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Half of U.S. adults exposed to harmful lead levels as children: Study
published in the Proceedings of the National Academy of Sciences.
In addition, the researchers found, 90% of children born in the United States between 1951 and 1980 had blood-lead levels higher than the Centers for Disease Control and Prevention threshold. On average, early childhood exposure to lead resulted in a 2.6-point drop in IQ per person.
“Most of what we think of as the Lost Generation and the Greatest Generation and Baby Boomers had a moderate amount of lead exposure,” Matt Hauer, PhD, one of the coauthors and an assistant professor of sociology at Florida State University, Tallahassee, said in a statement.
“Generation X was exposed to very high amounts of lead, and now Millennials and the generation following them have been exposed to very low amounts of lead,” he said.
The findings were “infuriating” because scientists have long known that lead exposure is harmful, Michael McFarland, PhD, coauthor and an associate professor of sociology at Florida State University, Tallahassee, told The Associated Press.
The research team analyzed blood-lead levels, census data, and the use of leaded gasoline to understand how widespread early childhood lead exposure was in the United States between 1940 and 2015. They looked mostly at exposure caused by leaded gasoline, which was the dominant form of exposure between the 1940s and 1980s.
They estimated that half of the U.S. adult population in 2015 had been exposed to lead levels that surpassed 5 micrograms per deciliter, which was the CDC threshold at the time. More than 54 million had been exposed to levels above 15 micrograms per deciliter, and 4.5 million were exposed to 30 micrograms per deciliter – or six times the threshold.
They found that estimated lead-linked deficits were greatest for the 21 million people born between 1966 and 1970, who had an average 5.9-point drop in IQ per person.
The United States has put in place tougher regulations to protect Americans from lead poisoning in recent decades, particularly from gasoline. The study team found that blood-lead levels were considerably lower than 5 micrograms per deciliter among those born since 2001.
At the same time, the public health effects of childhood exposure for older generations will last for years to come.
“Childhood lead exposure is not just here and now. It’s going to impact your lifelong health,” Abheet Solomon, a senior program manager at the United Nations Children’s Fund, told the AP.
Childhood lead exposure is known to affect the development of mental skills, and it raises the risk of hypertension, kidney damage, and heart disease. It has been linked to harm in pregnant women and developing children.
“The more tragic part is that we keep making the same … mistakes again,” Bruce Lanphear, MD, a health sciences professor at Simon Fraser University in Vancouver, B.C., told the AP.
Dr. Lanphear’s research on lead exposure has found loss of mental skills and IQ as well.
“First it was lead, then it was air pollution. Now it’s PFAS chemicals and phthalates (chemicals used to make plastics more durable),” he said. “And we can’t stop long enough to ask ourselves should we be regulating chemicals differently.”
A version of this article first appeared on WebMD.com.
published in the Proceedings of the National Academy of Sciences.
In addition, the researchers found, 90% of children born in the United States between 1951 and 1980 had blood-lead levels higher than the Centers for Disease Control and Prevention threshold. On average, early childhood exposure to lead resulted in a 2.6-point drop in IQ per person.
“Most of what we think of as the Lost Generation and the Greatest Generation and Baby Boomers had a moderate amount of lead exposure,” Matt Hauer, PhD, one of the coauthors and an assistant professor of sociology at Florida State University, Tallahassee, said in a statement.
“Generation X was exposed to very high amounts of lead, and now Millennials and the generation following them have been exposed to very low amounts of lead,” he said.
The findings were “infuriating” because scientists have long known that lead exposure is harmful, Michael McFarland, PhD, coauthor and an associate professor of sociology at Florida State University, Tallahassee, told The Associated Press.
The research team analyzed blood-lead levels, census data, and the use of leaded gasoline to understand how widespread early childhood lead exposure was in the United States between 1940 and 2015. They looked mostly at exposure caused by leaded gasoline, which was the dominant form of exposure between the 1940s and 1980s.
They estimated that half of the U.S. adult population in 2015 had been exposed to lead levels that surpassed 5 micrograms per deciliter, which was the CDC threshold at the time. More than 54 million had been exposed to levels above 15 micrograms per deciliter, and 4.5 million were exposed to 30 micrograms per deciliter – or six times the threshold.
They found that estimated lead-linked deficits were greatest for the 21 million people born between 1966 and 1970, who had an average 5.9-point drop in IQ per person.
The United States has put in place tougher regulations to protect Americans from lead poisoning in recent decades, particularly from gasoline. The study team found that blood-lead levels were considerably lower than 5 micrograms per deciliter among those born since 2001.
At the same time, the public health effects of childhood exposure for older generations will last for years to come.
“Childhood lead exposure is not just here and now. It’s going to impact your lifelong health,” Abheet Solomon, a senior program manager at the United Nations Children’s Fund, told the AP.
Childhood lead exposure is known to affect the development of mental skills, and it raises the risk of hypertension, kidney damage, and heart disease. It has been linked to harm in pregnant women and developing children.
“The more tragic part is that we keep making the same … mistakes again,” Bruce Lanphear, MD, a health sciences professor at Simon Fraser University in Vancouver, B.C., told the AP.
Dr. Lanphear’s research on lead exposure has found loss of mental skills and IQ as well.
“First it was lead, then it was air pollution. Now it’s PFAS chemicals and phthalates (chemicals used to make plastics more durable),” he said. “And we can’t stop long enough to ask ourselves should we be regulating chemicals differently.”
A version of this article first appeared on WebMD.com.
published in the Proceedings of the National Academy of Sciences.
In addition, the researchers found, 90% of children born in the United States between 1951 and 1980 had blood-lead levels higher than the Centers for Disease Control and Prevention threshold. On average, early childhood exposure to lead resulted in a 2.6-point drop in IQ per person.
“Most of what we think of as the Lost Generation and the Greatest Generation and Baby Boomers had a moderate amount of lead exposure,” Matt Hauer, PhD, one of the coauthors and an assistant professor of sociology at Florida State University, Tallahassee, said in a statement.
“Generation X was exposed to very high amounts of lead, and now Millennials and the generation following them have been exposed to very low amounts of lead,” he said.
The findings were “infuriating” because scientists have long known that lead exposure is harmful, Michael McFarland, PhD, coauthor and an associate professor of sociology at Florida State University, Tallahassee, told The Associated Press.
The research team analyzed blood-lead levels, census data, and the use of leaded gasoline to understand how widespread early childhood lead exposure was in the United States between 1940 and 2015. They looked mostly at exposure caused by leaded gasoline, which was the dominant form of exposure between the 1940s and 1980s.
They estimated that half of the U.S. adult population in 2015 had been exposed to lead levels that surpassed 5 micrograms per deciliter, which was the CDC threshold at the time. More than 54 million had been exposed to levels above 15 micrograms per deciliter, and 4.5 million were exposed to 30 micrograms per deciliter – or six times the threshold.
They found that estimated lead-linked deficits were greatest for the 21 million people born between 1966 and 1970, who had an average 5.9-point drop in IQ per person.
The United States has put in place tougher regulations to protect Americans from lead poisoning in recent decades, particularly from gasoline. The study team found that blood-lead levels were considerably lower than 5 micrograms per deciliter among those born since 2001.
At the same time, the public health effects of childhood exposure for older generations will last for years to come.
“Childhood lead exposure is not just here and now. It’s going to impact your lifelong health,” Abheet Solomon, a senior program manager at the United Nations Children’s Fund, told the AP.
Childhood lead exposure is known to affect the development of mental skills, and it raises the risk of hypertension, kidney damage, and heart disease. It has been linked to harm in pregnant women and developing children.
“The more tragic part is that we keep making the same … mistakes again,” Bruce Lanphear, MD, a health sciences professor at Simon Fraser University in Vancouver, B.C., told the AP.
Dr. Lanphear’s research on lead exposure has found loss of mental skills and IQ as well.
“First it was lead, then it was air pollution. Now it’s PFAS chemicals and phthalates (chemicals used to make plastics more durable),” he said. “And we can’t stop long enough to ask ourselves should we be regulating chemicals differently.”
A version of this article first appeared on WebMD.com.
Raise a glass to speed up the brain’s aging process
Drink a day could age your brain
There are many things we can do daily to improve our health: Exercise, read a book, eat an apple (supposedly). Not drink a glass of red wine. Wait, not drink? That’s right. We were told that a glass of red wine each night was doing something good for our hearts, but it’s doing something bad to our brains: Aging them prematurely.
According to a recent study in Nature Communications, drinking half a pint of beer a day could age the brain of a 50-year-old by 6 months. A pint of beer equaled 2 years of aging and a pint and a half aged participants’ brains by 3.5 years.
Compared with people who didn’t drink, those who averaged about two pints of beer or two glasses of wine daily had brains aged 10 years older!
The researchers’ analysis included MRI scans of about 37,000 middle-aged men in the United Kingdom, along with their medical information and drinking habits, Everyday Health reported. They determined volume reductions in two parts of the brain potentially impacted by daily consumption of alcohol: White matter, which controls the senses and communication, and gray matter, which controls cognitive functions such as movement, emotions, and memories.
Normal brain aging is bad enough: Stuff like forgetting why we walked into the kitchen or having a word we want to use on the tips of our tongues. Who knew that happy hour could be speeding up the process?
Bartender, make that mimosa a virgin.
A big dose of meta-cine
The metaverse is big news in the tech world. For those who are less technologically inclined or haven’t thrown a few hundred dollars at a clunky virtual reality headset, the metaverse is a vaguely defined artificial reality world, brought to you by Facebo-, excuse us, Meta, where you hang out with people using a virtual avatar and do various activities, all from the comfort of your own home.
That’s not the most helpful definition, if we’re being honest, and that’s partially because the metaverse, as it’s being pushed by companies such as Meta, is very new and kind of a Wild West. No one really knows what it’ll be used for, but that’s not going to stop big business from pushing to secure their own corners of a new and exciting market, and that brings us to CVS, which is looking to become the first pharmacy in the metaverse.
Specifically, the company is looking to provide the entirety of its health care services – nonemergency medical care, wellness programs, nutrition advice, and counseling – to the metaverse. That makes sense. Telemedicine has become big during the pandemic, and bringing that care to the metaverse could work. Probably overcomplicated, since the sort of person who couldn’t figure out a video call to a doctor probably won’t be spending much time in the metaverse, but hey, if they can make it work, more power to them.
Where things get a bit silly is the online store. CVS looking to sell not only NFTs (because of course it is), but also downloadable virtual goods, including “prescription drugs, health, wellness, beauty, and personal care products,” according to the company’s claim to the U.S. Patent Trade Office. What exactly is a downloadable virtual prescription drug? Excellent question. We’re picturing holographic meatloaf, but the true answer is bound to be sillier than anything SpongeBob and friends could conjure.
Please don’t eat the winner
Hello friends. LOTME Sports welcomes you to the University of Toledo’s Glass Bowl for the wackiest virtual sporting event since Usain Bolt raced against a cheetah.
Hi, I’m Jim Nantz, and we’re here to witness the brainchild of Toledo physics professor Scott Lee, PhD, who posed an unusual question to his students: Is Usain Bolt faster than a 900-pound dinosaur?
Before we get started, though, I’ve got a quick question for my partner in today’s broadcast, Hall of Fame quarterback Peyton Manning: Why is someone who practices physics called a physicist when someone who practices medicine is known as a physician?
Jim, I’m prepared to talk about how Dr. Lee’s students used the concepts of 1D kinematics – displacement, speed, velocity, and acceleration – to determine if a Jamaican sprinter could beat Dilophosaurus wetherilli in a hypothetical race. Heck, it took me 2 days to be able to pronounce Dilophosaurus wetherilli. Don’t get me started on etymology.
Fair enough, my friend. What else can you tell us?
In his article in The Physics Teacher, Dr. Lee noted that recent musculoskeletal models of vertebrate animals have shown that a dinosaur like Dilophosaurus could run about as fast as Usain Bolt when he set the world record of 9.58 seconds for 100 meters in 2009. You might remember Dilophosaurus from “Jurassic Park.” It was the one that attacked the guy who played Newman on “Seinfeld.”
Fascinating stuff, Peyton, but it looks like the race is about to start. And they’re off! Newton’s second law, which says that acceleration is determined by a combination of mass and force, gives the smaller Bolt an early advantage. The dinosaur takes longer to reach maximum running velocity and crosses the line 2 seconds behind the world’s fastest human. Amazing!
Be sure to tune in again next week, when tennis legend Serena Williams takes the court against a hungry velociraptor.
Turning back the egg timer
The idea of getting older can be scary. Wouldn’t it be nice if we could reverse the aging process? Nice, sure, but not possible. Well, it may just be possible for women undergoing assisted reproductive treatment.
It’s generally known that oocytes accumulate DNA damage over time as well, hindering fertility, but a lab in Jerusalem has found a way to reverse the age of eggs.
If you’re wondering how on Earth that was possible, here’s how. Scientists from the Hebrew University of Jerusalem said that they found a previously unknown aging mechanism, which they were able to reverse using antiviral medications, they reported in Aging Cell.
The experiment started on mice eggs, but soon real human eggs were donated. After the procedure, the treated eggs appeared younger, with less of the DNA damage that comes from age. Sperm has not yet been used to test fertility so it is unclear if this will result in something game changing, but the investigators have high hopes.
“Many women are trying to get pregnant aged 40 or over, and we think this could actually increase their level of fertility,” senior investigator Michael Klutstein, PhD, told the Times of Israel. “Within 10 years, we hope to use antiviral drugs to increase fertility among older women.”
We’re counting on you, science! Do your thing!
Drink a day could age your brain
There are many things we can do daily to improve our health: Exercise, read a book, eat an apple (supposedly). Not drink a glass of red wine. Wait, not drink? That’s right. We were told that a glass of red wine each night was doing something good for our hearts, but it’s doing something bad to our brains: Aging them prematurely.
According to a recent study in Nature Communications, drinking half a pint of beer a day could age the brain of a 50-year-old by 6 months. A pint of beer equaled 2 years of aging and a pint and a half aged participants’ brains by 3.5 years.
Compared with people who didn’t drink, those who averaged about two pints of beer or two glasses of wine daily had brains aged 10 years older!
The researchers’ analysis included MRI scans of about 37,000 middle-aged men in the United Kingdom, along with their medical information and drinking habits, Everyday Health reported. They determined volume reductions in two parts of the brain potentially impacted by daily consumption of alcohol: White matter, which controls the senses and communication, and gray matter, which controls cognitive functions such as movement, emotions, and memories.
Normal brain aging is bad enough: Stuff like forgetting why we walked into the kitchen or having a word we want to use on the tips of our tongues. Who knew that happy hour could be speeding up the process?
Bartender, make that mimosa a virgin.
A big dose of meta-cine
The metaverse is big news in the tech world. For those who are less technologically inclined or haven’t thrown a few hundred dollars at a clunky virtual reality headset, the metaverse is a vaguely defined artificial reality world, brought to you by Facebo-, excuse us, Meta, where you hang out with people using a virtual avatar and do various activities, all from the comfort of your own home.
That’s not the most helpful definition, if we’re being honest, and that’s partially because the metaverse, as it’s being pushed by companies such as Meta, is very new and kind of a Wild West. No one really knows what it’ll be used for, but that’s not going to stop big business from pushing to secure their own corners of a new and exciting market, and that brings us to CVS, which is looking to become the first pharmacy in the metaverse.
Specifically, the company is looking to provide the entirety of its health care services – nonemergency medical care, wellness programs, nutrition advice, and counseling – to the metaverse. That makes sense. Telemedicine has become big during the pandemic, and bringing that care to the metaverse could work. Probably overcomplicated, since the sort of person who couldn’t figure out a video call to a doctor probably won’t be spending much time in the metaverse, but hey, if they can make it work, more power to them.
Where things get a bit silly is the online store. CVS looking to sell not only NFTs (because of course it is), but also downloadable virtual goods, including “prescription drugs, health, wellness, beauty, and personal care products,” according to the company’s claim to the U.S. Patent Trade Office. What exactly is a downloadable virtual prescription drug? Excellent question. We’re picturing holographic meatloaf, but the true answer is bound to be sillier than anything SpongeBob and friends could conjure.
Please don’t eat the winner
Hello friends. LOTME Sports welcomes you to the University of Toledo’s Glass Bowl for the wackiest virtual sporting event since Usain Bolt raced against a cheetah.
Hi, I’m Jim Nantz, and we’re here to witness the brainchild of Toledo physics professor Scott Lee, PhD, who posed an unusual question to his students: Is Usain Bolt faster than a 900-pound dinosaur?
Before we get started, though, I’ve got a quick question for my partner in today’s broadcast, Hall of Fame quarterback Peyton Manning: Why is someone who practices physics called a physicist when someone who practices medicine is known as a physician?
Jim, I’m prepared to talk about how Dr. Lee’s students used the concepts of 1D kinematics – displacement, speed, velocity, and acceleration – to determine if a Jamaican sprinter could beat Dilophosaurus wetherilli in a hypothetical race. Heck, it took me 2 days to be able to pronounce Dilophosaurus wetherilli. Don’t get me started on etymology.
Fair enough, my friend. What else can you tell us?
In his article in The Physics Teacher, Dr. Lee noted that recent musculoskeletal models of vertebrate animals have shown that a dinosaur like Dilophosaurus could run about as fast as Usain Bolt when he set the world record of 9.58 seconds for 100 meters in 2009. You might remember Dilophosaurus from “Jurassic Park.” It was the one that attacked the guy who played Newman on “Seinfeld.”
Fascinating stuff, Peyton, but it looks like the race is about to start. And they’re off! Newton’s second law, which says that acceleration is determined by a combination of mass and force, gives the smaller Bolt an early advantage. The dinosaur takes longer to reach maximum running velocity and crosses the line 2 seconds behind the world’s fastest human. Amazing!
Be sure to tune in again next week, when tennis legend Serena Williams takes the court against a hungry velociraptor.
Turning back the egg timer
The idea of getting older can be scary. Wouldn’t it be nice if we could reverse the aging process? Nice, sure, but not possible. Well, it may just be possible for women undergoing assisted reproductive treatment.
It’s generally known that oocytes accumulate DNA damage over time as well, hindering fertility, but a lab in Jerusalem has found a way to reverse the age of eggs.
If you’re wondering how on Earth that was possible, here’s how. Scientists from the Hebrew University of Jerusalem said that they found a previously unknown aging mechanism, which they were able to reverse using antiviral medications, they reported in Aging Cell.
The experiment started on mice eggs, but soon real human eggs were donated. After the procedure, the treated eggs appeared younger, with less of the DNA damage that comes from age. Sperm has not yet been used to test fertility so it is unclear if this will result in something game changing, but the investigators have high hopes.
“Many women are trying to get pregnant aged 40 or over, and we think this could actually increase their level of fertility,” senior investigator Michael Klutstein, PhD, told the Times of Israel. “Within 10 years, we hope to use antiviral drugs to increase fertility among older women.”
We’re counting on you, science! Do your thing!
Drink a day could age your brain
There are many things we can do daily to improve our health: Exercise, read a book, eat an apple (supposedly). Not drink a glass of red wine. Wait, not drink? That’s right. We were told that a glass of red wine each night was doing something good for our hearts, but it’s doing something bad to our brains: Aging them prematurely.
According to a recent study in Nature Communications, drinking half a pint of beer a day could age the brain of a 50-year-old by 6 months. A pint of beer equaled 2 years of aging and a pint and a half aged participants’ brains by 3.5 years.
Compared with people who didn’t drink, those who averaged about two pints of beer or two glasses of wine daily had brains aged 10 years older!
The researchers’ analysis included MRI scans of about 37,000 middle-aged men in the United Kingdom, along with their medical information and drinking habits, Everyday Health reported. They determined volume reductions in two parts of the brain potentially impacted by daily consumption of alcohol: White matter, which controls the senses and communication, and gray matter, which controls cognitive functions such as movement, emotions, and memories.
Normal brain aging is bad enough: Stuff like forgetting why we walked into the kitchen or having a word we want to use on the tips of our tongues. Who knew that happy hour could be speeding up the process?
Bartender, make that mimosa a virgin.
A big dose of meta-cine
The metaverse is big news in the tech world. For those who are less technologically inclined or haven’t thrown a few hundred dollars at a clunky virtual reality headset, the metaverse is a vaguely defined artificial reality world, brought to you by Facebo-, excuse us, Meta, where you hang out with people using a virtual avatar and do various activities, all from the comfort of your own home.
That’s not the most helpful definition, if we’re being honest, and that’s partially because the metaverse, as it’s being pushed by companies such as Meta, is very new and kind of a Wild West. No one really knows what it’ll be used for, but that’s not going to stop big business from pushing to secure their own corners of a new and exciting market, and that brings us to CVS, which is looking to become the first pharmacy in the metaverse.
Specifically, the company is looking to provide the entirety of its health care services – nonemergency medical care, wellness programs, nutrition advice, and counseling – to the metaverse. That makes sense. Telemedicine has become big during the pandemic, and bringing that care to the metaverse could work. Probably overcomplicated, since the sort of person who couldn’t figure out a video call to a doctor probably won’t be spending much time in the metaverse, but hey, if they can make it work, more power to them.
Where things get a bit silly is the online store. CVS looking to sell not only NFTs (because of course it is), but also downloadable virtual goods, including “prescription drugs, health, wellness, beauty, and personal care products,” according to the company’s claim to the U.S. Patent Trade Office. What exactly is a downloadable virtual prescription drug? Excellent question. We’re picturing holographic meatloaf, but the true answer is bound to be sillier than anything SpongeBob and friends could conjure.
Please don’t eat the winner
Hello friends. LOTME Sports welcomes you to the University of Toledo’s Glass Bowl for the wackiest virtual sporting event since Usain Bolt raced against a cheetah.
Hi, I’m Jim Nantz, and we’re here to witness the brainchild of Toledo physics professor Scott Lee, PhD, who posed an unusual question to his students: Is Usain Bolt faster than a 900-pound dinosaur?
Before we get started, though, I’ve got a quick question for my partner in today’s broadcast, Hall of Fame quarterback Peyton Manning: Why is someone who practices physics called a physicist when someone who practices medicine is known as a physician?
Jim, I’m prepared to talk about how Dr. Lee’s students used the concepts of 1D kinematics – displacement, speed, velocity, and acceleration – to determine if a Jamaican sprinter could beat Dilophosaurus wetherilli in a hypothetical race. Heck, it took me 2 days to be able to pronounce Dilophosaurus wetherilli. Don’t get me started on etymology.
Fair enough, my friend. What else can you tell us?
In his article in The Physics Teacher, Dr. Lee noted that recent musculoskeletal models of vertebrate animals have shown that a dinosaur like Dilophosaurus could run about as fast as Usain Bolt when he set the world record of 9.58 seconds for 100 meters in 2009. You might remember Dilophosaurus from “Jurassic Park.” It was the one that attacked the guy who played Newman on “Seinfeld.”
Fascinating stuff, Peyton, but it looks like the race is about to start. And they’re off! Newton’s second law, which says that acceleration is determined by a combination of mass and force, gives the smaller Bolt an early advantage. The dinosaur takes longer to reach maximum running velocity and crosses the line 2 seconds behind the world’s fastest human. Amazing!
Be sure to tune in again next week, when tennis legend Serena Williams takes the court against a hungry velociraptor.
Turning back the egg timer
The idea of getting older can be scary. Wouldn’t it be nice if we could reverse the aging process? Nice, sure, but not possible. Well, it may just be possible for women undergoing assisted reproductive treatment.
It’s generally known that oocytes accumulate DNA damage over time as well, hindering fertility, but a lab in Jerusalem has found a way to reverse the age of eggs.
If you’re wondering how on Earth that was possible, here’s how. Scientists from the Hebrew University of Jerusalem said that they found a previously unknown aging mechanism, which they were able to reverse using antiviral medications, they reported in Aging Cell.
The experiment started on mice eggs, but soon real human eggs were donated. After the procedure, the treated eggs appeared younger, with less of the DNA damage that comes from age. Sperm has not yet been used to test fertility so it is unclear if this will result in something game changing, but the investigators have high hopes.
“Many women are trying to get pregnant aged 40 or over, and we think this could actually increase their level of fertility,” senior investigator Michael Klutstein, PhD, told the Times of Israel. “Within 10 years, we hope to use antiviral drugs to increase fertility among older women.”
We’re counting on you, science! Do your thing!
Why is there an increased risk of cancer in depressed patients?
LAS VEGAS – Is the relationship between major depressive disorder and the development of cancer, cardiovascular disease, and other medical conditions a coincidence, or is there more at play?
According to Charles B. Nemeroff, MD, PhD, a host of circumstances potentially underlies this association, including treatment of the medical disorder itself.
“The best example of that is probably the use of interferon-alpha for the treatment of malignant melanoma,” Dr. Nemeroff, professor and chair of the department of psychiatry and behavioral sciences at the University of Texas at Austin, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “Many patients treated with interferon-alpha ended up with very severe depression, including several documented suicides. Another possibility of the relationship between depression and medical disorders is that treating a patient for depression could result in a medical disorder. The best example of this is the use of 20 mg of olanzapine to augment the effects of an antidepressant, resulting in a 50-pound weight gain and the development of type 2 diabetes and metabolic syndrome. Both of those scenarios are well understood.”
Then there’s the behavioral aspects of the relationship, he continued, in which patients adopt the mindset that “I’m depressed. I don’t want to exercise. I’m a couch potato. I have been gaining a lot of weight. It’s bad for my heart.”
Converging biology is another possibility. “Is it possible that the biology of depression is linked to the biology of other disorders?” asked Dr. Nemeroff, who directs the university’s Institute for Early Life Adversity Research. “We can talk about this in relation to thyroid disease, a well known cause of depression, but we can also talk about the relationship to other disorders. There’s amazing epidemiologic evidence that patients with PTSD are much more likely to develop Alzheimer’s disease than patients without PTSD.”
Psychosocial issues also play a role. He recalled seeing patient in a clinic for the underserved who had underlying severe ulcerative colitis and anemia and couldn’t afford medical treatment. “The patient had a low hemoglobin, so it was impossible to distinguish between that and whether they had a primary depressive disorder or not,” he said.
In a study that explored the relationship between major depression and cancer, Dr. Nemeroff and colleagues found that the prevalence was highest in those with pancreatic cancer (50%), followed by oropharyngeal (40%), colon (13-25%), breast (18-25%), and gynecologic (23%), and Hodgkin’s lymphoma (17%) (Arch Gen Psychiatry 1995;52[2]:89-99). “Not all cancers have the same rate of depression,” he said. “One of the central questions is, not so much is the cancer patient depressed, but is depression a risk factor for developing cancer? The answer is a resounding yes. But what we don’t know is if you treat the depression aggressively, can you reduce that risk of either developing cancer or the progression of cancer?”
Dr. Nemeroff spotlighted several studies largely from the oncology literature, including a prospective survival analysis of 578 women with early-stage breast cancer (Lancet 1999;354:1331-6). After 5 years, 395 were alive and without relapse, 50 were alive with relapse, and 133 had died. The researchers found a significantly increased risk of death from all causes by 5 years in women with a high depression score (HR 3.59). There was a significantly increased risk of relapse or death at 5 years in women with high scores on helplessness and hopelessness measures.
In an analysis of the association between breast cancer and traumatic events, women who had severe stress or a traumatic event had lower rates of disease-free intervals (J Psychosomatic Res 2007;63:233-9). Another study by the same investigators found that a decrease in depression symptoms is associated with longer survival in patients with metastatic breast cancer (J Clin Oncol 2010;29:413-20). The median survival was 53.6 months for women with decreasing depression scores over 1 year and 25.1 months for women with increasing depression scores.
A more recent study of cervical cancer patients found that those exposed to psychological stress had an increased risk of cancer-specific mortality (HR 1.33) (Cancer Res 2019;79:3965-72). The association was mainly driven by distress experienced within 1 year before or after diagnosis (HR 1.30) but not afterward (HR 1.12). In addition, data from the large longitudinal Nurses’ Health Study II found that women with high PTSD symptoms had a twofold greater risk of ovarian cancer compared with women who had no trauma exposure (Cancer Res 2019;79:5113-20).
Authors of a separate study analyzed data from the Women’s Health Initiative to examine if depression precedes the development of a cancer diagnosis. They found that depression 3 years before a diagnosis of breast cancer was associated with all-cause mortality (HR 1.35) (Cancer 2017;123[16]:3107-15). Meanwhile, among women with late-stage breast cancer, newly developed depression at year 3 was significantly associated with all-cause mortality (HR 2.0) and breast cancer-specific mortality (HR 2.42). “That’s a pretty amazing finding,” Dr. Nemeroff said. “We have to think about depression as a systemic illness. What is depression doing that’s creating a fertile environment for cancer or worsening of cancer?”
He then discussed the risk of suicide in patients who are newly diagnosed with cancer. “No one ever talks about this, and I can’t get anybody to support research in this area,” he said. In one of the first studies on the topic, researchers conducted a case-control study of Medicare patients and determined risk of suicide among those with cancer was 2.3-fold higher compared with controls, even after adjustment for psychiatric illness and the risk of dying within a year (J Clin Oncol 2008;26[29]:4720-4). More recently, authors of a large population-based study in England found that the overall standardized mortality ratio for suicide was 1.20 (JAMA Psychiatry 2019;76[1]51-60). The risk was highest among patients with mesothelioma, with a 4.51-fold risk, followed by pancreatic (3.89-fold), esophageal (2.65-fold), lung (2.57-fold), and stomach cancer (2.20-fold). “They reported that the first 6 months after the diagnosis is associated with an increased risk of suicide – unrelated to prognosis,” Dr. Nemeroff said.
A separate analysis of SEER data from 1973-2014 and comprising more than 8.6 million cancer patients found that newly diagnosed cancer patients are 4.4 times more likely to die from suicide than patients in the same age group without cancer (Nat Commun 2019;10[1]:207). The highest risk was in lung cancer, followed by head and neck, testes, bladder, and Hodgkin’s lymphoma.
According to Dr. Nemeroff, For example, he said, if the depressed environment is associated with a marked increase in tumor necrosis factor, interleukin 6, and other inflammatory markers, “that probably contributes to the body’s ability to fight disease. Ironically, depression is associated with an increase in inflammation but a decreased in T cell function. Remember, there are two fundamental types of immunity: the antibody response and the cellular response. What’s odd about depression is that there’s an increase in inflammatory markers but a decrease in the ability of T cells to function in terms of cellular immunity.”
Dr. Nemeroff disclosed that he has served as a consultant and/or scientific adviser for numerous pharmaceutical companies. He has received research and grant support from the National Institutes of Health.
LAS VEGAS – Is the relationship between major depressive disorder and the development of cancer, cardiovascular disease, and other medical conditions a coincidence, or is there more at play?
According to Charles B. Nemeroff, MD, PhD, a host of circumstances potentially underlies this association, including treatment of the medical disorder itself.
“The best example of that is probably the use of interferon-alpha for the treatment of malignant melanoma,” Dr. Nemeroff, professor and chair of the department of psychiatry and behavioral sciences at the University of Texas at Austin, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “Many patients treated with interferon-alpha ended up with very severe depression, including several documented suicides. Another possibility of the relationship between depression and medical disorders is that treating a patient for depression could result in a medical disorder. The best example of this is the use of 20 mg of olanzapine to augment the effects of an antidepressant, resulting in a 50-pound weight gain and the development of type 2 diabetes and metabolic syndrome. Both of those scenarios are well understood.”
Then there’s the behavioral aspects of the relationship, he continued, in which patients adopt the mindset that “I’m depressed. I don’t want to exercise. I’m a couch potato. I have been gaining a lot of weight. It’s bad for my heart.”
Converging biology is another possibility. “Is it possible that the biology of depression is linked to the biology of other disorders?” asked Dr. Nemeroff, who directs the university’s Institute for Early Life Adversity Research. “We can talk about this in relation to thyroid disease, a well known cause of depression, but we can also talk about the relationship to other disorders. There’s amazing epidemiologic evidence that patients with PTSD are much more likely to develop Alzheimer’s disease than patients without PTSD.”
Psychosocial issues also play a role. He recalled seeing patient in a clinic for the underserved who had underlying severe ulcerative colitis and anemia and couldn’t afford medical treatment. “The patient had a low hemoglobin, so it was impossible to distinguish between that and whether they had a primary depressive disorder or not,” he said.
In a study that explored the relationship between major depression and cancer, Dr. Nemeroff and colleagues found that the prevalence was highest in those with pancreatic cancer (50%), followed by oropharyngeal (40%), colon (13-25%), breast (18-25%), and gynecologic (23%), and Hodgkin’s lymphoma (17%) (Arch Gen Psychiatry 1995;52[2]:89-99). “Not all cancers have the same rate of depression,” he said. “One of the central questions is, not so much is the cancer patient depressed, but is depression a risk factor for developing cancer? The answer is a resounding yes. But what we don’t know is if you treat the depression aggressively, can you reduce that risk of either developing cancer or the progression of cancer?”
Dr. Nemeroff spotlighted several studies largely from the oncology literature, including a prospective survival analysis of 578 women with early-stage breast cancer (Lancet 1999;354:1331-6). After 5 years, 395 were alive and without relapse, 50 were alive with relapse, and 133 had died. The researchers found a significantly increased risk of death from all causes by 5 years in women with a high depression score (HR 3.59). There was a significantly increased risk of relapse or death at 5 years in women with high scores on helplessness and hopelessness measures.
In an analysis of the association between breast cancer and traumatic events, women who had severe stress or a traumatic event had lower rates of disease-free intervals (J Psychosomatic Res 2007;63:233-9). Another study by the same investigators found that a decrease in depression symptoms is associated with longer survival in patients with metastatic breast cancer (J Clin Oncol 2010;29:413-20). The median survival was 53.6 months for women with decreasing depression scores over 1 year and 25.1 months for women with increasing depression scores.
A more recent study of cervical cancer patients found that those exposed to psychological stress had an increased risk of cancer-specific mortality (HR 1.33) (Cancer Res 2019;79:3965-72). The association was mainly driven by distress experienced within 1 year before or after diagnosis (HR 1.30) but not afterward (HR 1.12). In addition, data from the large longitudinal Nurses’ Health Study II found that women with high PTSD symptoms had a twofold greater risk of ovarian cancer compared with women who had no trauma exposure (Cancer Res 2019;79:5113-20).
Authors of a separate study analyzed data from the Women’s Health Initiative to examine if depression precedes the development of a cancer diagnosis. They found that depression 3 years before a diagnosis of breast cancer was associated with all-cause mortality (HR 1.35) (Cancer 2017;123[16]:3107-15). Meanwhile, among women with late-stage breast cancer, newly developed depression at year 3 was significantly associated with all-cause mortality (HR 2.0) and breast cancer-specific mortality (HR 2.42). “That’s a pretty amazing finding,” Dr. Nemeroff said. “We have to think about depression as a systemic illness. What is depression doing that’s creating a fertile environment for cancer or worsening of cancer?”
He then discussed the risk of suicide in patients who are newly diagnosed with cancer. “No one ever talks about this, and I can’t get anybody to support research in this area,” he said. In one of the first studies on the topic, researchers conducted a case-control study of Medicare patients and determined risk of suicide among those with cancer was 2.3-fold higher compared with controls, even after adjustment for psychiatric illness and the risk of dying within a year (J Clin Oncol 2008;26[29]:4720-4). More recently, authors of a large population-based study in England found that the overall standardized mortality ratio for suicide was 1.20 (JAMA Psychiatry 2019;76[1]51-60). The risk was highest among patients with mesothelioma, with a 4.51-fold risk, followed by pancreatic (3.89-fold), esophageal (2.65-fold), lung (2.57-fold), and stomach cancer (2.20-fold). “They reported that the first 6 months after the diagnosis is associated with an increased risk of suicide – unrelated to prognosis,” Dr. Nemeroff said.
A separate analysis of SEER data from 1973-2014 and comprising more than 8.6 million cancer patients found that newly diagnosed cancer patients are 4.4 times more likely to die from suicide than patients in the same age group without cancer (Nat Commun 2019;10[1]:207). The highest risk was in lung cancer, followed by head and neck, testes, bladder, and Hodgkin’s lymphoma.
According to Dr. Nemeroff, For example, he said, if the depressed environment is associated with a marked increase in tumor necrosis factor, interleukin 6, and other inflammatory markers, “that probably contributes to the body’s ability to fight disease. Ironically, depression is associated with an increase in inflammation but a decreased in T cell function. Remember, there are two fundamental types of immunity: the antibody response and the cellular response. What’s odd about depression is that there’s an increase in inflammatory markers but a decrease in the ability of T cells to function in terms of cellular immunity.”
Dr. Nemeroff disclosed that he has served as a consultant and/or scientific adviser for numerous pharmaceutical companies. He has received research and grant support from the National Institutes of Health.
LAS VEGAS – Is the relationship between major depressive disorder and the development of cancer, cardiovascular disease, and other medical conditions a coincidence, or is there more at play?
According to Charles B. Nemeroff, MD, PhD, a host of circumstances potentially underlies this association, including treatment of the medical disorder itself.
“The best example of that is probably the use of interferon-alpha for the treatment of malignant melanoma,” Dr. Nemeroff, professor and chair of the department of psychiatry and behavioral sciences at the University of Texas at Austin, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “Many patients treated with interferon-alpha ended up with very severe depression, including several documented suicides. Another possibility of the relationship between depression and medical disorders is that treating a patient for depression could result in a medical disorder. The best example of this is the use of 20 mg of olanzapine to augment the effects of an antidepressant, resulting in a 50-pound weight gain and the development of type 2 diabetes and metabolic syndrome. Both of those scenarios are well understood.”
Then there’s the behavioral aspects of the relationship, he continued, in which patients adopt the mindset that “I’m depressed. I don’t want to exercise. I’m a couch potato. I have been gaining a lot of weight. It’s bad for my heart.”
Converging biology is another possibility. “Is it possible that the biology of depression is linked to the biology of other disorders?” asked Dr. Nemeroff, who directs the university’s Institute for Early Life Adversity Research. “We can talk about this in relation to thyroid disease, a well known cause of depression, but we can also talk about the relationship to other disorders. There’s amazing epidemiologic evidence that patients with PTSD are much more likely to develop Alzheimer’s disease than patients without PTSD.”
Psychosocial issues also play a role. He recalled seeing patient in a clinic for the underserved who had underlying severe ulcerative colitis and anemia and couldn’t afford medical treatment. “The patient had a low hemoglobin, so it was impossible to distinguish between that and whether they had a primary depressive disorder or not,” he said.
In a study that explored the relationship between major depression and cancer, Dr. Nemeroff and colleagues found that the prevalence was highest in those with pancreatic cancer (50%), followed by oropharyngeal (40%), colon (13-25%), breast (18-25%), and gynecologic (23%), and Hodgkin’s lymphoma (17%) (Arch Gen Psychiatry 1995;52[2]:89-99). “Not all cancers have the same rate of depression,” he said. “One of the central questions is, not so much is the cancer patient depressed, but is depression a risk factor for developing cancer? The answer is a resounding yes. But what we don’t know is if you treat the depression aggressively, can you reduce that risk of either developing cancer or the progression of cancer?”
Dr. Nemeroff spotlighted several studies largely from the oncology literature, including a prospective survival analysis of 578 women with early-stage breast cancer (Lancet 1999;354:1331-6). After 5 years, 395 were alive and without relapse, 50 were alive with relapse, and 133 had died. The researchers found a significantly increased risk of death from all causes by 5 years in women with a high depression score (HR 3.59). There was a significantly increased risk of relapse or death at 5 years in women with high scores on helplessness and hopelessness measures.
In an analysis of the association between breast cancer and traumatic events, women who had severe stress or a traumatic event had lower rates of disease-free intervals (J Psychosomatic Res 2007;63:233-9). Another study by the same investigators found that a decrease in depression symptoms is associated with longer survival in patients with metastatic breast cancer (J Clin Oncol 2010;29:413-20). The median survival was 53.6 months for women with decreasing depression scores over 1 year and 25.1 months for women with increasing depression scores.
A more recent study of cervical cancer patients found that those exposed to psychological stress had an increased risk of cancer-specific mortality (HR 1.33) (Cancer Res 2019;79:3965-72). The association was mainly driven by distress experienced within 1 year before or after diagnosis (HR 1.30) but not afterward (HR 1.12). In addition, data from the large longitudinal Nurses’ Health Study II found that women with high PTSD symptoms had a twofold greater risk of ovarian cancer compared with women who had no trauma exposure (Cancer Res 2019;79:5113-20).
Authors of a separate study analyzed data from the Women’s Health Initiative to examine if depression precedes the development of a cancer diagnosis. They found that depression 3 years before a diagnosis of breast cancer was associated with all-cause mortality (HR 1.35) (Cancer 2017;123[16]:3107-15). Meanwhile, among women with late-stage breast cancer, newly developed depression at year 3 was significantly associated with all-cause mortality (HR 2.0) and breast cancer-specific mortality (HR 2.42). “That’s a pretty amazing finding,” Dr. Nemeroff said. “We have to think about depression as a systemic illness. What is depression doing that’s creating a fertile environment for cancer or worsening of cancer?”
He then discussed the risk of suicide in patients who are newly diagnosed with cancer. “No one ever talks about this, and I can’t get anybody to support research in this area,” he said. In one of the first studies on the topic, researchers conducted a case-control study of Medicare patients and determined risk of suicide among those with cancer was 2.3-fold higher compared with controls, even after adjustment for psychiatric illness and the risk of dying within a year (J Clin Oncol 2008;26[29]:4720-4). More recently, authors of a large population-based study in England found that the overall standardized mortality ratio for suicide was 1.20 (JAMA Psychiatry 2019;76[1]51-60). The risk was highest among patients with mesothelioma, with a 4.51-fold risk, followed by pancreatic (3.89-fold), esophageal (2.65-fold), lung (2.57-fold), and stomach cancer (2.20-fold). “They reported that the first 6 months after the diagnosis is associated with an increased risk of suicide – unrelated to prognosis,” Dr. Nemeroff said.
A separate analysis of SEER data from 1973-2014 and comprising more than 8.6 million cancer patients found that newly diagnosed cancer patients are 4.4 times more likely to die from suicide than patients in the same age group without cancer (Nat Commun 2019;10[1]:207). The highest risk was in lung cancer, followed by head and neck, testes, bladder, and Hodgkin’s lymphoma.
According to Dr. Nemeroff, For example, he said, if the depressed environment is associated with a marked increase in tumor necrosis factor, interleukin 6, and other inflammatory markers, “that probably contributes to the body’s ability to fight disease. Ironically, depression is associated with an increase in inflammation but a decreased in T cell function. Remember, there are two fundamental types of immunity: the antibody response and the cellular response. What’s odd about depression is that there’s an increase in inflammatory markers but a decrease in the ability of T cells to function in terms of cellular immunity.”
Dr. Nemeroff disclosed that he has served as a consultant and/or scientific adviser for numerous pharmaceutical companies. He has received research and grant support from the National Institutes of Health.
FROM NPA 2022
Cat ownership in childhood linked ‘conditionally’ to psychosis in adult males
Owning an outdoor cat as a child is associated with an increased risk of psychotic experiences in adulthood – but only in males, new research suggests.
Investigators found 
The suspected culprit is not the cat itself but rather exposure to Toxoplasma gondii, a common parasite carried by rodents and sometimes found in cat feces. The study adds to a growing evidence showing exposure to T. gondii may be a risk factor for schizophrenia and other psychotic disorders.
“These are small pieces of evidence but it’s interesting to consider that there might be combinations of risk factors at play,” lead author Vincent Paquin, MD, psychiatry resident at McGill University, Montreal, said in an interview.
“And even if the magnitude of the risk is small at the individual level,” he added, “cats and Toxoplasma gondii are so present in our society that if we add up all these small potential effects then it becomes a potential public health question.”
The study was published online Jan. 30, 2022, in the Journal of Psychiatric Research.
Inconsistent evidence
T. gondii infects about 30% of the human population and is usually transmitted by cats. Most infections are asymptomatic, but T. gondii can cause toxoplasmosis in humans, which has been linked to increased risk of schizophrenia, suicide attempts, and more recently, mild cognitive impairment.
Although some studies show an association between cat ownership and increased risk of mental illness, the research findings have been inconsistent.
“The evidence has been mixed about the association between cat ownership and psychosis expression, so our approach was to consider whether specific factors or combinations of factors could explain this mixed evidence,” Dr. Paquin said.
For the study, 2206 individuals aged 18-40 years completed the Community Assessment of Psychic Experiences (CAPE-42) and a questionnaire to gather information about cat ownership at any time between birth and age 13 and if the cats lived exclusively indoors (nonhunting) or if they were allowed outside (rodent hunting).
Participants were also asked about the number of residential moves between birth and age 15, date and place of birth, lifetime history of head trauma, and tobacco smoking history.
Rodent-hunting cat ownership was associated with higher risk of psychosis in male participants, compared with owning no cat or a nonhunting cat. When the investigators added head trauma and residential moves to rodent-hunting cat ownership, psychosis risk was elevated in both men and women.
Independent of cat ownership, younger age, moving more than three times as a child, a history of head trauma, and being a smoker were all associated with higher psychosis risk.
The study wasn’t designed to explore potential biological mechanisms to explain the sex differences in psychosis risk seen among rodent-hunting cat owners, but “one possible explanation based on the animal model literature is that the neurobiological effects of parasitic exposure may be greater with male sex,” senior author Suzanne King, PhD, professor of psychiatry at McGill, said in an interview.
The new study is part of a larger, long-term project called EnviroGen, led by Dr. King, examining the environmental and genetic risk factors for schizophrenia.
Need for replication
Commenting on the findings, E. Fuller Torrey, MD, who was among the first researchers to identify a link between cat ownership, T. gondii infection, and schizophrenia, said the study is “an interesting addition to the studies of cat ownership in childhood as a risk factor for psychosis.”
Of the approximately 10 published studies on the topic, about half suggest a link between cat ownership and psychosis later in life, said Dr. Torrey, associate director for research at the Stanley Medical Research Institute in Rockville, Md.
“The Canadian study is interesting in that it is the first study that separates exposure to permanently indoor cats from cats that are allowed to go outdoors, and the results were positive only for outdoor cats,” Dr. Torrey said.
The study has limitations, Dr. Torrey added, including its retrospective design and the use of a self-report questionnaire to assess psychotic experiences in adulthood.
Also commenting on findings, James Kirkbride, PhD, professor of psychiatric and social epidemiology, University College London, noted the same limitations.
Dr. Kirkbride is the lead author of a 2017 study that showed no link between cat ownership and serious mental illness that included nearly 5,000 people born in 1991 or 1992 and followed until age 18. In this study, there was no link between psychosis and cat ownership during pregnancy or at ages 4 or 10 years.
“Researchers have long been fascinated with the idea that cat ownership may affect mental health. This paper may have them chasing their own tail,” Dr. Kirkbride said.
“Evidence of any association is limited to certain subgroups without a strong theoretical basis for why this may be the case,” he added. “The retrospective and cross-sectional nature of the survey also raise the possibility that the results are impacted by differential recall bias, as well as the broader issues of chance and unobserved confounding.”
Dr. King noted that recall bias is a limitation the researchers highlighted in their study, but “considering the exposures are relatively objective and factual, we do not believe the potential for recall bias is substantial.”
“Nonetheless, we strongly believe that replication of our results in prospective, population-representative cohorts will be crucial to making firmer conclusions,” he added.
The study was funded by grants from the Quebec Health Research Fund. The study authors and Dr. Kirkbride disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Owning an outdoor cat as a child is associated with an increased risk of psychotic experiences in adulthood – but only in males, new research suggests.
Investigators found
The suspected culprit is not the cat itself but rather exposure to Toxoplasma gondii, a common parasite carried by rodents and sometimes found in cat feces. The study adds to a growing evidence showing exposure to T. gondii may be a risk factor for schizophrenia and other psychotic disorders.
“These are small pieces of evidence but it’s interesting to consider that there might be combinations of risk factors at play,” lead author Vincent Paquin, MD, psychiatry resident at McGill University, Montreal, said in an interview.
“And even if the magnitude of the risk is small at the individual level,” he added, “cats and Toxoplasma gondii are so present in our society that if we add up all these small potential effects then it becomes a potential public health question.”
The study was published online Jan. 30, 2022, in the Journal of Psychiatric Research.
Inconsistent evidence
T. gondii infects about 30% of the human population and is usually transmitted by cats. Most infections are asymptomatic, but T. gondii can cause toxoplasmosis in humans, which has been linked to increased risk of schizophrenia, suicide attempts, and more recently, mild cognitive impairment.
Although some studies show an association between cat ownership and increased risk of mental illness, the research findings have been inconsistent.
“The evidence has been mixed about the association between cat ownership and psychosis expression, so our approach was to consider whether specific factors or combinations of factors could explain this mixed evidence,” Dr. Paquin said.
For the study, 2206 individuals aged 18-40 years completed the Community Assessment of Psychic Experiences (CAPE-42) and a questionnaire to gather information about cat ownership at any time between birth and age 13 and if the cats lived exclusively indoors (nonhunting) or if they were allowed outside (rodent hunting).
Participants were also asked about the number of residential moves between birth and age 15, date and place of birth, lifetime history of head trauma, and tobacco smoking history.
Rodent-hunting cat ownership was associated with higher risk of psychosis in male participants, compared with owning no cat or a nonhunting cat. When the investigators added head trauma and residential moves to rodent-hunting cat ownership, psychosis risk was elevated in both men and women.
Independent of cat ownership, younger age, moving more than three times as a child, a history of head trauma, and being a smoker were all associated with higher psychosis risk.
The study wasn’t designed to explore potential biological mechanisms to explain the sex differences in psychosis risk seen among rodent-hunting cat owners, but “one possible explanation based on the animal model literature is that the neurobiological effects of parasitic exposure may be greater with male sex,” senior author Suzanne King, PhD, professor of psychiatry at McGill, said in an interview.
The new study is part of a larger, long-term project called EnviroGen, led by Dr. King, examining the environmental and genetic risk factors for schizophrenia.
Need for replication
Commenting on the findings, E. Fuller Torrey, MD, who was among the first researchers to identify a link between cat ownership, T. gondii infection, and schizophrenia, said the study is “an interesting addition to the studies of cat ownership in childhood as a risk factor for psychosis.”
Of the approximately 10 published studies on the topic, about half suggest a link between cat ownership and psychosis later in life, said Dr. Torrey, associate director for research at the Stanley Medical Research Institute in Rockville, Md.
“The Canadian study is interesting in that it is the first study that separates exposure to permanently indoor cats from cats that are allowed to go outdoors, and the results were positive only for outdoor cats,” Dr. Torrey said.
The study has limitations, Dr. Torrey added, including its retrospective design and the use of a self-report questionnaire to assess psychotic experiences in adulthood.
Also commenting on findings, James Kirkbride, PhD, professor of psychiatric and social epidemiology, University College London, noted the same limitations.
Dr. Kirkbride is the lead author of a 2017 study that showed no link between cat ownership and serious mental illness that included nearly 5,000 people born in 1991 or 1992 and followed until age 18. In this study, there was no link between psychosis and cat ownership during pregnancy or at ages 4 or 10 years.
“Researchers have long been fascinated with the idea that cat ownership may affect mental health. This paper may have them chasing their own tail,” Dr. Kirkbride said.
“Evidence of any association is limited to certain subgroups without a strong theoretical basis for why this may be the case,” he added. “The retrospective and cross-sectional nature of the survey also raise the possibility that the results are impacted by differential recall bias, as well as the broader issues of chance and unobserved confounding.”
Dr. King noted that recall bias is a limitation the researchers highlighted in their study, but “considering the exposures are relatively objective and factual, we do not believe the potential for recall bias is substantial.”
“Nonetheless, we strongly believe that replication of our results in prospective, population-representative cohorts will be crucial to making firmer conclusions,” he added.
The study was funded by grants from the Quebec Health Research Fund. The study authors and Dr. Kirkbride disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Owning an outdoor cat as a child is associated with an increased risk of psychotic experiences in adulthood – but only in males, new research suggests.
Investigators found
The suspected culprit is not the cat itself but rather exposure to Toxoplasma gondii, a common parasite carried by rodents and sometimes found in cat feces. The study adds to a growing evidence showing exposure to T. gondii may be a risk factor for schizophrenia and other psychotic disorders.
“These are small pieces of evidence but it’s interesting to consider that there might be combinations of risk factors at play,” lead author Vincent Paquin, MD, psychiatry resident at McGill University, Montreal, said in an interview.
“And even if the magnitude of the risk is small at the individual level,” he added, “cats and Toxoplasma gondii are so present in our society that if we add up all these small potential effects then it becomes a potential public health question.”
The study was published online Jan. 30, 2022, in the Journal of Psychiatric Research.
Inconsistent evidence
T. gondii infects about 30% of the human population and is usually transmitted by cats. Most infections are asymptomatic, but T. gondii can cause toxoplasmosis in humans, which has been linked to increased risk of schizophrenia, suicide attempts, and more recently, mild cognitive impairment.
Although some studies show an association between cat ownership and increased risk of mental illness, the research findings have been inconsistent.
“The evidence has been mixed about the association between cat ownership and psychosis expression, so our approach was to consider whether specific factors or combinations of factors could explain this mixed evidence,” Dr. Paquin said.
For the study, 2206 individuals aged 18-40 years completed the Community Assessment of Psychic Experiences (CAPE-42) and a questionnaire to gather information about cat ownership at any time between birth and age 13 and if the cats lived exclusively indoors (nonhunting) or if they were allowed outside (rodent hunting).
Participants were also asked about the number of residential moves between birth and age 15, date and place of birth, lifetime history of head trauma, and tobacco smoking history.
Rodent-hunting cat ownership was associated with higher risk of psychosis in male participants, compared with owning no cat or a nonhunting cat. When the investigators added head trauma and residential moves to rodent-hunting cat ownership, psychosis risk was elevated in both men and women.
Independent of cat ownership, younger age, moving more than three times as a child, a history of head trauma, and being a smoker were all associated with higher psychosis risk.
The study wasn’t designed to explore potential biological mechanisms to explain the sex differences in psychosis risk seen among rodent-hunting cat owners, but “one possible explanation based on the animal model literature is that the neurobiological effects of parasitic exposure may be greater with male sex,” senior author Suzanne King, PhD, professor of psychiatry at McGill, said in an interview.
The new study is part of a larger, long-term project called EnviroGen, led by Dr. King, examining the environmental and genetic risk factors for schizophrenia.
Need for replication
Commenting on the findings, E. Fuller Torrey, MD, who was among the first researchers to identify a link between cat ownership, T. gondii infection, and schizophrenia, said the study is “an interesting addition to the studies of cat ownership in childhood as a risk factor for psychosis.”
Of the approximately 10 published studies on the topic, about half suggest a link between cat ownership and psychosis later in life, said Dr. Torrey, associate director for research at the Stanley Medical Research Institute in Rockville, Md.
“The Canadian study is interesting in that it is the first study that separates exposure to permanently indoor cats from cats that are allowed to go outdoors, and the results were positive only for outdoor cats,” Dr. Torrey said.
The study has limitations, Dr. Torrey added, including its retrospective design and the use of a self-report questionnaire to assess psychotic experiences in adulthood.
Also commenting on findings, James Kirkbride, PhD, professor of psychiatric and social epidemiology, University College London, noted the same limitations.
Dr. Kirkbride is the lead author of a 2017 study that showed no link between cat ownership and serious mental illness that included nearly 5,000 people born in 1991 or 1992 and followed until age 18. In this study, there was no link between psychosis and cat ownership during pregnancy or at ages 4 or 10 years.
“Researchers have long been fascinated with the idea that cat ownership may affect mental health. This paper may have them chasing their own tail,” Dr. Kirkbride said.
“Evidence of any association is limited to certain subgroups without a strong theoretical basis for why this may be the case,” he added. “The retrospective and cross-sectional nature of the survey also raise the possibility that the results are impacted by differential recall bias, as well as the broader issues of chance and unobserved confounding.”
Dr. King noted that recall bias is a limitation the researchers highlighted in their study, but “considering the exposures are relatively objective and factual, we do not believe the potential for recall bias is substantial.”
“Nonetheless, we strongly believe that replication of our results in prospective, population-representative cohorts will be crucial to making firmer conclusions,” he added.
The study was funded by grants from the Quebec Health Research Fund. The study authors and Dr. Kirkbride disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF PSYCHIATRIC RESEARCH
Daylight Savings: How an imposed time change alters your brain, and what you can do
On March 13, most of the United States and Canada will advance the clock an hour to be on Daylight Saving Time. Most other countries in the Northern Hemisphere will do the same within a few weeks; and many countries across the Southern Hemisphere turn the clock back an hour around the same time. A friend of mine, who spent time on Capitol Hill, once told me that whether it’s adjusting to Daylight Saving Time (and losing an hour of sleep) or switching back to Standard Time (and picking up an hour), large numbers of Americans call their member of Congress every season to complain.
Why are so many of us annoyed by the semi-annual resetting of clocks? Those reasons also come into play when we change time zones as we travel, when we work on the night shift, or when we live at higher latitudes, where depressive symptoms from seasonal affective disorder (SAD) can plague us as the period of daylight progressively shortens in winter.
Our internal clock(s)
Each of us has a biological master clock keeping track of where we are in our 24-hour day, making ongoing time-of-day-appropriate physical and neurologic adjustments. We refer to those automatic adjustments as “circadian” rhythms – from the Latin, for “around a day” rhythms.
One of the most important regulated functions that is influenced by this time keeping is our sleep-wake cycle. Our brain’s hypothalamus has a kind of “master clock” that receives inputs directly from our eyes, which is how our brain sets our daily cycle period at about 24 hours.
This master clock turns on a tiny structure in our brains, called the pineal gland, to release more of a sleep-inducing chemical, called melatonin, about the same time every evening. The level of melatonin slowly increases to reach maximum deep sleep in the night, then slowly declines as you advance toward morning awakening. The shift from darkness to daylight in the morning, causing your initial morning awakening, releases the excitatory neuromodulator norepinephrine, which, with other chemicals, “turns on the lights” in your brain.
That works well most of the time – but no one told your brain that you were going to arbitrarily go to bed an hour earlier (or in the fall, later) on Circadian Rhythm Time!
We also obviously shift the time on the mechanical clock – requiring a reset of the brain’s master clock – when we travel across time zones or work the night shift. That type of desynchronization of our master clock from the mechanical clock puts our waking and sleeping behaviors out of sync with the production of brain chemicals that affect our alertness and mood. The result may be that you find yourself tired, but not sleepy, and often grumpy or even depressed. As an example, on average, people who work the night shift are just a little bit more anxious and depressed than people who get up to rise and shine with the sun every morning.
Seasonal affective disorder
An extreme example of this desynchronization of the master clock can manifest as SAD. SAD is a type of depression that’s related to seasonal transitions. The most commonly cited cases of SAD are for the fall-to-winter transition. In North America, its prevalence is significantly influenced by the distance of one’s place of residence from the equator – with about 12 times the impact in Alaska versus Florida. Of note, a weaker effect of latitude has been recorded in Europe, where more settled populations have had thousands of years to biologically and culturally adapt to their seasonal patterns.
What can we do about our clocks being messed with?
The most common treatment for SAD is light therapy, in which patients sit or work under artificial lights in an early-morning period, to try to advance the chemical signaling that controls sleeping and waking. Alas, light therapy doesn’t work for everyone.
Another approach, with or without the lights, is to engage in activities early in the day that produce brain chemicals to contribute to bright and cheerful waking. Those “raring-to-go” brain chemicals include norepinephrine (produced when you encounter novelty and are just having fun), acetylcholine (produced when you are carefully paying attention and are in a learning and remembering mode), serotonin (produced when you are feeling positive and just a little bit euphoric), and dopamine (produced when you feel happy and all is right with the world).
In fact, you would benefit from creating the habit of starting every day with activity that wakes up your brain. I begin my day with computerized brain exercises that are attentionally demanding, filled with novelty, and richly neurologically rewarding. I then take a brisk morning walk in which I vary my path for the sake of novelty (pumping norepinephrine), pay close attention to my surroundings (pumping acetylcholine and serotonin), and delight in all of the wonderful things out there in my world (pumping dopamine). My dog Doug enjoys this process of waking up brain and body almost as much as I do! Of course, there are a thousand other stimulating things that could help you get your day off to a lively start.
If you anticipate feeling altered by a time change, you could also think about preparing for it in advance. If it’s the semi-annual 1-hour change that throws you off kilter, you might adjust your bedtime by 10 minutes a day for the week before. If you are traveling 12 time zones (and flipping night and day), you may need to make larger adjustments over the preceding couple of weeks. Generally, without that preparation, it takes about 1 day per time zone crossed to naturally adjust your circadian rhythms.
If you’re a little lazier, like me, you might also adjust to jet lag by not forgetting to take along your little bottle of melatonin tablets, to give your pineal gland a little help. Still, that pineal gland will work hard to tell you to take a nap every day – just when you’ll probably want to be wide awake.
And if, after reading this column, you find yourself still annoyed by the upcoming 1-hour time change, you might just look around at what’s happening out there in the world and decide that your troubles are very small by comparison, and that you should delight in the “extra” hour of sunshine each evening!
Dr. Merzenich is professor emeritus, department of neuroscience, at the University of California, San Francisco. He reported serving in various positions and speaking for Posit Science and Stronger Brain, and has also received funding from the National Institutes of Health. A version of this article first appeared on Medscape.com.
On March 13, most of the United States and Canada will advance the clock an hour to be on Daylight Saving Time. Most other countries in the Northern Hemisphere will do the same within a few weeks; and many countries across the Southern Hemisphere turn the clock back an hour around the same time. A friend of mine, who spent time on Capitol Hill, once told me that whether it’s adjusting to Daylight Saving Time (and losing an hour of sleep) or switching back to Standard Time (and picking up an hour), large numbers of Americans call their member of Congress every season to complain.
Why are so many of us annoyed by the semi-annual resetting of clocks? Those reasons also come into play when we change time zones as we travel, when we work on the night shift, or when we live at higher latitudes, where depressive symptoms from seasonal affective disorder (SAD) can plague us as the period of daylight progressively shortens in winter.
Our internal clock(s)
Each of us has a biological master clock keeping track of where we are in our 24-hour day, making ongoing time-of-day-appropriate physical and neurologic adjustments. We refer to those automatic adjustments as “circadian” rhythms – from the Latin, for “around a day” rhythms.
One of the most important regulated functions that is influenced by this time keeping is our sleep-wake cycle. Our brain’s hypothalamus has a kind of “master clock” that receives inputs directly from our eyes, which is how our brain sets our daily cycle period at about 24 hours.
This master clock turns on a tiny structure in our brains, called the pineal gland, to release more of a sleep-inducing chemical, called melatonin, about the same time every evening. The level of melatonin slowly increases to reach maximum deep sleep in the night, then slowly declines as you advance toward morning awakening. The shift from darkness to daylight in the morning, causing your initial morning awakening, releases the excitatory neuromodulator norepinephrine, which, with other chemicals, “turns on the lights” in your brain.
That works well most of the time – but no one told your brain that you were going to arbitrarily go to bed an hour earlier (or in the fall, later) on Circadian Rhythm Time!
We also obviously shift the time on the mechanical clock – requiring a reset of the brain’s master clock – when we travel across time zones or work the night shift. That type of desynchronization of our master clock from the mechanical clock puts our waking and sleeping behaviors out of sync with the production of brain chemicals that affect our alertness and mood. The result may be that you find yourself tired, but not sleepy, and often grumpy or even depressed. As an example, on average, people who work the night shift are just a little bit more anxious and depressed than people who get up to rise and shine with the sun every morning.
Seasonal affective disorder
An extreme example of this desynchronization of the master clock can manifest as SAD. SAD is a type of depression that’s related to seasonal transitions. The most commonly cited cases of SAD are for the fall-to-winter transition. In North America, its prevalence is significantly influenced by the distance of one’s place of residence from the equator – with about 12 times the impact in Alaska versus Florida. Of note, a weaker effect of latitude has been recorded in Europe, where more settled populations have had thousands of years to biologically and culturally adapt to their seasonal patterns.
What can we do about our clocks being messed with?
The most common treatment for SAD is light therapy, in which patients sit or work under artificial lights in an early-morning period, to try to advance the chemical signaling that controls sleeping and waking. Alas, light therapy doesn’t work for everyone.
Another approach, with or without the lights, is to engage in activities early in the day that produce brain chemicals to contribute to bright and cheerful waking. Those “raring-to-go” brain chemicals include norepinephrine (produced when you encounter novelty and are just having fun), acetylcholine (produced when you are carefully paying attention and are in a learning and remembering mode), serotonin (produced when you are feeling positive and just a little bit euphoric), and dopamine (produced when you feel happy and all is right with the world).
In fact, you would benefit from creating the habit of starting every day with activity that wakes up your brain. I begin my day with computerized brain exercises that are attentionally demanding, filled with novelty, and richly neurologically rewarding. I then take a brisk morning walk in which I vary my path for the sake of novelty (pumping norepinephrine), pay close attention to my surroundings (pumping acetylcholine and serotonin), and delight in all of the wonderful things out there in my world (pumping dopamine). My dog Doug enjoys this process of waking up brain and body almost as much as I do! Of course, there are a thousand other stimulating things that could help you get your day off to a lively start.
If you anticipate feeling altered by a time change, you could also think about preparing for it in advance. If it’s the semi-annual 1-hour change that throws you off kilter, you might adjust your bedtime by 10 minutes a day for the week before. If you are traveling 12 time zones (and flipping night and day), you may need to make larger adjustments over the preceding couple of weeks. Generally, without that preparation, it takes about 1 day per time zone crossed to naturally adjust your circadian rhythms.
If you’re a little lazier, like me, you might also adjust to jet lag by not forgetting to take along your little bottle of melatonin tablets, to give your pineal gland a little help. Still, that pineal gland will work hard to tell you to take a nap every day – just when you’ll probably want to be wide awake.
And if, after reading this column, you find yourself still annoyed by the upcoming 1-hour time change, you might just look around at what’s happening out there in the world and decide that your troubles are very small by comparison, and that you should delight in the “extra” hour of sunshine each evening!
Dr. Merzenich is professor emeritus, department of neuroscience, at the University of California, San Francisco. He reported serving in various positions and speaking for Posit Science and Stronger Brain, and has also received funding from the National Institutes of Health. A version of this article first appeared on Medscape.com.
On March 13, most of the United States and Canada will advance the clock an hour to be on Daylight Saving Time. Most other countries in the Northern Hemisphere will do the same within a few weeks; and many countries across the Southern Hemisphere turn the clock back an hour around the same time. A friend of mine, who spent time on Capitol Hill, once told me that whether it’s adjusting to Daylight Saving Time (and losing an hour of sleep) or switching back to Standard Time (and picking up an hour), large numbers of Americans call their member of Congress every season to complain.
Why are so many of us annoyed by the semi-annual resetting of clocks? Those reasons also come into play when we change time zones as we travel, when we work on the night shift, or when we live at higher latitudes, where depressive symptoms from seasonal affective disorder (SAD) can plague us as the period of daylight progressively shortens in winter.
Our internal clock(s)
Each of us has a biological master clock keeping track of where we are in our 24-hour day, making ongoing time-of-day-appropriate physical and neurologic adjustments. We refer to those automatic adjustments as “circadian” rhythms – from the Latin, for “around a day” rhythms.
One of the most important regulated functions that is influenced by this time keeping is our sleep-wake cycle. Our brain’s hypothalamus has a kind of “master clock” that receives inputs directly from our eyes, which is how our brain sets our daily cycle period at about 24 hours.
This master clock turns on a tiny structure in our brains, called the pineal gland, to release more of a sleep-inducing chemical, called melatonin, about the same time every evening. The level of melatonin slowly increases to reach maximum deep sleep in the night, then slowly declines as you advance toward morning awakening. The shift from darkness to daylight in the morning, causing your initial morning awakening, releases the excitatory neuromodulator norepinephrine, which, with other chemicals, “turns on the lights” in your brain.
That works well most of the time – but no one told your brain that you were going to arbitrarily go to bed an hour earlier (or in the fall, later) on Circadian Rhythm Time!
We also obviously shift the time on the mechanical clock – requiring a reset of the brain’s master clock – when we travel across time zones or work the night shift. That type of desynchronization of our master clock from the mechanical clock puts our waking and sleeping behaviors out of sync with the production of brain chemicals that affect our alertness and mood. The result may be that you find yourself tired, but not sleepy, and often grumpy or even depressed. As an example, on average, people who work the night shift are just a little bit more anxious and depressed than people who get up to rise and shine with the sun every morning.
Seasonal affective disorder
An extreme example of this desynchronization of the master clock can manifest as SAD. SAD is a type of depression that’s related to seasonal transitions. The most commonly cited cases of SAD are for the fall-to-winter transition. In North America, its prevalence is significantly influenced by the distance of one’s place of residence from the equator – with about 12 times the impact in Alaska versus Florida. Of note, a weaker effect of latitude has been recorded in Europe, where more settled populations have had thousands of years to biologically and culturally adapt to their seasonal patterns.
What can we do about our clocks being messed with?
The most common treatment for SAD is light therapy, in which patients sit or work under artificial lights in an early-morning period, to try to advance the chemical signaling that controls sleeping and waking. Alas, light therapy doesn’t work for everyone.
Another approach, with or without the lights, is to engage in activities early in the day that produce brain chemicals to contribute to bright and cheerful waking. Those “raring-to-go” brain chemicals include norepinephrine (produced when you encounter novelty and are just having fun), acetylcholine (produced when you are carefully paying attention and are in a learning and remembering mode), serotonin (produced when you are feeling positive and just a little bit euphoric), and dopamine (produced when you feel happy and all is right with the world).
In fact, you would benefit from creating the habit of starting every day with activity that wakes up your brain. I begin my day with computerized brain exercises that are attentionally demanding, filled with novelty, and richly neurologically rewarding. I then take a brisk morning walk in which I vary my path for the sake of novelty (pumping norepinephrine), pay close attention to my surroundings (pumping acetylcholine and serotonin), and delight in all of the wonderful things out there in my world (pumping dopamine). My dog Doug enjoys this process of waking up brain and body almost as much as I do! Of course, there are a thousand other stimulating things that could help you get your day off to a lively start.
If you anticipate feeling altered by a time change, you could also think about preparing for it in advance. If it’s the semi-annual 1-hour change that throws you off kilter, you might adjust your bedtime by 10 minutes a day for the week before. If you are traveling 12 time zones (and flipping night and day), you may need to make larger adjustments over the preceding couple of weeks. Generally, without that preparation, it takes about 1 day per time zone crossed to naturally adjust your circadian rhythms.
If you’re a little lazier, like me, you might also adjust to jet lag by not forgetting to take along your little bottle of melatonin tablets, to give your pineal gland a little help. Still, that pineal gland will work hard to tell you to take a nap every day – just when you’ll probably want to be wide awake.
And if, after reading this column, you find yourself still annoyed by the upcoming 1-hour time change, you might just look around at what’s happening out there in the world and decide that your troubles are very small by comparison, and that you should delight in the “extra” hour of sunshine each evening!
Dr. Merzenich is professor emeritus, department of neuroscience, at the University of California, San Francisco. He reported serving in various positions and speaking for Posit Science and Stronger Brain, and has also received funding from the National Institutes of Health. A version of this article first appeared on Medscape.com.
If you’ve never had COVID, should you relax or worry?
If you’re among those people in the United States who never had COVID-19, how should you think about your risk?
According to the Centers for Disease Control and Prevention (CDC), more than half of people in the United States are in the never-got-COVID category.
The CDC estimated that by the end of January, 43.4% in the United States had developed antibodies to SARS-CoV-2 triggered by infection, not by vaccination — suggesting nearly 60% of people have never been infected.
Now mask mandates are lifting, and daily case and death numbers are plunging. According to the New York Times tracker, new cases are down 51% for the past 2 weeks, and deaths have fallen 30% in that period.
So as those who have so far escaped the virus venture further out into reopened environments, should they worry more or less about risk than their previously infected counterparts?
No “suit of armor”
William Schaffner, MD, an infectious disease expert at Vanderbilt University School of Medicine in Nashville, Tenn., said in an interview that science has not been able to determine why some people have been able to be stay COVID-free when the virus was raging and exposure was ubiquitous.
He said it’s important to remember that though some people think they have never had COVID, they may have been asymptomatic or attributed mild symptoms to something else.
“People may have conceivably — but we can’t define them yet — different capacities to ward off viruses or bacteria,” Dr. Schaffner said.
Could it be that some people have a better immune system or genetic component or environmental reason that they are less susceptible to infectious disease? “We can’t define that in 2022 medicine, but it could be,” he said.
More is known about why people with the same COVID exposure may have different levels of illness severity.
“They’re more likely to get seriously ill if they have a list of predisposing conditions — if they’re older, if they’re frail, if they have underlying illness or are obese. All of those things clearly impair the body’s response to virus,” Dr. Schaffner said.
He warns those who have never been infected, though, not to assume they have “a suit of armor.”
All should continue to follow guidance on getting vaccinated, and those vaccinated should continue to get boosted, Dr. Schaffner said.
“Clearly, the data show that if you are vaccinated and boosted, you’re protected much more securely against severe disease,” he said.
If the never-COVIDs develop a respiratory infection, they should still get tested for COVID, Dr. Schaffner said.
He said while both vaccines and previous natural infection offer protection, the duration of that protection is not yet known.
“We have to stay tuned,” Dr. Schaffner said. “There may be a recommendation in the future to get a booster annually or something like that. We need to be open to those down the road.”
Amesh Adalja, MD, senior scholar at the Johns Hopkins Center for Health Security in Baltimore, says it’s unclear why some people have been able to avoid COVID.
“The explanation is likely multifactorial and involves behaviors as well as possible idiosyncrasies with their immune systems that are genetically based,” he said. “It also may be the case that inapparent infections occurred and went undiagnosed.”
Dr. Adalja agrees, though, that this isn’t the time to get overconfident with risk-taking where COVID is concerned.
“People who have not knowingly been infected with COVID should be vaccinated, and after that, be assured that they are protected against serious disease from this virus,” he said.
Genetic protection?
A new study in Nature Genetics explains a potential genetic relationship. Study authors found evidence that levels of expression of angiotensin-converting enzyme 2 (ACE2) – which helps regulate blood pressure, wound healing, and inflammation, but has also been shown to serve as an entry point into cells for some coronaviruses like SARS-CoV-2 — influence COVID-19 risk.
Manuel A. Ferreira, PhD, an executive director for analytic genetics at Regeneron Pharmaceuticals, said in an interview that ACE2 receptors — what he calls the “gateways” for SARS-CoV-2 to enter the body — are different in people who have inherited a particular allele.
The researchers have found that that allele is associated with lower risk of SARS-CoV-2 infection.
“It’s quite substantial -- a 40% risk reduction if you carry the allele that reduces ACE2 expression,” he said. They were not able to discern from this study, however, whether that could predict severity of disease.
The team also looked at a series of six genetic variants elsewhere in the genome and developed a risk score to see if it was possible to predict who might be more susceptible to severe COVID.
Dr. Ferreira said the score only slightly improved predictive abilities beyond factors such as age, sex, weight, and comorbidities. Further information will help hone the ability to predict the likelihood of developing severe disease on the basis of genetics, Ferreira said.
“As we identify more genetic risk factors for COVID — variants like the ACE2 variant that will affect your risk of having COVID — the more informative the risk score will be,” he said.
Several authors of the Nature Genetics article are current and/or former employees of AncestryDNA and may hold equity in AncestryDNA. Several are Regeneron employees and/or hold stock in the company. Dr. Ferreira is an employee of Regeneron and holds stock in the company. Dr. Schaffner and Dr. Adalja report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
If you’re among those people in the United States who never had COVID-19, how should you think about your risk?
According to the Centers for Disease Control and Prevention (CDC), more than half of people in the United States are in the never-got-COVID category.
The CDC estimated that by the end of January, 43.4% in the United States had developed antibodies to SARS-CoV-2 triggered by infection, not by vaccination — suggesting nearly 60% of people have never been infected.
Now mask mandates are lifting, and daily case and death numbers are plunging. According to the New York Times tracker, new cases are down 51% for the past 2 weeks, and deaths have fallen 30% in that period.
So as those who have so far escaped the virus venture further out into reopened environments, should they worry more or less about risk than their previously infected counterparts?
No “suit of armor”
William Schaffner, MD, an infectious disease expert at Vanderbilt University School of Medicine in Nashville, Tenn., said in an interview that science has not been able to determine why some people have been able to be stay COVID-free when the virus was raging and exposure was ubiquitous.
He said it’s important to remember that though some people think they have never had COVID, they may have been asymptomatic or attributed mild symptoms to something else.
“People may have conceivably — but we can’t define them yet — different capacities to ward off viruses or bacteria,” Dr. Schaffner said.
Could it be that some people have a better immune system or genetic component or environmental reason that they are less susceptible to infectious disease? “We can’t define that in 2022 medicine, but it could be,” he said.
More is known about why people with the same COVID exposure may have different levels of illness severity.
“They’re more likely to get seriously ill if they have a list of predisposing conditions — if they’re older, if they’re frail, if they have underlying illness or are obese. All of those things clearly impair the body’s response to virus,” Dr. Schaffner said.
He warns those who have never been infected, though, not to assume they have “a suit of armor.”
All should continue to follow guidance on getting vaccinated, and those vaccinated should continue to get boosted, Dr. Schaffner said.
“Clearly, the data show that if you are vaccinated and boosted, you’re protected much more securely against severe disease,” he said.
If the never-COVIDs develop a respiratory infection, they should still get tested for COVID, Dr. Schaffner said.
He said while both vaccines and previous natural infection offer protection, the duration of that protection is not yet known.
“We have to stay tuned,” Dr. Schaffner said. “There may be a recommendation in the future to get a booster annually or something like that. We need to be open to those down the road.”
Amesh Adalja, MD, senior scholar at the Johns Hopkins Center for Health Security in Baltimore, says it’s unclear why some people have been able to avoid COVID.
“The explanation is likely multifactorial and involves behaviors as well as possible idiosyncrasies with their immune systems that are genetically based,” he said. “It also may be the case that inapparent infections occurred and went undiagnosed.”
Dr. Adalja agrees, though, that this isn’t the time to get overconfident with risk-taking where COVID is concerned.
“People who have not knowingly been infected with COVID should be vaccinated, and after that, be assured that they are protected against serious disease from this virus,” he said.
Genetic protection?
A new study in Nature Genetics explains a potential genetic relationship. Study authors found evidence that levels of expression of angiotensin-converting enzyme 2 (ACE2) – which helps regulate blood pressure, wound healing, and inflammation, but has also been shown to serve as an entry point into cells for some coronaviruses like SARS-CoV-2 — influence COVID-19 risk.
Manuel A. Ferreira, PhD, an executive director for analytic genetics at Regeneron Pharmaceuticals, said in an interview that ACE2 receptors — what he calls the “gateways” for SARS-CoV-2 to enter the body — are different in people who have inherited a particular allele.
The researchers have found that that allele is associated with lower risk of SARS-CoV-2 infection.
“It’s quite substantial -- a 40% risk reduction if you carry the allele that reduces ACE2 expression,” he said. They were not able to discern from this study, however, whether that could predict severity of disease.
The team also looked at a series of six genetic variants elsewhere in the genome and developed a risk score to see if it was possible to predict who might be more susceptible to severe COVID.
Dr. Ferreira said the score only slightly improved predictive abilities beyond factors such as age, sex, weight, and comorbidities. Further information will help hone the ability to predict the likelihood of developing severe disease on the basis of genetics, Ferreira said.
“As we identify more genetic risk factors for COVID — variants like the ACE2 variant that will affect your risk of having COVID — the more informative the risk score will be,” he said.
Several authors of the Nature Genetics article are current and/or former employees of AncestryDNA and may hold equity in AncestryDNA. Several are Regeneron employees and/or hold stock in the company. Dr. Ferreira is an employee of Regeneron and holds stock in the company. Dr. Schaffner and Dr. Adalja report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
If you’re among those people in the United States who never had COVID-19, how should you think about your risk?
According to the Centers for Disease Control and Prevention (CDC), more than half of people in the United States are in the never-got-COVID category.
The CDC estimated that by the end of January, 43.4% in the United States had developed antibodies to SARS-CoV-2 triggered by infection, not by vaccination — suggesting nearly 60% of people have never been infected.
Now mask mandates are lifting, and daily case and death numbers are plunging. According to the New York Times tracker, new cases are down 51% for the past 2 weeks, and deaths have fallen 30% in that period.
So as those who have so far escaped the virus venture further out into reopened environments, should they worry more or less about risk than their previously infected counterparts?
No “suit of armor”
William Schaffner, MD, an infectious disease expert at Vanderbilt University School of Medicine in Nashville, Tenn., said in an interview that science has not been able to determine why some people have been able to be stay COVID-free when the virus was raging and exposure was ubiquitous.
He said it’s important to remember that though some people think they have never had COVID, they may have been asymptomatic or attributed mild symptoms to something else.
“People may have conceivably — but we can’t define them yet — different capacities to ward off viruses or bacteria,” Dr. Schaffner said.
Could it be that some people have a better immune system or genetic component or environmental reason that they are less susceptible to infectious disease? “We can’t define that in 2022 medicine, but it could be,” he said.
More is known about why people with the same COVID exposure may have different levels of illness severity.
“They’re more likely to get seriously ill if they have a list of predisposing conditions — if they’re older, if they’re frail, if they have underlying illness or are obese. All of those things clearly impair the body’s response to virus,” Dr. Schaffner said.
He warns those who have never been infected, though, not to assume they have “a suit of armor.”
All should continue to follow guidance on getting vaccinated, and those vaccinated should continue to get boosted, Dr. Schaffner said.
“Clearly, the data show that if you are vaccinated and boosted, you’re protected much more securely against severe disease,” he said.
If the never-COVIDs develop a respiratory infection, they should still get tested for COVID, Dr. Schaffner said.
He said while both vaccines and previous natural infection offer protection, the duration of that protection is not yet known.
“We have to stay tuned,” Dr. Schaffner said. “There may be a recommendation in the future to get a booster annually or something like that. We need to be open to those down the road.”
Amesh Adalja, MD, senior scholar at the Johns Hopkins Center for Health Security in Baltimore, says it’s unclear why some people have been able to avoid COVID.
“The explanation is likely multifactorial and involves behaviors as well as possible idiosyncrasies with their immune systems that are genetically based,” he said. “It also may be the case that inapparent infections occurred and went undiagnosed.”
Dr. Adalja agrees, though, that this isn’t the time to get overconfident with risk-taking where COVID is concerned.
“People who have not knowingly been infected with COVID should be vaccinated, and after that, be assured that they are protected against serious disease from this virus,” he said.
Genetic protection?
A new study in Nature Genetics explains a potential genetic relationship. Study authors found evidence that levels of expression of angiotensin-converting enzyme 2 (ACE2) – which helps regulate blood pressure, wound healing, and inflammation, but has also been shown to serve as an entry point into cells for some coronaviruses like SARS-CoV-2 — influence COVID-19 risk.
Manuel A. Ferreira, PhD, an executive director for analytic genetics at Regeneron Pharmaceuticals, said in an interview that ACE2 receptors — what he calls the “gateways” for SARS-CoV-2 to enter the body — are different in people who have inherited a particular allele.
The researchers have found that that allele is associated with lower risk of SARS-CoV-2 infection.
“It’s quite substantial -- a 40% risk reduction if you carry the allele that reduces ACE2 expression,” he said. They were not able to discern from this study, however, whether that could predict severity of disease.
The team also looked at a series of six genetic variants elsewhere in the genome and developed a risk score to see if it was possible to predict who might be more susceptible to severe COVID.
Dr. Ferreira said the score only slightly improved predictive abilities beyond factors such as age, sex, weight, and comorbidities. Further information will help hone the ability to predict the likelihood of developing severe disease on the basis of genetics, Ferreira said.
“As we identify more genetic risk factors for COVID — variants like the ACE2 variant that will affect your risk of having COVID — the more informative the risk score will be,” he said.
Several authors of the Nature Genetics article are current and/or former employees of AncestryDNA and may hold equity in AncestryDNA. Several are Regeneron employees and/or hold stock in the company. Dr. Ferreira is an employee of Regeneron and holds stock in the company. Dr. Schaffner and Dr. Adalja report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
First ‘before-and-after’ COVID-19 brain imaging study shows structural changes
, a new imaging study shows.
In the first study to use magnetic resonance brain imaging, before and after COVID-19, investigators found “greater reduction in grey matter thickness and tissue-contrast in the orbitofrontal cortex and parahippocampal gyrus, greater changes in markers of tissue damage in regions functionally connected to the primary olfactory cortex and greater reduction in global brain size.” However, the researchers urge caution when interpreting the findings.
Gwenaëlle Douaud, PhD, Wellcome Center for Integrative Neuroimaging, Nuffield Department of Clinical Neurosciences, University of Oxford, England, and colleagues describe these brain changes as “modest.”
“Whether these abnormal changes are the hallmark of the spread of the pathogenic effects in the brain, or of the virus itself, and whether these may prefigure a future vulnerability of the limbic system in particular, including memory, for these participants, remains to be investigated,” the researchers wrote.
The findings were published online March 7 in the journal Nature.
Gray matter loss
The investigators analyzed data from the UK Biobank, a large-scale biomedical database with genetic and health information for about 500,000 individuals living in the UK. They identified 785 adults aged 51-81 years who had undergone two brain MRIs about 3 years apart. Of these, 401 tested positive for SARS-CoV-2 before the second scan.
Participants also completed cognitive tests at the time of both scans.
Biobank centers use identical MRI scans and scanning methods, including six types of MRI scans, to image distinct regions of the brain and brain function. Results showed that although some loss of gray matter over time is normal, individuals who were infected with SARS-CoV-2 showed a 0.2% to 2% brain tissue loss in the parahippocampal gyrus, the orbitofrontal cortex, and the insula – all of which are largely involved in the sense of smell.
Participants who had contracted COVID-19 also showed a greater reduction in overall brain volume and a decrease in cognitive function.
Most of those with COVID-19 had only mild or moderate symptoms. However, the findings held even after the researchers excluded patients who had been hospitalized.
More research needed
“These findings might help explain why some people experience brain symptoms long after the acute infection,” Max Taquet, PhD, National Institute for Health Research Oxford Health BRC senior research fellow, University of Oxford, said in a press release.
Dr. Taquet, who was not a part of the study, noted the causes of these brain changes remain to be determined. Questions remain as to “whether they can be prevented or even reverted, as well as whether similar changes are observed in hospitalized patients,” children, younger adults, and minority groups.
“It is possible that these brain changes are not caused by COVID-19 but represent the natural progression of a disease that itself increased the risk of COVID-19,” Dr. Taquet said.
Other experts expressed concern over the findings and emphasized the need for more research.
“I am very concerned by the alarming use of language in the report with terms such as ‘neurodegenerative,’ “ Alan Carson, MD, professor of neuropsychiatry at the Center for Clinical Brain Sciences at the University of Edinburgh, Scotland, said in a press release. “The size and magnitude of brain changes found is very modest and such changes can be caused by a simple change in mental experience,” Dr. Carson said.
“What this study almost certainly shows is the impact, in terms of neural changes, of being disconnected from one’s sense of smell,” he added.
The study was funded by the Wellcome Trust Collaborative. Full financial conflict information for the study authors is included in the original article. Dr. Taquet has collaborated previously with some of the investigators.
A version of this article first appeared on Medscape.com.
, a new imaging study shows.
In the first study to use magnetic resonance brain imaging, before and after COVID-19, investigators found “greater reduction in grey matter thickness and tissue-contrast in the orbitofrontal cortex and parahippocampal gyrus, greater changes in markers of tissue damage in regions functionally connected to the primary olfactory cortex and greater reduction in global brain size.” However, the researchers urge caution when interpreting the findings.
Gwenaëlle Douaud, PhD, Wellcome Center for Integrative Neuroimaging, Nuffield Department of Clinical Neurosciences, University of Oxford, England, and colleagues describe these brain changes as “modest.”
“Whether these abnormal changes are the hallmark of the spread of the pathogenic effects in the brain, or of the virus itself, and whether these may prefigure a future vulnerability of the limbic system in particular, including memory, for these participants, remains to be investigated,” the researchers wrote.
The findings were published online March 7 in the journal Nature.
Gray matter loss
The investigators analyzed data from the UK Biobank, a large-scale biomedical database with genetic and health information for about 500,000 individuals living in the UK. They identified 785 adults aged 51-81 years who had undergone two brain MRIs about 3 years apart. Of these, 401 tested positive for SARS-CoV-2 before the second scan.
Participants also completed cognitive tests at the time of both scans.
Biobank centers use identical MRI scans and scanning methods, including six types of MRI scans, to image distinct regions of the brain and brain function. Results showed that although some loss of gray matter over time is normal, individuals who were infected with SARS-CoV-2 showed a 0.2% to 2% brain tissue loss in the parahippocampal gyrus, the orbitofrontal cortex, and the insula – all of which are largely involved in the sense of smell.
Participants who had contracted COVID-19 also showed a greater reduction in overall brain volume and a decrease in cognitive function.
Most of those with COVID-19 had only mild or moderate symptoms. However, the findings held even after the researchers excluded patients who had been hospitalized.
More research needed
“These findings might help explain why some people experience brain symptoms long after the acute infection,” Max Taquet, PhD, National Institute for Health Research Oxford Health BRC senior research fellow, University of Oxford, said in a press release.
Dr. Taquet, who was not a part of the study, noted the causes of these brain changes remain to be determined. Questions remain as to “whether they can be prevented or even reverted, as well as whether similar changes are observed in hospitalized patients,” children, younger adults, and minority groups.
“It is possible that these brain changes are not caused by COVID-19 but represent the natural progression of a disease that itself increased the risk of COVID-19,” Dr. Taquet said.
Other experts expressed concern over the findings and emphasized the need for more research.
“I am very concerned by the alarming use of language in the report with terms such as ‘neurodegenerative,’ “ Alan Carson, MD, professor of neuropsychiatry at the Center for Clinical Brain Sciences at the University of Edinburgh, Scotland, said in a press release. “The size and magnitude of brain changes found is very modest and such changes can be caused by a simple change in mental experience,” Dr. Carson said.
“What this study almost certainly shows is the impact, in terms of neural changes, of being disconnected from one’s sense of smell,” he added.
The study was funded by the Wellcome Trust Collaborative. Full financial conflict information for the study authors is included in the original article. Dr. Taquet has collaborated previously with some of the investigators.
A version of this article first appeared on Medscape.com.
, a new imaging study shows.
In the first study to use magnetic resonance brain imaging, before and after COVID-19, investigators found “greater reduction in grey matter thickness and tissue-contrast in the orbitofrontal cortex and parahippocampal gyrus, greater changes in markers of tissue damage in regions functionally connected to the primary olfactory cortex and greater reduction in global brain size.” However, the researchers urge caution when interpreting the findings.
Gwenaëlle Douaud, PhD, Wellcome Center for Integrative Neuroimaging, Nuffield Department of Clinical Neurosciences, University of Oxford, England, and colleagues describe these brain changes as “modest.”
“Whether these abnormal changes are the hallmark of the spread of the pathogenic effects in the brain, or of the virus itself, and whether these may prefigure a future vulnerability of the limbic system in particular, including memory, for these participants, remains to be investigated,” the researchers wrote.
The findings were published online March 7 in the journal Nature.
Gray matter loss
The investigators analyzed data from the UK Biobank, a large-scale biomedical database with genetic and health information for about 500,000 individuals living in the UK. They identified 785 adults aged 51-81 years who had undergone two brain MRIs about 3 years apart. Of these, 401 tested positive for SARS-CoV-2 before the second scan.
Participants also completed cognitive tests at the time of both scans.
Biobank centers use identical MRI scans and scanning methods, including six types of MRI scans, to image distinct regions of the brain and brain function. Results showed that although some loss of gray matter over time is normal, individuals who were infected with SARS-CoV-2 showed a 0.2% to 2% brain tissue loss in the parahippocampal gyrus, the orbitofrontal cortex, and the insula – all of which are largely involved in the sense of smell.
Participants who had contracted COVID-19 also showed a greater reduction in overall brain volume and a decrease in cognitive function.
Most of those with COVID-19 had only mild or moderate symptoms. However, the findings held even after the researchers excluded patients who had been hospitalized.
More research needed
“These findings might help explain why some people experience brain symptoms long after the acute infection,” Max Taquet, PhD, National Institute for Health Research Oxford Health BRC senior research fellow, University of Oxford, said in a press release.
Dr. Taquet, who was not a part of the study, noted the causes of these brain changes remain to be determined. Questions remain as to “whether they can be prevented or even reverted, as well as whether similar changes are observed in hospitalized patients,” children, younger adults, and minority groups.
“It is possible that these brain changes are not caused by COVID-19 but represent the natural progression of a disease that itself increased the risk of COVID-19,” Dr. Taquet said.
Other experts expressed concern over the findings and emphasized the need for more research.
“I am very concerned by the alarming use of language in the report with terms such as ‘neurodegenerative,’ “ Alan Carson, MD, professor of neuropsychiatry at the Center for Clinical Brain Sciences at the University of Edinburgh, Scotland, said in a press release. “The size and magnitude of brain changes found is very modest and such changes can be caused by a simple change in mental experience,” Dr. Carson said.
“What this study almost certainly shows is the impact, in terms of neural changes, of being disconnected from one’s sense of smell,” he added.
The study was funded by the Wellcome Trust Collaborative. Full financial conflict information for the study authors is included in the original article. Dr. Taquet has collaborated previously with some of the investigators.
A version of this article first appeared on Medscape.com.
From Nature
FDA, DEA pushed to make gabapentin a controlled substance to stop ‘widespread misuse’
In a bid to stop abuse and diversion of the anticonvulsant gabapentin, a watchdog group is petitioning federal regulators to make the drug a controlled substance.
Gabapentin is a generic drug, best known under the brand name Neurontin. The petition also covers the related drug gabapentin enacarbil (Horizant).
Public Citizen requested that gabapentin come under the DEA’s Schedule V category, which already includes the similar drug pregabalin (Lyrica). Schedule V is the lowest rung on the DEA’s drug schedule, meaning it has lower potential for abuse then Schedule I through IV drugs. This tier also includes cough preparations with less than 200 milligrams of codeine.
Classifying gabapentin as a Schedule V drug would facilitate better tracking of the drug’s use and misuse and put in place educational and limitation requirements to mitigate the risk of addiction, overdose, and death, Michael Abrams, MPH, PhD, senior health researcher with Public Citizen’s Health Research Group, and colleagues write in the petition.
‘Widespread misuse’
There is “substantial evidence of widespread misuse” of gabapentin, plausibly helped by “extraordinary levels of off-label prescribing,” Public Citizen said in the petition.
Some estimates have pegged off-label use at more than 90%, with gabapentin prescribed for indications such as chronic cough, hiccups, postoperative pain, and postmenopausal hot flashes, the group said.
“Moreover, there are numerous reports indicating that gabapentin is widely used and diverted on the street to induce ‘highs’ or otherwise self-medicate,” Public Citizen said. “Both gabapentin and pregabalin have been empirically linked to the opioid overdose epidemic as drugs that potentiate the activity of these oftentimes deadly analgesics.”
This news organization tried several times to reach Azurity for comment but did not receive a response. Pfizer included gabapentin in the portfolio of drugs used to create the Viatris spin-off, which took place in 2020. Pfizer referred this news organization to Viatris for comment, but it also did not respond.
It is unclear how the FDA and DEA will respond to the petition. Public Citizen has received a reply from the FDA, in which the agency acknowledged receipt of the petition. However, the “acceptance of the petition for filing is a procedural matter and in no way reflects the agency’s decision on the substantive merits of the petition,” the FDA said in a letter.
As is common practice, the agency assigned a docket number for the petition, FDA-2022-P-0149. The docket’s website allows interested parties to track the issue.
‘Unnoticed’ abuse
There have been rising concerns about risks and abuse of gabapentin in recent years. In its petition, Public Citizen noted that the United Kingdom and several U.S. states have already sought tighter control of gabapentin prescriptions.
In 2019, the United Kingdom announced it would reclassify both pregabalin and gabapentin as class C controlled substances because of the rising numbers of deaths linked to the drugs.
As of November 2020, seven states – Alabama, Kentucky, Michigan, North Dakota, Tennessee, Virginia, and West Virginia – had classified gabapentin as a schedule V drug, while another 12 states required prescription monitoring of the drug, Public Citizen noted.
In 2018, researchers at the University of Louisville, Kentucky, a state that has been hit particularly hard by the opioid crisis, tried to draw more attention to the risks of gabapentin.
“Amid the opioid epidemic, abuse of a different prescription painkiller has widely gone unnoticed,” the University said in a press release at the time.
The release highlighted a study led by Rachel Vickers Smith, PhD, assistant professor in the University of Louisville School of Nursing that was published in Psychology of Addictive Behaviors.
It included 33 individuals who reported recent recreational use of gabapentin. Use of the drug was combined with buprenorphine, other opioids, cocaine, and caffeine to produce effects such as muscle relaxation, pain reduction, sleep induction, feeling drunk, and feeling “high.”
In the press release, Dr. Vickers Smith said individuals who abuse gabapentin often mix it with opioids, marijuana, cocaine, and opioid treatment medication, compounding side effects to the central nervous system that include euphoria and sedation.
In addition, some individuals who primarily abused opioid pain medication have turned to gabapentin after law-enforcement actions made it more difficult to obtain prescription opioids, she noted.
“People are looking for other drugs to substitute for opioids, and gabapentin has filled that place for some,” Dr. Vickers Smith said. “Some have said it gives them a high similar to opioids.”
FDA 2019 warning
In 2019, the FDA issued a warning about serious breathing difficulties associated with gabapentin and pregabalin in patients with respiratory risk factors.
These factors include opioid use and other drugs that depress the central nervous system, as well as conditions such as chronic obstructive pulmonary disease that reduce lung function. Older patients are also at higher risk, the FDA said.
The agency noted that gabapentinoids are often co-prescribed with opioids for for medical conditions and abused in combination with opioids. Data collected in 2016 from an office-based physician survey showed 14% of patient encounters involving gabapentin also involved opioids, the FDA said.
“Our evaluation shows that the use of these medicines, often referred to as gabapentinoids, has been growing for prescribed medical use, as well as misuse and abuse,” the agency said in its 2019 alert.
A version of this article first appeared on Medscape.com.
In a bid to stop abuse and diversion of the anticonvulsant gabapentin, a watchdog group is petitioning federal regulators to make the drug a controlled substance.
Gabapentin is a generic drug, best known under the brand name Neurontin. The petition also covers the related drug gabapentin enacarbil (Horizant).
Public Citizen requested that gabapentin come under the DEA’s Schedule V category, which already includes the similar drug pregabalin (Lyrica). Schedule V is the lowest rung on the DEA’s drug schedule, meaning it has lower potential for abuse then Schedule I through IV drugs. This tier also includes cough preparations with less than 200 milligrams of codeine.
Classifying gabapentin as a Schedule V drug would facilitate better tracking of the drug’s use and misuse and put in place educational and limitation requirements to mitigate the risk of addiction, overdose, and death, Michael Abrams, MPH, PhD, senior health researcher with Public Citizen’s Health Research Group, and colleagues write in the petition.
‘Widespread misuse’
There is “substantial evidence of widespread misuse” of gabapentin, plausibly helped by “extraordinary levels of off-label prescribing,” Public Citizen said in the petition.
Some estimates have pegged off-label use at more than 90%, with gabapentin prescribed for indications such as chronic cough, hiccups, postoperative pain, and postmenopausal hot flashes, the group said.
“Moreover, there are numerous reports indicating that gabapentin is widely used and diverted on the street to induce ‘highs’ or otherwise self-medicate,” Public Citizen said. “Both gabapentin and pregabalin have been empirically linked to the opioid overdose epidemic as drugs that potentiate the activity of these oftentimes deadly analgesics.”
This news organization tried several times to reach Azurity for comment but did not receive a response. Pfizer included gabapentin in the portfolio of drugs used to create the Viatris spin-off, which took place in 2020. Pfizer referred this news organization to Viatris for comment, but it also did not respond.
It is unclear how the FDA and DEA will respond to the petition. Public Citizen has received a reply from the FDA, in which the agency acknowledged receipt of the petition. However, the “acceptance of the petition for filing is a procedural matter and in no way reflects the agency’s decision on the substantive merits of the petition,” the FDA said in a letter.
As is common practice, the agency assigned a docket number for the petition, FDA-2022-P-0149. The docket’s website allows interested parties to track the issue.
‘Unnoticed’ abuse
There have been rising concerns about risks and abuse of gabapentin in recent years. In its petition, Public Citizen noted that the United Kingdom and several U.S. states have already sought tighter control of gabapentin prescriptions.
In 2019, the United Kingdom announced it would reclassify both pregabalin and gabapentin as class C controlled substances because of the rising numbers of deaths linked to the drugs.
As of November 2020, seven states – Alabama, Kentucky, Michigan, North Dakota, Tennessee, Virginia, and West Virginia – had classified gabapentin as a schedule V drug, while another 12 states required prescription monitoring of the drug, Public Citizen noted.
In 2018, researchers at the University of Louisville, Kentucky, a state that has been hit particularly hard by the opioid crisis, tried to draw more attention to the risks of gabapentin.
“Amid the opioid epidemic, abuse of a different prescription painkiller has widely gone unnoticed,” the University said in a press release at the time.
The release highlighted a study led by Rachel Vickers Smith, PhD, assistant professor in the University of Louisville School of Nursing that was published in Psychology of Addictive Behaviors.
It included 33 individuals who reported recent recreational use of gabapentin. Use of the drug was combined with buprenorphine, other opioids, cocaine, and caffeine to produce effects such as muscle relaxation, pain reduction, sleep induction, feeling drunk, and feeling “high.”
In the press release, Dr. Vickers Smith said individuals who abuse gabapentin often mix it with opioids, marijuana, cocaine, and opioid treatment medication, compounding side effects to the central nervous system that include euphoria and sedation.
In addition, some individuals who primarily abused opioid pain medication have turned to gabapentin after law-enforcement actions made it more difficult to obtain prescription opioids, she noted.
“People are looking for other drugs to substitute for opioids, and gabapentin has filled that place for some,” Dr. Vickers Smith said. “Some have said it gives them a high similar to opioids.”
FDA 2019 warning
In 2019, the FDA issued a warning about serious breathing difficulties associated with gabapentin and pregabalin in patients with respiratory risk factors.
These factors include opioid use and other drugs that depress the central nervous system, as well as conditions such as chronic obstructive pulmonary disease that reduce lung function. Older patients are also at higher risk, the FDA said.
The agency noted that gabapentinoids are often co-prescribed with opioids for for medical conditions and abused in combination with opioids. Data collected in 2016 from an office-based physician survey showed 14% of patient encounters involving gabapentin also involved opioids, the FDA said.
“Our evaluation shows that the use of these medicines, often referred to as gabapentinoids, has been growing for prescribed medical use, as well as misuse and abuse,” the agency said in its 2019 alert.
A version of this article first appeared on Medscape.com.
In a bid to stop abuse and diversion of the anticonvulsant gabapentin, a watchdog group is petitioning federal regulators to make the drug a controlled substance.
Gabapentin is a generic drug, best known under the brand name Neurontin. The petition also covers the related drug gabapentin enacarbil (Horizant).
Public Citizen requested that gabapentin come under the DEA’s Schedule V category, which already includes the similar drug pregabalin (Lyrica). Schedule V is the lowest rung on the DEA’s drug schedule, meaning it has lower potential for abuse then Schedule I through IV drugs. This tier also includes cough preparations with less than 200 milligrams of codeine.
Classifying gabapentin as a Schedule V drug would facilitate better tracking of the drug’s use and misuse and put in place educational and limitation requirements to mitigate the risk of addiction, overdose, and death, Michael Abrams, MPH, PhD, senior health researcher with Public Citizen’s Health Research Group, and colleagues write in the petition.
‘Widespread misuse’
There is “substantial evidence of widespread misuse” of gabapentin, plausibly helped by “extraordinary levels of off-label prescribing,” Public Citizen said in the petition.
Some estimates have pegged off-label use at more than 90%, with gabapentin prescribed for indications such as chronic cough, hiccups, postoperative pain, and postmenopausal hot flashes, the group said.
“Moreover, there are numerous reports indicating that gabapentin is widely used and diverted on the street to induce ‘highs’ or otherwise self-medicate,” Public Citizen said. “Both gabapentin and pregabalin have been empirically linked to the opioid overdose epidemic as drugs that potentiate the activity of these oftentimes deadly analgesics.”
This news organization tried several times to reach Azurity for comment but did not receive a response. Pfizer included gabapentin in the portfolio of drugs used to create the Viatris spin-off, which took place in 2020. Pfizer referred this news organization to Viatris for comment, but it also did not respond.
It is unclear how the FDA and DEA will respond to the petition. Public Citizen has received a reply from the FDA, in which the agency acknowledged receipt of the petition. However, the “acceptance of the petition for filing is a procedural matter and in no way reflects the agency’s decision on the substantive merits of the petition,” the FDA said in a letter.
As is common practice, the agency assigned a docket number for the petition, FDA-2022-P-0149. The docket’s website allows interested parties to track the issue.
‘Unnoticed’ abuse
There have been rising concerns about risks and abuse of gabapentin in recent years. In its petition, Public Citizen noted that the United Kingdom and several U.S. states have already sought tighter control of gabapentin prescriptions.
In 2019, the United Kingdom announced it would reclassify both pregabalin and gabapentin as class C controlled substances because of the rising numbers of deaths linked to the drugs.
As of November 2020, seven states – Alabama, Kentucky, Michigan, North Dakota, Tennessee, Virginia, and West Virginia – had classified gabapentin as a schedule V drug, while another 12 states required prescription monitoring of the drug, Public Citizen noted.
In 2018, researchers at the University of Louisville, Kentucky, a state that has been hit particularly hard by the opioid crisis, tried to draw more attention to the risks of gabapentin.
“Amid the opioid epidemic, abuse of a different prescription painkiller has widely gone unnoticed,” the University said in a press release at the time.
The release highlighted a study led by Rachel Vickers Smith, PhD, assistant professor in the University of Louisville School of Nursing that was published in Psychology of Addictive Behaviors.
It included 33 individuals who reported recent recreational use of gabapentin. Use of the drug was combined with buprenorphine, other opioids, cocaine, and caffeine to produce effects such as muscle relaxation, pain reduction, sleep induction, feeling drunk, and feeling “high.”
In the press release, Dr. Vickers Smith said individuals who abuse gabapentin often mix it with opioids, marijuana, cocaine, and opioid treatment medication, compounding side effects to the central nervous system that include euphoria and sedation.
In addition, some individuals who primarily abused opioid pain medication have turned to gabapentin after law-enforcement actions made it more difficult to obtain prescription opioids, she noted.
“People are looking for other drugs to substitute for opioids, and gabapentin has filled that place for some,” Dr. Vickers Smith said. “Some have said it gives them a high similar to opioids.”
FDA 2019 warning
In 2019, the FDA issued a warning about serious breathing difficulties associated with gabapentin and pregabalin in patients with respiratory risk factors.
These factors include opioid use and other drugs that depress the central nervous system, as well as conditions such as chronic obstructive pulmonary disease that reduce lung function. Older patients are also at higher risk, the FDA said.
The agency noted that gabapentinoids are often co-prescribed with opioids for for medical conditions and abused in combination with opioids. Data collected in 2016 from an office-based physician survey showed 14% of patient encounters involving gabapentin also involved opioids, the FDA said.
“Our evaluation shows that the use of these medicines, often referred to as gabapentinoids, has been growing for prescribed medical use, as well as misuse and abuse,” the agency said in its 2019 alert.
A version of this article first appeared on Medscape.com.
Physicians beware: Feds start tracking information-blocking claims
The federal government’s efforts to thwart information blocking are underway. As such,
Recently, the Office of the National Coordinator revealed that the Department of Health & Humans Services has received 299 reports of information blocking since inviting anyone who suspected that health care providers, IT developers, or health information networks/exchanges might have interfered with access, exchange, or use of EHI through the Report Information Blocking Portal on April 5, 2021.
The vast majority of these claims – 211 – were filed against providers, while 46 alleged incidents of information blocking were by health IT developers, and two claims point to health information networks/ exchanges. The other 25 claims did not appear to present a claim of information blocking.
Of the 274 possible claims of information blocking recently released by ONC, 176 were made by patients.
The ONC has sent all possible claims to the HHS’s Office of the Inspector General. The claims have not yet been investigated and substantiated.
Do the stats tell the story?
The numbers in the recent ONC report do not shed much light on how much impact the regulations are having on information sharing. Health care providers, including physicians, might not yet be complying with the rules because monetary penalties are not in place.
Indeed, HHS has yet to spell out exactly what the disincentives on providers will be, though the 21st Century Cures Act stipulates that regulators could fine up to $1 million per information-blocking incident.
“Some providers might be saying, ‘I’m not going to be penalized at this point … so I can take a little bit longer to think about how I come into compliance.’ That could be just one factor of a host of many that are affecting compliance. We also are still in the middle of a public health emergency. So it’s hard to say at this point” exactly how the regulations will affect information blocking, Lauren Riplinger, vice president of policy and public affairs at the American Health Information Management Association, Chicago, said in an interview.
A long time coming
The government first zeroed in on ensuring that patients have access to their information in 2016 when President Obama signed the Cures Act into law. The legislation directed ONC to implement a standardized process for the public to report claims of possible information blocking.
The initiative appears to be picking up steam. The ONC is expected to release monthly reports on the cumulative number of information-blocking claims. The announcement of associated penalties is expected sometime in the future.
Industry leaders are advising health care providers to brush up on compliance. Physicians can look to professional groups such as the American Medical Association, the Medical Group Management Association, and other specialty associations for guidance. In addition, the ONC is educating providers on the rule.
“The ONC has provided a lot of great content for the past couple months, not only in terms of putting out FAQs to help clarify some of the gray areas in the rule, but they also have produced a series of provider-specific webinars where they walk through a potential scenario and address the extent to the rules apply,” Ms. Riplinger said.
With education, more is better
These efforts, however, could be expanded, according to MGMA.
“There is a general awareness of the rules, but we encourage ONC to continue educating the provider community: More FAQs and educational webinars would be helpful,” Claire Ernst, director of government affairs for MGMA, said in an interview. “A June 2021 MGMA poll found that 51% of medical groups said they needed more government guidance on complying with the new information-blocking rules.”
Although ONC already has provided some “scenario-based” education, more of this type of guidance could prove valuable.
“This rule is that it is very circumstance based. … and so it’s those more nuanced cases that I think are more challenging for providers to know whether or not they are engaging in information blocking,” Ms. Riplinger noted.
For example, a physician might choose to not upload lab test results to a patient portal and prefer to wait to discuss the results directly with the patient, which could potentially be construed as information blocking under the regulations.
The MGMA is requesting that ONC take a second look at these situations – and possibly adjust the regulations.
“MGMA has heard concerns about the impact of providing immediate results to patients before medical groups have the time to thoroughly review test results and discuss them compassionately with their patients,” Ms. Ernst said. “To address this, ONC could expand the current definition of harm to account for other unintended consequences, such as emotional distress, or provide more flexibility in terms of the time frame.”
A version of this article first appeared on Medscape.com.
The federal government’s efforts to thwart information blocking are underway. As such,
Recently, the Office of the National Coordinator revealed that the Department of Health & Humans Services has received 299 reports of information blocking since inviting anyone who suspected that health care providers, IT developers, or health information networks/exchanges might have interfered with access, exchange, or use of EHI through the Report Information Blocking Portal on April 5, 2021.
The vast majority of these claims – 211 – were filed against providers, while 46 alleged incidents of information blocking were by health IT developers, and two claims point to health information networks/ exchanges. The other 25 claims did not appear to present a claim of information blocking.
Of the 274 possible claims of information blocking recently released by ONC, 176 were made by patients.
The ONC has sent all possible claims to the HHS’s Office of the Inspector General. The claims have not yet been investigated and substantiated.
Do the stats tell the story?
The numbers in the recent ONC report do not shed much light on how much impact the regulations are having on information sharing. Health care providers, including physicians, might not yet be complying with the rules because monetary penalties are not in place.
Indeed, HHS has yet to spell out exactly what the disincentives on providers will be, though the 21st Century Cures Act stipulates that regulators could fine up to $1 million per information-blocking incident.
“Some providers might be saying, ‘I’m not going to be penalized at this point … so I can take a little bit longer to think about how I come into compliance.’ That could be just one factor of a host of many that are affecting compliance. We also are still in the middle of a public health emergency. So it’s hard to say at this point” exactly how the regulations will affect information blocking, Lauren Riplinger, vice president of policy and public affairs at the American Health Information Management Association, Chicago, said in an interview.
A long time coming
The government first zeroed in on ensuring that patients have access to their information in 2016 when President Obama signed the Cures Act into law. The legislation directed ONC to implement a standardized process for the public to report claims of possible information blocking.
The initiative appears to be picking up steam. The ONC is expected to release monthly reports on the cumulative number of information-blocking claims. The announcement of associated penalties is expected sometime in the future.
Industry leaders are advising health care providers to brush up on compliance. Physicians can look to professional groups such as the American Medical Association, the Medical Group Management Association, and other specialty associations for guidance. In addition, the ONC is educating providers on the rule.
“The ONC has provided a lot of great content for the past couple months, not only in terms of putting out FAQs to help clarify some of the gray areas in the rule, but they also have produced a series of provider-specific webinars where they walk through a potential scenario and address the extent to the rules apply,” Ms. Riplinger said.
With education, more is better
These efforts, however, could be expanded, according to MGMA.
“There is a general awareness of the rules, but we encourage ONC to continue educating the provider community: More FAQs and educational webinars would be helpful,” Claire Ernst, director of government affairs for MGMA, said in an interview. “A June 2021 MGMA poll found that 51% of medical groups said they needed more government guidance on complying with the new information-blocking rules.”
Although ONC already has provided some “scenario-based” education, more of this type of guidance could prove valuable.
“This rule is that it is very circumstance based. … and so it’s those more nuanced cases that I think are more challenging for providers to know whether or not they are engaging in information blocking,” Ms. Riplinger noted.
For example, a physician might choose to not upload lab test results to a patient portal and prefer to wait to discuss the results directly with the patient, which could potentially be construed as information blocking under the regulations.
The MGMA is requesting that ONC take a second look at these situations – and possibly adjust the regulations.
“MGMA has heard concerns about the impact of providing immediate results to patients before medical groups have the time to thoroughly review test results and discuss them compassionately with their patients,” Ms. Ernst said. “To address this, ONC could expand the current definition of harm to account for other unintended consequences, such as emotional distress, or provide more flexibility in terms of the time frame.”
A version of this article first appeared on Medscape.com.
The federal government’s efforts to thwart information blocking are underway. As such,
Recently, the Office of the National Coordinator revealed that the Department of Health & Humans Services has received 299 reports of information blocking since inviting anyone who suspected that health care providers, IT developers, or health information networks/exchanges might have interfered with access, exchange, or use of EHI through the Report Information Blocking Portal on April 5, 2021.
The vast majority of these claims – 211 – were filed against providers, while 46 alleged incidents of information blocking were by health IT developers, and two claims point to health information networks/ exchanges. The other 25 claims did not appear to present a claim of information blocking.
Of the 274 possible claims of information blocking recently released by ONC, 176 were made by patients.
The ONC has sent all possible claims to the HHS’s Office of the Inspector General. The claims have not yet been investigated and substantiated.
Do the stats tell the story?
The numbers in the recent ONC report do not shed much light on how much impact the regulations are having on information sharing. Health care providers, including physicians, might not yet be complying with the rules because monetary penalties are not in place.
Indeed, HHS has yet to spell out exactly what the disincentives on providers will be, though the 21st Century Cures Act stipulates that regulators could fine up to $1 million per information-blocking incident.
“Some providers might be saying, ‘I’m not going to be penalized at this point … so I can take a little bit longer to think about how I come into compliance.’ That could be just one factor of a host of many that are affecting compliance. We also are still in the middle of a public health emergency. So it’s hard to say at this point” exactly how the regulations will affect information blocking, Lauren Riplinger, vice president of policy and public affairs at the American Health Information Management Association, Chicago, said in an interview.
A long time coming
The government first zeroed in on ensuring that patients have access to their information in 2016 when President Obama signed the Cures Act into law. The legislation directed ONC to implement a standardized process for the public to report claims of possible information blocking.
The initiative appears to be picking up steam. The ONC is expected to release monthly reports on the cumulative number of information-blocking claims. The announcement of associated penalties is expected sometime in the future.
Industry leaders are advising health care providers to brush up on compliance. Physicians can look to professional groups such as the American Medical Association, the Medical Group Management Association, and other specialty associations for guidance. In addition, the ONC is educating providers on the rule.
“The ONC has provided a lot of great content for the past couple months, not only in terms of putting out FAQs to help clarify some of the gray areas in the rule, but they also have produced a series of provider-specific webinars where they walk through a potential scenario and address the extent to the rules apply,” Ms. Riplinger said.
With education, more is better
These efforts, however, could be expanded, according to MGMA.
“There is a general awareness of the rules, but we encourage ONC to continue educating the provider community: More FAQs and educational webinars would be helpful,” Claire Ernst, director of government affairs for MGMA, said in an interview. “A June 2021 MGMA poll found that 51% of medical groups said they needed more government guidance on complying with the new information-blocking rules.”
Although ONC already has provided some “scenario-based” education, more of this type of guidance could prove valuable.
“This rule is that it is very circumstance based. … and so it’s those more nuanced cases that I think are more challenging for providers to know whether or not they are engaging in information blocking,” Ms. Riplinger noted.
For example, a physician might choose to not upload lab test results to a patient portal and prefer to wait to discuss the results directly with the patient, which could potentially be construed as information blocking under the regulations.
The MGMA is requesting that ONC take a second look at these situations – and possibly adjust the regulations.
“MGMA has heard concerns about the impact of providing immediate results to patients before medical groups have the time to thoroughly review test results and discuss them compassionately with their patients,” Ms. Ernst said. “To address this, ONC could expand the current definition of harm to account for other unintended consequences, such as emotional distress, or provide more flexibility in terms of the time frame.”
A version of this article first appeared on Medscape.com.
Dietary fiber tied to lower dementia risk
, new research shows.
Investigators administered a dietary survey to 3,700 healthy adults at midlife and then followed them for up to 20 years. They found that participants who consumed the most fiber had approximately a 25% lower risk of developing dementia in later life.
“This study showed that people with a high intake of dietary fiber, especially soluble fiber, have a lower risk of dementia,” study investigator Kazumasa Yamagishi, MD, PhD, professor, department of public health medicine, faculty of medicine and health, Services Research and Development Center, University of Tsukuba, Japan, said in an interview.
“There are still many unknowns about the causes of dementia, and it is not appropriate to determine causality based on the results of a single cohort study. However, the results of this study can be said to be one of the findings that will lead to the prevention of dementia,” Dr. Yamagishi said.
The study was published online Feb. 6 in Nutritional Neuroscience.
Brain-gut interaction
Brain-gut interaction has recently received attention for its potential involvement in the development of dementia. “The concept of brain-gut interaction emerged from the idea that the central nervous system communicates bidirectionally with the gastrointestinal tract, suggesting that the gut microbiome may influence brain plasticity and cognitive function,” the authors wrote.
A diet high in soluble fiber attenuates neuroinflammation in mouse models. Other animal studies have suggested that insoluble fiber might also have a beneficial effect on the microbiome.
The researchers wanted to see whether dietary fiber intake – especially soluble fiber – is associated with a reduced risk of dementia. They also investigated whether there was any difference between dementia in patients with vs. without a history of stroke.
In a previous study, these same researchers reported an inverse association between eating beans, which are high in fiber, and risk of disabling dementia. In the current study, the researchers extended the analyses to dietary fiber intake of total, soluble, and insoluble fibers, as well as other fiber-containing foods, such potatoes, vegetables, and fruits. However, they distinguished potatoes from other vegetables because the composition of starch in potatoes differs.
“Dietary fiber is a nutrient found in grains, potatoes, vegetables, and fruits and is known to affect intestinal bacteria,” Dr. Yamagishi said. “Recently, some experimental studies have shown that intestinal bacteria may be involved in cognitive functions as well as diseases of the digestive tract. However, there have been no studies that have actually examined the relationship between dietary fiber intake and the subsequent risk of dementia in large numbers of general people.”
The researchers turned to participants in the Circulatory Risk in Communities Study (CIRCS), an ongoing dynamic community cohort study involving five communities in Japan. The current study focused on communities where disabling dementia surveillance is conducted.
Participants (n = 3,739) ranged in age from 40 to 64 years (mean age, 51 years) at the time they completed the 24-hour dietary recall survey, and they participated in annual health checkups from 1985 to 1999. Potential risk factors for disabling dementia were measured at the time the dietary surveys were conducted. Participants were then followed for a median of 19.7 years (1999-2020) to confirm incident, disabling dementia.
“Disabling dementia” was defined as dementia that required care under the National Long-Term Care Insurance System and was further categorized on the basis of having a history or not having a history of stroke.
The researchers divided participants into quartiles, based on the amount of total, soluble, and insoluble intake reported in their surveys. They found that men tended to consume less total fiber compared to women.
Unclear mechanism
During follow-up, 670 participants developed disabling dementia.
Total fiber intake was “inversely and linearly” associated with risk of incident dementia, the authors reported, with each successive quartile associated with a lower risk compared to the lowest quartile (P for trend = .03).
The association remained after adjustment for potential factors that might affect dementia onset, such as body mass index, systolic blood pressure, antihypertensive medication use, serum total cholesterol, cholesterol-lowering medication, and diabetes (P for trend = .05).
“The inverse association was more evident for soluble fiber intake and was confined to dementia without a history of stroke,” the authors reported. Moreover, potatoes, not vegetables or fruits, showed a similar association.
“The mechanisms are currently unknown but might involve the interactions that take place between the gut and the brain,” Dr. Yamagishi said in a release.
“One possibility is that soluble fiber regulates the composition of gut bacteria. This composition may affect neuroinflammation, which plays a role in the onset of dementia,” he suggested. “It’s also possible that dietary fiber may reduce other risk factors for dementia, such as body weight, blood pressure, lipids, and glucose levels.”
The authors noted several limitations. For example, they did not distinguish between Alzheimer’s and non-Alzheimer’s dementia. Moreover, they classified dietary habits on the basis of a single survey, and participants’ dietary patterns might have changed over the study period.
In addition, Dr. Yamagishi noted, it is “important to confirm the association in other populations.”
Balance is key
In an interview, Uma Naidoo, MD, director of nutritional and lifestyle psychiatry, Massachusetts General Hospital, and nutrition educator at Harvard Medical School, both in Boston, said the study “adds to the growing pool of evidence suggesting that a diet rich in colorful, plant-based foods can benefit our neurological and psychiatric health, especially as we age.”
Dr. Naidoo, a chef and the author of “This Is Your Brain on Food,” who was not involved in the study, continued, “In nutritional psychiatry, balance is key and therefore consuming a well-rounded diet including ample amounts of fiber – particularly from sources like steel-cut oats, beans, lentils, and numerous other fruits and vegetables – can be part of a healthy lifestyle and prevention against cognitive decline in later years.
“While the study authors admit to limitations within the study, in my opinion, eating healthier has so many mental and physical health benefits that it’s a nutritional psychiatry no-brainer,” she added.
The study was partly supported by Health and Labour Science Research Grants for Dementia from the Ministry of Health, Labour and Welfare of Japan; JSPS Kakenhi; FULLHAP; and the Osaka University International Joint Research Promotion Programme with University College London. The authors and Dr. Naidoo report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research shows.
Investigators administered a dietary survey to 3,700 healthy adults at midlife and then followed them for up to 20 years. They found that participants who consumed the most fiber had approximately a 25% lower risk of developing dementia in later life.
“This study showed that people with a high intake of dietary fiber, especially soluble fiber, have a lower risk of dementia,” study investigator Kazumasa Yamagishi, MD, PhD, professor, department of public health medicine, faculty of medicine and health, Services Research and Development Center, University of Tsukuba, Japan, said in an interview.
“There are still many unknowns about the causes of dementia, and it is not appropriate to determine causality based on the results of a single cohort study. However, the results of this study can be said to be one of the findings that will lead to the prevention of dementia,” Dr. Yamagishi said.
The study was published online Feb. 6 in Nutritional Neuroscience.
Brain-gut interaction
Brain-gut interaction has recently received attention for its potential involvement in the development of dementia. “The concept of brain-gut interaction emerged from the idea that the central nervous system communicates bidirectionally with the gastrointestinal tract, suggesting that the gut microbiome may influence brain plasticity and cognitive function,” the authors wrote.
A diet high in soluble fiber attenuates neuroinflammation in mouse models. Other animal studies have suggested that insoluble fiber might also have a beneficial effect on the microbiome.
The researchers wanted to see whether dietary fiber intake – especially soluble fiber – is associated with a reduced risk of dementia. They also investigated whether there was any difference between dementia in patients with vs. without a history of stroke.
In a previous study, these same researchers reported an inverse association between eating beans, which are high in fiber, and risk of disabling dementia. In the current study, the researchers extended the analyses to dietary fiber intake of total, soluble, and insoluble fibers, as well as other fiber-containing foods, such potatoes, vegetables, and fruits. However, they distinguished potatoes from other vegetables because the composition of starch in potatoes differs.
“Dietary fiber is a nutrient found in grains, potatoes, vegetables, and fruits and is known to affect intestinal bacteria,” Dr. Yamagishi said. “Recently, some experimental studies have shown that intestinal bacteria may be involved in cognitive functions as well as diseases of the digestive tract. However, there have been no studies that have actually examined the relationship between dietary fiber intake and the subsequent risk of dementia in large numbers of general people.”
The researchers turned to participants in the Circulatory Risk in Communities Study (CIRCS), an ongoing dynamic community cohort study involving five communities in Japan. The current study focused on communities where disabling dementia surveillance is conducted.
Participants (n = 3,739) ranged in age from 40 to 64 years (mean age, 51 years) at the time they completed the 24-hour dietary recall survey, and they participated in annual health checkups from 1985 to 1999. Potential risk factors for disabling dementia were measured at the time the dietary surveys were conducted. Participants were then followed for a median of 19.7 years (1999-2020) to confirm incident, disabling dementia.
“Disabling dementia” was defined as dementia that required care under the National Long-Term Care Insurance System and was further categorized on the basis of having a history or not having a history of stroke.
The researchers divided participants into quartiles, based on the amount of total, soluble, and insoluble intake reported in their surveys. They found that men tended to consume less total fiber compared to women.
Unclear mechanism
During follow-up, 670 participants developed disabling dementia.
Total fiber intake was “inversely and linearly” associated with risk of incident dementia, the authors reported, with each successive quartile associated with a lower risk compared to the lowest quartile (P for trend = .03).
The association remained after adjustment for potential factors that might affect dementia onset, such as body mass index, systolic blood pressure, antihypertensive medication use, serum total cholesterol, cholesterol-lowering medication, and diabetes (P for trend = .05).
“The inverse association was more evident for soluble fiber intake and was confined to dementia without a history of stroke,” the authors reported. Moreover, potatoes, not vegetables or fruits, showed a similar association.
“The mechanisms are currently unknown but might involve the interactions that take place between the gut and the brain,” Dr. Yamagishi said in a release.
“One possibility is that soluble fiber regulates the composition of gut bacteria. This composition may affect neuroinflammation, which plays a role in the onset of dementia,” he suggested. “It’s also possible that dietary fiber may reduce other risk factors for dementia, such as body weight, blood pressure, lipids, and glucose levels.”
The authors noted several limitations. For example, they did not distinguish between Alzheimer’s and non-Alzheimer’s dementia. Moreover, they classified dietary habits on the basis of a single survey, and participants’ dietary patterns might have changed over the study period.
In addition, Dr. Yamagishi noted, it is “important to confirm the association in other populations.”
Balance is key
In an interview, Uma Naidoo, MD, director of nutritional and lifestyle psychiatry, Massachusetts General Hospital, and nutrition educator at Harvard Medical School, both in Boston, said the study “adds to the growing pool of evidence suggesting that a diet rich in colorful, plant-based foods can benefit our neurological and psychiatric health, especially as we age.”
Dr. Naidoo, a chef and the author of “This Is Your Brain on Food,” who was not involved in the study, continued, “In nutritional psychiatry, balance is key and therefore consuming a well-rounded diet including ample amounts of fiber – particularly from sources like steel-cut oats, beans, lentils, and numerous other fruits and vegetables – can be part of a healthy lifestyle and prevention against cognitive decline in later years.
“While the study authors admit to limitations within the study, in my opinion, eating healthier has so many mental and physical health benefits that it’s a nutritional psychiatry no-brainer,” she added.
The study was partly supported by Health and Labour Science Research Grants for Dementia from the Ministry of Health, Labour and Welfare of Japan; JSPS Kakenhi; FULLHAP; and the Osaka University International Joint Research Promotion Programme with University College London. The authors and Dr. Naidoo report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research shows.
Investigators administered a dietary survey to 3,700 healthy adults at midlife and then followed them for up to 20 years. They found that participants who consumed the most fiber had approximately a 25% lower risk of developing dementia in later life.
“This study showed that people with a high intake of dietary fiber, especially soluble fiber, have a lower risk of dementia,” study investigator Kazumasa Yamagishi, MD, PhD, professor, department of public health medicine, faculty of medicine and health, Services Research and Development Center, University of Tsukuba, Japan, said in an interview.
“There are still many unknowns about the causes of dementia, and it is not appropriate to determine causality based on the results of a single cohort study. However, the results of this study can be said to be one of the findings that will lead to the prevention of dementia,” Dr. Yamagishi said.
The study was published online Feb. 6 in Nutritional Neuroscience.
Brain-gut interaction
Brain-gut interaction has recently received attention for its potential involvement in the development of dementia. “The concept of brain-gut interaction emerged from the idea that the central nervous system communicates bidirectionally with the gastrointestinal tract, suggesting that the gut microbiome may influence brain plasticity and cognitive function,” the authors wrote.
A diet high in soluble fiber attenuates neuroinflammation in mouse models. Other animal studies have suggested that insoluble fiber might also have a beneficial effect on the microbiome.
The researchers wanted to see whether dietary fiber intake – especially soluble fiber – is associated with a reduced risk of dementia. They also investigated whether there was any difference between dementia in patients with vs. without a history of stroke.
In a previous study, these same researchers reported an inverse association between eating beans, which are high in fiber, and risk of disabling dementia. In the current study, the researchers extended the analyses to dietary fiber intake of total, soluble, and insoluble fibers, as well as other fiber-containing foods, such potatoes, vegetables, and fruits. However, they distinguished potatoes from other vegetables because the composition of starch in potatoes differs.
“Dietary fiber is a nutrient found in grains, potatoes, vegetables, and fruits and is known to affect intestinal bacteria,” Dr. Yamagishi said. “Recently, some experimental studies have shown that intestinal bacteria may be involved in cognitive functions as well as diseases of the digestive tract. However, there have been no studies that have actually examined the relationship between dietary fiber intake and the subsequent risk of dementia in large numbers of general people.”
The researchers turned to participants in the Circulatory Risk in Communities Study (CIRCS), an ongoing dynamic community cohort study involving five communities in Japan. The current study focused on communities where disabling dementia surveillance is conducted.
Participants (n = 3,739) ranged in age from 40 to 64 years (mean age, 51 years) at the time they completed the 24-hour dietary recall survey, and they participated in annual health checkups from 1985 to 1999. Potential risk factors for disabling dementia were measured at the time the dietary surveys were conducted. Participants were then followed for a median of 19.7 years (1999-2020) to confirm incident, disabling dementia.
“Disabling dementia” was defined as dementia that required care under the National Long-Term Care Insurance System and was further categorized on the basis of having a history or not having a history of stroke.
The researchers divided participants into quartiles, based on the amount of total, soluble, and insoluble intake reported in their surveys. They found that men tended to consume less total fiber compared to women.
Unclear mechanism
During follow-up, 670 participants developed disabling dementia.
Total fiber intake was “inversely and linearly” associated with risk of incident dementia, the authors reported, with each successive quartile associated with a lower risk compared to the lowest quartile (P for trend = .03).
The association remained after adjustment for potential factors that might affect dementia onset, such as body mass index, systolic blood pressure, antihypertensive medication use, serum total cholesterol, cholesterol-lowering medication, and diabetes (P for trend = .05).
“The inverse association was more evident for soluble fiber intake and was confined to dementia without a history of stroke,” the authors reported. Moreover, potatoes, not vegetables or fruits, showed a similar association.
“The mechanisms are currently unknown but might involve the interactions that take place between the gut and the brain,” Dr. Yamagishi said in a release.
“One possibility is that soluble fiber regulates the composition of gut bacteria. This composition may affect neuroinflammation, which plays a role in the onset of dementia,” he suggested. “It’s also possible that dietary fiber may reduce other risk factors for dementia, such as body weight, blood pressure, lipids, and glucose levels.”
The authors noted several limitations. For example, they did not distinguish between Alzheimer’s and non-Alzheimer’s dementia. Moreover, they classified dietary habits on the basis of a single survey, and participants’ dietary patterns might have changed over the study period.
In addition, Dr. Yamagishi noted, it is “important to confirm the association in other populations.”
Balance is key
In an interview, Uma Naidoo, MD, director of nutritional and lifestyle psychiatry, Massachusetts General Hospital, and nutrition educator at Harvard Medical School, both in Boston, said the study “adds to the growing pool of evidence suggesting that a diet rich in colorful, plant-based foods can benefit our neurological and psychiatric health, especially as we age.”
Dr. Naidoo, a chef and the author of “This Is Your Brain on Food,” who was not involved in the study, continued, “In nutritional psychiatry, balance is key and therefore consuming a well-rounded diet including ample amounts of fiber – particularly from sources like steel-cut oats, beans, lentils, and numerous other fruits and vegetables – can be part of a healthy lifestyle and prevention against cognitive decline in later years.
“While the study authors admit to limitations within the study, in my opinion, eating healthier has so many mental and physical health benefits that it’s a nutritional psychiatry no-brainer,” she added.
The study was partly supported by Health and Labour Science Research Grants for Dementia from the Ministry of Health, Labour and Welfare of Japan; JSPS Kakenhi; FULLHAP; and the Osaka University International Joint Research Promotion Programme with University College London. The authors and Dr. Naidoo report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NUTRITIONAL NEUROSCIENCE