic agents, frequently metformin, and 7 were taking insulin.
- Rates of tumors with PD‐L1 expression above 50% were not significantly different among patients with diabetes and those without.
TAKEAWAY:
- Overall, among patients with diabetes, median progression-free survival (PFS) was significantly shorter than among patients without diabetes (5.9 vs. 7.1 months), as was overall survival (12 vs. 21 months).
- Shorter overall survival was more pronounced among those with diabetes who received pembrolizumab alone (12 vs. 27 months) in comparison with patients who received pembrolizumab plus chemotherapy (14.3 vs. 19.4 months).
- After adjusting for potential confounders, multivariate analysis confirmed that diabetes was an independent risk factor for shorter PFS (hazard ratio, 1.67) and shorter overall survival (HR, 1.73) for patients with NSCLC.
- In a validation cohort of 452 patients with metastatic NSCLC, only 19.6% of those with diabetes continued to take pembrolizumab at 12 months versus 31.7% of those without diabetes.
IN PRACTICE:
“As NSCLC patients with [diabetes] constitute a significant subgroup, there is an urgent need to validate our findings and explore whether outcomes in these patients can be improved by better glycemic control,” the authors said, adding that “chemotherapy may offset some of the deleterious effects” of diabetes.
SOURCE:
The study was led by Yasmin Leshem, MD, PhD, of the Tel Aviv Sourasky Medical Center, and was published in Cancer.
LIMITATIONS:
- Without access to blood test results outside the hospital, the researchers could not determine whether better glycemic control might have improved outcomes.
- The incidence of type 1 or 2 diabetes was not well documented.
DISCLOSURES:
- No funding source was reported.
- Two investigators reported receiving consulting and/or other fees from Bristol-Myers Squibb, Roche, Merck, Novartis, and Merck Sharp and Dohme.
A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Investigators reviewed the medical records of 203 consecutive patients with metastatic NSCLC who received first-line pembrolizumab either alone or in combination with chemotherapy at a single tertiary center in Israel.
- Overall, 1 in 4 patients (n = 51) had diabetes mellitus; most (n = 42) were being treated with oral hypoglycemic agents, frequently metformin, and 7 were taking insulin.
- Rates of tumors with PD‐L1 expression above 50% were not significantly different among patients with diabetes and those without.
TAKEAWAY:
- Overall, among patients with diabetes, median progression-free survival (PFS) was significantly shorter than among patients without diabetes (5.9 vs. 7.1 months), as was overall survival (12 vs. 21 months).
- Shorter overall survival was more pronounced among those with diabetes who received pembrolizumab alone (12 vs. 27 months) in comparison with patients who received pembrolizumab plus chemotherapy (14.3 vs. 19.4 months).
- After adjusting for potential confounders, multivariate analysis confirmed that diabetes was an independent risk factor for shorter PFS (hazard ratio, 1.67) and shorter overall survival (HR, 1.73) for patients with NSCLC.
- In a validation cohort of 452 patients with metastatic NSCLC, only 19.6% of those with diabetes continued to take pembrolizumab at 12 months versus 31.7% of those without diabetes.
IN PRACTICE:
“As NSCLC patients with [diabetes] constitute a significant subgroup, there is an urgent need to validate our findings and explore whether outcomes in these patients can be improved by better glycemic control,” the authors said, adding that “chemotherapy may offset some of the deleterious effects” of diabetes.
SOURCE:
The study was led by Yasmin Leshem, MD, PhD, of the Tel Aviv Sourasky Medical Center, and was published in Cancer.
LIMITATIONS:
- Without access to blood test results outside the hospital, the researchers could not determine whether better glycemic control might have improved outcomes.
- The incidence of type 1 or 2 diabetes was not well documented.
DISCLOSURES:
- No funding source was reported.
- Two investigators reported receiving consulting and/or other fees from Bristol-Myers Squibb, Roche, Merck, Novartis, and Merck Sharp and Dohme.
A version of this article first appeared on Medscape.com.
Cannabis for cancer symptoms: Perceived or real benefit?
TOPLINE:
METHODOLOGY:
- Participants included 267 adults (mean age, 58 years; 70% women; 88% White) undergoing treatment for cancer, most commonly breast (47%) and ovarian (29%).
- Participants completed online surveys to characterize cannabis use, reasons for using it, perceived benefits and harms, and physical/psychological symptoms.
- Participants who had used cannabis for more than 1 day during the previous 30 days were compared with those who had not.
TAKEAWAY:
- Overall, 26% of respondents reported cannabis use in the past 30 days, most often edibles (65%) or smoked cannabis (51%).
- Cannabis users were more likely to be younger, male, Black, to have lower income, worse physical/psychological symptoms, and to be disabled or unable to work in comparison with nonusers.
- Cannabis was used to treat pain, cancer, sleep problems, anxiety, nausea, and poor appetite; perceived benefits were greatest with respect to sleep, nausea, pain, muscle spasms, and anxiety.
- Despite perceived benefits, cannabis users reported worse overall distress, anxiety, sleep disturbances, appetite, nausea, fatigue, and pain.
IN PRACTICE:
“The study findings indicate that patients with cancer perceived benefits to using cannabis for many symptoms” but also revealed that “those who used cannabis in the past 30 days had significantly worse symptom profiles overall than those who did not use cannabis,” the authors wrote.
SOURCE:
The study, led by Desiree R. Azizoddin, PsyD, University of Oklahoma Health Science Center, Oklahoma City, was published online in Cancer.
LIMITATIONS:
It’s not known whether adults who used cannabis had significantly worse symptoms at the outset, which may have prompted cannabis use, or whether cannabis use may have exacerbated their symptoms.
DISCLOSURES:
Funding for the study was provided by grants from the National Cancer Institute and the Oklahoma Tobacco Settlement Endowment Trust. Nine of the 10 authors have disclosed no relevant conflicts of interest. One author has relationships with various pharmaceutical companies involved in oncology.
A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Participants included 267 adults (mean age, 58 years; 70% women; 88% White) undergoing treatment for cancer, most commonly breast (47%) and ovarian (29%).
- Participants completed online surveys to characterize cannabis use, reasons for using it, perceived benefits and harms, and physical/psychological symptoms.
- Participants who had used cannabis for more than 1 day during the previous 30 days were compared with those who had not.
TAKEAWAY:
- Overall, 26% of respondents reported cannabis use in the past 30 days, most often edibles (65%) or smoked cannabis (51%).
- Cannabis users were more likely to be younger, male, Black, to have lower income, worse physical/psychological symptoms, and to be disabled or unable to work in comparison with nonusers.
- Cannabis was used to treat pain, cancer, sleep problems, anxiety, nausea, and poor appetite; perceived benefits were greatest with respect to sleep, nausea, pain, muscle spasms, and anxiety.
- Despite perceived benefits, cannabis users reported worse overall distress, anxiety, sleep disturbances, appetite, nausea, fatigue, and pain.
IN PRACTICE:
“The study findings indicate that patients with cancer perceived benefits to using cannabis for many symptoms” but also revealed that “those who used cannabis in the past 30 days had significantly worse symptom profiles overall than those who did not use cannabis,” the authors wrote.
SOURCE:
The study, led by Desiree R. Azizoddin, PsyD, University of Oklahoma Health Science Center, Oklahoma City, was published online in Cancer.
LIMITATIONS:
It’s not known whether adults who used cannabis had significantly worse symptoms at the outset, which may have prompted cannabis use, or whether cannabis use may have exacerbated their symptoms.
DISCLOSURES:
Funding for the study was provided by grants from the National Cancer Institute and the Oklahoma Tobacco Settlement Endowment Trust. Nine of the 10 authors have disclosed no relevant conflicts of interest. One author has relationships with various pharmaceutical companies involved in oncology.
A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Participants included 267 adults (mean age, 58 years; 70% women; 88% White) undergoing treatment for cancer, most commonly breast (47%) and ovarian (29%).
- Participants completed online surveys to characterize cannabis use, reasons for using it, perceived benefits and harms, and physical/psychological symptoms.
- Participants who had used cannabis for more than 1 day during the previous 30 days were compared with those who had not.
TAKEAWAY:
- Overall, 26% of respondents reported cannabis use in the past 30 days, most often edibles (65%) or smoked cannabis (51%).
- Cannabis users were more likely to be younger, male, Black, to have lower income, worse physical/psychological symptoms, and to be disabled or unable to work in comparison with nonusers.
- Cannabis was used to treat pain, cancer, sleep problems, anxiety, nausea, and poor appetite; perceived benefits were greatest with respect to sleep, nausea, pain, muscle spasms, and anxiety.
- Despite perceived benefits, cannabis users reported worse overall distress, anxiety, sleep disturbances, appetite, nausea, fatigue, and pain.
IN PRACTICE:
“The study findings indicate that patients with cancer perceived benefits to using cannabis for many symptoms” but also revealed that “those who used cannabis in the past 30 days had significantly worse symptom profiles overall than those who did not use cannabis,” the authors wrote.
SOURCE:
The study, led by Desiree R. Azizoddin, PsyD, University of Oklahoma Health Science Center, Oklahoma City, was published online in Cancer.
LIMITATIONS:
It’s not known whether adults who used cannabis had significantly worse symptoms at the outset, which may have prompted cannabis use, or whether cannabis use may have exacerbated their symptoms.
DISCLOSURES:
Funding for the study was provided by grants from the National Cancer Institute and the Oklahoma Tobacco Settlement Endowment Trust. Nine of the 10 authors have disclosed no relevant conflicts of interest. One author has relationships with various pharmaceutical companies involved in oncology.
A version of this article first appeared on Medscape.com.