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Sexual activities in seniors: Experts advise on what to ask
Sexual activity in older adults is something of a taboo, rarely discussed and largely ignored by researchers.
But failing to address human sexuality in old age can lead doctors to ask seniors the wrong questions about sex – if they ask at all.
When researchers do look at the issue, they find surprises, as Janie Steckenrider, PhD, has learned. In a new study presented at the annual scientific meeting of the Gerontological Society of America, Dr. Steckenrider, a professor of political science at Loyola Marymount University, Los Angeles, found that previous attempts to qualify the sexual activities of seniors appear to be limited largely to partnered sex – despite the fact that many older people tend to practice “solo sex,” another term for masturbation.
“Maybe they don’t have a partner, or their partner has sexual dysfunction, or has died. There could be pain involved,” Dr. Steckenrider said. “In the hierarchy of sexual activity, penetrative sex is the cultural norm. As people get older, penetrative sex becomes less important. The hierarchy shifts to include more emotional intimacy like touching and fondling.”
Of the 17 survey questionnaires Dr. Steckenrider analyzed, 11 had questions that focused exclusively on sex with a partner. Nine defined sexual activity and just five included questions about masturbation.
Take, for example, a 2018 poll by researchers at the University of Michigan, Ann Arbor, who found that 40% of people ages 65-80 said they were sexually active. Meanwhile, nearly two thirds of older adults said they were interested in sex, and more than half said sex was important to their quality of life.
But Dr. Steckenrider said this poll, like others, left the term “sexually active” undefined – raising questions about the meaning of the findings.
Sheryl A. Kingsberg, PhD, chief of behavioral medicine in the department of obstetrics and gynecology at University Hospitals Cleveland Medical Center, said she was surprised so few of the studies analyzed by Dr. Steckenrider included masturbation in their definition of sex.
“Clinical trials of potential treatments for female sexual problems, like hypoactive sexual desire disorder or painful sex, include both definitions of sexual activity and questions about masturbation, she said. “Definitions also should not assume partnered sex is male or female,” she added.
Dr. Steckenrider and Dr. Kingsberg encouraged healthcare providers to address the sexual health of their patients by asking questions about their sexual health and concerns.
“Health care professionals cannot address sexual concerns if they don’t acknowledge their patients as sexual beings and inquire about sexual problems,” Dr. Kingsberg said.
The key, according to Dr. Steckenrider, is for clinicians to ask the right questions. But which ones?
Detail is crucial.
“I think that’s far better than asking whether they are sexually active, yes or no,” she said. “Ask: ‘How often have you engaged in these types of sexual activities?’ If you are looking for frequency, and be specific about the types of sex: kissing, fondling, or masturbation.”
A version of this article first appeared on Medscape.com.
Sexual activity in older adults is something of a taboo, rarely discussed and largely ignored by researchers.
But failing to address human sexuality in old age can lead doctors to ask seniors the wrong questions about sex – if they ask at all.
When researchers do look at the issue, they find surprises, as Janie Steckenrider, PhD, has learned. In a new study presented at the annual scientific meeting of the Gerontological Society of America, Dr. Steckenrider, a professor of political science at Loyola Marymount University, Los Angeles, found that previous attempts to qualify the sexual activities of seniors appear to be limited largely to partnered sex – despite the fact that many older people tend to practice “solo sex,” another term for masturbation.
“Maybe they don’t have a partner, or their partner has sexual dysfunction, or has died. There could be pain involved,” Dr. Steckenrider said. “In the hierarchy of sexual activity, penetrative sex is the cultural norm. As people get older, penetrative sex becomes less important. The hierarchy shifts to include more emotional intimacy like touching and fondling.”
Of the 17 survey questionnaires Dr. Steckenrider analyzed, 11 had questions that focused exclusively on sex with a partner. Nine defined sexual activity and just five included questions about masturbation.
Take, for example, a 2018 poll by researchers at the University of Michigan, Ann Arbor, who found that 40% of people ages 65-80 said they were sexually active. Meanwhile, nearly two thirds of older adults said they were interested in sex, and more than half said sex was important to their quality of life.
But Dr. Steckenrider said this poll, like others, left the term “sexually active” undefined – raising questions about the meaning of the findings.
Sheryl A. Kingsberg, PhD, chief of behavioral medicine in the department of obstetrics and gynecology at University Hospitals Cleveland Medical Center, said she was surprised so few of the studies analyzed by Dr. Steckenrider included masturbation in their definition of sex.
“Clinical trials of potential treatments for female sexual problems, like hypoactive sexual desire disorder or painful sex, include both definitions of sexual activity and questions about masturbation, she said. “Definitions also should not assume partnered sex is male or female,” she added.
Dr. Steckenrider and Dr. Kingsberg encouraged healthcare providers to address the sexual health of their patients by asking questions about their sexual health and concerns.
“Health care professionals cannot address sexual concerns if they don’t acknowledge their patients as sexual beings and inquire about sexual problems,” Dr. Kingsberg said.
The key, according to Dr. Steckenrider, is for clinicians to ask the right questions. But which ones?
Detail is crucial.
“I think that’s far better than asking whether they are sexually active, yes or no,” she said. “Ask: ‘How often have you engaged in these types of sexual activities?’ If you are looking for frequency, and be specific about the types of sex: kissing, fondling, or masturbation.”
A version of this article first appeared on Medscape.com.
Sexual activity in older adults is something of a taboo, rarely discussed and largely ignored by researchers.
But failing to address human sexuality in old age can lead doctors to ask seniors the wrong questions about sex – if they ask at all.
When researchers do look at the issue, they find surprises, as Janie Steckenrider, PhD, has learned. In a new study presented at the annual scientific meeting of the Gerontological Society of America, Dr. Steckenrider, a professor of political science at Loyola Marymount University, Los Angeles, found that previous attempts to qualify the sexual activities of seniors appear to be limited largely to partnered sex – despite the fact that many older people tend to practice “solo sex,” another term for masturbation.
“Maybe they don’t have a partner, or their partner has sexual dysfunction, or has died. There could be pain involved,” Dr. Steckenrider said. “In the hierarchy of sexual activity, penetrative sex is the cultural norm. As people get older, penetrative sex becomes less important. The hierarchy shifts to include more emotional intimacy like touching and fondling.”
Of the 17 survey questionnaires Dr. Steckenrider analyzed, 11 had questions that focused exclusively on sex with a partner. Nine defined sexual activity and just five included questions about masturbation.
Take, for example, a 2018 poll by researchers at the University of Michigan, Ann Arbor, who found that 40% of people ages 65-80 said they were sexually active. Meanwhile, nearly two thirds of older adults said they were interested in sex, and more than half said sex was important to their quality of life.
But Dr. Steckenrider said this poll, like others, left the term “sexually active” undefined – raising questions about the meaning of the findings.
Sheryl A. Kingsberg, PhD, chief of behavioral medicine in the department of obstetrics and gynecology at University Hospitals Cleveland Medical Center, said she was surprised so few of the studies analyzed by Dr. Steckenrider included masturbation in their definition of sex.
“Clinical trials of potential treatments for female sexual problems, like hypoactive sexual desire disorder or painful sex, include both definitions of sexual activity and questions about masturbation, she said. “Definitions also should not assume partnered sex is male or female,” she added.
Dr. Steckenrider and Dr. Kingsberg encouraged healthcare providers to address the sexual health of their patients by asking questions about their sexual health and concerns.
“Health care professionals cannot address sexual concerns if they don’t acknowledge their patients as sexual beings and inquire about sexual problems,” Dr. Kingsberg said.
The key, according to Dr. Steckenrider, is for clinicians to ask the right questions. But which ones?
Detail is crucial.
“I think that’s far better than asking whether they are sexually active, yes or no,” she said. “Ask: ‘How often have you engaged in these types of sexual activities?’ If you are looking for frequency, and be specific about the types of sex: kissing, fondling, or masturbation.”
A version of this article first appeared on Medscape.com.
Microplastics and health risks: What do we really know?
You eat a credit card’s worth of plastic in a week. That may bother you. But does it harm you?
The answer depends on who you ask. Awareness of microplastics in general is certainly increasing; the most recent news is the detection of microplastics in human breast milk. Other research has suggested that we may be consuming up to 5 grams of plastic each week from our food, water, and certain consumer products.
The World Health Organization has been releasing reports on microplastics and human health since 2019. Their most recent report was released in late August 2022.
“Although the limited data provide little evidence that nano- and microplastic particles have adverse effects in humans, there is increasing public awareness and an overwhelming consensus among all stakeholders that plastics do not belong in the environment, and measures should be taken to mitigate exposure,” the WHO said at the time.
The WHO can’t go beyond what the data shows, of course. If microplastics are wreaking long-term havoc in our bodies as we speak, science hasn’t connected the dots enough to definitively say “this is the problem.”
But some researchers are willing to speculate – and, at the very least, the risks are becoming impossible to ignore. Dick Vethaak, PhD, a microplastics researcher and emeritus professor of ecotoxicology at Vrije Universiteit, Amsterdam, is blunt, calling them “a plastic time bomb.”
The plastic problem
Every piece of plastic that has ever been created is still on our planet today, apart from what has been burned. Past estimates show we only recycle about 9% of all plastic, leaving 9 billion tons in our landfills, oceans, and ecosystems. For context, that amount is 1,500 times heavier than the Great Pyramid of Khufu.
New data is even more dire. A 2022 report from Greenpeace showed a 5% U.S. recycling rate in 2021, with a large portion of what consumers think of as “recycled” still winding up in garbage piles or bodies of water.
And this plastic doesn’t disappear. Instead, it breaks down into smaller and smaller pieces known as microplastics and nanoplastics.
Microplastics have been confirmed in human blood, lung tissue, colons, placentas, stool, and breast milk. But how they impact our health is still unknown.
To assess risk, we must ask: “How hazardous is the material?” said Flemming Cassee, PhD, professor of inhalation toxicology at Utrecht (the Netherlands) University and coauthor of the WHO’s recent microplastics report.
There are three potential hazards of microplastics: their physical presence in our bodies, what they’re made of, and what they carry. To determine the extent of these risks, we need to know how much we’re exposed to, said Dr. Cassee.
The first initiative to research the impact of microplastics on human health came from the European Union in 2018. Although microplastics were around before then, we were unable to detect them, said Dr. Cassee.
That’s the real problem: warned Dr. Vethaak.
What, exactly, are microplastics?
Microplastics are plastic particles between 5 mm and 100 nm in diameter, or the width of a pencil eraser and something 10 times thinner than a human hair. Anything smaller than that is known as a nanoplastic.
“Microplastics include a wide range of different materials, different sizes, different shapes, different densities, and different colors,” said Evangelos Danopoulos, PhD, a microplastics researcher at Hull York (England) Medical School.
“Primary” microplastics are manufactured to be small and used in things like cosmetics and paints. “Secondary” microplastics result from the breaking down of larger plastic materials, like water bottles and plastic bags.
Secondary microplastics are more diverse than primary microplastics and can take forms ranging from fibers shed from synthetic clothing (like polyester) to pieces of a plastic spoon left in our rivers, lakes, and oceans. Any plastic in the environment will eventually become a secondary microplastic as natural forces such as wind, water currents, and UV radiation break it down into smaller and smaller pieces.
Plastic is a diverse material. Heather Leslie, PhD, senior researcher in Vrije Universiteit’s department of environment and health, likens it to spaghetti with sauce. The noodles are the long polymer backbone that all plastic shares. The sauces are “the pigments, the antioxidants, the flame retardants, etc., that make it functional,” she said.
What makes microplastics dangerous?
There are more than 10,000 different chemicals, or “sauces,” used to alter a plastic’s physical characteristics – making it softer, more rigid, or more flexible, said Hanna Dusza, PhD, of the Institute for Risk Assessment Sciences at Utrecht University.
As plastics degrade and become microplastics, these chemicals likely remain. Recent research has shown that microplastics leach these chemicals locally in human tissues, or other areas of accumulation, said Dr. Dusza. Some 2,400 of the 10,000 chemical additives were classified as substances of potential concern, meeting the European Union’s criteria for persistence, bioaccumulation, or toxicity.
Many of these chemicals also act as endocrine-disrupting compounds, or toxicants that imitate hormones when they enter the body. Hormones are active at very low concentrations in your bloodstream, explained Dr. Leslie. To your body, some chemical additives in plastic resemble hormones, so the body responds.
“Sometimes even a low dose of some of these additives can cause unwanted effects,” said Dr. Leslie.
Bisphenol A (BPA), for example, is one of the more infamous endocrine disruptors. It is used as an additive to make plastics more rigid and can be found in any number of plastic products, though areas of concern have been plastic water bottles, baby bottles, and the protective coatings in canned foods.
BPA may mimic estrogen, the female sex hormone essential for reproduction, neurodevelopment, and bone density. In men, estrogen regulates sperm count, sex drive, and erectile function. BPA exposure has been linked with – but not proven to cause – multiple cancer types, ADHD, obesity, and low sperm count. Most everyone has some amount of BPA circulating within their blood, but microplastics may retain BPA as they degrade, potentially increasing our exposure, leading to its unwanted consequences, said Dr. Dusza.
And BPA is just one of those 2,400 substances of “potential concern.”
The inflammation problem
A potentially larger health issue emerges from our bodies yet again doing what they are supposed to do when encountering microplastics. Particles can trigger an immune response when they enter your bloodstream, explains Nienke Vrisekoop, PhD, assistant professor at UMC Utrecht.
White blood cells have no issue breaking down things like bacteria, but microplastics cannot be degraded. When a white blood cell engulfs a certain mass of microplastics – either many small particles or a singular large one – it dies, releasing its enzymes and causing local inflammation.
Meanwhile, the plastic particle remains. So more white blood cells attack.
“This triggers continual activation that can result in various adverse effects, including oxidative stress and the release of cytokines that trigger inflammatory reactions, said Dr. Vethaak.
And “chronic inflammation is the prelude to chronic diseases,” said Dr. Leslie. “Every chronic disease, like cancer, heart disease, and even neuropsychiatric diseases like Parkinson’s or major depression, begins with inflammation.”
Meanwhile, inhaling microplastic particles can lead to respiratory diseases and cancer.
“The smallest particles – less than one-tenth of a micrometer – penetrate deep into the lungs and even into the bloodstream, causing damage to the heart, blood vessels and brain,” said Dr. Vetaak. “The only direct evidence comes from workers in the textile and plastic industries that had been exposed to very high amounts of plastic fibrous dust.”
Microplastics as carriers
Microplastics can also pick up harmful substances and deliver them into your body.
“When they’re in an environment, they basically can suck up [chemicals] like a sponge,” said Dr. Dusza. “These chemicals are known environmental pollutants, like pesticides, fluorinated compounds, flame retardants, and so on.”
Once in the body, these chemicals can be released, potentially leading to cancer, chronic inflammation, or other unknown effects.
Particles can also act as a vector for microbes, bacteria, and viruses. A September 2022 study found that infectious viruses can survive for 3 days in fresh water by “hitchhiking” on microplastics. Their porous nature provides microbes with a perfect environment in which to live and reproduce, said Dr. Dusza. If you ingest the plastics, you ingest the microbes.
How to minimize exposure
There is no way to avoid microplastics. They’re in the air we breathe, the products we use, the water we drink, and the food we eat.
Dr. Danopoulos reviewed 72 studies to quantify our consumption of microplastics in drinking water, salt, and seafood.
“We are exposed to millions of microplastics every year, and I was only looking at three food sources, so there are really a lot more,” he said. “Once plastic waste is mismanaged and it enters the environment, there is very little we can do to extract it.”
That said, we can take steps to lower our exposure and keep the problem from getting worse.
Water filtration is one option, though it is not perfect. Research has shown that municipal water treatment can be effective. An October 2021 study found that two methods – electrocoagulation-electroflotation and membrane filtration – can be 100% effective in removing microplastics from treated water. The problem? Not all municipal water treatment uses these methods – and you would have to investigate to find out if your locality does.
As for at-home filtration methods, they can be effective but can also be dicey. Some consumer brands claim they remove microplastics, but how well depends on not just the type of filter but the size of the particles in the water. Meanwhile, how do you know if a filter is working on your water without testing it, something few people will do? Best not to take a brand’s claims on face-value, but look for independent testing on at-home brands.
A longer-term project: Reduce our risk by reusing and recycling plastic waste. Limiting our consumption of plastic, especially single use plastic, decreases the amount available to become micro- and nanoplastics.
We must all learn to not treat plastic as waste, but rather as a renewable material, said Dr. Cassee. But if that seems like a tall order, it’s because it is.
“You’re a human being and you have a voice and there are a lot of other humans out there with voices,” said Dr. Leslie.
“You sign a petition in your community. You talk about it with your friends at the pub. If you’re a teacher, you discuss it in your class. You call your elected representatives and tell them what you think and how you want them to vote on bills.”
When people start working together, you can really amplify that voice, said Dr. Leslie.
What’s the bottom line right now, today?
Numerous sources have declared microplastics do not impact human health. But that’s largely because no direct evidence of this exists yet.
Even the WHO in its report suggests that progress must happen if we’re to fully understand the scope of the problem.
“Strengthening of the evidence necessary for reliable characterization and quantification of the risks to human health posed by [nano- and microplastics] will require active participation by all stakeholders,” it said.
All researchers interviewed for this article agree we don’t have enough evidence to draw any definite conclusions. But “if you look at the wrong endpoints, things will look safe, until you look at the endpoint where it’s really causing the problem,” said Dr. Leslie.
We must research our blind spots and continually ask: Where could we be wrong?
“It is a problem; it’s not going to go away,” said Dr. Danopoulos. “It’s going to get worse, and will continue to get worse, not by something that we are doing now but by something we did 5 years ago.”
Perhaps the question to be asked, then, is the hardest to answer: Are we willing to wait for the science?
A version of this article first appeared on WebMD.com.
You eat a credit card’s worth of plastic in a week. That may bother you. But does it harm you?
The answer depends on who you ask. Awareness of microplastics in general is certainly increasing; the most recent news is the detection of microplastics in human breast milk. Other research has suggested that we may be consuming up to 5 grams of plastic each week from our food, water, and certain consumer products.
The World Health Organization has been releasing reports on microplastics and human health since 2019. Their most recent report was released in late August 2022.
“Although the limited data provide little evidence that nano- and microplastic particles have adverse effects in humans, there is increasing public awareness and an overwhelming consensus among all stakeholders that plastics do not belong in the environment, and measures should be taken to mitigate exposure,” the WHO said at the time.
The WHO can’t go beyond what the data shows, of course. If microplastics are wreaking long-term havoc in our bodies as we speak, science hasn’t connected the dots enough to definitively say “this is the problem.”
But some researchers are willing to speculate – and, at the very least, the risks are becoming impossible to ignore. Dick Vethaak, PhD, a microplastics researcher and emeritus professor of ecotoxicology at Vrije Universiteit, Amsterdam, is blunt, calling them “a plastic time bomb.”
The plastic problem
Every piece of plastic that has ever been created is still on our planet today, apart from what has been burned. Past estimates show we only recycle about 9% of all plastic, leaving 9 billion tons in our landfills, oceans, and ecosystems. For context, that amount is 1,500 times heavier than the Great Pyramid of Khufu.
New data is even more dire. A 2022 report from Greenpeace showed a 5% U.S. recycling rate in 2021, with a large portion of what consumers think of as “recycled” still winding up in garbage piles or bodies of water.
And this plastic doesn’t disappear. Instead, it breaks down into smaller and smaller pieces known as microplastics and nanoplastics.
Microplastics have been confirmed in human blood, lung tissue, colons, placentas, stool, and breast milk. But how they impact our health is still unknown.
To assess risk, we must ask: “How hazardous is the material?” said Flemming Cassee, PhD, professor of inhalation toxicology at Utrecht (the Netherlands) University and coauthor of the WHO’s recent microplastics report.
There are three potential hazards of microplastics: their physical presence in our bodies, what they’re made of, and what they carry. To determine the extent of these risks, we need to know how much we’re exposed to, said Dr. Cassee.
The first initiative to research the impact of microplastics on human health came from the European Union in 2018. Although microplastics were around before then, we were unable to detect them, said Dr. Cassee.
That’s the real problem: warned Dr. Vethaak.
What, exactly, are microplastics?
Microplastics are plastic particles between 5 mm and 100 nm in diameter, or the width of a pencil eraser and something 10 times thinner than a human hair. Anything smaller than that is known as a nanoplastic.
“Microplastics include a wide range of different materials, different sizes, different shapes, different densities, and different colors,” said Evangelos Danopoulos, PhD, a microplastics researcher at Hull York (England) Medical School.
“Primary” microplastics are manufactured to be small and used in things like cosmetics and paints. “Secondary” microplastics result from the breaking down of larger plastic materials, like water bottles and plastic bags.
Secondary microplastics are more diverse than primary microplastics and can take forms ranging from fibers shed from synthetic clothing (like polyester) to pieces of a plastic spoon left in our rivers, lakes, and oceans. Any plastic in the environment will eventually become a secondary microplastic as natural forces such as wind, water currents, and UV radiation break it down into smaller and smaller pieces.
Plastic is a diverse material. Heather Leslie, PhD, senior researcher in Vrije Universiteit’s department of environment and health, likens it to spaghetti with sauce. The noodles are the long polymer backbone that all plastic shares. The sauces are “the pigments, the antioxidants, the flame retardants, etc., that make it functional,” she said.
What makes microplastics dangerous?
There are more than 10,000 different chemicals, or “sauces,” used to alter a plastic’s physical characteristics – making it softer, more rigid, or more flexible, said Hanna Dusza, PhD, of the Institute for Risk Assessment Sciences at Utrecht University.
As plastics degrade and become microplastics, these chemicals likely remain. Recent research has shown that microplastics leach these chemicals locally in human tissues, or other areas of accumulation, said Dr. Dusza. Some 2,400 of the 10,000 chemical additives were classified as substances of potential concern, meeting the European Union’s criteria for persistence, bioaccumulation, or toxicity.
Many of these chemicals also act as endocrine-disrupting compounds, or toxicants that imitate hormones when they enter the body. Hormones are active at very low concentrations in your bloodstream, explained Dr. Leslie. To your body, some chemical additives in plastic resemble hormones, so the body responds.
“Sometimes even a low dose of some of these additives can cause unwanted effects,” said Dr. Leslie.
Bisphenol A (BPA), for example, is one of the more infamous endocrine disruptors. It is used as an additive to make plastics more rigid and can be found in any number of plastic products, though areas of concern have been plastic water bottles, baby bottles, and the protective coatings in canned foods.
BPA may mimic estrogen, the female sex hormone essential for reproduction, neurodevelopment, and bone density. In men, estrogen regulates sperm count, sex drive, and erectile function. BPA exposure has been linked with – but not proven to cause – multiple cancer types, ADHD, obesity, and low sperm count. Most everyone has some amount of BPA circulating within their blood, but microplastics may retain BPA as they degrade, potentially increasing our exposure, leading to its unwanted consequences, said Dr. Dusza.
And BPA is just one of those 2,400 substances of “potential concern.”
The inflammation problem
A potentially larger health issue emerges from our bodies yet again doing what they are supposed to do when encountering microplastics. Particles can trigger an immune response when they enter your bloodstream, explains Nienke Vrisekoop, PhD, assistant professor at UMC Utrecht.
White blood cells have no issue breaking down things like bacteria, but microplastics cannot be degraded. When a white blood cell engulfs a certain mass of microplastics – either many small particles or a singular large one – it dies, releasing its enzymes and causing local inflammation.
Meanwhile, the plastic particle remains. So more white blood cells attack.
“This triggers continual activation that can result in various adverse effects, including oxidative stress and the release of cytokines that trigger inflammatory reactions, said Dr. Vethaak.
And “chronic inflammation is the prelude to chronic diseases,” said Dr. Leslie. “Every chronic disease, like cancer, heart disease, and even neuropsychiatric diseases like Parkinson’s or major depression, begins with inflammation.”
Meanwhile, inhaling microplastic particles can lead to respiratory diseases and cancer.
“The smallest particles – less than one-tenth of a micrometer – penetrate deep into the lungs and even into the bloodstream, causing damage to the heart, blood vessels and brain,” said Dr. Vetaak. “The only direct evidence comes from workers in the textile and plastic industries that had been exposed to very high amounts of plastic fibrous dust.”
Microplastics as carriers
Microplastics can also pick up harmful substances and deliver them into your body.
“When they’re in an environment, they basically can suck up [chemicals] like a sponge,” said Dr. Dusza. “These chemicals are known environmental pollutants, like pesticides, fluorinated compounds, flame retardants, and so on.”
Once in the body, these chemicals can be released, potentially leading to cancer, chronic inflammation, or other unknown effects.
Particles can also act as a vector for microbes, bacteria, and viruses. A September 2022 study found that infectious viruses can survive for 3 days in fresh water by “hitchhiking” on microplastics. Their porous nature provides microbes with a perfect environment in which to live and reproduce, said Dr. Dusza. If you ingest the plastics, you ingest the microbes.
How to minimize exposure
There is no way to avoid microplastics. They’re in the air we breathe, the products we use, the water we drink, and the food we eat.
Dr. Danopoulos reviewed 72 studies to quantify our consumption of microplastics in drinking water, salt, and seafood.
“We are exposed to millions of microplastics every year, and I was only looking at three food sources, so there are really a lot more,” he said. “Once plastic waste is mismanaged and it enters the environment, there is very little we can do to extract it.”
That said, we can take steps to lower our exposure and keep the problem from getting worse.
Water filtration is one option, though it is not perfect. Research has shown that municipal water treatment can be effective. An October 2021 study found that two methods – electrocoagulation-electroflotation and membrane filtration – can be 100% effective in removing microplastics from treated water. The problem? Not all municipal water treatment uses these methods – and you would have to investigate to find out if your locality does.
As for at-home filtration methods, they can be effective but can also be dicey. Some consumer brands claim they remove microplastics, but how well depends on not just the type of filter but the size of the particles in the water. Meanwhile, how do you know if a filter is working on your water without testing it, something few people will do? Best not to take a brand’s claims on face-value, but look for independent testing on at-home brands.
A longer-term project: Reduce our risk by reusing and recycling plastic waste. Limiting our consumption of plastic, especially single use plastic, decreases the amount available to become micro- and nanoplastics.
We must all learn to not treat plastic as waste, but rather as a renewable material, said Dr. Cassee. But if that seems like a tall order, it’s because it is.
“You’re a human being and you have a voice and there are a lot of other humans out there with voices,” said Dr. Leslie.
“You sign a petition in your community. You talk about it with your friends at the pub. If you’re a teacher, you discuss it in your class. You call your elected representatives and tell them what you think and how you want them to vote on bills.”
When people start working together, you can really amplify that voice, said Dr. Leslie.
What’s the bottom line right now, today?
Numerous sources have declared microplastics do not impact human health. But that’s largely because no direct evidence of this exists yet.
Even the WHO in its report suggests that progress must happen if we’re to fully understand the scope of the problem.
“Strengthening of the evidence necessary for reliable characterization and quantification of the risks to human health posed by [nano- and microplastics] will require active participation by all stakeholders,” it said.
All researchers interviewed for this article agree we don’t have enough evidence to draw any definite conclusions. But “if you look at the wrong endpoints, things will look safe, until you look at the endpoint where it’s really causing the problem,” said Dr. Leslie.
We must research our blind spots and continually ask: Where could we be wrong?
“It is a problem; it’s not going to go away,” said Dr. Danopoulos. “It’s going to get worse, and will continue to get worse, not by something that we are doing now but by something we did 5 years ago.”
Perhaps the question to be asked, then, is the hardest to answer: Are we willing to wait for the science?
A version of this article first appeared on WebMD.com.
You eat a credit card’s worth of plastic in a week. That may bother you. But does it harm you?
The answer depends on who you ask. Awareness of microplastics in general is certainly increasing; the most recent news is the detection of microplastics in human breast milk. Other research has suggested that we may be consuming up to 5 grams of plastic each week from our food, water, and certain consumer products.
The World Health Organization has been releasing reports on microplastics and human health since 2019. Their most recent report was released in late August 2022.
“Although the limited data provide little evidence that nano- and microplastic particles have adverse effects in humans, there is increasing public awareness and an overwhelming consensus among all stakeholders that plastics do not belong in the environment, and measures should be taken to mitigate exposure,” the WHO said at the time.
The WHO can’t go beyond what the data shows, of course. If microplastics are wreaking long-term havoc in our bodies as we speak, science hasn’t connected the dots enough to definitively say “this is the problem.”
But some researchers are willing to speculate – and, at the very least, the risks are becoming impossible to ignore. Dick Vethaak, PhD, a microplastics researcher and emeritus professor of ecotoxicology at Vrije Universiteit, Amsterdam, is blunt, calling them “a plastic time bomb.”
The plastic problem
Every piece of plastic that has ever been created is still on our planet today, apart from what has been burned. Past estimates show we only recycle about 9% of all plastic, leaving 9 billion tons in our landfills, oceans, and ecosystems. For context, that amount is 1,500 times heavier than the Great Pyramid of Khufu.
New data is even more dire. A 2022 report from Greenpeace showed a 5% U.S. recycling rate in 2021, with a large portion of what consumers think of as “recycled” still winding up in garbage piles or bodies of water.
And this plastic doesn’t disappear. Instead, it breaks down into smaller and smaller pieces known as microplastics and nanoplastics.
Microplastics have been confirmed in human blood, lung tissue, colons, placentas, stool, and breast milk. But how they impact our health is still unknown.
To assess risk, we must ask: “How hazardous is the material?” said Flemming Cassee, PhD, professor of inhalation toxicology at Utrecht (the Netherlands) University and coauthor of the WHO’s recent microplastics report.
There are three potential hazards of microplastics: their physical presence in our bodies, what they’re made of, and what they carry. To determine the extent of these risks, we need to know how much we’re exposed to, said Dr. Cassee.
The first initiative to research the impact of microplastics on human health came from the European Union in 2018. Although microplastics were around before then, we were unable to detect them, said Dr. Cassee.
That’s the real problem: warned Dr. Vethaak.
What, exactly, are microplastics?
Microplastics are plastic particles between 5 mm and 100 nm in diameter, or the width of a pencil eraser and something 10 times thinner than a human hair. Anything smaller than that is known as a nanoplastic.
“Microplastics include a wide range of different materials, different sizes, different shapes, different densities, and different colors,” said Evangelos Danopoulos, PhD, a microplastics researcher at Hull York (England) Medical School.
“Primary” microplastics are manufactured to be small and used in things like cosmetics and paints. “Secondary” microplastics result from the breaking down of larger plastic materials, like water bottles and plastic bags.
Secondary microplastics are more diverse than primary microplastics and can take forms ranging from fibers shed from synthetic clothing (like polyester) to pieces of a plastic spoon left in our rivers, lakes, and oceans. Any plastic in the environment will eventually become a secondary microplastic as natural forces such as wind, water currents, and UV radiation break it down into smaller and smaller pieces.
Plastic is a diverse material. Heather Leslie, PhD, senior researcher in Vrije Universiteit’s department of environment and health, likens it to spaghetti with sauce. The noodles are the long polymer backbone that all plastic shares. The sauces are “the pigments, the antioxidants, the flame retardants, etc., that make it functional,” she said.
What makes microplastics dangerous?
There are more than 10,000 different chemicals, or “sauces,” used to alter a plastic’s physical characteristics – making it softer, more rigid, or more flexible, said Hanna Dusza, PhD, of the Institute for Risk Assessment Sciences at Utrecht University.
As plastics degrade and become microplastics, these chemicals likely remain. Recent research has shown that microplastics leach these chemicals locally in human tissues, or other areas of accumulation, said Dr. Dusza. Some 2,400 of the 10,000 chemical additives were classified as substances of potential concern, meeting the European Union’s criteria for persistence, bioaccumulation, or toxicity.
Many of these chemicals also act as endocrine-disrupting compounds, or toxicants that imitate hormones when they enter the body. Hormones are active at very low concentrations in your bloodstream, explained Dr. Leslie. To your body, some chemical additives in plastic resemble hormones, so the body responds.
“Sometimes even a low dose of some of these additives can cause unwanted effects,” said Dr. Leslie.
Bisphenol A (BPA), for example, is one of the more infamous endocrine disruptors. It is used as an additive to make plastics more rigid and can be found in any number of plastic products, though areas of concern have been plastic water bottles, baby bottles, and the protective coatings in canned foods.
BPA may mimic estrogen, the female sex hormone essential for reproduction, neurodevelopment, and bone density. In men, estrogen regulates sperm count, sex drive, and erectile function. BPA exposure has been linked with – but not proven to cause – multiple cancer types, ADHD, obesity, and low sperm count. Most everyone has some amount of BPA circulating within their blood, but microplastics may retain BPA as they degrade, potentially increasing our exposure, leading to its unwanted consequences, said Dr. Dusza.
And BPA is just one of those 2,400 substances of “potential concern.”
The inflammation problem
A potentially larger health issue emerges from our bodies yet again doing what they are supposed to do when encountering microplastics. Particles can trigger an immune response when they enter your bloodstream, explains Nienke Vrisekoop, PhD, assistant professor at UMC Utrecht.
White blood cells have no issue breaking down things like bacteria, but microplastics cannot be degraded. When a white blood cell engulfs a certain mass of microplastics – either many small particles or a singular large one – it dies, releasing its enzymes and causing local inflammation.
Meanwhile, the plastic particle remains. So more white blood cells attack.
“This triggers continual activation that can result in various adverse effects, including oxidative stress and the release of cytokines that trigger inflammatory reactions, said Dr. Vethaak.
And “chronic inflammation is the prelude to chronic diseases,” said Dr. Leslie. “Every chronic disease, like cancer, heart disease, and even neuropsychiatric diseases like Parkinson’s or major depression, begins with inflammation.”
Meanwhile, inhaling microplastic particles can lead to respiratory diseases and cancer.
“The smallest particles – less than one-tenth of a micrometer – penetrate deep into the lungs and even into the bloodstream, causing damage to the heart, blood vessels and brain,” said Dr. Vetaak. “The only direct evidence comes from workers in the textile and plastic industries that had been exposed to very high amounts of plastic fibrous dust.”
Microplastics as carriers
Microplastics can also pick up harmful substances and deliver them into your body.
“When they’re in an environment, they basically can suck up [chemicals] like a sponge,” said Dr. Dusza. “These chemicals are known environmental pollutants, like pesticides, fluorinated compounds, flame retardants, and so on.”
Once in the body, these chemicals can be released, potentially leading to cancer, chronic inflammation, or other unknown effects.
Particles can also act as a vector for microbes, bacteria, and viruses. A September 2022 study found that infectious viruses can survive for 3 days in fresh water by “hitchhiking” on microplastics. Their porous nature provides microbes with a perfect environment in which to live and reproduce, said Dr. Dusza. If you ingest the plastics, you ingest the microbes.
How to minimize exposure
There is no way to avoid microplastics. They’re in the air we breathe, the products we use, the water we drink, and the food we eat.
Dr. Danopoulos reviewed 72 studies to quantify our consumption of microplastics in drinking water, salt, and seafood.
“We are exposed to millions of microplastics every year, and I was only looking at three food sources, so there are really a lot more,” he said. “Once plastic waste is mismanaged and it enters the environment, there is very little we can do to extract it.”
That said, we can take steps to lower our exposure and keep the problem from getting worse.
Water filtration is one option, though it is not perfect. Research has shown that municipal water treatment can be effective. An October 2021 study found that two methods – electrocoagulation-electroflotation and membrane filtration – can be 100% effective in removing microplastics from treated water. The problem? Not all municipal water treatment uses these methods – and you would have to investigate to find out if your locality does.
As for at-home filtration methods, they can be effective but can also be dicey. Some consumer brands claim they remove microplastics, but how well depends on not just the type of filter but the size of the particles in the water. Meanwhile, how do you know if a filter is working on your water without testing it, something few people will do? Best not to take a brand’s claims on face-value, but look for independent testing on at-home brands.
A longer-term project: Reduce our risk by reusing and recycling plastic waste. Limiting our consumption of plastic, especially single use plastic, decreases the amount available to become micro- and nanoplastics.
We must all learn to not treat plastic as waste, but rather as a renewable material, said Dr. Cassee. But if that seems like a tall order, it’s because it is.
“You’re a human being and you have a voice and there are a lot of other humans out there with voices,” said Dr. Leslie.
“You sign a petition in your community. You talk about it with your friends at the pub. If you’re a teacher, you discuss it in your class. You call your elected representatives and tell them what you think and how you want them to vote on bills.”
When people start working together, you can really amplify that voice, said Dr. Leslie.
What’s the bottom line right now, today?
Numerous sources have declared microplastics do not impact human health. But that’s largely because no direct evidence of this exists yet.
Even the WHO in its report suggests that progress must happen if we’re to fully understand the scope of the problem.
“Strengthening of the evidence necessary for reliable characterization and quantification of the risks to human health posed by [nano- and microplastics] will require active participation by all stakeholders,” it said.
All researchers interviewed for this article agree we don’t have enough evidence to draw any definite conclusions. But “if you look at the wrong endpoints, things will look safe, until you look at the endpoint where it’s really causing the problem,” said Dr. Leslie.
We must research our blind spots and continually ask: Where could we be wrong?
“It is a problem; it’s not going to go away,” said Dr. Danopoulos. “It’s going to get worse, and will continue to get worse, not by something that we are doing now but by something we did 5 years ago.”
Perhaps the question to be asked, then, is the hardest to answer: Are we willing to wait for the science?
A version of this article first appeared on WebMD.com.
The truth of alcohol consequences
Bad drinking consequence No. 87: Joining the LOTME team
Alcohol and college students go together like peanut butter and jelly. Or peanut butter and chocolate. Or peanut butter and toothpaste. Peanut butter goes with a lot of things.
Naturally, when you combine alcohol and college students, bad decisions are sure to follow. But have you ever wondered just how many bad decisions alcohol causes? A team of researchers from Penn State University, the undisputed champion of poor drinking decisions (trust us, we know), sure has. They’ve even conducted a 4-year study of 1,700 students as they carved a drunken swath through the many fine local drinking establishments, such as East Halls or that one frat house that hosts medieval battle–style ping pong tournaments.
The students were surveyed twice a year throughout the study, and the researchers compiled a list of all the various consequences their subjects experienced. Ultimately, college students will experience an average of 102 consequences from drinking during their 4-year college careers, which is an impressive number. Try thinking up a hundred consequences for anything.
Some consequences are less common than others – we imagine “missing the Renaissance Faire because you felt drunker the morning after than while you were drinking” is pretty low on the list – but more than 96% of students reported that they’d experienced a hangover and that drinking had caused them to say or do embarrassing things. Also, more than 70% said they needed additional alcohol to feel any effect, a potential sign of alcohol use disorder.
Once they had their list, the researchers focused on 12 of the more common and severe consequences, such as blacking out, hangovers, and missing work/class, and asked the study participants how their parents would react to their drinking and those specific consequences. Students who believed their parents would disapprove of alcohol-related consequences actually experienced fewer consequences overall.
College students, it seems, really do care what their parents think, even if they don’t express it, the researchers said. That gives space for parents to offer advice about the consequences of hard drinking, making decisions while drunk, or bringing godawful Fireball whiskey to parties. Seriously, don’t do that. Stuff’s bad, and you should feel bad for bringing it. Your parents raised you better than that.
COVID ‘expert’ discusses data sharing
We interrupt our regularly scheduled programming to bring you this special news event. Elon Musk, the world’s second-most annoying human, is holding a press conference to discuss, of all things, COVID-19.
Reporter: Hey, Mr. Musketeer, what qualifies you to talk about a global pandemic?
EM: As the official king of the Twitterverse, I’m pretty much an expert on any topic.
Reporter: Okay then, Mr. Muskmelon, what can you tell us about the new study in Agricultural Economics, which looked at consumers’ knowledge of local COVID infection rates and their willingness to eat at restaurants?
EM: Well, I know that one of the investigators, Rigoberto Lopez, PhD, of the University of Connecticut, said “no news is bad news.” Restaurants located in cities where local regulations required COVID tracking recovered faster than those in areas that did not, according to data from 87 restaurants in 10 Chinese cities that were gathered between Dec. 1, 2019, and March 27, 2020. Having access to local infection rate data made customers more comfortable going out to eat, the investigators explained.
Second reporter: Interesting, Mr. Muskox, but how about this headline from CNN: “Workers flee China’s biggest iPhone factory over Covid outbreak”? Do you agree with analysts, who said that “the chaos at Zhengzhou could jeopardize Apple and Foxconn’s output in the coming weeks,” as CNN put it?
EM: I did see that a manager at Foxconn, which owns the factory and is known to its friends as Hon Hai Precision Industry, told a Chinese media outlet that “workers are panicking over the spread of the virus at the factory and lack of access to official information.” As we’ve already discussed, no news is bad news.
That’s all the time I have to chat with you today. I’m off to fire some more Twitter employees.
In case you hadn’t already guessed, Vlad Putin is officially more annoying than Elon Musk. We now return to this week’s typical LOTME shenanigans, already in progress.
The deadliest month
With climate change making the world hotter, leading to more heat stroke and organ failure, you would think the summer months would be the most deadly. In reality, though, it’s quite the opposite.
There are multiple factors that make January the most deadly month out of the year, as LiveScience discovered in a recent analysis.
Let’s go through them, shall we?
Respiratory viruses: Robert Glatter, MD, of Lenox Hill Hospital in New York, told LiveScence that winter is the time for illnesses like the flu, bacterial pneumonia, and RSV. Millions of people worldwide die from the flu, according to the CDC. And the World Health Organization reported lower respiratory infections as the fourth-leading cause of death worldwide before COVID came along.
Heart disease: Heart conditions are actually more fatal in the winter months, according to a study published in Circulation. The cold puts more stress on the heart to keep the body warm, which can be a challenge for people who already have preexisting heart conditions.
Space heaters: Dr. Glatter also told Live Science that the use of space heaters could be a factor in the cold winter months since they can lead to carbon monoxide poisoning and even fires. Silent killers.
Holiday season: A time for joy and merriment, certainly, but Christmas et al. have their downsides. By January we’re coming off a 3-month food and alcohol binge, which leads to cardiac stress. There’s also the psychological stress that comes with the season. Sometimes the most wonderful time of the year just isn’t.
So even though summer is hot, fall has hurricanes, and spring tends to have the highest suicide rate, winter still ends up being the deadliest season.
Bad drinking consequence No. 87: Joining the LOTME team
Alcohol and college students go together like peanut butter and jelly. Or peanut butter and chocolate. Or peanut butter and toothpaste. Peanut butter goes with a lot of things.
Naturally, when you combine alcohol and college students, bad decisions are sure to follow. But have you ever wondered just how many bad decisions alcohol causes? A team of researchers from Penn State University, the undisputed champion of poor drinking decisions (trust us, we know), sure has. They’ve even conducted a 4-year study of 1,700 students as they carved a drunken swath through the many fine local drinking establishments, such as East Halls or that one frat house that hosts medieval battle–style ping pong tournaments.
The students were surveyed twice a year throughout the study, and the researchers compiled a list of all the various consequences their subjects experienced. Ultimately, college students will experience an average of 102 consequences from drinking during their 4-year college careers, which is an impressive number. Try thinking up a hundred consequences for anything.
Some consequences are less common than others – we imagine “missing the Renaissance Faire because you felt drunker the morning after than while you were drinking” is pretty low on the list – but more than 96% of students reported that they’d experienced a hangover and that drinking had caused them to say or do embarrassing things. Also, more than 70% said they needed additional alcohol to feel any effect, a potential sign of alcohol use disorder.
Once they had their list, the researchers focused on 12 of the more common and severe consequences, such as blacking out, hangovers, and missing work/class, and asked the study participants how their parents would react to their drinking and those specific consequences. Students who believed their parents would disapprove of alcohol-related consequences actually experienced fewer consequences overall.
College students, it seems, really do care what their parents think, even if they don’t express it, the researchers said. That gives space for parents to offer advice about the consequences of hard drinking, making decisions while drunk, or bringing godawful Fireball whiskey to parties. Seriously, don’t do that. Stuff’s bad, and you should feel bad for bringing it. Your parents raised you better than that.
COVID ‘expert’ discusses data sharing
We interrupt our regularly scheduled programming to bring you this special news event. Elon Musk, the world’s second-most annoying human, is holding a press conference to discuss, of all things, COVID-19.
Reporter: Hey, Mr. Musketeer, what qualifies you to talk about a global pandemic?
EM: As the official king of the Twitterverse, I’m pretty much an expert on any topic.
Reporter: Okay then, Mr. Muskmelon, what can you tell us about the new study in Agricultural Economics, which looked at consumers’ knowledge of local COVID infection rates and their willingness to eat at restaurants?
EM: Well, I know that one of the investigators, Rigoberto Lopez, PhD, of the University of Connecticut, said “no news is bad news.” Restaurants located in cities where local regulations required COVID tracking recovered faster than those in areas that did not, according to data from 87 restaurants in 10 Chinese cities that were gathered between Dec. 1, 2019, and March 27, 2020. Having access to local infection rate data made customers more comfortable going out to eat, the investigators explained.
Second reporter: Interesting, Mr. Muskox, but how about this headline from CNN: “Workers flee China’s biggest iPhone factory over Covid outbreak”? Do you agree with analysts, who said that “the chaos at Zhengzhou could jeopardize Apple and Foxconn’s output in the coming weeks,” as CNN put it?
EM: I did see that a manager at Foxconn, which owns the factory and is known to its friends as Hon Hai Precision Industry, told a Chinese media outlet that “workers are panicking over the spread of the virus at the factory and lack of access to official information.” As we’ve already discussed, no news is bad news.
That’s all the time I have to chat with you today. I’m off to fire some more Twitter employees.
In case you hadn’t already guessed, Vlad Putin is officially more annoying than Elon Musk. We now return to this week’s typical LOTME shenanigans, already in progress.
The deadliest month
With climate change making the world hotter, leading to more heat stroke and organ failure, you would think the summer months would be the most deadly. In reality, though, it’s quite the opposite.
There are multiple factors that make January the most deadly month out of the year, as LiveScience discovered in a recent analysis.
Let’s go through them, shall we?
Respiratory viruses: Robert Glatter, MD, of Lenox Hill Hospital in New York, told LiveScence that winter is the time for illnesses like the flu, bacterial pneumonia, and RSV. Millions of people worldwide die from the flu, according to the CDC. And the World Health Organization reported lower respiratory infections as the fourth-leading cause of death worldwide before COVID came along.
Heart disease: Heart conditions are actually more fatal in the winter months, according to a study published in Circulation. The cold puts more stress on the heart to keep the body warm, which can be a challenge for people who already have preexisting heart conditions.
Space heaters: Dr. Glatter also told Live Science that the use of space heaters could be a factor in the cold winter months since they can lead to carbon monoxide poisoning and even fires. Silent killers.
Holiday season: A time for joy and merriment, certainly, but Christmas et al. have their downsides. By January we’re coming off a 3-month food and alcohol binge, which leads to cardiac stress. There’s also the psychological stress that comes with the season. Sometimes the most wonderful time of the year just isn’t.
So even though summer is hot, fall has hurricanes, and spring tends to have the highest suicide rate, winter still ends up being the deadliest season.
Bad drinking consequence No. 87: Joining the LOTME team
Alcohol and college students go together like peanut butter and jelly. Or peanut butter and chocolate. Or peanut butter and toothpaste. Peanut butter goes with a lot of things.
Naturally, when you combine alcohol and college students, bad decisions are sure to follow. But have you ever wondered just how many bad decisions alcohol causes? A team of researchers from Penn State University, the undisputed champion of poor drinking decisions (trust us, we know), sure has. They’ve even conducted a 4-year study of 1,700 students as they carved a drunken swath through the many fine local drinking establishments, such as East Halls or that one frat house that hosts medieval battle–style ping pong tournaments.
The students were surveyed twice a year throughout the study, and the researchers compiled a list of all the various consequences their subjects experienced. Ultimately, college students will experience an average of 102 consequences from drinking during their 4-year college careers, which is an impressive number. Try thinking up a hundred consequences for anything.
Some consequences are less common than others – we imagine “missing the Renaissance Faire because you felt drunker the morning after than while you were drinking” is pretty low on the list – but more than 96% of students reported that they’d experienced a hangover and that drinking had caused them to say or do embarrassing things. Also, more than 70% said they needed additional alcohol to feel any effect, a potential sign of alcohol use disorder.
Once they had their list, the researchers focused on 12 of the more common and severe consequences, such as blacking out, hangovers, and missing work/class, and asked the study participants how their parents would react to their drinking and those specific consequences. Students who believed their parents would disapprove of alcohol-related consequences actually experienced fewer consequences overall.
College students, it seems, really do care what their parents think, even if they don’t express it, the researchers said. That gives space for parents to offer advice about the consequences of hard drinking, making decisions while drunk, or bringing godawful Fireball whiskey to parties. Seriously, don’t do that. Stuff’s bad, and you should feel bad for bringing it. Your parents raised you better than that.
COVID ‘expert’ discusses data sharing
We interrupt our regularly scheduled programming to bring you this special news event. Elon Musk, the world’s second-most annoying human, is holding a press conference to discuss, of all things, COVID-19.
Reporter: Hey, Mr. Musketeer, what qualifies you to talk about a global pandemic?
EM: As the official king of the Twitterverse, I’m pretty much an expert on any topic.
Reporter: Okay then, Mr. Muskmelon, what can you tell us about the new study in Agricultural Economics, which looked at consumers’ knowledge of local COVID infection rates and their willingness to eat at restaurants?
EM: Well, I know that one of the investigators, Rigoberto Lopez, PhD, of the University of Connecticut, said “no news is bad news.” Restaurants located in cities where local regulations required COVID tracking recovered faster than those in areas that did not, according to data from 87 restaurants in 10 Chinese cities that were gathered between Dec. 1, 2019, and March 27, 2020. Having access to local infection rate data made customers more comfortable going out to eat, the investigators explained.
Second reporter: Interesting, Mr. Muskox, but how about this headline from CNN: “Workers flee China’s biggest iPhone factory over Covid outbreak”? Do you agree with analysts, who said that “the chaos at Zhengzhou could jeopardize Apple and Foxconn’s output in the coming weeks,” as CNN put it?
EM: I did see that a manager at Foxconn, which owns the factory and is known to its friends as Hon Hai Precision Industry, told a Chinese media outlet that “workers are panicking over the spread of the virus at the factory and lack of access to official information.” As we’ve already discussed, no news is bad news.
That’s all the time I have to chat with you today. I’m off to fire some more Twitter employees.
In case you hadn’t already guessed, Vlad Putin is officially more annoying than Elon Musk. We now return to this week’s typical LOTME shenanigans, already in progress.
The deadliest month
With climate change making the world hotter, leading to more heat stroke and organ failure, you would think the summer months would be the most deadly. In reality, though, it’s quite the opposite.
There are multiple factors that make January the most deadly month out of the year, as LiveScience discovered in a recent analysis.
Let’s go through them, shall we?
Respiratory viruses: Robert Glatter, MD, of Lenox Hill Hospital in New York, told LiveScence that winter is the time for illnesses like the flu, bacterial pneumonia, and RSV. Millions of people worldwide die from the flu, according to the CDC. And the World Health Organization reported lower respiratory infections as the fourth-leading cause of death worldwide before COVID came along.
Heart disease: Heart conditions are actually more fatal in the winter months, according to a study published in Circulation. The cold puts more stress on the heart to keep the body warm, which can be a challenge for people who already have preexisting heart conditions.
Space heaters: Dr. Glatter also told Live Science that the use of space heaters could be a factor in the cold winter months since they can lead to carbon monoxide poisoning and even fires. Silent killers.
Holiday season: A time for joy and merriment, certainly, but Christmas et al. have their downsides. By January we’re coming off a 3-month food and alcohol binge, which leads to cardiac stress. There’s also the psychological stress that comes with the season. Sometimes the most wonderful time of the year just isn’t.
So even though summer is hot, fall has hurricanes, and spring tends to have the highest suicide rate, winter still ends up being the deadliest season.
How to prevent a feared complication after joint replacement
Knee and hip replacements can improve how well patients get around and can significantly increase their quality of life. But if a bone near the new joint breaks, the injury can be a major setback for the patient’s mobility, and the consequences can be life-threatening.
The proportion of patients who experience a periprosthetic fracture within 5 years of total hip arthroplasty is 0.9%. After total knee arthroplasty (TKA), the proportion is 0.6%, research shows.
Those rates might seem low. But given that more than a million of these joint replacement surgeries are performed each year in the United States – they are the most common inpatient surgical procedures among people aged 65 and older – thousands of revision surgeries due to periprosthetic fractures occur each year.
Primary care clinicians who make their patients’ bone health a priority early on – years before surgery, ideally – may help patients enjoy the benefits of new joints long term.
At the 2022 annual Santa Fe Bone Symposium this summer, Susan V. Bukata, MD, professor and chair of orthopedics at the University of California, San Diego, showed an image of “what we’re trying to avoid” – a patient with a broken bone and infection. Unfortunately, Dr. Bukata said, the patient’s clinicians had not adequately addressed her skeletal health before the injury.
“This is a complete disaster for this person who went in having a total hip to improve their function and now will probably never walk normally on that leg,” Dr. Bukata said at the meeting.
The patient eventually underwent total femur replacement. Five surgeries were required to clear the infection.
Medical and surgical advances have allowed more people – including older patients and those with other medical conditions – to undergo joint replacement surgery, including replacement of knees, hips, and shoulders.
The surgeries often are performed for adults whose bones are thinning. Sometimes surgeons don’t realize just how thin a patient’s bone is until they are operating.
Prioritizing bone health
In patients with osteoporosis, the bone surrounding the new joint is weaker than the metal of the prosthesis, and the metal can rip out of the bone, Dr. Bukata told this news organization. A periprosthetic fracture should be recognized as an osteoporotic fracture, too, although these fractures have not typically been categorized that way, she said.
People live with total joints in place for as long as 40 years, and fractures around the implants are “one of the fastest growing injuries that we are seeing in older patients,” Dr. Bukata said. “People don’t think of those as osteoporotic fractures. But a 90-year-old who falls and breaks next to their total knee, if they didn’t have that total knee in place, everybody would be, like, ‘Oh, that’s an osteoporotic fracture.’ ”
Periprosthetic fractures tend not to occur right after surgery but rather after the bone continues to lose density as the patient ages, Dr. Bukata said.
Missed chances
One approach to preventing periprosthetic fractures could involve prioritizing bone health earlier in life and diagnosing and treating osteoporosis well before a patient is scheduled for surgery.
A patient’s initial visit to their primary care doctor because of joint pain is an opportunity to check on and promote their bone health, given that they might be a candidate for surgery in the future, Dr. Bukata said.
Ahead of a scheduled surgery, patients can see endocrinologists or rheumatologists to receive medication to try to strengthen bones. Doctors may be limited in how much of a difference they can make in a matter of several weeks or months with these drugs, however. These patients still likely will need to be treated as if they have osteoporosis, Dr. Bukata said.
When surgeons realize that a patient has weaker bones while they are in the middle of an operation, they should emphasize the importance of bone health after the procedure, Dr. Bukata said.
Strengthening, maintaining, and protecting bone should be seen as a long-term investment in the patient’s success after a joint replacement. That said, “There is no clear evidence or protocol for us to follow,” she said. “The mantra at UCSD now is, let’s keep it simple. Get the patient on track. And then we can always refine things as we continue to treat the patient.”
Health systems should establish routines in which bone health is discussed before surgery in the way patient education programs address smoking cessation, nutrition, and weight management, Dr. Bukata said. Another step in the right direction could involve setting electronic medical records to automatically order assessments of bone health when a surgeon books a case.
Linda A. Russell, MD, rheumatologist and director of perioperative medicine at the Hospital for Special Surgery in New York, said periprosthetic fractures are a “complication we fear.”
“It’s a big deal to try to repair it,” Dr. Russell said. “Sometimes you need to revise the joint, or sometimes you need to put lots more hardware in.” Surgeons increasingly appreciate the need to pay attention to the quality of the bone before they operate, she said.
Nevertheless, Dr. Russell does not necessarily say that such cases call for alarm or particularly aggressive treatment regimens – just regular bone health evaluations before and after surgery to see whether patients have osteoporosis and are candidates for treatment.
Lifelong effort
In some ways, to address bone health at the time of surgery may be too late.
Bone health “is not something that you can have as an afterthought when you’re 75 years old,” said Elizabeth Matzkin, MD, chief of women’s sports medicine at Brigham and Women’s Hospital, in Boston.
The chance of being able to rebuild bone mass at that age is slim. If patients maximize bone density when they are young, they can afford to lose some bone mass each year as they age.
To that end, a healthy diet, exercise, not smoking, and cutting back on alcohol can help, she said.
For Dr. Matzkin, a fragility fracture is a red flag that the patient’s bone density is probably not optimal. In such cases, she prepares for various scenarios during surgery, such as a screw not holding in a low-density bone.
Recently published research reflects that prior fragility fractures are a significant risk factor for complications after surgery, including periprosthetic fractures.
Edward J. Testa, MD, of Brown University, Providence, R.I., and colleagues analyzed insurance claims to compare outcomes for 24,398 patients who had experienced a fragility fracture – that is, a break caused by low-velocity trauma such as a fall – during the 3 years before their TKA procedure and a matched group of patients who were similar in many respects but who had not had a fragility fracture in the 3 years before surgery.
Dr. Testa’s group found that a history of fragility fracture was associated with higher rates of complications in the year after surgery, including hospital readmissions (hazard ratio = 1.30; 95% CI, 1.22-1.38), periprosthetic fractures (odds ratio = 2.72; 95% CI, 1.89-3.99), and secondary fragility fractures (OR = 4.62; 95% CI, 4.19-5.12). Patients who had previously experienced fragility fractures also experienced dislocated prostheses (OR = 1.76; 95% CI, 1.22-2.56) and periprosthetic infections (OR = 1.49; 95% CI, 1.29-1.71) at higher rates.
The rates of complications were similar regardless of whether patients had filled a prescription for medications used to treat osteoporosis, including bisphosphonates, vitamin D replacement, raloxifene, and denosumab, the researchers reported.
The lack of a clear association between these treatments and patient outcomes could be related to an insufficient duration of pharmacotherapy before or after TKA, poor medication adherence, or small sample sizes, Dr. Testa said.
Given the findings, which were published online in the Journal of Arthroplasty, “patients with a history of fragility fracture should be identified and counseled appropriately for a possible increased risk of the aforementioned complications, and optimized when possible, prior to undergoing TKA,” Dr. Testa told this news organization. “Ultimately, the decision to move forward with surgery is far more complex than the identification of this sole, yet important, risk factor for certain postoperative, implant-related complications.”
Treatment gaps
Prior research has shown that women aged 70 years and older are at higher risk for periprosthetic fractures. Many women in this age group who could receive treatment for osteoporosis do not, and major treatment gaps exist worldwide, noted Neil Binkley, MD, with the University of Wisconsin–Madison, in a separate talk at the Santa Fe Bone Symposium.
Ensuring adequate protein intake and addressing the risk of falling are other measures that clinicians can take to promote healthy bones, apart from prescribing drugs, he said.
Unpublished data from one group show that nearly 90% of periprosthetic fractures may result from falls, while about 8% may be spontaneous. “We need to be thinking about falls,” Dr. Binkley said.
Dr. Bukata has consulted for Amgen, Radius, and Solarea Bio and has served on a speakers bureau for Radius. She also is a board member for the Orthopaedic Research Society and the American Academy of Orthopaedic Surgeons Board of Specialty Societies. Dr. Binkley has received research support from Radius and has consulted for Amgen.
A version of this article first appeared on Medscape.com.
Knee and hip replacements can improve how well patients get around and can significantly increase their quality of life. But if a bone near the new joint breaks, the injury can be a major setback for the patient’s mobility, and the consequences can be life-threatening.
The proportion of patients who experience a periprosthetic fracture within 5 years of total hip arthroplasty is 0.9%. After total knee arthroplasty (TKA), the proportion is 0.6%, research shows.
Those rates might seem low. But given that more than a million of these joint replacement surgeries are performed each year in the United States – they are the most common inpatient surgical procedures among people aged 65 and older – thousands of revision surgeries due to periprosthetic fractures occur each year.
Primary care clinicians who make their patients’ bone health a priority early on – years before surgery, ideally – may help patients enjoy the benefits of new joints long term.
At the 2022 annual Santa Fe Bone Symposium this summer, Susan V. Bukata, MD, professor and chair of orthopedics at the University of California, San Diego, showed an image of “what we’re trying to avoid” – a patient with a broken bone and infection. Unfortunately, Dr. Bukata said, the patient’s clinicians had not adequately addressed her skeletal health before the injury.
“This is a complete disaster for this person who went in having a total hip to improve their function and now will probably never walk normally on that leg,” Dr. Bukata said at the meeting.
The patient eventually underwent total femur replacement. Five surgeries were required to clear the infection.
Medical and surgical advances have allowed more people – including older patients and those with other medical conditions – to undergo joint replacement surgery, including replacement of knees, hips, and shoulders.
The surgeries often are performed for adults whose bones are thinning. Sometimes surgeons don’t realize just how thin a patient’s bone is until they are operating.
Prioritizing bone health
In patients with osteoporosis, the bone surrounding the new joint is weaker than the metal of the prosthesis, and the metal can rip out of the bone, Dr. Bukata told this news organization. A periprosthetic fracture should be recognized as an osteoporotic fracture, too, although these fractures have not typically been categorized that way, she said.
People live with total joints in place for as long as 40 years, and fractures around the implants are “one of the fastest growing injuries that we are seeing in older patients,” Dr. Bukata said. “People don’t think of those as osteoporotic fractures. But a 90-year-old who falls and breaks next to their total knee, if they didn’t have that total knee in place, everybody would be, like, ‘Oh, that’s an osteoporotic fracture.’ ”
Periprosthetic fractures tend not to occur right after surgery but rather after the bone continues to lose density as the patient ages, Dr. Bukata said.
Missed chances
One approach to preventing periprosthetic fractures could involve prioritizing bone health earlier in life and diagnosing and treating osteoporosis well before a patient is scheduled for surgery.
A patient’s initial visit to their primary care doctor because of joint pain is an opportunity to check on and promote their bone health, given that they might be a candidate for surgery in the future, Dr. Bukata said.
Ahead of a scheduled surgery, patients can see endocrinologists or rheumatologists to receive medication to try to strengthen bones. Doctors may be limited in how much of a difference they can make in a matter of several weeks or months with these drugs, however. These patients still likely will need to be treated as if they have osteoporosis, Dr. Bukata said.
When surgeons realize that a patient has weaker bones while they are in the middle of an operation, they should emphasize the importance of bone health after the procedure, Dr. Bukata said.
Strengthening, maintaining, and protecting bone should be seen as a long-term investment in the patient’s success after a joint replacement. That said, “There is no clear evidence or protocol for us to follow,” she said. “The mantra at UCSD now is, let’s keep it simple. Get the patient on track. And then we can always refine things as we continue to treat the patient.”
Health systems should establish routines in which bone health is discussed before surgery in the way patient education programs address smoking cessation, nutrition, and weight management, Dr. Bukata said. Another step in the right direction could involve setting electronic medical records to automatically order assessments of bone health when a surgeon books a case.
Linda A. Russell, MD, rheumatologist and director of perioperative medicine at the Hospital for Special Surgery in New York, said periprosthetic fractures are a “complication we fear.”
“It’s a big deal to try to repair it,” Dr. Russell said. “Sometimes you need to revise the joint, or sometimes you need to put lots more hardware in.” Surgeons increasingly appreciate the need to pay attention to the quality of the bone before they operate, she said.
Nevertheless, Dr. Russell does not necessarily say that such cases call for alarm or particularly aggressive treatment regimens – just regular bone health evaluations before and after surgery to see whether patients have osteoporosis and are candidates for treatment.
Lifelong effort
In some ways, to address bone health at the time of surgery may be too late.
Bone health “is not something that you can have as an afterthought when you’re 75 years old,” said Elizabeth Matzkin, MD, chief of women’s sports medicine at Brigham and Women’s Hospital, in Boston.
The chance of being able to rebuild bone mass at that age is slim. If patients maximize bone density when they are young, they can afford to lose some bone mass each year as they age.
To that end, a healthy diet, exercise, not smoking, and cutting back on alcohol can help, she said.
For Dr. Matzkin, a fragility fracture is a red flag that the patient’s bone density is probably not optimal. In such cases, she prepares for various scenarios during surgery, such as a screw not holding in a low-density bone.
Recently published research reflects that prior fragility fractures are a significant risk factor for complications after surgery, including periprosthetic fractures.
Edward J. Testa, MD, of Brown University, Providence, R.I., and colleagues analyzed insurance claims to compare outcomes for 24,398 patients who had experienced a fragility fracture – that is, a break caused by low-velocity trauma such as a fall – during the 3 years before their TKA procedure and a matched group of patients who were similar in many respects but who had not had a fragility fracture in the 3 years before surgery.
Dr. Testa’s group found that a history of fragility fracture was associated with higher rates of complications in the year after surgery, including hospital readmissions (hazard ratio = 1.30; 95% CI, 1.22-1.38), periprosthetic fractures (odds ratio = 2.72; 95% CI, 1.89-3.99), and secondary fragility fractures (OR = 4.62; 95% CI, 4.19-5.12). Patients who had previously experienced fragility fractures also experienced dislocated prostheses (OR = 1.76; 95% CI, 1.22-2.56) and periprosthetic infections (OR = 1.49; 95% CI, 1.29-1.71) at higher rates.
The rates of complications were similar regardless of whether patients had filled a prescription for medications used to treat osteoporosis, including bisphosphonates, vitamin D replacement, raloxifene, and denosumab, the researchers reported.
The lack of a clear association between these treatments and patient outcomes could be related to an insufficient duration of pharmacotherapy before or after TKA, poor medication adherence, or small sample sizes, Dr. Testa said.
Given the findings, which were published online in the Journal of Arthroplasty, “patients with a history of fragility fracture should be identified and counseled appropriately for a possible increased risk of the aforementioned complications, and optimized when possible, prior to undergoing TKA,” Dr. Testa told this news organization. “Ultimately, the decision to move forward with surgery is far more complex than the identification of this sole, yet important, risk factor for certain postoperative, implant-related complications.”
Treatment gaps
Prior research has shown that women aged 70 years and older are at higher risk for periprosthetic fractures. Many women in this age group who could receive treatment for osteoporosis do not, and major treatment gaps exist worldwide, noted Neil Binkley, MD, with the University of Wisconsin–Madison, in a separate talk at the Santa Fe Bone Symposium.
Ensuring adequate protein intake and addressing the risk of falling are other measures that clinicians can take to promote healthy bones, apart from prescribing drugs, he said.
Unpublished data from one group show that nearly 90% of periprosthetic fractures may result from falls, while about 8% may be spontaneous. “We need to be thinking about falls,” Dr. Binkley said.
Dr. Bukata has consulted for Amgen, Radius, and Solarea Bio and has served on a speakers bureau for Radius. She also is a board member for the Orthopaedic Research Society and the American Academy of Orthopaedic Surgeons Board of Specialty Societies. Dr. Binkley has received research support from Radius and has consulted for Amgen.
A version of this article first appeared on Medscape.com.
Knee and hip replacements can improve how well patients get around and can significantly increase their quality of life. But if a bone near the new joint breaks, the injury can be a major setback for the patient’s mobility, and the consequences can be life-threatening.
The proportion of patients who experience a periprosthetic fracture within 5 years of total hip arthroplasty is 0.9%. After total knee arthroplasty (TKA), the proportion is 0.6%, research shows.
Those rates might seem low. But given that more than a million of these joint replacement surgeries are performed each year in the United States – they are the most common inpatient surgical procedures among people aged 65 and older – thousands of revision surgeries due to periprosthetic fractures occur each year.
Primary care clinicians who make their patients’ bone health a priority early on – years before surgery, ideally – may help patients enjoy the benefits of new joints long term.
At the 2022 annual Santa Fe Bone Symposium this summer, Susan V. Bukata, MD, professor and chair of orthopedics at the University of California, San Diego, showed an image of “what we’re trying to avoid” – a patient with a broken bone and infection. Unfortunately, Dr. Bukata said, the patient’s clinicians had not adequately addressed her skeletal health before the injury.
“This is a complete disaster for this person who went in having a total hip to improve their function and now will probably never walk normally on that leg,” Dr. Bukata said at the meeting.
The patient eventually underwent total femur replacement. Five surgeries were required to clear the infection.
Medical and surgical advances have allowed more people – including older patients and those with other medical conditions – to undergo joint replacement surgery, including replacement of knees, hips, and shoulders.
The surgeries often are performed for adults whose bones are thinning. Sometimes surgeons don’t realize just how thin a patient’s bone is until they are operating.
Prioritizing bone health
In patients with osteoporosis, the bone surrounding the new joint is weaker than the metal of the prosthesis, and the metal can rip out of the bone, Dr. Bukata told this news organization. A periprosthetic fracture should be recognized as an osteoporotic fracture, too, although these fractures have not typically been categorized that way, she said.
People live with total joints in place for as long as 40 years, and fractures around the implants are “one of the fastest growing injuries that we are seeing in older patients,” Dr. Bukata said. “People don’t think of those as osteoporotic fractures. But a 90-year-old who falls and breaks next to their total knee, if they didn’t have that total knee in place, everybody would be, like, ‘Oh, that’s an osteoporotic fracture.’ ”
Periprosthetic fractures tend not to occur right after surgery but rather after the bone continues to lose density as the patient ages, Dr. Bukata said.
Missed chances
One approach to preventing periprosthetic fractures could involve prioritizing bone health earlier in life and diagnosing and treating osteoporosis well before a patient is scheduled for surgery.
A patient’s initial visit to their primary care doctor because of joint pain is an opportunity to check on and promote their bone health, given that they might be a candidate for surgery in the future, Dr. Bukata said.
Ahead of a scheduled surgery, patients can see endocrinologists or rheumatologists to receive medication to try to strengthen bones. Doctors may be limited in how much of a difference they can make in a matter of several weeks or months with these drugs, however. These patients still likely will need to be treated as if they have osteoporosis, Dr. Bukata said.
When surgeons realize that a patient has weaker bones while they are in the middle of an operation, they should emphasize the importance of bone health after the procedure, Dr. Bukata said.
Strengthening, maintaining, and protecting bone should be seen as a long-term investment in the patient’s success after a joint replacement. That said, “There is no clear evidence or protocol for us to follow,” she said. “The mantra at UCSD now is, let’s keep it simple. Get the patient on track. And then we can always refine things as we continue to treat the patient.”
Health systems should establish routines in which bone health is discussed before surgery in the way patient education programs address smoking cessation, nutrition, and weight management, Dr. Bukata said. Another step in the right direction could involve setting electronic medical records to automatically order assessments of bone health when a surgeon books a case.
Linda A. Russell, MD, rheumatologist and director of perioperative medicine at the Hospital for Special Surgery in New York, said periprosthetic fractures are a “complication we fear.”
“It’s a big deal to try to repair it,” Dr. Russell said. “Sometimes you need to revise the joint, or sometimes you need to put lots more hardware in.” Surgeons increasingly appreciate the need to pay attention to the quality of the bone before they operate, she said.
Nevertheless, Dr. Russell does not necessarily say that such cases call for alarm or particularly aggressive treatment regimens – just regular bone health evaluations before and after surgery to see whether patients have osteoporosis and are candidates for treatment.
Lifelong effort
In some ways, to address bone health at the time of surgery may be too late.
Bone health “is not something that you can have as an afterthought when you’re 75 years old,” said Elizabeth Matzkin, MD, chief of women’s sports medicine at Brigham and Women’s Hospital, in Boston.
The chance of being able to rebuild bone mass at that age is slim. If patients maximize bone density when they are young, they can afford to lose some bone mass each year as they age.
To that end, a healthy diet, exercise, not smoking, and cutting back on alcohol can help, she said.
For Dr. Matzkin, a fragility fracture is a red flag that the patient’s bone density is probably not optimal. In such cases, she prepares for various scenarios during surgery, such as a screw not holding in a low-density bone.
Recently published research reflects that prior fragility fractures are a significant risk factor for complications after surgery, including periprosthetic fractures.
Edward J. Testa, MD, of Brown University, Providence, R.I., and colleagues analyzed insurance claims to compare outcomes for 24,398 patients who had experienced a fragility fracture – that is, a break caused by low-velocity trauma such as a fall – during the 3 years before their TKA procedure and a matched group of patients who were similar in many respects but who had not had a fragility fracture in the 3 years before surgery.
Dr. Testa’s group found that a history of fragility fracture was associated with higher rates of complications in the year after surgery, including hospital readmissions (hazard ratio = 1.30; 95% CI, 1.22-1.38), periprosthetic fractures (odds ratio = 2.72; 95% CI, 1.89-3.99), and secondary fragility fractures (OR = 4.62; 95% CI, 4.19-5.12). Patients who had previously experienced fragility fractures also experienced dislocated prostheses (OR = 1.76; 95% CI, 1.22-2.56) and periprosthetic infections (OR = 1.49; 95% CI, 1.29-1.71) at higher rates.
The rates of complications were similar regardless of whether patients had filled a prescription for medications used to treat osteoporosis, including bisphosphonates, vitamin D replacement, raloxifene, and denosumab, the researchers reported.
The lack of a clear association between these treatments and patient outcomes could be related to an insufficient duration of pharmacotherapy before or after TKA, poor medication adherence, or small sample sizes, Dr. Testa said.
Given the findings, which were published online in the Journal of Arthroplasty, “patients with a history of fragility fracture should be identified and counseled appropriately for a possible increased risk of the aforementioned complications, and optimized when possible, prior to undergoing TKA,” Dr. Testa told this news organization. “Ultimately, the decision to move forward with surgery is far more complex than the identification of this sole, yet important, risk factor for certain postoperative, implant-related complications.”
Treatment gaps
Prior research has shown that women aged 70 years and older are at higher risk for periprosthetic fractures. Many women in this age group who could receive treatment for osteoporosis do not, and major treatment gaps exist worldwide, noted Neil Binkley, MD, with the University of Wisconsin–Madison, in a separate talk at the Santa Fe Bone Symposium.
Ensuring adequate protein intake and addressing the risk of falling are other measures that clinicians can take to promote healthy bones, apart from prescribing drugs, he said.
Unpublished data from one group show that nearly 90% of periprosthetic fractures may result from falls, while about 8% may be spontaneous. “We need to be thinking about falls,” Dr. Binkley said.
Dr. Bukata has consulted for Amgen, Radius, and Solarea Bio and has served on a speakers bureau for Radius. She also is a board member for the Orthopaedic Research Society and the American Academy of Orthopaedic Surgeons Board of Specialty Societies. Dr. Binkley has received research support from Radius and has consulted for Amgen.
A version of this article first appeared on Medscape.com.
Studies provide compelling momentum for mucosal origins hypothesis of rheumatoid arthritis
A newly discovered strain of bacteria could play a role in the development of rheumatoid arthritis, according to findings recently published in Science Translational Medicine.
Mice colonized with a strain of Subdoligranulum bacteria in their gut – a strain previously unidentified but now named Subdoligranulum didolesgii – developed joint swelling and inflammation as well as antibodies and T-cell responses similar to what is seen in RA, researchers reported.
“This was the first time that anyone has observed arthritis developing in a mouse that was not otherwise immunologically stimulated with an adjuvant of some kind, or genetically manipulated,” said Kristine Kuhn, MD, PhD, associate professor of rheumatology at the University of Colorado at Denver, Aurora, who led a team of researchers that also included investigators from Stanford (Calif.) University and Benaroya Research Institute in Seattle.
The findings offer the latest evidence – and perhaps the most compelling evidence – for the mucosal origins hypothesis, the idea that rheumatoid arthritis can start with an immune response somewhere in the mucosa because of environmental interactions, and then becomes systemic, resulting in symptoms in the joints. Anti-citrullinated protein antibodies (ACPA), hallmarks of RA, have been found at mucosal surfaces in the periodontium and the lungs, and there have been reports of them in the intestine and cervicovaginal mucosa as well.
The latest findings that implicate the new bacterium build on previous findings in which people at risk of RA, but without symptoms yet, had an expansion of B cells producing immunoglobulin A (IgA), an antibody found in the mucosa. A closer look at these B cells, using variable region sequencing, found that they arose from a family that includes both IgA and IgG members. Because IgG antibodies are systemic, this suggested a kind of evolution from an IgA-based, mucosal immune response to one that is systemic and could target the joints.
Researchers mixed monoclonal antibodies from these B cells with a pool of bacteria from the stool of a broad population of people, and then pulled out the bacteria bound by these antibodies, and sequenced them. They found that the antibodies had bound almost exclusively to Ruminococcaceae and Lachnospiraceae.
They then cultured the stool of an individual at risk of developing RA and ended up with five isolates within Ruminococcaceae – “all of which belonged to the Subdoligranulum genus,” Dr. Kuhn said. When they sequenced these, they found that they had a new strain, which was named by Meagan Chriswell, an MD-PhD candidate and member of the Cherokee Nation of Oklahoma, who chose a term based on the Cherokee word for rheumatism.
Researchers at Benaroya then mixed this strain with T cells of people with RA, and those of controls, and only the T cells of those with RA were stimulated by the bacterium, they found.
“When intestines of germ-free mice were colonized with the strain, we found that they were getting arthritis,” Dr. Kuhn said. Photos of the joints show a striking contrast between the swollen joints of the mice given Subdoligranulum didolesgii and those injected with Prevotella copri, another strain suspected of having a link to RA, as well as with another Subdoligranulum strain and a sterile media. Dr. Kuhn noted that the P. copri strain did not come from an RA-affected individual.
“We thought that our results closed the loop nicely to show that these immune responses truly were toward the Subdoligranulum, and also stimulating arthritis,” she said.
The researchers then assessed the prevalence of the strain in people at risk for RA or with RA, and in controls. They found it in 17% of those with or at risk for RA but didn’t see it at all in the healthy control population.
Dr. Kuhn and her research team, she said, are now looking at the prevalence of the strain in a larger population and doing more investigating into the link with RA.
“Does it really associate with the development of immune responses and the development of rheumatoid arthritis?” she said.
Potential etiologic role of P. copri
Another paper, published in Arthritis & Rheumatology by some of the same investigators a week before the study describing the Subdoligranulum findings, tried to ascertain the point at which individuals might develop antibodies to P. copri, which for about a decade has been suspected of having a link to the development of RA.
They found that those with early RA had higher median values of IgG anti–P. copri (Pc) antibodies, compared with matched controls. People with established RA also had higher values of IgA anti-Pc antibodies. Those with ACPA, but not rheumatoid factor (RF), showed a trend toward higher IgG anti-Pc antibodies. Those who were ACPA-positive and RF-positive had significantly increased levels of IgA anti-Pc antibodies and a trend toward higher levels of IgG anti-Pc antibodies, compared with matched controls.
The findings, according to the researchers, “support a potential etiologic role for this microorganism in both RA preclinical evolution and the subsequent pathogenesis of synovitis.”
Dr. Kuhn and others in the field say it’s likely that many microbes play a role in the development of RA, and that the P. copri findings only add evidence of that relationship.
“Maybe the bacteria are involved at different parts of the pathway, and maybe they’re involved in triggering different parts of the immune responses,” she said. “Those are all to be determined.”
Dan Littman, MD, PhD, professor of rheumatology at New York University, who wrote a commentary reflecting on the findings of the Subdoligranulum study, said the results are “another piece of data” adding to the evidence base for the mucosal origins hypothesis.
“It’s by no means proven that this is the way pathogenesis in RA can occur, but it’s certainly a very solid study,” said Dr. Littman, who with colleagues published findings in 2013 linking P. copri to RA. “What makes it most compelling is that they seem to be able to show some evidence of causality in the mouse model.”
Before the findings could lead to therapy, he said, more evidence is needed to show that there is a causal link, and on the mechanism at work, such as whether this is something that occurs at the outset of disease or is something that “fuels the disease” by continually activating immune cells contributing to RA.
“If it’s only something that’s involved in the initiation of the disease, you need to catch it very early,” he said. “But if it’s something that continues to provide fuel for the disease, you may be able to catch it later and still be effective. Those are really critical items.”
Eventually, if these questions are answered, bacteriophages could be developed to snuff out problematic strains, or the regulatory response could be targeted to prevent the activation of the B cells that give rise to autoimmunity, he suggested.
“There are multiple steps to get to a therapeutic here, and I think we’re still a long ways from that,” he said. Still, he said, “I think it’s an important paper because it will encourage more people to look at this mechanism more closely and determine whether it really is representative of what happens in a lot of RA patients.”
The study in Science Translational Medicine was supported by grants from the National Institutes of Health, a Pfizer ASPIRE grant, and a grant from the Rheumatology Research Foundation. The Arthritis & Rheumatology study was supported in part by grants from the National Institutes of Health; the American College of Rheumatology Innovative Grant Program; the Ounsworth-Fitzgerald Foundation; Mathers Foundation; English, Bonter, Mitchell Foundation; Littauer Foundation; Lillian B. Davey Foundation; and the Eshe Fund. None of the researchers in either study had relevant financial disclosures. Dr. Littman is scientific cofounder and member of the scientific advisory board of Vedanta Biosciences, which studies microbiota therapeutics.
A newly discovered strain of bacteria could play a role in the development of rheumatoid arthritis, according to findings recently published in Science Translational Medicine.
Mice colonized with a strain of Subdoligranulum bacteria in their gut – a strain previously unidentified but now named Subdoligranulum didolesgii – developed joint swelling and inflammation as well as antibodies and T-cell responses similar to what is seen in RA, researchers reported.
“This was the first time that anyone has observed arthritis developing in a mouse that was not otherwise immunologically stimulated with an adjuvant of some kind, or genetically manipulated,” said Kristine Kuhn, MD, PhD, associate professor of rheumatology at the University of Colorado at Denver, Aurora, who led a team of researchers that also included investigators from Stanford (Calif.) University and Benaroya Research Institute in Seattle.
The findings offer the latest evidence – and perhaps the most compelling evidence – for the mucosal origins hypothesis, the idea that rheumatoid arthritis can start with an immune response somewhere in the mucosa because of environmental interactions, and then becomes systemic, resulting in symptoms in the joints. Anti-citrullinated protein antibodies (ACPA), hallmarks of RA, have been found at mucosal surfaces in the periodontium and the lungs, and there have been reports of them in the intestine and cervicovaginal mucosa as well.
The latest findings that implicate the new bacterium build on previous findings in which people at risk of RA, but without symptoms yet, had an expansion of B cells producing immunoglobulin A (IgA), an antibody found in the mucosa. A closer look at these B cells, using variable region sequencing, found that they arose from a family that includes both IgA and IgG members. Because IgG antibodies are systemic, this suggested a kind of evolution from an IgA-based, mucosal immune response to one that is systemic and could target the joints.
Researchers mixed monoclonal antibodies from these B cells with a pool of bacteria from the stool of a broad population of people, and then pulled out the bacteria bound by these antibodies, and sequenced them. They found that the antibodies had bound almost exclusively to Ruminococcaceae and Lachnospiraceae.
They then cultured the stool of an individual at risk of developing RA and ended up with five isolates within Ruminococcaceae – “all of which belonged to the Subdoligranulum genus,” Dr. Kuhn said. When they sequenced these, they found that they had a new strain, which was named by Meagan Chriswell, an MD-PhD candidate and member of the Cherokee Nation of Oklahoma, who chose a term based on the Cherokee word for rheumatism.
Researchers at Benaroya then mixed this strain with T cells of people with RA, and those of controls, and only the T cells of those with RA were stimulated by the bacterium, they found.
“When intestines of germ-free mice were colonized with the strain, we found that they were getting arthritis,” Dr. Kuhn said. Photos of the joints show a striking contrast between the swollen joints of the mice given Subdoligranulum didolesgii and those injected with Prevotella copri, another strain suspected of having a link to RA, as well as with another Subdoligranulum strain and a sterile media. Dr. Kuhn noted that the P. copri strain did not come from an RA-affected individual.
“We thought that our results closed the loop nicely to show that these immune responses truly were toward the Subdoligranulum, and also stimulating arthritis,” she said.
The researchers then assessed the prevalence of the strain in people at risk for RA or with RA, and in controls. They found it in 17% of those with or at risk for RA but didn’t see it at all in the healthy control population.
Dr. Kuhn and her research team, she said, are now looking at the prevalence of the strain in a larger population and doing more investigating into the link with RA.
“Does it really associate with the development of immune responses and the development of rheumatoid arthritis?” she said.
Potential etiologic role of P. copri
Another paper, published in Arthritis & Rheumatology by some of the same investigators a week before the study describing the Subdoligranulum findings, tried to ascertain the point at which individuals might develop antibodies to P. copri, which for about a decade has been suspected of having a link to the development of RA.
They found that those with early RA had higher median values of IgG anti–P. copri (Pc) antibodies, compared with matched controls. People with established RA also had higher values of IgA anti-Pc antibodies. Those with ACPA, but not rheumatoid factor (RF), showed a trend toward higher IgG anti-Pc antibodies. Those who were ACPA-positive and RF-positive had significantly increased levels of IgA anti-Pc antibodies and a trend toward higher levels of IgG anti-Pc antibodies, compared with matched controls.
The findings, according to the researchers, “support a potential etiologic role for this microorganism in both RA preclinical evolution and the subsequent pathogenesis of synovitis.”
Dr. Kuhn and others in the field say it’s likely that many microbes play a role in the development of RA, and that the P. copri findings only add evidence of that relationship.
“Maybe the bacteria are involved at different parts of the pathway, and maybe they’re involved in triggering different parts of the immune responses,” she said. “Those are all to be determined.”
Dan Littman, MD, PhD, professor of rheumatology at New York University, who wrote a commentary reflecting on the findings of the Subdoligranulum study, said the results are “another piece of data” adding to the evidence base for the mucosal origins hypothesis.
“It’s by no means proven that this is the way pathogenesis in RA can occur, but it’s certainly a very solid study,” said Dr. Littman, who with colleagues published findings in 2013 linking P. copri to RA. “What makes it most compelling is that they seem to be able to show some evidence of causality in the mouse model.”
Before the findings could lead to therapy, he said, more evidence is needed to show that there is a causal link, and on the mechanism at work, such as whether this is something that occurs at the outset of disease or is something that “fuels the disease” by continually activating immune cells contributing to RA.
“If it’s only something that’s involved in the initiation of the disease, you need to catch it very early,” he said. “But if it’s something that continues to provide fuel for the disease, you may be able to catch it later and still be effective. Those are really critical items.”
Eventually, if these questions are answered, bacteriophages could be developed to snuff out problematic strains, or the regulatory response could be targeted to prevent the activation of the B cells that give rise to autoimmunity, he suggested.
“There are multiple steps to get to a therapeutic here, and I think we’re still a long ways from that,” he said. Still, he said, “I think it’s an important paper because it will encourage more people to look at this mechanism more closely and determine whether it really is representative of what happens in a lot of RA patients.”
The study in Science Translational Medicine was supported by grants from the National Institutes of Health, a Pfizer ASPIRE grant, and a grant from the Rheumatology Research Foundation. The Arthritis & Rheumatology study was supported in part by grants from the National Institutes of Health; the American College of Rheumatology Innovative Grant Program; the Ounsworth-Fitzgerald Foundation; Mathers Foundation; English, Bonter, Mitchell Foundation; Littauer Foundation; Lillian B. Davey Foundation; and the Eshe Fund. None of the researchers in either study had relevant financial disclosures. Dr. Littman is scientific cofounder and member of the scientific advisory board of Vedanta Biosciences, which studies microbiota therapeutics.
A newly discovered strain of bacteria could play a role in the development of rheumatoid arthritis, according to findings recently published in Science Translational Medicine.
Mice colonized with a strain of Subdoligranulum bacteria in their gut – a strain previously unidentified but now named Subdoligranulum didolesgii – developed joint swelling and inflammation as well as antibodies and T-cell responses similar to what is seen in RA, researchers reported.
“This was the first time that anyone has observed arthritis developing in a mouse that was not otherwise immunologically stimulated with an adjuvant of some kind, or genetically manipulated,” said Kristine Kuhn, MD, PhD, associate professor of rheumatology at the University of Colorado at Denver, Aurora, who led a team of researchers that also included investigators from Stanford (Calif.) University and Benaroya Research Institute in Seattle.
The findings offer the latest evidence – and perhaps the most compelling evidence – for the mucosal origins hypothesis, the idea that rheumatoid arthritis can start with an immune response somewhere in the mucosa because of environmental interactions, and then becomes systemic, resulting in symptoms in the joints. Anti-citrullinated protein antibodies (ACPA), hallmarks of RA, have been found at mucosal surfaces in the periodontium and the lungs, and there have been reports of them in the intestine and cervicovaginal mucosa as well.
The latest findings that implicate the new bacterium build on previous findings in which people at risk of RA, but without symptoms yet, had an expansion of B cells producing immunoglobulin A (IgA), an antibody found in the mucosa. A closer look at these B cells, using variable region sequencing, found that they arose from a family that includes both IgA and IgG members. Because IgG antibodies are systemic, this suggested a kind of evolution from an IgA-based, mucosal immune response to one that is systemic and could target the joints.
Researchers mixed monoclonal antibodies from these B cells with a pool of bacteria from the stool of a broad population of people, and then pulled out the bacteria bound by these antibodies, and sequenced them. They found that the antibodies had bound almost exclusively to Ruminococcaceae and Lachnospiraceae.
They then cultured the stool of an individual at risk of developing RA and ended up with five isolates within Ruminococcaceae – “all of which belonged to the Subdoligranulum genus,” Dr. Kuhn said. When they sequenced these, they found that they had a new strain, which was named by Meagan Chriswell, an MD-PhD candidate and member of the Cherokee Nation of Oklahoma, who chose a term based on the Cherokee word for rheumatism.
Researchers at Benaroya then mixed this strain with T cells of people with RA, and those of controls, and only the T cells of those with RA were stimulated by the bacterium, they found.
“When intestines of germ-free mice were colonized with the strain, we found that they were getting arthritis,” Dr. Kuhn said. Photos of the joints show a striking contrast between the swollen joints of the mice given Subdoligranulum didolesgii and those injected with Prevotella copri, another strain suspected of having a link to RA, as well as with another Subdoligranulum strain and a sterile media. Dr. Kuhn noted that the P. copri strain did not come from an RA-affected individual.
“We thought that our results closed the loop nicely to show that these immune responses truly were toward the Subdoligranulum, and also stimulating arthritis,” she said.
The researchers then assessed the prevalence of the strain in people at risk for RA or with RA, and in controls. They found it in 17% of those with or at risk for RA but didn’t see it at all in the healthy control population.
Dr. Kuhn and her research team, she said, are now looking at the prevalence of the strain in a larger population and doing more investigating into the link with RA.
“Does it really associate with the development of immune responses and the development of rheumatoid arthritis?” she said.
Potential etiologic role of P. copri
Another paper, published in Arthritis & Rheumatology by some of the same investigators a week before the study describing the Subdoligranulum findings, tried to ascertain the point at which individuals might develop antibodies to P. copri, which for about a decade has been suspected of having a link to the development of RA.
They found that those with early RA had higher median values of IgG anti–P. copri (Pc) antibodies, compared with matched controls. People with established RA also had higher values of IgA anti-Pc antibodies. Those with ACPA, but not rheumatoid factor (RF), showed a trend toward higher IgG anti-Pc antibodies. Those who were ACPA-positive and RF-positive had significantly increased levels of IgA anti-Pc antibodies and a trend toward higher levels of IgG anti-Pc antibodies, compared with matched controls.
The findings, according to the researchers, “support a potential etiologic role for this microorganism in both RA preclinical evolution and the subsequent pathogenesis of synovitis.”
Dr. Kuhn and others in the field say it’s likely that many microbes play a role in the development of RA, and that the P. copri findings only add evidence of that relationship.
“Maybe the bacteria are involved at different parts of the pathway, and maybe they’re involved in triggering different parts of the immune responses,” she said. “Those are all to be determined.”
Dan Littman, MD, PhD, professor of rheumatology at New York University, who wrote a commentary reflecting on the findings of the Subdoligranulum study, said the results are “another piece of data” adding to the evidence base for the mucosal origins hypothesis.
“It’s by no means proven that this is the way pathogenesis in RA can occur, but it’s certainly a very solid study,” said Dr. Littman, who with colleagues published findings in 2013 linking P. copri to RA. “What makes it most compelling is that they seem to be able to show some evidence of causality in the mouse model.”
Before the findings could lead to therapy, he said, more evidence is needed to show that there is a causal link, and on the mechanism at work, such as whether this is something that occurs at the outset of disease or is something that “fuels the disease” by continually activating immune cells contributing to RA.
“If it’s only something that’s involved in the initiation of the disease, you need to catch it very early,” he said. “But if it’s something that continues to provide fuel for the disease, you may be able to catch it later and still be effective. Those are really critical items.”
Eventually, if these questions are answered, bacteriophages could be developed to snuff out problematic strains, or the regulatory response could be targeted to prevent the activation of the B cells that give rise to autoimmunity, he suggested.
“There are multiple steps to get to a therapeutic here, and I think we’re still a long ways from that,” he said. Still, he said, “I think it’s an important paper because it will encourage more people to look at this mechanism more closely and determine whether it really is representative of what happens in a lot of RA patients.”
The study in Science Translational Medicine was supported by grants from the National Institutes of Health, a Pfizer ASPIRE grant, and a grant from the Rheumatology Research Foundation. The Arthritis & Rheumatology study was supported in part by grants from the National Institutes of Health; the American College of Rheumatology Innovative Grant Program; the Ounsworth-Fitzgerald Foundation; Mathers Foundation; English, Bonter, Mitchell Foundation; Littauer Foundation; Lillian B. Davey Foundation; and the Eshe Fund. None of the researchers in either study had relevant financial disclosures. Dr. Littman is scientific cofounder and member of the scientific advisory board of Vedanta Biosciences, which studies microbiota therapeutics.
FROM SCIENCE TRANSLATIONAL MEDICINE AND ARTHRITIS & RHEUMATOLOGY
Don’t wait for patients to bring up their GI symptoms
Nearly three-quarters of Americans would wait before discussing GI symptoms with a health care provider if their bowel frequency or symptoms changed, with more than a quarter overall waiting for symptoms to become severe, according to a new survey from the American Gastroenterological Association.
Nearly 40% of people said GI symptoms had disrupted everyday activities such as exercising, running errands, and spending time with family or friends, but despite these disruptions, 30% of people said they would only discuss their bowel-related concerns if their doctor brought it up first. In response, the AGA launched “Trust Your Gut,” an awareness campaign aimed at shortening the time from the onset of bowel symptoms to discussions with health care providers.
“So many patients are either fearful or embarrassed about discussing their digestive symptoms such that they delay care unless the health care provider brings it up,” said Rajeev Jain, MD, a gastroenterologist with Texas Digestive Disease Consultants, AGA patient education adviser and a Trust Your Gut spokesperson.
“This potential delay could be detrimental in some cases, such as bleeding related to colon cancer,” he said. “If diagnosed sooner, an operation or chemotherapy could lead to treatment and a cure in those cases, versus advanced cancer that may be incurable.”
The AGA Trust Your Gut survey, conducted by Kelton Global during May 9-11, 2022, included 1,010 respondents from a nationally representative sample of U.S. adults.
Struggling with the issue
About 28% of respondents said they would see a clinician immediately if their bowel frequency or symptoms changed. However, 72% said they would wait, and on top of that, 27% said they would wait until the condition became severe or didn’t resolve over time. Women were more likely than men to say they would wait, at 72% versus 64%.
Overall, 39% of respondents said bowel issues have stopped them from doing some type of activity in the past year. Men were more likely than women to say that bowel issues have affected their ability to do an activity, at 44% versus 35%.
“Typically, when it comes to functional or motility disorders or bowel dysfunction, we tend to see a higher prevalence in women, so this was somewhat surprising to see,” said Andrea Shin, MD, a gastroenterology specialist and assistant professor of medicine at Indiana University, Indianapolis, and AGA patient education adviser designate.
“Part of this difference may be related to the communication barrier and how sex or gender affects that relationship between a clinician and a patient,” she said.
The reasons for patients’ reluctance varies, but themes of uncertainty and embarrassment are prevalent. About 33% said they’re not sure whether the symptoms are a problem, 31% said they hope the symptoms improve on their own, 23% said it’s embarrassing, and 12% don’t know what to tell the doctor. Men were more likely than women to say they don’t know what to say to a doctor about their symptoms, at 15% versus 9%.
Starting the conversation
From a young age, many respondents were raised to avoid the topic of bowel issues. About 23% said their parents encouraged them not to mention bathroom-related health issues, and 10% said they didn’t talk about bowel issues at all. Another 32% said they could talk about it but had to use code words, such as “go to the bathroom” or “potty.”
“What this highlights is that patients are culturally taught not to talk about their digestive tract, or they’re embarrassed or uncertain,” Dr. Jain said. “At the end of the day, we need to destigmatize discussions about digestive function and normalize it as part of overall health.”
The survey respondents said they’d feel most comfortable talking about bowel issues with doctors (63%) and nurses (41%), as well as a significant other (44%), parent (32%), or friend (27%). Women were more likely than men to feel comfortable turning to a nurse practitioner or physician’s assistant (47% versus 35%) or a friend (30% versus 24%).
To feel more comfortable with these conversations, 42% of survey participants said they would like their doctor or clinician to describe what’s normal. About 30% want to know the appropriate terms to describe their situation.
Health care providers should also consider the cultural and social factors that may affect a patient’s disease experience, as well as how they interact with the health care system, Shin said.
“Understanding these differences might help us to better engage with a community that is diverse,” she said. “In general, we also need to be more proactive about drawing these conversations out of patients, who may not mention it unless we ask because they find it so personal.”
The AGA Trust Your Gut campaign is supported by a sponsorship from Janssen. Dr. Jain and Dr. Shin reported to relevant disclosures.
Help your patients learn more by encouraging them to visit https://patient.gastro.org/trust-your-gut/.
Nearly three-quarters of Americans would wait before discussing GI symptoms with a health care provider if their bowel frequency or symptoms changed, with more than a quarter overall waiting for symptoms to become severe, according to a new survey from the American Gastroenterological Association.
Nearly 40% of people said GI symptoms had disrupted everyday activities such as exercising, running errands, and spending time with family or friends, but despite these disruptions, 30% of people said they would only discuss their bowel-related concerns if their doctor brought it up first. In response, the AGA launched “Trust Your Gut,” an awareness campaign aimed at shortening the time from the onset of bowel symptoms to discussions with health care providers.
“So many patients are either fearful or embarrassed about discussing their digestive symptoms such that they delay care unless the health care provider brings it up,” said Rajeev Jain, MD, a gastroenterologist with Texas Digestive Disease Consultants, AGA patient education adviser and a Trust Your Gut spokesperson.
“This potential delay could be detrimental in some cases, such as bleeding related to colon cancer,” he said. “If diagnosed sooner, an operation or chemotherapy could lead to treatment and a cure in those cases, versus advanced cancer that may be incurable.”
The AGA Trust Your Gut survey, conducted by Kelton Global during May 9-11, 2022, included 1,010 respondents from a nationally representative sample of U.S. adults.
Struggling with the issue
About 28% of respondents said they would see a clinician immediately if their bowel frequency or symptoms changed. However, 72% said they would wait, and on top of that, 27% said they would wait until the condition became severe or didn’t resolve over time. Women were more likely than men to say they would wait, at 72% versus 64%.
Overall, 39% of respondents said bowel issues have stopped them from doing some type of activity in the past year. Men were more likely than women to say that bowel issues have affected their ability to do an activity, at 44% versus 35%.
“Typically, when it comes to functional or motility disorders or bowel dysfunction, we tend to see a higher prevalence in women, so this was somewhat surprising to see,” said Andrea Shin, MD, a gastroenterology specialist and assistant professor of medicine at Indiana University, Indianapolis, and AGA patient education adviser designate.
“Part of this difference may be related to the communication barrier and how sex or gender affects that relationship between a clinician and a patient,” she said.
The reasons for patients’ reluctance varies, but themes of uncertainty and embarrassment are prevalent. About 33% said they’re not sure whether the symptoms are a problem, 31% said they hope the symptoms improve on their own, 23% said it’s embarrassing, and 12% don’t know what to tell the doctor. Men were more likely than women to say they don’t know what to say to a doctor about their symptoms, at 15% versus 9%.
Starting the conversation
From a young age, many respondents were raised to avoid the topic of bowel issues. About 23% said their parents encouraged them not to mention bathroom-related health issues, and 10% said they didn’t talk about bowel issues at all. Another 32% said they could talk about it but had to use code words, such as “go to the bathroom” or “potty.”
“What this highlights is that patients are culturally taught not to talk about their digestive tract, or they’re embarrassed or uncertain,” Dr. Jain said. “At the end of the day, we need to destigmatize discussions about digestive function and normalize it as part of overall health.”
The survey respondents said they’d feel most comfortable talking about bowel issues with doctors (63%) and nurses (41%), as well as a significant other (44%), parent (32%), or friend (27%). Women were more likely than men to feel comfortable turning to a nurse practitioner or physician’s assistant (47% versus 35%) or a friend (30% versus 24%).
To feel more comfortable with these conversations, 42% of survey participants said they would like their doctor or clinician to describe what’s normal. About 30% want to know the appropriate terms to describe their situation.
Health care providers should also consider the cultural and social factors that may affect a patient’s disease experience, as well as how they interact with the health care system, Shin said.
“Understanding these differences might help us to better engage with a community that is diverse,” she said. “In general, we also need to be more proactive about drawing these conversations out of patients, who may not mention it unless we ask because they find it so personal.”
The AGA Trust Your Gut campaign is supported by a sponsorship from Janssen. Dr. Jain and Dr. Shin reported to relevant disclosures.
Help your patients learn more by encouraging them to visit https://patient.gastro.org/trust-your-gut/.
Nearly three-quarters of Americans would wait before discussing GI symptoms with a health care provider if their bowel frequency or symptoms changed, with more than a quarter overall waiting for symptoms to become severe, according to a new survey from the American Gastroenterological Association.
Nearly 40% of people said GI symptoms had disrupted everyday activities such as exercising, running errands, and spending time with family or friends, but despite these disruptions, 30% of people said they would only discuss their bowel-related concerns if their doctor brought it up first. In response, the AGA launched “Trust Your Gut,” an awareness campaign aimed at shortening the time from the onset of bowel symptoms to discussions with health care providers.
“So many patients are either fearful or embarrassed about discussing their digestive symptoms such that they delay care unless the health care provider brings it up,” said Rajeev Jain, MD, a gastroenterologist with Texas Digestive Disease Consultants, AGA patient education adviser and a Trust Your Gut spokesperson.
“This potential delay could be detrimental in some cases, such as bleeding related to colon cancer,” he said. “If diagnosed sooner, an operation or chemotherapy could lead to treatment and a cure in those cases, versus advanced cancer that may be incurable.”
The AGA Trust Your Gut survey, conducted by Kelton Global during May 9-11, 2022, included 1,010 respondents from a nationally representative sample of U.S. adults.
Struggling with the issue
About 28% of respondents said they would see a clinician immediately if their bowel frequency or symptoms changed. However, 72% said they would wait, and on top of that, 27% said they would wait until the condition became severe or didn’t resolve over time. Women were more likely than men to say they would wait, at 72% versus 64%.
Overall, 39% of respondents said bowel issues have stopped them from doing some type of activity in the past year. Men were more likely than women to say that bowel issues have affected their ability to do an activity, at 44% versus 35%.
“Typically, when it comes to functional or motility disorders or bowel dysfunction, we tend to see a higher prevalence in women, so this was somewhat surprising to see,” said Andrea Shin, MD, a gastroenterology specialist and assistant professor of medicine at Indiana University, Indianapolis, and AGA patient education adviser designate.
“Part of this difference may be related to the communication barrier and how sex or gender affects that relationship between a clinician and a patient,” she said.
The reasons for patients’ reluctance varies, but themes of uncertainty and embarrassment are prevalent. About 33% said they’re not sure whether the symptoms are a problem, 31% said they hope the symptoms improve on their own, 23% said it’s embarrassing, and 12% don’t know what to tell the doctor. Men were more likely than women to say they don’t know what to say to a doctor about their symptoms, at 15% versus 9%.
Starting the conversation
From a young age, many respondents were raised to avoid the topic of bowel issues. About 23% said their parents encouraged them not to mention bathroom-related health issues, and 10% said they didn’t talk about bowel issues at all. Another 32% said they could talk about it but had to use code words, such as “go to the bathroom” or “potty.”
“What this highlights is that patients are culturally taught not to talk about their digestive tract, or they’re embarrassed or uncertain,” Dr. Jain said. “At the end of the day, we need to destigmatize discussions about digestive function and normalize it as part of overall health.”
The survey respondents said they’d feel most comfortable talking about bowel issues with doctors (63%) and nurses (41%), as well as a significant other (44%), parent (32%), or friend (27%). Women were more likely than men to feel comfortable turning to a nurse practitioner or physician’s assistant (47% versus 35%) or a friend (30% versus 24%).
To feel more comfortable with these conversations, 42% of survey participants said they would like their doctor or clinician to describe what’s normal. About 30% want to know the appropriate terms to describe their situation.
Health care providers should also consider the cultural and social factors that may affect a patient’s disease experience, as well as how they interact with the health care system, Shin said.
“Understanding these differences might help us to better engage with a community that is diverse,” she said. “In general, we also need to be more proactive about drawing these conversations out of patients, who may not mention it unless we ask because they find it so personal.”
The AGA Trust Your Gut campaign is supported by a sponsorship from Janssen. Dr. Jain and Dr. Shin reported to relevant disclosures.
Help your patients learn more by encouraging them to visit https://patient.gastro.org/trust-your-gut/.
Scientists identify new genetic links to dyslexia
Dyslexia occurs in 5%-17% of the general population, depending on the diagnostic criteria, and has been linked with speech and language disorders, as well as ADHD, Catherine Doust, PhD, of the University of Edinburgh and colleagues wrote.
However, previous studies of the genetics of dyslexia are limited, corresponding author Michelle Luciano, PhD, said in an interview. “So much progress has been made in understanding the genetics of behavior and health, but only a small genomewide study of dyslexia existed before ours.”
Currently, genetic testing for dyslexia alone is not done.
“You couldn’t order a genetic test for dyslexia unless it were part of another genetic panel,” according to Herschel Lessin, MD, of Children’s Medical Group, Poughkeepsie, N.Y.
There are also known associations with some genes and autism, but none are definitive, and testing requires a workup of which a genetic panel may be a part. Such tests are expensive, and rarely covered by insurance, the pediatrician explained.
Experts recommend genetic screening for every child with developmental delay, but most insurance won’t cover it, Dr. Lessin continued.
In the new genomewide association study published in Nature Genetics, the researchers reviewed data from 51,800 adults aged 18 years and older with a self-reported dyslexia diagnosis and 1,087,070 controls. All study participants are enrolled in ongoing research with 23andMe, the personal genetics company.
The researchers investigated the genetic correlations with reading and related skills and evaluated evidence for genes previously associated with dyslexia. The mean ages of the dyslexia cases and controls were 49.6 years and 51.7 years, respectively.
The researchers identified 42 independent genetic variants (genomewide significant loci) associated with dyslexia; 15 of these loci were in genes previously associated with cognitive ability and educational attainment, and 27 were newly identified as specifically associated with dyslexia. The researchers further determined that 12 of the newly identified genes were associated with proficiency in reading and spelling in English and European languages, and 1 in a Chinese-language population.
A polygenic risk score is a way to characterize an individual’s risk of developing a disease, based on the total number of genetic changes related to the disease; the researchers used this score to validate their results. Dyslexia polygenic scores were used to predict reading and spelling in additional population-based and reading disorder–enriched samples outside of the study population; these genetic measures explained up to 6% of variance in reading traits, the researchers noted. Ultimately, these scores may be a tool to help identify children with a predisposition for dyslexia so reading skills support can begin early.
The researchers also found that many of the genes associated with dyslexia are also associated with ADHD, (24% of dyslexia patients reporting ADHD vs. 9% of controls), and with a moderate correlation, which suggests possible shared genetic components for deficits in working memory and attention.
The study findings were limited by the inability to prove causality, and by the potential bias in the study sample, but were strengthened by the large study population, the researchers noted.
Potential implications for reading and spelling
“We were surprised that none of the previous dyslexia candidate genes were genomewide significant in our study; all of our discoveries were in new genes that had not been previously implicated in dyslexia,” Dr. Luciano said in an interview. “Some of these genes have been found to be associated with general cognitive ability, but most were novel and may represent genes specifically related to cognitive processes dominant in reading and spelling.
“We were also surprised that there was little genetic correlation (or overlap) with brain MRI variables, given that brain regions have been linked to reading skill. This suggests that the link is environmental in origin,” she added.
“Our results do not directly feed into clinical practice,” said Dr. Luciano. However, “the moderate genetic overlap with ADHD suggests that broader assessments of behavior are important when a child presents with dyslexia, as co-occurrence with other conditions might influence the intervention chosen. Asking about family history of dyslexia might also help in identification.
With more research, genetic studies may find a place in the clinical setting, said Dr. Luciano.
“As genomewide association studies become larger and the findings more stable, genetic information might be used as an adjunct to what is known about the child’s environment and their performance on standardized tests of reading. The key advantage of genetic information is that it could allow much earlier identification of children who would benefit from extra learning support,” she said.
More research is needed to understand the interaction between genes and the environment, Dr. Luciano said. “It is essential that we understand what environmental learning support can minimize genetic predisposition to dyslexia.”
Too soon for clinical utility
The study findings are an important foundation for additional research, but not yet clinically useful, Dr. Lessin said in an interview.
“Dyslexia is a tough diagnosis,” that requires assessment by a developmental pediatrician or a pediatric neurologist and these specialists are often not accessible to many parents, Dr. Lessin noted.
In the current study, the researchers found a number of genes potentially associated with dyslexia, but the study does not prove causality, he emphasized. The findings simply mean that some of these genes may have something to do with dyslexia, and further research might identify a genetic cause.
“No one is going to make a diagnosis of dyslexia based on genes just yet,” said Dr. Lessin. In the meantime, clinicians should be aware that good research is being conducted, and that the genetic foundations for dyslexia are being explored.
Lead author Dr. Doust and corresponding author Dr. Luciano had no financial conflicts to disclose. Several coauthors disclosed support from the Max Planck Society (Germany), the National Natural Science Foundation of China, Funds for Humanities and Social Sciences Research of the Ministry of Education, and General Project of Shaanxi Natural Science Basic Research Program. Two coauthors are employed by and hold stock or stock options in 23andMe. Dr. Lessin had no financial conflicts to disclose, but serves on the editorial advisory board of Pediatric News.
Dyslexia occurs in 5%-17% of the general population, depending on the diagnostic criteria, and has been linked with speech and language disorders, as well as ADHD, Catherine Doust, PhD, of the University of Edinburgh and colleagues wrote.
However, previous studies of the genetics of dyslexia are limited, corresponding author Michelle Luciano, PhD, said in an interview. “So much progress has been made in understanding the genetics of behavior and health, but only a small genomewide study of dyslexia existed before ours.”
Currently, genetic testing for dyslexia alone is not done.
“You couldn’t order a genetic test for dyslexia unless it were part of another genetic panel,” according to Herschel Lessin, MD, of Children’s Medical Group, Poughkeepsie, N.Y.
There are also known associations with some genes and autism, but none are definitive, and testing requires a workup of which a genetic panel may be a part. Such tests are expensive, and rarely covered by insurance, the pediatrician explained.
Experts recommend genetic screening for every child with developmental delay, but most insurance won’t cover it, Dr. Lessin continued.
In the new genomewide association study published in Nature Genetics, the researchers reviewed data from 51,800 adults aged 18 years and older with a self-reported dyslexia diagnosis and 1,087,070 controls. All study participants are enrolled in ongoing research with 23andMe, the personal genetics company.
The researchers investigated the genetic correlations with reading and related skills and evaluated evidence for genes previously associated with dyslexia. The mean ages of the dyslexia cases and controls were 49.6 years and 51.7 years, respectively.
The researchers identified 42 independent genetic variants (genomewide significant loci) associated with dyslexia; 15 of these loci were in genes previously associated with cognitive ability and educational attainment, and 27 were newly identified as specifically associated with dyslexia. The researchers further determined that 12 of the newly identified genes were associated with proficiency in reading and spelling in English and European languages, and 1 in a Chinese-language population.
A polygenic risk score is a way to characterize an individual’s risk of developing a disease, based on the total number of genetic changes related to the disease; the researchers used this score to validate their results. Dyslexia polygenic scores were used to predict reading and spelling in additional population-based and reading disorder–enriched samples outside of the study population; these genetic measures explained up to 6% of variance in reading traits, the researchers noted. Ultimately, these scores may be a tool to help identify children with a predisposition for dyslexia so reading skills support can begin early.
The researchers also found that many of the genes associated with dyslexia are also associated with ADHD, (24% of dyslexia patients reporting ADHD vs. 9% of controls), and with a moderate correlation, which suggests possible shared genetic components for deficits in working memory and attention.
The study findings were limited by the inability to prove causality, and by the potential bias in the study sample, but were strengthened by the large study population, the researchers noted.
Potential implications for reading and spelling
“We were surprised that none of the previous dyslexia candidate genes were genomewide significant in our study; all of our discoveries were in new genes that had not been previously implicated in dyslexia,” Dr. Luciano said in an interview. “Some of these genes have been found to be associated with general cognitive ability, but most were novel and may represent genes specifically related to cognitive processes dominant in reading and spelling.
“We were also surprised that there was little genetic correlation (or overlap) with brain MRI variables, given that brain regions have been linked to reading skill. This suggests that the link is environmental in origin,” she added.
“Our results do not directly feed into clinical practice,” said Dr. Luciano. However, “the moderate genetic overlap with ADHD suggests that broader assessments of behavior are important when a child presents with dyslexia, as co-occurrence with other conditions might influence the intervention chosen. Asking about family history of dyslexia might also help in identification.
With more research, genetic studies may find a place in the clinical setting, said Dr. Luciano.
“As genomewide association studies become larger and the findings more stable, genetic information might be used as an adjunct to what is known about the child’s environment and their performance on standardized tests of reading. The key advantage of genetic information is that it could allow much earlier identification of children who would benefit from extra learning support,” she said.
More research is needed to understand the interaction between genes and the environment, Dr. Luciano said. “It is essential that we understand what environmental learning support can minimize genetic predisposition to dyslexia.”
Too soon for clinical utility
The study findings are an important foundation for additional research, but not yet clinically useful, Dr. Lessin said in an interview.
“Dyslexia is a tough diagnosis,” that requires assessment by a developmental pediatrician or a pediatric neurologist and these specialists are often not accessible to many parents, Dr. Lessin noted.
In the current study, the researchers found a number of genes potentially associated with dyslexia, but the study does not prove causality, he emphasized. The findings simply mean that some of these genes may have something to do with dyslexia, and further research might identify a genetic cause.
“No one is going to make a diagnosis of dyslexia based on genes just yet,” said Dr. Lessin. In the meantime, clinicians should be aware that good research is being conducted, and that the genetic foundations for dyslexia are being explored.
Lead author Dr. Doust and corresponding author Dr. Luciano had no financial conflicts to disclose. Several coauthors disclosed support from the Max Planck Society (Germany), the National Natural Science Foundation of China, Funds for Humanities and Social Sciences Research of the Ministry of Education, and General Project of Shaanxi Natural Science Basic Research Program. Two coauthors are employed by and hold stock or stock options in 23andMe. Dr. Lessin had no financial conflicts to disclose, but serves on the editorial advisory board of Pediatric News.
Dyslexia occurs in 5%-17% of the general population, depending on the diagnostic criteria, and has been linked with speech and language disorders, as well as ADHD, Catherine Doust, PhD, of the University of Edinburgh and colleagues wrote.
However, previous studies of the genetics of dyslexia are limited, corresponding author Michelle Luciano, PhD, said in an interview. “So much progress has been made in understanding the genetics of behavior and health, but only a small genomewide study of dyslexia existed before ours.”
Currently, genetic testing for dyslexia alone is not done.
“You couldn’t order a genetic test for dyslexia unless it were part of another genetic panel,” according to Herschel Lessin, MD, of Children’s Medical Group, Poughkeepsie, N.Y.
There are also known associations with some genes and autism, but none are definitive, and testing requires a workup of which a genetic panel may be a part. Such tests are expensive, and rarely covered by insurance, the pediatrician explained.
Experts recommend genetic screening for every child with developmental delay, but most insurance won’t cover it, Dr. Lessin continued.
In the new genomewide association study published in Nature Genetics, the researchers reviewed data from 51,800 adults aged 18 years and older with a self-reported dyslexia diagnosis and 1,087,070 controls. All study participants are enrolled in ongoing research with 23andMe, the personal genetics company.
The researchers investigated the genetic correlations with reading and related skills and evaluated evidence for genes previously associated with dyslexia. The mean ages of the dyslexia cases and controls were 49.6 years and 51.7 years, respectively.
The researchers identified 42 independent genetic variants (genomewide significant loci) associated with dyslexia; 15 of these loci were in genes previously associated with cognitive ability and educational attainment, and 27 were newly identified as specifically associated with dyslexia. The researchers further determined that 12 of the newly identified genes were associated with proficiency in reading and spelling in English and European languages, and 1 in a Chinese-language population.
A polygenic risk score is a way to characterize an individual’s risk of developing a disease, based on the total number of genetic changes related to the disease; the researchers used this score to validate their results. Dyslexia polygenic scores were used to predict reading and spelling in additional population-based and reading disorder–enriched samples outside of the study population; these genetic measures explained up to 6% of variance in reading traits, the researchers noted. Ultimately, these scores may be a tool to help identify children with a predisposition for dyslexia so reading skills support can begin early.
The researchers also found that many of the genes associated with dyslexia are also associated with ADHD, (24% of dyslexia patients reporting ADHD vs. 9% of controls), and with a moderate correlation, which suggests possible shared genetic components for deficits in working memory and attention.
The study findings were limited by the inability to prove causality, and by the potential bias in the study sample, but were strengthened by the large study population, the researchers noted.
Potential implications for reading and spelling
“We were surprised that none of the previous dyslexia candidate genes were genomewide significant in our study; all of our discoveries were in new genes that had not been previously implicated in dyslexia,” Dr. Luciano said in an interview. “Some of these genes have been found to be associated with general cognitive ability, but most were novel and may represent genes specifically related to cognitive processes dominant in reading and spelling.
“We were also surprised that there was little genetic correlation (or overlap) with brain MRI variables, given that brain regions have been linked to reading skill. This suggests that the link is environmental in origin,” she added.
“Our results do not directly feed into clinical practice,” said Dr. Luciano. However, “the moderate genetic overlap with ADHD suggests that broader assessments of behavior are important when a child presents with dyslexia, as co-occurrence with other conditions might influence the intervention chosen. Asking about family history of dyslexia might also help in identification.
With more research, genetic studies may find a place in the clinical setting, said Dr. Luciano.
“As genomewide association studies become larger and the findings more stable, genetic information might be used as an adjunct to what is known about the child’s environment and their performance on standardized tests of reading. The key advantage of genetic information is that it could allow much earlier identification of children who would benefit from extra learning support,” she said.
More research is needed to understand the interaction between genes and the environment, Dr. Luciano said. “It is essential that we understand what environmental learning support can minimize genetic predisposition to dyslexia.”
Too soon for clinical utility
The study findings are an important foundation for additional research, but not yet clinically useful, Dr. Lessin said in an interview.
“Dyslexia is a tough diagnosis,” that requires assessment by a developmental pediatrician or a pediatric neurologist and these specialists are often not accessible to many parents, Dr. Lessin noted.
In the current study, the researchers found a number of genes potentially associated with dyslexia, but the study does not prove causality, he emphasized. The findings simply mean that some of these genes may have something to do with dyslexia, and further research might identify a genetic cause.
“No one is going to make a diagnosis of dyslexia based on genes just yet,” said Dr. Lessin. In the meantime, clinicians should be aware that good research is being conducted, and that the genetic foundations for dyslexia are being explored.
Lead author Dr. Doust and corresponding author Dr. Luciano had no financial conflicts to disclose. Several coauthors disclosed support from the Max Planck Society (Germany), the National Natural Science Foundation of China, Funds for Humanities and Social Sciences Research of the Ministry of Education, and General Project of Shaanxi Natural Science Basic Research Program. Two coauthors are employed by and hold stock or stock options in 23andMe. Dr. Lessin had no financial conflicts to disclose, but serves on the editorial advisory board of Pediatric News.
FROM NATURE GENETICS
Kidney function may help docs pick antiplatelet mix after stroke
Renal function should be considered when determining whether to pick ticagrelor-aspirin or clopidogrel-aspirin as the antiplatelet therapy for patients with minor stroke, according to new research.
The study, which was conducted in 202 centers in China and published in Annals of Internal Medicine, indicates that when patients had normal kidney function, ticagrelor-aspirin, compared with clopidogrel-aspirin, substantially reduced the risk for recurrent stroke within 90 days of follow-up.
However, this effect was not seen in patients with mildly, moderately or severely decreased kidney function.
Rates of severe or moderate bleeding did not differ substantially between the two treatments.
Results gleaned from CHANCE-2 data
The researchers, led by Anxin Wang, PhD, from Capital Medical University in Beijing, conducted a post hoc analysis of the CHANCE-2 (Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events-II) trial.
The trial included 6,378 patients who carried cytochrome P450 2C19 (CYP2C19) loss-of-function (LOF) alleles who had experienced a minor stroke or transient ischemic attack.
Patients received either ticagrelor-aspirin or clopidogrel-aspirin, and their renal function was measured by estimated glomerular filtration rate. The authors listed as a limitation that no data were available on the presence of albuminuria or proteinuria.
The researchers investigated what effect renal function had on the efficacy and safety of the therapies.
Differences in the therapies
Clopidogrel-aspirin is often recommended for preventing stroke. It can reduce thrombotic risk in patients with impaired kidney function, the authors noted. Ticagrelor can provide greater, faster, and more consistent P2Y12 inhibition than clopidogrel, and evidence shows it is effective in preventing stroke recurrence, particularly in people carrying CYP2C19 LOF alleles.
When people have reduced kidney function, clopidogrel may be harder to clear than ticagrelor and there may be increased plasma concentrations, so function is important to consider when choosing an antiplatelet therapy, the authors wrote.
Choice may come down to cost
Geoffrey Barnes, MD, MSc, associate professor of vascular and cardiovascular medicine at University of Michigan Medicine in Ann Arbor, said in an interview that there has been momentum toward ticagrelor as a more potent choice than clopidogrel not just in populations with minor stroke but for people with MI and coronary stents.
He said he found the results surprising and was intrigued that this paper suggests looking more skeptically at ticagrelor when kidney function is impaired.
Still, the choice may also come down to what the patient can afford at the pharmacy, he said.
“The reality is many patients still get clopidogrel either because that’s what their physicians have been prescribing for well over a decade or because of cost issues, and clopidogrel, for many patients, can be less expensive,” Dr. Barnes noted.
He said he would like to see more study in different populations as the prevalence of people carrying CYP2C19 allele differs by race and results might be different in a non-Asian population. That allele is thought to affect how clopidogrel is metabolized.
Study should spur more research
Nada El Husseini, MD, associate professor of neurology and Duke Telestroke Medical Director at Duke University Medical Center, Durham, N.C., said the study is hypothesis generating, but shouldn’t be thought of as the last word on the subject.
She pointed out some additional limitations of the study, including that it was a post hoc analysis. She explained that the question researchers asked in this study – about effect of kidney function on the safety and efficacy of the therapies – was not the focus of the original CHANCE-2 study, and, as such, the post hoc study may have been underpowered to answer the renal function question.
The authors acknowledged that limitation, noting that “the proportion of patients with severely decreased renal function was low.”
Among 6,378 patients, 4,050 (63.5%) had normal kidney function, 2,010 (31.5%) had mildly decreased function, and 318 (5.0%) had moderately to severely decreased function.
The study was funded by the Ministry of Science and Technology of the People’s Republic of China, the Beijing Municipal Science and Technology Commission, the Chinese Stroke Association, the National Science and Technology Major Project and the Beijing Municipal Administration of Hospitals Incubating Program). Salubris Pharmaceuticals contributed ticagrelor and, clopidogrel at no cost and with no restrictions. Dr. Wang reported no relevant financial relationships. Dr. Barnes and Dr. El Husseini reported no relevant financial relationships.
Renal function should be considered when determining whether to pick ticagrelor-aspirin or clopidogrel-aspirin as the antiplatelet therapy for patients with minor stroke, according to new research.
The study, which was conducted in 202 centers in China and published in Annals of Internal Medicine, indicates that when patients had normal kidney function, ticagrelor-aspirin, compared with clopidogrel-aspirin, substantially reduced the risk for recurrent stroke within 90 days of follow-up.
However, this effect was not seen in patients with mildly, moderately or severely decreased kidney function.
Rates of severe or moderate bleeding did not differ substantially between the two treatments.
Results gleaned from CHANCE-2 data
The researchers, led by Anxin Wang, PhD, from Capital Medical University in Beijing, conducted a post hoc analysis of the CHANCE-2 (Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events-II) trial.
The trial included 6,378 patients who carried cytochrome P450 2C19 (CYP2C19) loss-of-function (LOF) alleles who had experienced a minor stroke or transient ischemic attack.
Patients received either ticagrelor-aspirin or clopidogrel-aspirin, and their renal function was measured by estimated glomerular filtration rate. The authors listed as a limitation that no data were available on the presence of albuminuria or proteinuria.
The researchers investigated what effect renal function had on the efficacy and safety of the therapies.
Differences in the therapies
Clopidogrel-aspirin is often recommended for preventing stroke. It can reduce thrombotic risk in patients with impaired kidney function, the authors noted. Ticagrelor can provide greater, faster, and more consistent P2Y12 inhibition than clopidogrel, and evidence shows it is effective in preventing stroke recurrence, particularly in people carrying CYP2C19 LOF alleles.
When people have reduced kidney function, clopidogrel may be harder to clear than ticagrelor and there may be increased plasma concentrations, so function is important to consider when choosing an antiplatelet therapy, the authors wrote.
Choice may come down to cost
Geoffrey Barnes, MD, MSc, associate professor of vascular and cardiovascular medicine at University of Michigan Medicine in Ann Arbor, said in an interview that there has been momentum toward ticagrelor as a more potent choice than clopidogrel not just in populations with minor stroke but for people with MI and coronary stents.
He said he found the results surprising and was intrigued that this paper suggests looking more skeptically at ticagrelor when kidney function is impaired.
Still, the choice may also come down to what the patient can afford at the pharmacy, he said.
“The reality is many patients still get clopidogrel either because that’s what their physicians have been prescribing for well over a decade or because of cost issues, and clopidogrel, for many patients, can be less expensive,” Dr. Barnes noted.
He said he would like to see more study in different populations as the prevalence of people carrying CYP2C19 allele differs by race and results might be different in a non-Asian population. That allele is thought to affect how clopidogrel is metabolized.
Study should spur more research
Nada El Husseini, MD, associate professor of neurology and Duke Telestroke Medical Director at Duke University Medical Center, Durham, N.C., said the study is hypothesis generating, but shouldn’t be thought of as the last word on the subject.
She pointed out some additional limitations of the study, including that it was a post hoc analysis. She explained that the question researchers asked in this study – about effect of kidney function on the safety and efficacy of the therapies – was not the focus of the original CHANCE-2 study, and, as such, the post hoc study may have been underpowered to answer the renal function question.
The authors acknowledged that limitation, noting that “the proportion of patients with severely decreased renal function was low.”
Among 6,378 patients, 4,050 (63.5%) had normal kidney function, 2,010 (31.5%) had mildly decreased function, and 318 (5.0%) had moderately to severely decreased function.
The study was funded by the Ministry of Science and Technology of the People’s Republic of China, the Beijing Municipal Science and Technology Commission, the Chinese Stroke Association, the National Science and Technology Major Project and the Beijing Municipal Administration of Hospitals Incubating Program). Salubris Pharmaceuticals contributed ticagrelor and, clopidogrel at no cost and with no restrictions. Dr. Wang reported no relevant financial relationships. Dr. Barnes and Dr. El Husseini reported no relevant financial relationships.
Renal function should be considered when determining whether to pick ticagrelor-aspirin or clopidogrel-aspirin as the antiplatelet therapy for patients with minor stroke, according to new research.
The study, which was conducted in 202 centers in China and published in Annals of Internal Medicine, indicates that when patients had normal kidney function, ticagrelor-aspirin, compared with clopidogrel-aspirin, substantially reduced the risk for recurrent stroke within 90 days of follow-up.
However, this effect was not seen in patients with mildly, moderately or severely decreased kidney function.
Rates of severe or moderate bleeding did not differ substantially between the two treatments.
Results gleaned from CHANCE-2 data
The researchers, led by Anxin Wang, PhD, from Capital Medical University in Beijing, conducted a post hoc analysis of the CHANCE-2 (Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events-II) trial.
The trial included 6,378 patients who carried cytochrome P450 2C19 (CYP2C19) loss-of-function (LOF) alleles who had experienced a minor stroke or transient ischemic attack.
Patients received either ticagrelor-aspirin or clopidogrel-aspirin, and their renal function was measured by estimated glomerular filtration rate. The authors listed as a limitation that no data were available on the presence of albuminuria or proteinuria.
The researchers investigated what effect renal function had on the efficacy and safety of the therapies.
Differences in the therapies
Clopidogrel-aspirin is often recommended for preventing stroke. It can reduce thrombotic risk in patients with impaired kidney function, the authors noted. Ticagrelor can provide greater, faster, and more consistent P2Y12 inhibition than clopidogrel, and evidence shows it is effective in preventing stroke recurrence, particularly in people carrying CYP2C19 LOF alleles.
When people have reduced kidney function, clopidogrel may be harder to clear than ticagrelor and there may be increased plasma concentrations, so function is important to consider when choosing an antiplatelet therapy, the authors wrote.
Choice may come down to cost
Geoffrey Barnes, MD, MSc, associate professor of vascular and cardiovascular medicine at University of Michigan Medicine in Ann Arbor, said in an interview that there has been momentum toward ticagrelor as a more potent choice than clopidogrel not just in populations with minor stroke but for people with MI and coronary stents.
He said he found the results surprising and was intrigued that this paper suggests looking more skeptically at ticagrelor when kidney function is impaired.
Still, the choice may also come down to what the patient can afford at the pharmacy, he said.
“The reality is many patients still get clopidogrel either because that’s what their physicians have been prescribing for well over a decade or because of cost issues, and clopidogrel, for many patients, can be less expensive,” Dr. Barnes noted.
He said he would like to see more study in different populations as the prevalence of people carrying CYP2C19 allele differs by race and results might be different in a non-Asian population. That allele is thought to affect how clopidogrel is metabolized.
Study should spur more research
Nada El Husseini, MD, associate professor of neurology and Duke Telestroke Medical Director at Duke University Medical Center, Durham, N.C., said the study is hypothesis generating, but shouldn’t be thought of as the last word on the subject.
She pointed out some additional limitations of the study, including that it was a post hoc analysis. She explained that the question researchers asked in this study – about effect of kidney function on the safety and efficacy of the therapies – was not the focus of the original CHANCE-2 study, and, as such, the post hoc study may have been underpowered to answer the renal function question.
The authors acknowledged that limitation, noting that “the proportion of patients with severely decreased renal function was low.”
Among 6,378 patients, 4,050 (63.5%) had normal kidney function, 2,010 (31.5%) had mildly decreased function, and 318 (5.0%) had moderately to severely decreased function.
The study was funded by the Ministry of Science and Technology of the People’s Republic of China, the Beijing Municipal Science and Technology Commission, the Chinese Stroke Association, the National Science and Technology Major Project and the Beijing Municipal Administration of Hospitals Incubating Program). Salubris Pharmaceuticals contributed ticagrelor and, clopidogrel at no cost and with no restrictions. Dr. Wang reported no relevant financial relationships. Dr. Barnes and Dr. El Husseini reported no relevant financial relationships.
FROM ANNALS OF INTERNAL MEDICINE
Post Roe, pregnant SCD patients facing “dire” risks
When maternal-fetal medicine specialist Andra James, MD, MPH, trained as a midwife decades ago, women with sickle cell disease (SCD) were urged to never get pregnant. If they did, termination was considered the best option.
“If they did carry a pregnancy, the baby would not survive to the point of viability,” Dr. James, emeritus professor of obstetrics and gynecology at Duke University, Durham, N.C., recalled in an interview.
The fates of women with SCD have transformed dramatically since those grim days. In general, this blood disorder no longer robs patients of decades of life, and many women with SCD bear healthy children. But their pregnancies are still considered high risk with significant potential for health crises and death. Now, there’s a new complication: The overturning of Roe v. Wade.
For example, women with SCD may be unable able to seek elective abortions in some states even if their pregnancies pose a danger to their lives. And abortion restrictions are imperiling access to a medication that’s used to treat miscarriages, which are more common in women with SCD.
“The situation with Dobbs is dire, and maternal health care is being compromised,” Johns Hopkins University pediatric hematologist Lydia Pecker, MD, who treats young people with SCD and studies its impact on pregnancy, said in an interview. “Women with sickle cell disease who are pregnant constitute an underserved and understudied population with special health care needs, and the Dobbs decision will only make providing their care even more difficult in many parts of the country.”
For her part, Dr. James described the risk to pregnant women with SCD this way: In the wake of the court ruling, “we increase the opportunity for them to lose their lives and for their babies to die.”
SCD’s impact on pregnancy
While physicians no longer advise women with SCD to avoid motherhood, pregnancy is still uniquely dangerous for them. “Most of them have babies and children who are thriving, but it’s not easy for them,” University of North Carolina at Chapel Hill hematologist and SCD specialist Jane Little, MD, said in an interview. And in some cases, she said, pregnancies “do not end well.”
For a 2022 report, Dr. Pecker and colleagues analyzed 2012-2018 data for 6,610 U.S. hospital admissions among women with SCD (87% of whom were Black). These women were more likely than were unaffected women to suffer severe maternal morbidity (odds ratio[OR], 4.63, 95% confidence interval [CI], 4.16-5.16, P < .001). Cerebrovascular event were especially more common in SCD (OR, 13.94, P < .001).
According to a 2019 report, pregnant women with SCD “are more likely to develop a host of complications, particularly hypertensive syndromes (such as preeclampsia), venous thromboembolism (VTE), preterm labor, and fetal loss. Newborns are more likely to have growth problems and prematurity.”
Although data are sparse, experts say it’s also clear that women with SCD face significantly higher risk of death in pregnancy compared to other women. In fact, the maternal mortality rate for females with SCD “is higher than for Black females without SCD, who already suffer from a higher mortality rate than White females during pregnancy and childbirth,” Andrea Roe, MD, MPH, assistant professor of obstetrics and gynecology at the Hospital of the University of Pennsylvania, Philadelphia, said in an interview.
Women with SCD also are more likely to have premature and stillborn births.
Some of the health challenges in pregnant women with SCD stem from the body’s inability to boost blood production in order to supply the placenta, said Dr. James, the Duke University emeritus professor. “Her bone marrow is already turning out red blood cells as fast as it can.”
In addition, she said, these women are more susceptible to infection, blood clots, and damage to the kidneys and lungs.
Still, in most cases of SCD in pregnancy, “we counsel a woman that we can get you safely through it,” Dr. James said. “But there is a subset of patients that will have organ damage from their sickle cell disease and should not become pregnant or stay pregnant if they become pregnant.”
Court ruling limits options in some states
The Dobbs ruling affects pregnant women with SCD in two ways: It allows states to restrict or ban abortion to greater extents than were possible over the last 50 years, and it has spawned further limitations on access to mifepristone, which is commonly used to treat early miscarriages.
In some cases, Dr. James said, abortions in this population are elective. “People with sickle cell disease are frequently in pain, they are frequently hospitalized. They may have suffered strokes or subclinical strokes or have some cognitive impairment, and they don’t have the mental and physical fortitude [to tolerate pregnancy and birth].”
In other cases, abortions are medically necessary to preserve the mother’s life. The American Society of Hematology highlighted the risks posed by SCD to maternal health in a June 24 statement that criticized the Dobbs ruling. “In some cases, denying women their right to terminate a pregnancy puts them at risk of serious illness or death,” wrote Jane N. Winter, MD, president of ASH and professor of medicine at Northwestern University, Chicago.
There do not appear to be any statistics about abortion rates among women with SCD in the United States or whether the rates are higher than in other groups.
As for miscarriages in SCD, an analysis of first pregnancies in California women with SCD from 1991 to 2016 found that about 16% were “incomplete,” mainly (59.3%) from miscarriage.
The Dobbs ruling allows states to further restrict the drug combination of mifepristone and misoprostol, which is used to trigger abortions and to treat early pregnancy loss. Access to mifepristone was already limited prior to the ruling due to tight regulation, and advocates say it’s now even harder to get.
What now? Physicians urge focus on contraception
As the ramifications of the Dobbs ruling sink in, SCD specialists are emphasizing the importance of providing gynecological and contraceptive care to help women with the condition avoid unwanted pregnancies. At the University of North Carolina, “we’re pretty aggressive about trying to give women the option to see a gynecologist to get the best care they can,” Dr. Little said. “We have a shared gynecology and sickle cell clinic because we really want women to be making the choice [to become pregnant] when they are ready because it’s a strain on their health and their lives.”
Dr. Pecker, the Johns Hopkins University pediatric hematologist, urged colleagues to partner with maternal-fetal medicine specialists so they can quickly get help for pregnant patients when needed. “That way they can get high-quality pregnancy care and help to end pregnancies that need to be ended.”
She recommended “highly effective” progesterone-based birth control as the best first-line contraceptive for women with SCD. And, she said, every woman of child-bearing age with SCD should be assessed annually for their intentions regarding pregnancy. As she put it, “there’s so much that we can do to reduce harms.”
Dr. Pecker disclosed financial relationships with the National Institutes of Health, American Society of Hematology, Doris Duke Charitable Foundation, the Mellon Foundation, Global Blood Therapeutics, and Novo Nordisk. Dr. Little disclosed financial relationships with Global Blood Therapeutics, Bluebird Bio, and Forma Therapeutics. Dr. Roe has no disclosures.
When maternal-fetal medicine specialist Andra James, MD, MPH, trained as a midwife decades ago, women with sickle cell disease (SCD) were urged to never get pregnant. If they did, termination was considered the best option.
“If they did carry a pregnancy, the baby would not survive to the point of viability,” Dr. James, emeritus professor of obstetrics and gynecology at Duke University, Durham, N.C., recalled in an interview.
The fates of women with SCD have transformed dramatically since those grim days. In general, this blood disorder no longer robs patients of decades of life, and many women with SCD bear healthy children. But their pregnancies are still considered high risk with significant potential for health crises and death. Now, there’s a new complication: The overturning of Roe v. Wade.
For example, women with SCD may be unable able to seek elective abortions in some states even if their pregnancies pose a danger to their lives. And abortion restrictions are imperiling access to a medication that’s used to treat miscarriages, which are more common in women with SCD.
“The situation with Dobbs is dire, and maternal health care is being compromised,” Johns Hopkins University pediatric hematologist Lydia Pecker, MD, who treats young people with SCD and studies its impact on pregnancy, said in an interview. “Women with sickle cell disease who are pregnant constitute an underserved and understudied population with special health care needs, and the Dobbs decision will only make providing their care even more difficult in many parts of the country.”
For her part, Dr. James described the risk to pregnant women with SCD this way: In the wake of the court ruling, “we increase the opportunity for them to lose their lives and for their babies to die.”
SCD’s impact on pregnancy
While physicians no longer advise women with SCD to avoid motherhood, pregnancy is still uniquely dangerous for them. “Most of them have babies and children who are thriving, but it’s not easy for them,” University of North Carolina at Chapel Hill hematologist and SCD specialist Jane Little, MD, said in an interview. And in some cases, she said, pregnancies “do not end well.”
For a 2022 report, Dr. Pecker and colleagues analyzed 2012-2018 data for 6,610 U.S. hospital admissions among women with SCD (87% of whom were Black). These women were more likely than were unaffected women to suffer severe maternal morbidity (odds ratio[OR], 4.63, 95% confidence interval [CI], 4.16-5.16, P < .001). Cerebrovascular event were especially more common in SCD (OR, 13.94, P < .001).
According to a 2019 report, pregnant women with SCD “are more likely to develop a host of complications, particularly hypertensive syndromes (such as preeclampsia), venous thromboembolism (VTE), preterm labor, and fetal loss. Newborns are more likely to have growth problems and prematurity.”
Although data are sparse, experts say it’s also clear that women with SCD face significantly higher risk of death in pregnancy compared to other women. In fact, the maternal mortality rate for females with SCD “is higher than for Black females without SCD, who already suffer from a higher mortality rate than White females during pregnancy and childbirth,” Andrea Roe, MD, MPH, assistant professor of obstetrics and gynecology at the Hospital of the University of Pennsylvania, Philadelphia, said in an interview.
Women with SCD also are more likely to have premature and stillborn births.
Some of the health challenges in pregnant women with SCD stem from the body’s inability to boost blood production in order to supply the placenta, said Dr. James, the Duke University emeritus professor. “Her bone marrow is already turning out red blood cells as fast as it can.”
In addition, she said, these women are more susceptible to infection, blood clots, and damage to the kidneys and lungs.
Still, in most cases of SCD in pregnancy, “we counsel a woman that we can get you safely through it,” Dr. James said. “But there is a subset of patients that will have organ damage from their sickle cell disease and should not become pregnant or stay pregnant if they become pregnant.”
Court ruling limits options in some states
The Dobbs ruling affects pregnant women with SCD in two ways: It allows states to restrict or ban abortion to greater extents than were possible over the last 50 years, and it has spawned further limitations on access to mifepristone, which is commonly used to treat early miscarriages.
In some cases, Dr. James said, abortions in this population are elective. “People with sickle cell disease are frequently in pain, they are frequently hospitalized. They may have suffered strokes or subclinical strokes or have some cognitive impairment, and they don’t have the mental and physical fortitude [to tolerate pregnancy and birth].”
In other cases, abortions are medically necessary to preserve the mother’s life. The American Society of Hematology highlighted the risks posed by SCD to maternal health in a June 24 statement that criticized the Dobbs ruling. “In some cases, denying women their right to terminate a pregnancy puts them at risk of serious illness or death,” wrote Jane N. Winter, MD, president of ASH and professor of medicine at Northwestern University, Chicago.
There do not appear to be any statistics about abortion rates among women with SCD in the United States or whether the rates are higher than in other groups.
As for miscarriages in SCD, an analysis of first pregnancies in California women with SCD from 1991 to 2016 found that about 16% were “incomplete,” mainly (59.3%) from miscarriage.
The Dobbs ruling allows states to further restrict the drug combination of mifepristone and misoprostol, which is used to trigger abortions and to treat early pregnancy loss. Access to mifepristone was already limited prior to the ruling due to tight regulation, and advocates say it’s now even harder to get.
What now? Physicians urge focus on contraception
As the ramifications of the Dobbs ruling sink in, SCD specialists are emphasizing the importance of providing gynecological and contraceptive care to help women with the condition avoid unwanted pregnancies. At the University of North Carolina, “we’re pretty aggressive about trying to give women the option to see a gynecologist to get the best care they can,” Dr. Little said. “We have a shared gynecology and sickle cell clinic because we really want women to be making the choice [to become pregnant] when they are ready because it’s a strain on their health and their lives.”
Dr. Pecker, the Johns Hopkins University pediatric hematologist, urged colleagues to partner with maternal-fetal medicine specialists so they can quickly get help for pregnant patients when needed. “That way they can get high-quality pregnancy care and help to end pregnancies that need to be ended.”
She recommended “highly effective” progesterone-based birth control as the best first-line contraceptive for women with SCD. And, she said, every woman of child-bearing age with SCD should be assessed annually for their intentions regarding pregnancy. As she put it, “there’s so much that we can do to reduce harms.”
Dr. Pecker disclosed financial relationships with the National Institutes of Health, American Society of Hematology, Doris Duke Charitable Foundation, the Mellon Foundation, Global Blood Therapeutics, and Novo Nordisk. Dr. Little disclosed financial relationships with Global Blood Therapeutics, Bluebird Bio, and Forma Therapeutics. Dr. Roe has no disclosures.
When maternal-fetal medicine specialist Andra James, MD, MPH, trained as a midwife decades ago, women with sickle cell disease (SCD) were urged to never get pregnant. If they did, termination was considered the best option.
“If they did carry a pregnancy, the baby would not survive to the point of viability,” Dr. James, emeritus professor of obstetrics and gynecology at Duke University, Durham, N.C., recalled in an interview.
The fates of women with SCD have transformed dramatically since those grim days. In general, this blood disorder no longer robs patients of decades of life, and many women with SCD bear healthy children. But their pregnancies are still considered high risk with significant potential for health crises and death. Now, there’s a new complication: The overturning of Roe v. Wade.
For example, women with SCD may be unable able to seek elective abortions in some states even if their pregnancies pose a danger to their lives. And abortion restrictions are imperiling access to a medication that’s used to treat miscarriages, which are more common in women with SCD.
“The situation with Dobbs is dire, and maternal health care is being compromised,” Johns Hopkins University pediatric hematologist Lydia Pecker, MD, who treats young people with SCD and studies its impact on pregnancy, said in an interview. “Women with sickle cell disease who are pregnant constitute an underserved and understudied population with special health care needs, and the Dobbs decision will only make providing their care even more difficult in many parts of the country.”
For her part, Dr. James described the risk to pregnant women with SCD this way: In the wake of the court ruling, “we increase the opportunity for them to lose their lives and for their babies to die.”
SCD’s impact on pregnancy
While physicians no longer advise women with SCD to avoid motherhood, pregnancy is still uniquely dangerous for them. “Most of them have babies and children who are thriving, but it’s not easy for them,” University of North Carolina at Chapel Hill hematologist and SCD specialist Jane Little, MD, said in an interview. And in some cases, she said, pregnancies “do not end well.”
For a 2022 report, Dr. Pecker and colleagues analyzed 2012-2018 data for 6,610 U.S. hospital admissions among women with SCD (87% of whom were Black). These women were more likely than were unaffected women to suffer severe maternal morbidity (odds ratio[OR], 4.63, 95% confidence interval [CI], 4.16-5.16, P < .001). Cerebrovascular event were especially more common in SCD (OR, 13.94, P < .001).
According to a 2019 report, pregnant women with SCD “are more likely to develop a host of complications, particularly hypertensive syndromes (such as preeclampsia), venous thromboembolism (VTE), preterm labor, and fetal loss. Newborns are more likely to have growth problems and prematurity.”
Although data are sparse, experts say it’s also clear that women with SCD face significantly higher risk of death in pregnancy compared to other women. In fact, the maternal mortality rate for females with SCD “is higher than for Black females without SCD, who already suffer from a higher mortality rate than White females during pregnancy and childbirth,” Andrea Roe, MD, MPH, assistant professor of obstetrics and gynecology at the Hospital of the University of Pennsylvania, Philadelphia, said in an interview.
Women with SCD also are more likely to have premature and stillborn births.
Some of the health challenges in pregnant women with SCD stem from the body’s inability to boost blood production in order to supply the placenta, said Dr. James, the Duke University emeritus professor. “Her bone marrow is already turning out red blood cells as fast as it can.”
In addition, she said, these women are more susceptible to infection, blood clots, and damage to the kidneys and lungs.
Still, in most cases of SCD in pregnancy, “we counsel a woman that we can get you safely through it,” Dr. James said. “But there is a subset of patients that will have organ damage from their sickle cell disease and should not become pregnant or stay pregnant if they become pregnant.”
Court ruling limits options in some states
The Dobbs ruling affects pregnant women with SCD in two ways: It allows states to restrict or ban abortion to greater extents than were possible over the last 50 years, and it has spawned further limitations on access to mifepristone, which is commonly used to treat early miscarriages.
In some cases, Dr. James said, abortions in this population are elective. “People with sickle cell disease are frequently in pain, they are frequently hospitalized. They may have suffered strokes or subclinical strokes or have some cognitive impairment, and they don’t have the mental and physical fortitude [to tolerate pregnancy and birth].”
In other cases, abortions are medically necessary to preserve the mother’s life. The American Society of Hematology highlighted the risks posed by SCD to maternal health in a June 24 statement that criticized the Dobbs ruling. “In some cases, denying women their right to terminate a pregnancy puts them at risk of serious illness or death,” wrote Jane N. Winter, MD, president of ASH and professor of medicine at Northwestern University, Chicago.
There do not appear to be any statistics about abortion rates among women with SCD in the United States or whether the rates are higher than in other groups.
As for miscarriages in SCD, an analysis of first pregnancies in California women with SCD from 1991 to 2016 found that about 16% were “incomplete,” mainly (59.3%) from miscarriage.
The Dobbs ruling allows states to further restrict the drug combination of mifepristone and misoprostol, which is used to trigger abortions and to treat early pregnancy loss. Access to mifepristone was already limited prior to the ruling due to tight regulation, and advocates say it’s now even harder to get.
What now? Physicians urge focus on contraception
As the ramifications of the Dobbs ruling sink in, SCD specialists are emphasizing the importance of providing gynecological and contraceptive care to help women with the condition avoid unwanted pregnancies. At the University of North Carolina, “we’re pretty aggressive about trying to give women the option to see a gynecologist to get the best care they can,” Dr. Little said. “We have a shared gynecology and sickle cell clinic because we really want women to be making the choice [to become pregnant] when they are ready because it’s a strain on their health and their lives.”
Dr. Pecker, the Johns Hopkins University pediatric hematologist, urged colleagues to partner with maternal-fetal medicine specialists so they can quickly get help for pregnant patients when needed. “That way they can get high-quality pregnancy care and help to end pregnancies that need to be ended.”
She recommended “highly effective” progesterone-based birth control as the best first-line contraceptive for women with SCD. And, she said, every woman of child-bearing age with SCD should be assessed annually for their intentions regarding pregnancy. As she put it, “there’s so much that we can do to reduce harms.”
Dr. Pecker disclosed financial relationships with the National Institutes of Health, American Society of Hematology, Doris Duke Charitable Foundation, the Mellon Foundation, Global Blood Therapeutics, and Novo Nordisk. Dr. Little disclosed financial relationships with Global Blood Therapeutics, Bluebird Bio, and Forma Therapeutics. Dr. Roe has no disclosures.
Despite Katie Couric’s advice, doctors say ultrasound breast exams may not be needed
When Katie Couric shared the news of her breast cancer diagnosis, the former co-host of NBC’s “Today” show said she considered this new health challenge to be a teachable moment to encourage people to get needed cancer screenings.
“Please get your annual mammogram,” she wrote on her website in September. “But just as importantly, please find out if you need additional screening.”
In the essay, Couric, 65, explained that because she tends to have dense breast tissue, she gets an ultrasound test in addition to a mammogram when screening for breast cancer. A breast ultrasound, sometimes called a sonogram, uses sound waves to take images of the breast tissue. It can sometimes identify malignancies that are hard to spot on a mammogram in women whose breasts are dense – that is, having a high proportion of fibrous tissue and glands vs. fatty tissue.
Ms. Couric, who famously underwent a colonoscopy on live television after her first husband died of colon cancer and who lost her sister to pancreatic cancer, has long pushed for cancer screening and better detection options.
“We don’t have evidence that auxiliary screening reduces breast cancer mortality or improves quality of life,” said Dr. Carol Mangione, a professor of medicine and public health at the University of California, Los Angeles, who chairs the U.S. Preventive Services Task Force, a group of medical experts who make recommendations for preventive services after weighing their benefits and harms.
Ms. Couric’s office did not respond to requests for comment.
In addition to an annual mammogram, some women with dense breasts get a breast ultrasound or MRI to help identify cancerous cells missed by the mammogram. Dense fibrous tissue appears white on a mammogram and makes it harder to see cancers, which also appear white. Fatty breast tissue, which appears dark on the mammogram, doesn’t obscure breast malignancies.
As digital breast tomosynthesis, or 3-D mammography, has become more widely available, a growing number of women are getting that screening test rather than the standard 2-D mammography. The 3-D mammography has been found to reduce the number of false-positive results and identify more cancers in some women with dense breasts, though the impact on mortality is unknown.
The task force gives an “I” rating to supplemental screening for women with dense breasts whose mammogram results don’t indicate a problem. That means the current evidence is “insufficient” to assess whether the benefits outweigh the harms of the extra screening. (The task force is updating its recommendation for breast cancer screening, including supplemental screening for women with dense breasts.)
One key harm that researchers are concerned about, besides the possible extra cost, is the chance of a false-positive result. Supplemental imaging in women who aren’t at high risk for breast cancer may identify potential trouble spots, which can lead to follow-up testing such as breast biopsies that are invasive and raise cancer fears for many patients. But research has found that very often these results turn out to be false alarms.
If 1,000 women with dense breasts get an ultrasound after a negative mammogram, the ultrasound will identify two to three cancers, studies show. But the extra imaging will also identify up to 117 potential problems that lead to recall visits and tests but are ultimately determined to be false positives.
“On the one hand, we want to do everything we can to improve detection,” said Dr. Sharon Mass, an ob.gyn. in Morristown, N.J., and the former chair of the American College of Obstetricians and Gynecologists’ New Jersey section. “But on the other hand, there are lots of costs and emotional distress” associated with false-positive results.
The professional group doesn’t recommend supplemental screening for women with dense breasts who don’t have any additional risk factors for cancer.
Many other professional groups take a similar position.
“We recommend having a conversation with a health care provider, and for patients to understand whether their breasts are dense,” Dr. Mass said. “But we do not recommend everyone get tested.”
In particular, for the roughly 8% of women who have extremely dense breasts, it’s worth having a conversation with a doctor about additional screening, said Dr. Mass.
Similarly, for women with dense breasts who have additional risk factors for breast cancer, such as a family history of the disease or a personal history of breast biopsies to check suspected cancers, supplemental screening may make sense, she said.
Dense breasts are relatively common. In the United States, an estimated 43% of women 40 and older have breasts that are considered dense or extremely dense. In addition to making it harder to interpret mammograms, women with dense breasts are up to twice as likely to develop breast cancer as women with average-density breasts, research shows.
Studies have shown that mammograms reduce breast cancer mortality. But even though it seems intuitive that more testing would improve someone’s odds of beating cancer, research hasn’t found that women are any less likely to die from breast cancer if they get a supplemental ultrasound or MRI after a negative mammogram result.
A few studies have found that women with dense or very dense breasts who got an ultrasound or an MRI in addition to a mammogram had fewer so-called interval cancers between regular screening mammograms. But it’s unclear whether those results have any effect on their risk of dying from breast cancer.
“Not every small abnormality is going to lead to something that needs treatment,” said Dr. Mangione.
Thirty-eight states and the District of Columbia have laws requiring that patients be notified about breast density after a mammogram, though some require only a general notice rather than mandate that individual women be informed about their own status. Some states require insurers to cover supplemental testing, but others do not.
In 2019, the FDA proposed that information about breast density be incorporated into the letters patients receive after a mammogram. That rule hasn’t yet been finalized, but the agency told lawmakers that it expects to issue the rule no later than early next year.
In a statement to KHN, FDA spokesperson Carly Kempler said, “The FDA is committed to improving mammography services for patients and working diligently to finalize the rule to amend the existing mammography regulations.”
The cost of additional testing is another factor to consider. Because the Preventive Services Task Force recommends women get regular screening mammograms, health plans are generally required to cover them without charging people anything out-of-pocket. That’s not the case with supplemental screening for women with dense breasts, which the task force does not recommend. Some states require insurance coverage of those tests, but those laws don’t apply to the many plans in which employers “self-fund” workers’ benefits rather than buy state-regulated insurance coverage.
Supplemental imaging can be pricey if your health plan doesn’t cover it. A screening ultrasound might cost $250 out-of-pocket while a breast MRI could cost $1,084, according to the Brem Foundation to Defeat Breast Cancer.
Rep. Rosa DeLauro (D-Conn.) recently tweeted that she is working on a bill with Ms. Couric that would cover MRIs and ultrasounds for women with dense breasts without any out-of-pocket costs.
Some doctors recommend other steps that may be more effective than extra screening for women with dense breasts who want to reduce their breast cancer risk.
“If you really want to help yourself, lose weight,” said Dr. Karla Kerlikowske, a professor of medicine and epidemiology/biostatistics at the University of California, San Francisco, who has worked with other researchers to develop calculators that help providers assess patients’ breast cancer risk. “Moderate your alcohol intake and avoid long-term hormone replacement. Those are things you can control.”
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.
When Katie Couric shared the news of her breast cancer diagnosis, the former co-host of NBC’s “Today” show said she considered this new health challenge to be a teachable moment to encourage people to get needed cancer screenings.
“Please get your annual mammogram,” she wrote on her website in September. “But just as importantly, please find out if you need additional screening.”
In the essay, Couric, 65, explained that because she tends to have dense breast tissue, she gets an ultrasound test in addition to a mammogram when screening for breast cancer. A breast ultrasound, sometimes called a sonogram, uses sound waves to take images of the breast tissue. It can sometimes identify malignancies that are hard to spot on a mammogram in women whose breasts are dense – that is, having a high proportion of fibrous tissue and glands vs. fatty tissue.
Ms. Couric, who famously underwent a colonoscopy on live television after her first husband died of colon cancer and who lost her sister to pancreatic cancer, has long pushed for cancer screening and better detection options.
“We don’t have evidence that auxiliary screening reduces breast cancer mortality or improves quality of life,” said Dr. Carol Mangione, a professor of medicine and public health at the University of California, Los Angeles, who chairs the U.S. Preventive Services Task Force, a group of medical experts who make recommendations for preventive services after weighing their benefits and harms.
Ms. Couric’s office did not respond to requests for comment.
In addition to an annual mammogram, some women with dense breasts get a breast ultrasound or MRI to help identify cancerous cells missed by the mammogram. Dense fibrous tissue appears white on a mammogram and makes it harder to see cancers, which also appear white. Fatty breast tissue, which appears dark on the mammogram, doesn’t obscure breast malignancies.
As digital breast tomosynthesis, or 3-D mammography, has become more widely available, a growing number of women are getting that screening test rather than the standard 2-D mammography. The 3-D mammography has been found to reduce the number of false-positive results and identify more cancers in some women with dense breasts, though the impact on mortality is unknown.
The task force gives an “I” rating to supplemental screening for women with dense breasts whose mammogram results don’t indicate a problem. That means the current evidence is “insufficient” to assess whether the benefits outweigh the harms of the extra screening. (The task force is updating its recommendation for breast cancer screening, including supplemental screening for women with dense breasts.)
One key harm that researchers are concerned about, besides the possible extra cost, is the chance of a false-positive result. Supplemental imaging in women who aren’t at high risk for breast cancer may identify potential trouble spots, which can lead to follow-up testing such as breast biopsies that are invasive and raise cancer fears for many patients. But research has found that very often these results turn out to be false alarms.
If 1,000 women with dense breasts get an ultrasound after a negative mammogram, the ultrasound will identify two to three cancers, studies show. But the extra imaging will also identify up to 117 potential problems that lead to recall visits and tests but are ultimately determined to be false positives.
“On the one hand, we want to do everything we can to improve detection,” said Dr. Sharon Mass, an ob.gyn. in Morristown, N.J., and the former chair of the American College of Obstetricians and Gynecologists’ New Jersey section. “But on the other hand, there are lots of costs and emotional distress” associated with false-positive results.
The professional group doesn’t recommend supplemental screening for women with dense breasts who don’t have any additional risk factors for cancer.
Many other professional groups take a similar position.
“We recommend having a conversation with a health care provider, and for patients to understand whether their breasts are dense,” Dr. Mass said. “But we do not recommend everyone get tested.”
In particular, for the roughly 8% of women who have extremely dense breasts, it’s worth having a conversation with a doctor about additional screening, said Dr. Mass.
Similarly, for women with dense breasts who have additional risk factors for breast cancer, such as a family history of the disease or a personal history of breast biopsies to check suspected cancers, supplemental screening may make sense, she said.
Dense breasts are relatively common. In the United States, an estimated 43% of women 40 and older have breasts that are considered dense or extremely dense. In addition to making it harder to interpret mammograms, women with dense breasts are up to twice as likely to develop breast cancer as women with average-density breasts, research shows.
Studies have shown that mammograms reduce breast cancer mortality. But even though it seems intuitive that more testing would improve someone’s odds of beating cancer, research hasn’t found that women are any less likely to die from breast cancer if they get a supplemental ultrasound or MRI after a negative mammogram result.
A few studies have found that women with dense or very dense breasts who got an ultrasound or an MRI in addition to a mammogram had fewer so-called interval cancers between regular screening mammograms. But it’s unclear whether those results have any effect on their risk of dying from breast cancer.
“Not every small abnormality is going to lead to something that needs treatment,” said Dr. Mangione.
Thirty-eight states and the District of Columbia have laws requiring that patients be notified about breast density after a mammogram, though some require only a general notice rather than mandate that individual women be informed about their own status. Some states require insurers to cover supplemental testing, but others do not.
In 2019, the FDA proposed that information about breast density be incorporated into the letters patients receive after a mammogram. That rule hasn’t yet been finalized, but the agency told lawmakers that it expects to issue the rule no later than early next year.
In a statement to KHN, FDA spokesperson Carly Kempler said, “The FDA is committed to improving mammography services for patients and working diligently to finalize the rule to amend the existing mammography regulations.”
The cost of additional testing is another factor to consider. Because the Preventive Services Task Force recommends women get regular screening mammograms, health plans are generally required to cover them without charging people anything out-of-pocket. That’s not the case with supplemental screening for women with dense breasts, which the task force does not recommend. Some states require insurance coverage of those tests, but those laws don’t apply to the many plans in which employers “self-fund” workers’ benefits rather than buy state-regulated insurance coverage.
Supplemental imaging can be pricey if your health plan doesn’t cover it. A screening ultrasound might cost $250 out-of-pocket while a breast MRI could cost $1,084, according to the Brem Foundation to Defeat Breast Cancer.
Rep. Rosa DeLauro (D-Conn.) recently tweeted that she is working on a bill with Ms. Couric that would cover MRIs and ultrasounds for women with dense breasts without any out-of-pocket costs.
Some doctors recommend other steps that may be more effective than extra screening for women with dense breasts who want to reduce their breast cancer risk.
“If you really want to help yourself, lose weight,” said Dr. Karla Kerlikowske, a professor of medicine and epidemiology/biostatistics at the University of California, San Francisco, who has worked with other researchers to develop calculators that help providers assess patients’ breast cancer risk. “Moderate your alcohol intake and avoid long-term hormone replacement. Those are things you can control.”
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.
When Katie Couric shared the news of her breast cancer diagnosis, the former co-host of NBC’s “Today” show said she considered this new health challenge to be a teachable moment to encourage people to get needed cancer screenings.
“Please get your annual mammogram,” she wrote on her website in September. “But just as importantly, please find out if you need additional screening.”
In the essay, Couric, 65, explained that because she tends to have dense breast tissue, she gets an ultrasound test in addition to a mammogram when screening for breast cancer. A breast ultrasound, sometimes called a sonogram, uses sound waves to take images of the breast tissue. It can sometimes identify malignancies that are hard to spot on a mammogram in women whose breasts are dense – that is, having a high proportion of fibrous tissue and glands vs. fatty tissue.
Ms. Couric, who famously underwent a colonoscopy on live television after her first husband died of colon cancer and who lost her sister to pancreatic cancer, has long pushed for cancer screening and better detection options.
“We don’t have evidence that auxiliary screening reduces breast cancer mortality or improves quality of life,” said Dr. Carol Mangione, a professor of medicine and public health at the University of California, Los Angeles, who chairs the U.S. Preventive Services Task Force, a group of medical experts who make recommendations for preventive services after weighing their benefits and harms.
Ms. Couric’s office did not respond to requests for comment.
In addition to an annual mammogram, some women with dense breasts get a breast ultrasound or MRI to help identify cancerous cells missed by the mammogram. Dense fibrous tissue appears white on a mammogram and makes it harder to see cancers, which also appear white. Fatty breast tissue, which appears dark on the mammogram, doesn’t obscure breast malignancies.
As digital breast tomosynthesis, or 3-D mammography, has become more widely available, a growing number of women are getting that screening test rather than the standard 2-D mammography. The 3-D mammography has been found to reduce the number of false-positive results and identify more cancers in some women with dense breasts, though the impact on mortality is unknown.
The task force gives an “I” rating to supplemental screening for women with dense breasts whose mammogram results don’t indicate a problem. That means the current evidence is “insufficient” to assess whether the benefits outweigh the harms of the extra screening. (The task force is updating its recommendation for breast cancer screening, including supplemental screening for women with dense breasts.)
One key harm that researchers are concerned about, besides the possible extra cost, is the chance of a false-positive result. Supplemental imaging in women who aren’t at high risk for breast cancer may identify potential trouble spots, which can lead to follow-up testing such as breast biopsies that are invasive and raise cancer fears for many patients. But research has found that very often these results turn out to be false alarms.
If 1,000 women with dense breasts get an ultrasound after a negative mammogram, the ultrasound will identify two to three cancers, studies show. But the extra imaging will also identify up to 117 potential problems that lead to recall visits and tests but are ultimately determined to be false positives.
“On the one hand, we want to do everything we can to improve detection,” said Dr. Sharon Mass, an ob.gyn. in Morristown, N.J., and the former chair of the American College of Obstetricians and Gynecologists’ New Jersey section. “But on the other hand, there are lots of costs and emotional distress” associated with false-positive results.
The professional group doesn’t recommend supplemental screening for women with dense breasts who don’t have any additional risk factors for cancer.
Many other professional groups take a similar position.
“We recommend having a conversation with a health care provider, and for patients to understand whether their breasts are dense,” Dr. Mass said. “But we do not recommend everyone get tested.”
In particular, for the roughly 8% of women who have extremely dense breasts, it’s worth having a conversation with a doctor about additional screening, said Dr. Mass.
Similarly, for women with dense breasts who have additional risk factors for breast cancer, such as a family history of the disease or a personal history of breast biopsies to check suspected cancers, supplemental screening may make sense, she said.
Dense breasts are relatively common. In the United States, an estimated 43% of women 40 and older have breasts that are considered dense or extremely dense. In addition to making it harder to interpret mammograms, women with dense breasts are up to twice as likely to develop breast cancer as women with average-density breasts, research shows.
Studies have shown that mammograms reduce breast cancer mortality. But even though it seems intuitive that more testing would improve someone’s odds of beating cancer, research hasn’t found that women are any less likely to die from breast cancer if they get a supplemental ultrasound or MRI after a negative mammogram result.
A few studies have found that women with dense or very dense breasts who got an ultrasound or an MRI in addition to a mammogram had fewer so-called interval cancers between regular screening mammograms. But it’s unclear whether those results have any effect on their risk of dying from breast cancer.
“Not every small abnormality is going to lead to something that needs treatment,” said Dr. Mangione.
Thirty-eight states and the District of Columbia have laws requiring that patients be notified about breast density after a mammogram, though some require only a general notice rather than mandate that individual women be informed about their own status. Some states require insurers to cover supplemental testing, but others do not.
In 2019, the FDA proposed that information about breast density be incorporated into the letters patients receive after a mammogram. That rule hasn’t yet been finalized, but the agency told lawmakers that it expects to issue the rule no later than early next year.
In a statement to KHN, FDA spokesperson Carly Kempler said, “The FDA is committed to improving mammography services for patients and working diligently to finalize the rule to amend the existing mammography regulations.”
The cost of additional testing is another factor to consider. Because the Preventive Services Task Force recommends women get regular screening mammograms, health plans are generally required to cover them without charging people anything out-of-pocket. That’s not the case with supplemental screening for women with dense breasts, which the task force does not recommend. Some states require insurance coverage of those tests, but those laws don’t apply to the many plans in which employers “self-fund” workers’ benefits rather than buy state-regulated insurance coverage.
Supplemental imaging can be pricey if your health plan doesn’t cover it. A screening ultrasound might cost $250 out-of-pocket while a breast MRI could cost $1,084, according to the Brem Foundation to Defeat Breast Cancer.
Rep. Rosa DeLauro (D-Conn.) recently tweeted that she is working on a bill with Ms. Couric that would cover MRIs and ultrasounds for women with dense breasts without any out-of-pocket costs.
Some doctors recommend other steps that may be more effective than extra screening for women with dense breasts who want to reduce their breast cancer risk.
“If you really want to help yourself, lose weight,” said Dr. Karla Kerlikowske, a professor of medicine and epidemiology/biostatistics at the University of California, San Francisco, who has worked with other researchers to develop calculators that help providers assess patients’ breast cancer risk. “Moderate your alcohol intake and avoid long-term hormone replacement. Those are things you can control.”
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.