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FDA orders Juul to stop selling E-cigarettes
The marketing denial order covers all the company’s products in the United States, which means Juul must stop distributing the products and remove everything on the market. That includes the Juul device and flavor replacement pods in the tobacco and menthol flavors.
“Today’s action is further progress on the FDA’s commitment to ensuring that all e-cigarette and electronic nicotine delivery system products currently being marketed to consumers meet our public health standards,” Robert Califf, MD, the FDA commissioner, said in the announcement.
“The agency has dedicated significant resources to review products from the companies that account for most of the U.S. market,” he said. “We recognize these make up a significant part of the available products and many have played a disproportionate role in the rise in youth vaping.”
The marketing denial order covers only the commercial distribution and retail sale of Juul’s products and doesn’t restrict consumer possession or use. The FDA “cannot and will not” enforce actions against consumers, the agency said.
The order comes after a 2-year review of the company’s application seeking authorization to continue selling non–fruit-flavored products, such as menthol and tobacco. The FDA determined the application “lacked sufficient evidence regarding the toxicological profile of the products to demonstrate that marketing of the products would be appropriate for the protection of the public health.”
Some of Juul’s study findings raised concerns because of “insufficient and conflicting data,” the FDA said, including potentially harmful chemicals leaching from the Juul liquid replacement pods.
“To date, the FDA has not received clinical information to suggest an immediate hazard associated with the use of the JUUL device or JUUL pods,” the agency said. “However, the [orders] issued today reflect FDA’s determination that there is insufficient evidence to assess the potential toxicological risks of using the JUUL products.”
Juul is expected to appeal the FDA’s decision, according to The New York Times.
In recent years, the FDA has reviewed marketing applications from Juul and other e-cigarette companies as anti-tobacco groups have called for new rules to limit products that led to a surge in youth vaping during the past decade. At the same time, advocates of e-cigarettes and nicotine-delivery devices have said the products help adult smokers to quit cigarettes and other tobacco products.
Juul, in particular, has been blamed for fueling the surge in underage vaping due to fruity flavors and hip marketing, according to The Wall Street Journal. The company removed sweet and fruity flavors from shelves in 2019 and has been trying to repair its reputation by limiting its marketing and focusing on adult cigarette smokers.
In 2020, all e-cigarette manufacturers in the United States were required to submit their products for FDA review to stay on the market, the newspaper reported. The agency has been weighing the potential benefits for adult cigarette smokers against the harms for young people.
The FDA banned the sale of fruit- and mint-flavored cartridges and juice pods in 2020, but menthol and tobacco-flavored products were left on the market, according to USA Today. In September 2021, the agency also banned the sale of hundreds of thousands of vaping and e-cigarette products but didn’t rule on Juul.
Meanwhile, the FDA has cleared Reynolds American and NJOY Holdings – two of Juul’s biggest rivals – to keep tobacco-flavored products on the market. Industry experts expected Juul to receive similar clearance, the Journal reported.
Juul, which was at the top of the U.S. e-cigarette market in 2018, has moved to second place behind Reynolds’s Vuse brand, the newspaper reported. The United States represents most of the company’s revenue, though its products are also available in Canada, the United Kingdom, France, Italy, and the Philippines.
Underage vaping has fallen in the United States since federal restrictions raised the legal purchase age for tobacco products to 21 and banned the sale of sweet and fruity cartridges, according to the Journal. Juul’s popularity has also dropped among youth, with other products such as Puff Bar, Vuse, and Smok becoming more popular among e-cigarette users in high school.
In a separate decision announced this week, the FDA is also moving forward with a plan to reduce the amount of nicotine in cigarettes. The decision, which has been years in the making, is aimed at prompting millions of cigarette users to quit smoking or switch to alternatives such as e-cigarettes, as well as limit the number of users who pick up smoking at an early age.
A version of this article first appeared on WebMD.com .
The marketing denial order covers all the company’s products in the United States, which means Juul must stop distributing the products and remove everything on the market. That includes the Juul device and flavor replacement pods in the tobacco and menthol flavors.
“Today’s action is further progress on the FDA’s commitment to ensuring that all e-cigarette and electronic nicotine delivery system products currently being marketed to consumers meet our public health standards,” Robert Califf, MD, the FDA commissioner, said in the announcement.
“The agency has dedicated significant resources to review products from the companies that account for most of the U.S. market,” he said. “We recognize these make up a significant part of the available products and many have played a disproportionate role in the rise in youth vaping.”
The marketing denial order covers only the commercial distribution and retail sale of Juul’s products and doesn’t restrict consumer possession or use. The FDA “cannot and will not” enforce actions against consumers, the agency said.
The order comes after a 2-year review of the company’s application seeking authorization to continue selling non–fruit-flavored products, such as menthol and tobacco. The FDA determined the application “lacked sufficient evidence regarding the toxicological profile of the products to demonstrate that marketing of the products would be appropriate for the protection of the public health.”
Some of Juul’s study findings raised concerns because of “insufficient and conflicting data,” the FDA said, including potentially harmful chemicals leaching from the Juul liquid replacement pods.
“To date, the FDA has not received clinical information to suggest an immediate hazard associated with the use of the JUUL device or JUUL pods,” the agency said. “However, the [orders] issued today reflect FDA’s determination that there is insufficient evidence to assess the potential toxicological risks of using the JUUL products.”
Juul is expected to appeal the FDA’s decision, according to The New York Times.
In recent years, the FDA has reviewed marketing applications from Juul and other e-cigarette companies as anti-tobacco groups have called for new rules to limit products that led to a surge in youth vaping during the past decade. At the same time, advocates of e-cigarettes and nicotine-delivery devices have said the products help adult smokers to quit cigarettes and other tobacco products.
Juul, in particular, has been blamed for fueling the surge in underage vaping due to fruity flavors and hip marketing, according to The Wall Street Journal. The company removed sweet and fruity flavors from shelves in 2019 and has been trying to repair its reputation by limiting its marketing and focusing on adult cigarette smokers.
In 2020, all e-cigarette manufacturers in the United States were required to submit their products for FDA review to stay on the market, the newspaper reported. The agency has been weighing the potential benefits for adult cigarette smokers against the harms for young people.
The FDA banned the sale of fruit- and mint-flavored cartridges and juice pods in 2020, but menthol and tobacco-flavored products were left on the market, according to USA Today. In September 2021, the agency also banned the sale of hundreds of thousands of vaping and e-cigarette products but didn’t rule on Juul.
Meanwhile, the FDA has cleared Reynolds American and NJOY Holdings – two of Juul’s biggest rivals – to keep tobacco-flavored products on the market. Industry experts expected Juul to receive similar clearance, the Journal reported.
Juul, which was at the top of the U.S. e-cigarette market in 2018, has moved to second place behind Reynolds’s Vuse brand, the newspaper reported. The United States represents most of the company’s revenue, though its products are also available in Canada, the United Kingdom, France, Italy, and the Philippines.
Underage vaping has fallen in the United States since federal restrictions raised the legal purchase age for tobacco products to 21 and banned the sale of sweet and fruity cartridges, according to the Journal. Juul’s popularity has also dropped among youth, with other products such as Puff Bar, Vuse, and Smok becoming more popular among e-cigarette users in high school.
In a separate decision announced this week, the FDA is also moving forward with a plan to reduce the amount of nicotine in cigarettes. The decision, which has been years in the making, is aimed at prompting millions of cigarette users to quit smoking or switch to alternatives such as e-cigarettes, as well as limit the number of users who pick up smoking at an early age.
A version of this article first appeared on WebMD.com .
The marketing denial order covers all the company’s products in the United States, which means Juul must stop distributing the products and remove everything on the market. That includes the Juul device and flavor replacement pods in the tobacco and menthol flavors.
“Today’s action is further progress on the FDA’s commitment to ensuring that all e-cigarette and electronic nicotine delivery system products currently being marketed to consumers meet our public health standards,” Robert Califf, MD, the FDA commissioner, said in the announcement.
“The agency has dedicated significant resources to review products from the companies that account for most of the U.S. market,” he said. “We recognize these make up a significant part of the available products and many have played a disproportionate role in the rise in youth vaping.”
The marketing denial order covers only the commercial distribution and retail sale of Juul’s products and doesn’t restrict consumer possession or use. The FDA “cannot and will not” enforce actions against consumers, the agency said.
The order comes after a 2-year review of the company’s application seeking authorization to continue selling non–fruit-flavored products, such as menthol and tobacco. The FDA determined the application “lacked sufficient evidence regarding the toxicological profile of the products to demonstrate that marketing of the products would be appropriate for the protection of the public health.”
Some of Juul’s study findings raised concerns because of “insufficient and conflicting data,” the FDA said, including potentially harmful chemicals leaching from the Juul liquid replacement pods.
“To date, the FDA has not received clinical information to suggest an immediate hazard associated with the use of the JUUL device or JUUL pods,” the agency said. “However, the [orders] issued today reflect FDA’s determination that there is insufficient evidence to assess the potential toxicological risks of using the JUUL products.”
Juul is expected to appeal the FDA’s decision, according to The New York Times.
In recent years, the FDA has reviewed marketing applications from Juul and other e-cigarette companies as anti-tobacco groups have called for new rules to limit products that led to a surge in youth vaping during the past decade. At the same time, advocates of e-cigarettes and nicotine-delivery devices have said the products help adult smokers to quit cigarettes and other tobacco products.
Juul, in particular, has been blamed for fueling the surge in underage vaping due to fruity flavors and hip marketing, according to The Wall Street Journal. The company removed sweet and fruity flavors from shelves in 2019 and has been trying to repair its reputation by limiting its marketing and focusing on adult cigarette smokers.
In 2020, all e-cigarette manufacturers in the United States were required to submit their products for FDA review to stay on the market, the newspaper reported. The agency has been weighing the potential benefits for adult cigarette smokers against the harms for young people.
The FDA banned the sale of fruit- and mint-flavored cartridges and juice pods in 2020, but menthol and tobacco-flavored products were left on the market, according to USA Today. In September 2021, the agency also banned the sale of hundreds of thousands of vaping and e-cigarette products but didn’t rule on Juul.
Meanwhile, the FDA has cleared Reynolds American and NJOY Holdings – two of Juul’s biggest rivals – to keep tobacco-flavored products on the market. Industry experts expected Juul to receive similar clearance, the Journal reported.
Juul, which was at the top of the U.S. e-cigarette market in 2018, has moved to second place behind Reynolds’s Vuse brand, the newspaper reported. The United States represents most of the company’s revenue, though its products are also available in Canada, the United Kingdom, France, Italy, and the Philippines.
Underage vaping has fallen in the United States since federal restrictions raised the legal purchase age for tobacco products to 21 and banned the sale of sweet and fruity cartridges, according to the Journal. Juul’s popularity has also dropped among youth, with other products such as Puff Bar, Vuse, and Smok becoming more popular among e-cigarette users in high school.
In a separate decision announced this week, the FDA is also moving forward with a plan to reduce the amount of nicotine in cigarettes. The decision, which has been years in the making, is aimed at prompting millions of cigarette users to quit smoking or switch to alternatives such as e-cigarettes, as well as limit the number of users who pick up smoking at an early age.
A version of this article first appeared on WebMD.com .
A doctor’s missed diagnosis results in mega award
, according to a story from WCCO CBS Minnesota, among other news outlets. The award has been called the largest judgment of its kind in Minnesota history.
In January 2017, Nepalese immigrant Anuj Thapa was playing in an indoor soccer game at St. Cloud State University when another player tackled him. His left leg badly injured, Mr. Thapa was taken by ambulance to CentraCare’s St. Cloud Hospital. The orthopedic surgeon on call that day was Chad Holien, MD, who is affiliated with St. Cloud Orthopedics, a private clinic in nearby Sartell, Minn. Following preparations, and with the help of a physician assistant, Dr. Holien operated on the patient’s broken leg.
But Mr. Thapa experienced post-surgical complications – severe pain, numbness, burning, and muscle issues. Despite the complications, he was discharged from the hospital that afternoon and sent home.
Six days later, Mr. Thapa returned to St. Cloud Hospital, still complaining of severe pain. A second orthopedic surgeon operated and found that Mr. Thapa had “acute compartment syndrome,” the result of internal pressure that had built up in his leg muscles.
Over time, Mr. Thapa underwent more than 20 surgeries on his leg to deal with the ongoing pain and other complications, according to WCCO.
In 2019, he filed a medical malpractice suit in U.S. district court against St. Cloud Orthopedics, the private practice that employed the surgeon and the PA. (Under Minnesota law, an employer is responsible for the actions of its employees.)
In his complaint, Mr. Thapa alleged that in treating him, “the defendants departed from accepted standards of medical practice.” Among other things, he claimed that Dr. Holien and the PA had not properly evaluated his postoperative symptoms, failed to diagnose and treat his compartment syndrome, and improperly discharged him from the hospital. These lapses, Mr. Thapa said, led to his “severe, permanent, and disabling injuries.”
The federal jury agreed. After a weeklong trial, it awarded the plaintiff $100 million for future “pain, disability, disfigurement, embarrassment, and emotional distress.” It also gave him $10 million for past suffering and a little more than $1 million for past and future medical bills.
In a postverdict statement, Mr. Thapa’s attorney said that, while the surgeon and PA are undoubtedly good providers, they made mistakes in this case.
A defense attorney for St. Cloud Orthopedics disputes this: “We maintain the care provided in this case was in accordance with accepted standards of care.”
At press time, the defense had not determined whether to appeal the jury’s $111 million verdict. “St. Cloud continues to support its providers,” said the clinic’s defense attorney. “We are evaluating our options regarding this verdict.”
The content contained in this article is for informational purposes only and does not constitute legal advice. Reliance on any information provided in this article is solely at your own risk.
A version of this article first appeared on Medscape.com.
, according to a story from WCCO CBS Minnesota, among other news outlets. The award has been called the largest judgment of its kind in Minnesota history.
In January 2017, Nepalese immigrant Anuj Thapa was playing in an indoor soccer game at St. Cloud State University when another player tackled him. His left leg badly injured, Mr. Thapa was taken by ambulance to CentraCare’s St. Cloud Hospital. The orthopedic surgeon on call that day was Chad Holien, MD, who is affiliated with St. Cloud Orthopedics, a private clinic in nearby Sartell, Minn. Following preparations, and with the help of a physician assistant, Dr. Holien operated on the patient’s broken leg.
But Mr. Thapa experienced post-surgical complications – severe pain, numbness, burning, and muscle issues. Despite the complications, he was discharged from the hospital that afternoon and sent home.
Six days later, Mr. Thapa returned to St. Cloud Hospital, still complaining of severe pain. A second orthopedic surgeon operated and found that Mr. Thapa had “acute compartment syndrome,” the result of internal pressure that had built up in his leg muscles.
Over time, Mr. Thapa underwent more than 20 surgeries on his leg to deal with the ongoing pain and other complications, according to WCCO.
In 2019, he filed a medical malpractice suit in U.S. district court against St. Cloud Orthopedics, the private practice that employed the surgeon and the PA. (Under Minnesota law, an employer is responsible for the actions of its employees.)
In his complaint, Mr. Thapa alleged that in treating him, “the defendants departed from accepted standards of medical practice.” Among other things, he claimed that Dr. Holien and the PA had not properly evaluated his postoperative symptoms, failed to diagnose and treat his compartment syndrome, and improperly discharged him from the hospital. These lapses, Mr. Thapa said, led to his “severe, permanent, and disabling injuries.”
The federal jury agreed. After a weeklong trial, it awarded the plaintiff $100 million for future “pain, disability, disfigurement, embarrassment, and emotional distress.” It also gave him $10 million for past suffering and a little more than $1 million for past and future medical bills.
In a postverdict statement, Mr. Thapa’s attorney said that, while the surgeon and PA are undoubtedly good providers, they made mistakes in this case.
A defense attorney for St. Cloud Orthopedics disputes this: “We maintain the care provided in this case was in accordance with accepted standards of care.”
At press time, the defense had not determined whether to appeal the jury’s $111 million verdict. “St. Cloud continues to support its providers,” said the clinic’s defense attorney. “We are evaluating our options regarding this verdict.”
The content contained in this article is for informational purposes only and does not constitute legal advice. Reliance on any information provided in this article is solely at your own risk.
A version of this article first appeared on Medscape.com.
, according to a story from WCCO CBS Minnesota, among other news outlets. The award has been called the largest judgment of its kind in Minnesota history.
In January 2017, Nepalese immigrant Anuj Thapa was playing in an indoor soccer game at St. Cloud State University when another player tackled him. His left leg badly injured, Mr. Thapa was taken by ambulance to CentraCare’s St. Cloud Hospital. The orthopedic surgeon on call that day was Chad Holien, MD, who is affiliated with St. Cloud Orthopedics, a private clinic in nearby Sartell, Minn. Following preparations, and with the help of a physician assistant, Dr. Holien operated on the patient’s broken leg.
But Mr. Thapa experienced post-surgical complications – severe pain, numbness, burning, and muscle issues. Despite the complications, he was discharged from the hospital that afternoon and sent home.
Six days later, Mr. Thapa returned to St. Cloud Hospital, still complaining of severe pain. A second orthopedic surgeon operated and found that Mr. Thapa had “acute compartment syndrome,” the result of internal pressure that had built up in his leg muscles.
Over time, Mr. Thapa underwent more than 20 surgeries on his leg to deal with the ongoing pain and other complications, according to WCCO.
In 2019, he filed a medical malpractice suit in U.S. district court against St. Cloud Orthopedics, the private practice that employed the surgeon and the PA. (Under Minnesota law, an employer is responsible for the actions of its employees.)
In his complaint, Mr. Thapa alleged that in treating him, “the defendants departed from accepted standards of medical practice.” Among other things, he claimed that Dr. Holien and the PA had not properly evaluated his postoperative symptoms, failed to diagnose and treat his compartment syndrome, and improperly discharged him from the hospital. These lapses, Mr. Thapa said, led to his “severe, permanent, and disabling injuries.”
The federal jury agreed. After a weeklong trial, it awarded the plaintiff $100 million for future “pain, disability, disfigurement, embarrassment, and emotional distress.” It also gave him $10 million for past suffering and a little more than $1 million for past and future medical bills.
In a postverdict statement, Mr. Thapa’s attorney said that, while the surgeon and PA are undoubtedly good providers, they made mistakes in this case.
A defense attorney for St. Cloud Orthopedics disputes this: “We maintain the care provided in this case was in accordance with accepted standards of care.”
At press time, the defense had not determined whether to appeal the jury’s $111 million verdict. “St. Cloud continues to support its providers,” said the clinic’s defense attorney. “We are evaluating our options regarding this verdict.”
The content contained in this article is for informational purposes only and does not constitute legal advice. Reliance on any information provided in this article is solely at your own risk.
A version of this article first appeared on Medscape.com.
Microbiome’s new happy place: The beer gut
Your gut microbiome will thank you later
A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?
In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.
Beer? Yes. Beer.
We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?
In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.
So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
We’ve lost our minds, but at least we know how fast they’re going
The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”
When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.
To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.
That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.
The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
Missing links: A real fish story
Dear LOTME:
Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?
Restless in Roswell
Dear Restless:
The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.
For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?
The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.
“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.
In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.
So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
Can you lend me an ear?
If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?
Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?
“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.
And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”
The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!
Your gut microbiome will thank you later
A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?
In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.
Beer? Yes. Beer.
We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?
In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.
So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
We’ve lost our minds, but at least we know how fast they’re going
The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”
When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.
To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.
That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.
The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
Missing links: A real fish story
Dear LOTME:
Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?
Restless in Roswell
Dear Restless:
The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.
For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?
The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.
“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.
In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.
So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
Can you lend me an ear?
If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?
Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?
“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.
And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”
The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!
Your gut microbiome will thank you later
A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?
In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.
Beer? Yes. Beer.
We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?
In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.
So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
We’ve lost our minds, but at least we know how fast they’re going
The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”
When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.
To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.
That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.
The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
Missing links: A real fish story
Dear LOTME:
Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?
Restless in Roswell
Dear Restless:
The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.
For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?
The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.
“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.
In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.
So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
Can you lend me an ear?
If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?
Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?
“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.
And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”
The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!
Can too much sleep raise the risk of cancer?
The findings reveal that sleeping 10-plus hours may increase a woman’s risk of getting cancer and both men and women’s risk of dying from cancer.
The researchers say their findings may help refine sleep recommendations in Japan, which currently advise working, middle-aged adults to sleep “as long as they can.”
Based on the new findings, a sleep duration of 6-8 hours for men and 6-9 hours for women “may be the safest” regarding cancer incidence and mortality risk among Japanese adults, the authors conclude.
The findings were published online in the International Journal of Cancer.
The literature on sleep time and cancer risk is mixed. A trio of meta-analyses conducted between 2016 and 2019 found that long sleep duration, but not short, was associated with a slightly elevated risk of all cancer mortality in Asians.
A separate meta-analysis conducted in 2018 found that both short and long sleep durations were not related to cancer incidence. But in the stratified analysis, shorter sleep time was associated with 36% increased cancer risk among Asians.
To investigate further, the researchers pooled data from six population-based cohorts that included 271,694 adults – 126,930 men and 144,764 women – with 40,751 total incident cancer cases and 18,323 total cancer deaths during a follow-up lasting about 5.9 million person-years.
In the multivariable analysis, longer sleep duration was not associated with total cancer incidence in men. In women, however, sleeping 10 or more hours vs. 7 was associated with a 19% increased risk of cancer.
In addition, sleeping 10 or more hours was associated with an increased risk of dying from cancer in women (hazard ratio, 1.44) and men (HR, 1.18).
Sleeping for 5 hours or fewer, compared with 7, was not associated with cancer incidence and mortality. However, among postmenopausal women, shorter sleep durations did increase the risk of dying from cancer (HR, 1.15).
The authors highlight several strengths of the analysis, including a large sample size as well as stratification of the results by body mass index and menopause status, which has rarely been done in previous studies.
Limitations include self-reported sleep durations and lack of data on sleep quality. The researchers note that the mechanism by which sleep time may influence cancer incidence and mortality is unclear but likely to be complex and cancer site specific.
It’s also possible that reverse causation could explain associations between sleep duration and cancer occurrence and mortality – with pain from cancer, for instance, impairing sleep duration and quality. However, the sensitivity analysis found no evidence of reverse causality or other confounding factors.
Based on these findings, the researchers say sleep duration “may be an important variable to include in cancer incidence and mortality risk prediction models.”
The study had no specific funding. The authors declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The findings reveal that sleeping 10-plus hours may increase a woman’s risk of getting cancer and both men and women’s risk of dying from cancer.
The researchers say their findings may help refine sleep recommendations in Japan, which currently advise working, middle-aged adults to sleep “as long as they can.”
Based on the new findings, a sleep duration of 6-8 hours for men and 6-9 hours for women “may be the safest” regarding cancer incidence and mortality risk among Japanese adults, the authors conclude.
The findings were published online in the International Journal of Cancer.
The literature on sleep time and cancer risk is mixed. A trio of meta-analyses conducted between 2016 and 2019 found that long sleep duration, but not short, was associated with a slightly elevated risk of all cancer mortality in Asians.
A separate meta-analysis conducted in 2018 found that both short and long sleep durations were not related to cancer incidence. But in the stratified analysis, shorter sleep time was associated with 36% increased cancer risk among Asians.
To investigate further, the researchers pooled data from six population-based cohorts that included 271,694 adults – 126,930 men and 144,764 women – with 40,751 total incident cancer cases and 18,323 total cancer deaths during a follow-up lasting about 5.9 million person-years.
In the multivariable analysis, longer sleep duration was not associated with total cancer incidence in men. In women, however, sleeping 10 or more hours vs. 7 was associated with a 19% increased risk of cancer.
In addition, sleeping 10 or more hours was associated with an increased risk of dying from cancer in women (hazard ratio, 1.44) and men (HR, 1.18).
Sleeping for 5 hours or fewer, compared with 7, was not associated with cancer incidence and mortality. However, among postmenopausal women, shorter sleep durations did increase the risk of dying from cancer (HR, 1.15).
The authors highlight several strengths of the analysis, including a large sample size as well as stratification of the results by body mass index and menopause status, which has rarely been done in previous studies.
Limitations include self-reported sleep durations and lack of data on sleep quality. The researchers note that the mechanism by which sleep time may influence cancer incidence and mortality is unclear but likely to be complex and cancer site specific.
It’s also possible that reverse causation could explain associations between sleep duration and cancer occurrence and mortality – with pain from cancer, for instance, impairing sleep duration and quality. However, the sensitivity analysis found no evidence of reverse causality or other confounding factors.
Based on these findings, the researchers say sleep duration “may be an important variable to include in cancer incidence and mortality risk prediction models.”
The study had no specific funding. The authors declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The findings reveal that sleeping 10-plus hours may increase a woman’s risk of getting cancer and both men and women’s risk of dying from cancer.
The researchers say their findings may help refine sleep recommendations in Japan, which currently advise working, middle-aged adults to sleep “as long as they can.”
Based on the new findings, a sleep duration of 6-8 hours for men and 6-9 hours for women “may be the safest” regarding cancer incidence and mortality risk among Japanese adults, the authors conclude.
The findings were published online in the International Journal of Cancer.
The literature on sleep time and cancer risk is mixed. A trio of meta-analyses conducted between 2016 and 2019 found that long sleep duration, but not short, was associated with a slightly elevated risk of all cancer mortality in Asians.
A separate meta-analysis conducted in 2018 found that both short and long sleep durations were not related to cancer incidence. But in the stratified analysis, shorter sleep time was associated with 36% increased cancer risk among Asians.
To investigate further, the researchers pooled data from six population-based cohorts that included 271,694 adults – 126,930 men and 144,764 women – with 40,751 total incident cancer cases and 18,323 total cancer deaths during a follow-up lasting about 5.9 million person-years.
In the multivariable analysis, longer sleep duration was not associated with total cancer incidence in men. In women, however, sleeping 10 or more hours vs. 7 was associated with a 19% increased risk of cancer.
In addition, sleeping 10 or more hours was associated with an increased risk of dying from cancer in women (hazard ratio, 1.44) and men (HR, 1.18).
Sleeping for 5 hours or fewer, compared with 7, was not associated with cancer incidence and mortality. However, among postmenopausal women, shorter sleep durations did increase the risk of dying from cancer (HR, 1.15).
The authors highlight several strengths of the analysis, including a large sample size as well as stratification of the results by body mass index and menopause status, which has rarely been done in previous studies.
Limitations include self-reported sleep durations and lack of data on sleep quality. The researchers note that the mechanism by which sleep time may influence cancer incidence and mortality is unclear but likely to be complex and cancer site specific.
It’s also possible that reverse causation could explain associations between sleep duration and cancer occurrence and mortality – with pain from cancer, for instance, impairing sleep duration and quality. However, the sensitivity analysis found no evidence of reverse causality or other confounding factors.
Based on these findings, the researchers say sleep duration “may be an important variable to include in cancer incidence and mortality risk prediction models.”
The study had no specific funding. The authors declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
FROM THE INTERNATIONAL JOURNAL OF CANCER
Physician convicted in $10M veteran insurance fraud scheme
A federal jury found Alexander, Ark., family physician Joe David May, MD, known locally as “Jay,” guilty on all 22 counts for which he was indicted in a multi-million-dollar conspiracy to defraud TRICARE, the federal insurance program for U.S. veterans.
. A pharmacy promoter paid recruiters to find TRICARE beneficiaries, then paid Dr. May and other medical professionals to rubber-stamp prescriptions for pain cream, whether or not the patients needed it.
As a result of this scheme, TRICARE paid more than $12 million for compounded drugs. Dr. May, according to evidence presented at the trial, wrote 226 prescriptions over the course of 10 months, costing TRICARE $4.63 million. All but one of these prescriptions were supplied by pharmaceutical sales representatives Glenn Hudson and Derek Clifton, according to federal officials. The sales reps passed the prescriptions to the providers, including Dr. May.
Dr. May accepted $15,000 in cash bribes and signed off on the prescriptions without consulting or examining patients to determine whether or not the prescriptions were needed. Mr. Hudson and Mr. Clifton have pleaded guilty in the scheme, according to the U.S. Department of Justice.
The conspiracy was complex and involved recruiting patients. According to prosecutors, one recruiter, for example, hosted a meeting at the Fisher Armory in North Little Rock, Ark., where he signed up patients for the drugs and offered to pay them $1,000. Thirteen of the patients from this meeting were sent to Dr. May, who signed the prescriptions. This group alone cost the veterans’ insurance program $370,000, say prosecutors. When the conspirators learned that reimbursements from TRICARE were set to decrease in May 2015, they rushed to profit from the scheme while there was still time. In April 2015 alone, Dr. May signed 59 prescriptions, contributing to the bilking of TRICARE for another $1.4 million.
According to a report in the Arkansas Democrat Gazette, Dr. May and Mr. Clifton, a former basketball coach, were longtime friends. Alexander Morgan, U.S. Attorney and one of the prosecutors in the case, said that Dr. May signed the prescriptions at the behest of Mr. Clifton. According to the Gazette report, Mr. Morgan said the scheme was successful for as long as it was because “TRICARE is not in the business of catching fraud. Tricare is in the business of delivering health care to our nation’s veterans. They trust the professionals to do the right thing.”
Dr. May is currently licensed in Arkansas to practice family medicine and emergency medicine and as a hospitalist. His license expires in September.
Dr. May is free pending a presentencing report. In addition to sentences imposed for fraud, mail fraud, falsifying records, and violation of anti kickback laws, for which he faces up to 20 years in prison, Dr. May will serve an additional 4 years for convictions on two counts of aggravated identity theft.
A version of this article first appeared on Medscape.com.
A federal jury found Alexander, Ark., family physician Joe David May, MD, known locally as “Jay,” guilty on all 22 counts for which he was indicted in a multi-million-dollar conspiracy to defraud TRICARE, the federal insurance program for U.S. veterans.
. A pharmacy promoter paid recruiters to find TRICARE beneficiaries, then paid Dr. May and other medical professionals to rubber-stamp prescriptions for pain cream, whether or not the patients needed it.
As a result of this scheme, TRICARE paid more than $12 million for compounded drugs. Dr. May, according to evidence presented at the trial, wrote 226 prescriptions over the course of 10 months, costing TRICARE $4.63 million. All but one of these prescriptions were supplied by pharmaceutical sales representatives Glenn Hudson and Derek Clifton, according to federal officials. The sales reps passed the prescriptions to the providers, including Dr. May.
Dr. May accepted $15,000 in cash bribes and signed off on the prescriptions without consulting or examining patients to determine whether or not the prescriptions were needed. Mr. Hudson and Mr. Clifton have pleaded guilty in the scheme, according to the U.S. Department of Justice.
The conspiracy was complex and involved recruiting patients. According to prosecutors, one recruiter, for example, hosted a meeting at the Fisher Armory in North Little Rock, Ark., where he signed up patients for the drugs and offered to pay them $1,000. Thirteen of the patients from this meeting were sent to Dr. May, who signed the prescriptions. This group alone cost the veterans’ insurance program $370,000, say prosecutors. When the conspirators learned that reimbursements from TRICARE were set to decrease in May 2015, they rushed to profit from the scheme while there was still time. In April 2015 alone, Dr. May signed 59 prescriptions, contributing to the bilking of TRICARE for another $1.4 million.
According to a report in the Arkansas Democrat Gazette, Dr. May and Mr. Clifton, a former basketball coach, were longtime friends. Alexander Morgan, U.S. Attorney and one of the prosecutors in the case, said that Dr. May signed the prescriptions at the behest of Mr. Clifton. According to the Gazette report, Mr. Morgan said the scheme was successful for as long as it was because “TRICARE is not in the business of catching fraud. Tricare is in the business of delivering health care to our nation’s veterans. They trust the professionals to do the right thing.”
Dr. May is currently licensed in Arkansas to practice family medicine and emergency medicine and as a hospitalist. His license expires in September.
Dr. May is free pending a presentencing report. In addition to sentences imposed for fraud, mail fraud, falsifying records, and violation of anti kickback laws, for which he faces up to 20 years in prison, Dr. May will serve an additional 4 years for convictions on two counts of aggravated identity theft.
A version of this article first appeared on Medscape.com.
A federal jury found Alexander, Ark., family physician Joe David May, MD, known locally as “Jay,” guilty on all 22 counts for which he was indicted in a multi-million-dollar conspiracy to defraud TRICARE, the federal insurance program for U.S. veterans.
. A pharmacy promoter paid recruiters to find TRICARE beneficiaries, then paid Dr. May and other medical professionals to rubber-stamp prescriptions for pain cream, whether or not the patients needed it.
As a result of this scheme, TRICARE paid more than $12 million for compounded drugs. Dr. May, according to evidence presented at the trial, wrote 226 prescriptions over the course of 10 months, costing TRICARE $4.63 million. All but one of these prescriptions were supplied by pharmaceutical sales representatives Glenn Hudson and Derek Clifton, according to federal officials. The sales reps passed the prescriptions to the providers, including Dr. May.
Dr. May accepted $15,000 in cash bribes and signed off on the prescriptions without consulting or examining patients to determine whether or not the prescriptions were needed. Mr. Hudson and Mr. Clifton have pleaded guilty in the scheme, according to the U.S. Department of Justice.
The conspiracy was complex and involved recruiting patients. According to prosecutors, one recruiter, for example, hosted a meeting at the Fisher Armory in North Little Rock, Ark., where he signed up patients for the drugs and offered to pay them $1,000. Thirteen of the patients from this meeting were sent to Dr. May, who signed the prescriptions. This group alone cost the veterans’ insurance program $370,000, say prosecutors. When the conspirators learned that reimbursements from TRICARE were set to decrease in May 2015, they rushed to profit from the scheme while there was still time. In April 2015 alone, Dr. May signed 59 prescriptions, contributing to the bilking of TRICARE for another $1.4 million.
According to a report in the Arkansas Democrat Gazette, Dr. May and Mr. Clifton, a former basketball coach, were longtime friends. Alexander Morgan, U.S. Attorney and one of the prosecutors in the case, said that Dr. May signed the prescriptions at the behest of Mr. Clifton. According to the Gazette report, Mr. Morgan said the scheme was successful for as long as it was because “TRICARE is not in the business of catching fraud. Tricare is in the business of delivering health care to our nation’s veterans. They trust the professionals to do the right thing.”
Dr. May is currently licensed in Arkansas to practice family medicine and emergency medicine and as a hospitalist. His license expires in September.
Dr. May is free pending a presentencing report. In addition to sentences imposed for fraud, mail fraud, falsifying records, and violation of anti kickback laws, for which he faces up to 20 years in prison, Dr. May will serve an additional 4 years for convictions on two counts of aggravated identity theft.
A version of this article first appeared on Medscape.com.
Opioid use in the elderly a dementia risk factor?
in new findings that suggest exposure to these drugs may be another modifiable risk factor for dementia.
“Clinicians and others may want to consider that opioid exposure in those aged 75-80 increases dementia risk, and to balance the potential benefits of opioid use in old age with adverse side effects,” said Stephen Z. Levine, PhD, professor, department of community mental health, University of Haifa (Israel).
The study was published online in the American Journal of Geriatric Psychiatry.
Widespread use
Evidence points to a relatively high rate of opioid prescriptions among older adults. A Morbidity and Mortality Weekly Report noted 19.2% of the U.S. adult population filled an opioid prescription in 2018, with the rate in those over 65 double that of adults aged 20-24 years (25% vs. 11.2%).
Disorders and illnesses for which opioids might be prescribed, including cancer and some pain conditions, “are far more prevalent in old age than at a younger age,” said Dr. Levine.
This high rate of opioid use underscores the need to consider the risks of opioid use in old age, said Dr. Levine. “Unfortunately, studies of the association between opioid use and dementia risk in old age are few, and their results are inconsistent.”
The study included 91,307 Israeli citizens aged 60 and over without dementia who were enrolled in the Meuhedet Healthcare Services, a nonprofit health maintenance organization (HMO) serving 14% of the country’s population. Meuhedet has maintained an up-to-date dementia registry since 2002.
The average age of the study sample was 68.29 years at the start of the study (in 2012).
In Israel, opioids are prescribed for a 30-day period. In this study, opioid exposure was defined as opioid medication fills covering 60 days (or two prescriptions) within a 120-day interval.
The primary outcome was incident dementia during follow-up from Jan. 1, 2013 to Oct. 30, 2017. The analysis controlled for a number of factors, including age, sex, smoking status, health conditions such as arthritis, depression, diabetes, osteoporosis, cognitive decline, vitamin deficiencies, cancer, cardiovascular conditions, and hospitalizations for falls.
Researchers also accounted for the competing risk of mortality.
During the study, 3.1% of subjects were exposed to opioids at a mean age of 73.94 years, and 5.8% of subjects developed dementia at an average age of 78.07 years.
Increased dementia risk
The risk of incident dementia was significantly increased in those exposed to opioids versus unexposed individuals in the 75- to 80-year age group (adjusted hazard ratio, 1.39; 95% confidence interval, 1.01-1.92; z statistic = 2.02; P < .05).
The authors noted the effect size for opioid exposure in this elderly age group is like other potentially modifiable risk factors for dementia, including body mass index and smoking.
The current study could not determine the biological explanation for the increased dementia risk among older opioid users. “Causal notions are challenging in observational studies and should be viewed with caution,” Dr. Levine noted.
However, a plausible mechanism highlighted in the literature is that opioids promote apoptosis of microglia and neurons that contribute to neurodegenerative diseases, he said.
The study included 14 sensitivity analyses, including those that looked at females, subjects older than 70, smokers, and groups with and without comorbid health conditions. The only sensitivity analysis that didn’t have similar findings to the primary analysis looked at dementia risk restricted to subjects without a vitamin deficiency.
“It’s reassuring that 13 or 14 sensitivity analyses found a significant association between opioid exposure and dementia risk,” said Dr. Levine.
Some prior studies did not show an association between opioid exposure and dementia risk. One possible reason for the discrepancy with the current findings is that the previous research didn’t account for age-specific opioid use effects, or the competing risk of mortality, said Dr. Levine.
Clinicians have a number of potential alternatives to opioids to treat various conditions including acetaminophen, non-steroidal anti-inflammatory drugs, amine reuptake inhibitors (ARIs), membrane stabilizers, muscle relaxants, topical capsaicin, botulinum toxin, cannabinoids, and steroids.
A limitation of the study was that it didn’t adjust for all possible comorbid health conditions, including vascular conditions, or for use of benzodiazepines, and surgical procedures.
In addition, since up to 50% of dementia cases are undetected, it’s possible some in the unexposed opioid group may actually have undiagnosed dementia, thereby reducing the effect sizes in the results.
Reverse causality is also a possibility as the neuropathological process associated with dementia could have started prior to opioid exposure. In addition, the results are limited to prolonged opioid exposure.
Interpret with caution
Commenting on the study, David Knopman, MD, a neurologist at Mayo Clinic in Rochester, Minn., whose research involves late-life cognitive disorders, was skeptical.
“On the face of it, the fact that an association was seen only in one narrow age range – 75+ to 80 years – ought to raise serious suspicion about the reliability and validity of the claim that opioid use is a risk factor for dementia, he said.
Although the researchers performed several sensitivity analyses, including accounting for mortality, “pharmacoepidemiological studies are terribly sensitive to residual biases” related to physician and patient choices related to medication use, added Dr. Knopman.
The claim that opioids are a dementia risk “should be viewed with great caution” and should not influence use of opioids where they’re truly indicated, he said.
“It would be a great pity if patients with pain requiring opioids avoid them because of fears about dementia based on the dubious relationship between age and opioid use.”
Dr. Levine and Dr. Knopman report no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
in new findings that suggest exposure to these drugs may be another modifiable risk factor for dementia.
“Clinicians and others may want to consider that opioid exposure in those aged 75-80 increases dementia risk, and to balance the potential benefits of opioid use in old age with adverse side effects,” said Stephen Z. Levine, PhD, professor, department of community mental health, University of Haifa (Israel).
The study was published online in the American Journal of Geriatric Psychiatry.
Widespread use
Evidence points to a relatively high rate of opioid prescriptions among older adults. A Morbidity and Mortality Weekly Report noted 19.2% of the U.S. adult population filled an opioid prescription in 2018, with the rate in those over 65 double that of adults aged 20-24 years (25% vs. 11.2%).
Disorders and illnesses for which opioids might be prescribed, including cancer and some pain conditions, “are far more prevalent in old age than at a younger age,” said Dr. Levine.
This high rate of opioid use underscores the need to consider the risks of opioid use in old age, said Dr. Levine. “Unfortunately, studies of the association between opioid use and dementia risk in old age are few, and their results are inconsistent.”
The study included 91,307 Israeli citizens aged 60 and over without dementia who were enrolled in the Meuhedet Healthcare Services, a nonprofit health maintenance organization (HMO) serving 14% of the country’s population. Meuhedet has maintained an up-to-date dementia registry since 2002.
The average age of the study sample was 68.29 years at the start of the study (in 2012).
In Israel, opioids are prescribed for a 30-day period. In this study, opioid exposure was defined as opioid medication fills covering 60 days (or two prescriptions) within a 120-day interval.
The primary outcome was incident dementia during follow-up from Jan. 1, 2013 to Oct. 30, 2017. The analysis controlled for a number of factors, including age, sex, smoking status, health conditions such as arthritis, depression, diabetes, osteoporosis, cognitive decline, vitamin deficiencies, cancer, cardiovascular conditions, and hospitalizations for falls.
Researchers also accounted for the competing risk of mortality.
During the study, 3.1% of subjects were exposed to opioids at a mean age of 73.94 years, and 5.8% of subjects developed dementia at an average age of 78.07 years.
Increased dementia risk
The risk of incident dementia was significantly increased in those exposed to opioids versus unexposed individuals in the 75- to 80-year age group (adjusted hazard ratio, 1.39; 95% confidence interval, 1.01-1.92; z statistic = 2.02; P < .05).
The authors noted the effect size for opioid exposure in this elderly age group is like other potentially modifiable risk factors for dementia, including body mass index and smoking.
The current study could not determine the biological explanation for the increased dementia risk among older opioid users. “Causal notions are challenging in observational studies and should be viewed with caution,” Dr. Levine noted.
However, a plausible mechanism highlighted in the literature is that opioids promote apoptosis of microglia and neurons that contribute to neurodegenerative diseases, he said.
The study included 14 sensitivity analyses, including those that looked at females, subjects older than 70, smokers, and groups with and without comorbid health conditions. The only sensitivity analysis that didn’t have similar findings to the primary analysis looked at dementia risk restricted to subjects without a vitamin deficiency.
“It’s reassuring that 13 or 14 sensitivity analyses found a significant association between opioid exposure and dementia risk,” said Dr. Levine.
Some prior studies did not show an association between opioid exposure and dementia risk. One possible reason for the discrepancy with the current findings is that the previous research didn’t account for age-specific opioid use effects, or the competing risk of mortality, said Dr. Levine.
Clinicians have a number of potential alternatives to opioids to treat various conditions including acetaminophen, non-steroidal anti-inflammatory drugs, amine reuptake inhibitors (ARIs), membrane stabilizers, muscle relaxants, topical capsaicin, botulinum toxin, cannabinoids, and steroids.
A limitation of the study was that it didn’t adjust for all possible comorbid health conditions, including vascular conditions, or for use of benzodiazepines, and surgical procedures.
In addition, since up to 50% of dementia cases are undetected, it’s possible some in the unexposed opioid group may actually have undiagnosed dementia, thereby reducing the effect sizes in the results.
Reverse causality is also a possibility as the neuropathological process associated with dementia could have started prior to opioid exposure. In addition, the results are limited to prolonged opioid exposure.
Interpret with caution
Commenting on the study, David Knopman, MD, a neurologist at Mayo Clinic in Rochester, Minn., whose research involves late-life cognitive disorders, was skeptical.
“On the face of it, the fact that an association was seen only in one narrow age range – 75+ to 80 years – ought to raise serious suspicion about the reliability and validity of the claim that opioid use is a risk factor for dementia, he said.
Although the researchers performed several sensitivity analyses, including accounting for mortality, “pharmacoepidemiological studies are terribly sensitive to residual biases” related to physician and patient choices related to medication use, added Dr. Knopman.
The claim that opioids are a dementia risk “should be viewed with great caution” and should not influence use of opioids where they’re truly indicated, he said.
“It would be a great pity if patients with pain requiring opioids avoid them because of fears about dementia based on the dubious relationship between age and opioid use.”
Dr. Levine and Dr. Knopman report no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
in new findings that suggest exposure to these drugs may be another modifiable risk factor for dementia.
“Clinicians and others may want to consider that opioid exposure in those aged 75-80 increases dementia risk, and to balance the potential benefits of opioid use in old age with adverse side effects,” said Stephen Z. Levine, PhD, professor, department of community mental health, University of Haifa (Israel).
The study was published online in the American Journal of Geriatric Psychiatry.
Widespread use
Evidence points to a relatively high rate of opioid prescriptions among older adults. A Morbidity and Mortality Weekly Report noted 19.2% of the U.S. adult population filled an opioid prescription in 2018, with the rate in those over 65 double that of adults aged 20-24 years (25% vs. 11.2%).
Disorders and illnesses for which opioids might be prescribed, including cancer and some pain conditions, “are far more prevalent in old age than at a younger age,” said Dr. Levine.
This high rate of opioid use underscores the need to consider the risks of opioid use in old age, said Dr. Levine. “Unfortunately, studies of the association between opioid use and dementia risk in old age are few, and their results are inconsistent.”
The study included 91,307 Israeli citizens aged 60 and over without dementia who were enrolled in the Meuhedet Healthcare Services, a nonprofit health maintenance organization (HMO) serving 14% of the country’s population. Meuhedet has maintained an up-to-date dementia registry since 2002.
The average age of the study sample was 68.29 years at the start of the study (in 2012).
In Israel, opioids are prescribed for a 30-day period. In this study, opioid exposure was defined as opioid medication fills covering 60 days (or two prescriptions) within a 120-day interval.
The primary outcome was incident dementia during follow-up from Jan. 1, 2013 to Oct. 30, 2017. The analysis controlled for a number of factors, including age, sex, smoking status, health conditions such as arthritis, depression, diabetes, osteoporosis, cognitive decline, vitamin deficiencies, cancer, cardiovascular conditions, and hospitalizations for falls.
Researchers also accounted for the competing risk of mortality.
During the study, 3.1% of subjects were exposed to opioids at a mean age of 73.94 years, and 5.8% of subjects developed dementia at an average age of 78.07 years.
Increased dementia risk
The risk of incident dementia was significantly increased in those exposed to opioids versus unexposed individuals in the 75- to 80-year age group (adjusted hazard ratio, 1.39; 95% confidence interval, 1.01-1.92; z statistic = 2.02; P < .05).
The authors noted the effect size for opioid exposure in this elderly age group is like other potentially modifiable risk factors for dementia, including body mass index and smoking.
The current study could not determine the biological explanation for the increased dementia risk among older opioid users. “Causal notions are challenging in observational studies and should be viewed with caution,” Dr. Levine noted.
However, a plausible mechanism highlighted in the literature is that opioids promote apoptosis of microglia and neurons that contribute to neurodegenerative diseases, he said.
The study included 14 sensitivity analyses, including those that looked at females, subjects older than 70, smokers, and groups with and without comorbid health conditions. The only sensitivity analysis that didn’t have similar findings to the primary analysis looked at dementia risk restricted to subjects without a vitamin deficiency.
“It’s reassuring that 13 or 14 sensitivity analyses found a significant association between opioid exposure and dementia risk,” said Dr. Levine.
Some prior studies did not show an association between opioid exposure and dementia risk. One possible reason for the discrepancy with the current findings is that the previous research didn’t account for age-specific opioid use effects, or the competing risk of mortality, said Dr. Levine.
Clinicians have a number of potential alternatives to opioids to treat various conditions including acetaminophen, non-steroidal anti-inflammatory drugs, amine reuptake inhibitors (ARIs), membrane stabilizers, muscle relaxants, topical capsaicin, botulinum toxin, cannabinoids, and steroids.
A limitation of the study was that it didn’t adjust for all possible comorbid health conditions, including vascular conditions, or for use of benzodiazepines, and surgical procedures.
In addition, since up to 50% of dementia cases are undetected, it’s possible some in the unexposed opioid group may actually have undiagnosed dementia, thereby reducing the effect sizes in the results.
Reverse causality is also a possibility as the neuropathological process associated with dementia could have started prior to opioid exposure. In addition, the results are limited to prolonged opioid exposure.
Interpret with caution
Commenting on the study, David Knopman, MD, a neurologist at Mayo Clinic in Rochester, Minn., whose research involves late-life cognitive disorders, was skeptical.
“On the face of it, the fact that an association was seen only in one narrow age range – 75+ to 80 years – ought to raise serious suspicion about the reliability and validity of the claim that opioid use is a risk factor for dementia, he said.
Although the researchers performed several sensitivity analyses, including accounting for mortality, “pharmacoepidemiological studies are terribly sensitive to residual biases” related to physician and patient choices related to medication use, added Dr. Knopman.
The claim that opioids are a dementia risk “should be viewed with great caution” and should not influence use of opioids where they’re truly indicated, he said.
“It would be a great pity if patients with pain requiring opioids avoid them because of fears about dementia based on the dubious relationship between age and opioid use.”
Dr. Levine and Dr. Knopman report no relevant financial disclosures.
A version of this article first appeared on Medscape.com.
FROM AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
Genetic testing for best antidepressant accurate, cost effective
new research suggests.
CYP2D6 and CYP2C19, from the cytochrome P450 family, are involved in the metabolism and elimination of various molecules, including medications. Variants in the genes encoding these enzymes affect the speed at which drugs are metabolized, altering their pharmacokinetic profiles.
The researchers studied 125 patients with MDD and used CYP2D6 and CYP2C19 genotyping to determine the presence of actionable phenotypes in line with Food and Drug Administration labeling.
They found that, in many cases, pharmacogenetic testing could have predicted poor response to the initial treatment selection and could have helped guide subsequent choices to improve outcomes.
In addition, a pharmacoeconomic evaluation that combined direct and indirect costs resulting from MDD with the prevalence of CYP2D6 and CYP2C19 phenotypes showed that testing for functional variants in both genes would be cost effective at a national level.
Had psychiatrists who treated patients in the study known about their metabolizing profiles, it “might have contributed to switches in medication” and could have reduced “delays in response,” said lead researcher Alessio Squassina, PhD, associate professor of pharmacology at the University of Cagliari (Italy).
The findings were presented at the European Psychiatric Association 2022 Congress.
Highly variable response rates
Dr. Squassina noted that the response to antidepressants is a “highly variable trait,” and while it is known that genetics play a role, their contribution is “still not completely understood.”
He explained that the use of pharmacogenetics, which leverages genetic information to guide treatment decision-making, has increased significantly.
While regulatory bodies, including the FDA, have been “very active” in defining strict criteria for interpreting the information from pharmacogenetic tests, there remains some “discrepancy” in their clinical utility.
Dr. Squassina said the FDA provides guidance on use of genetic testing on the labels of 34 psychiatric medications. Of these, 79% relate to CYP2D6, 12% relate to CYP2C19, and 9% relate to other genes.
These labels provide guidance on when genetic testing is recommended or required, as well as potentially clinically actionable gene-drug associations in patients with certain functional alleles.
However, Dr. Squassina noted that the distribution of such alleles is not the same across Europe, so it’s possible that a psychiatrist in Italy may be less likely to treat a patient with a phenotype affecting response to treatment or risk of adverse events than one in Norway or Sweden.
For the study, the investigators examined the frequency of CYP2D6 and CYP2C19 phenotypes in psychiatric patients in Sardinia and their relationship with pharmacologic treatment and cost-effectiveness.
They set out to recruit 200 patients with MDD who had a documented 5-year medical and treatment history, including alterations in treatment, adverse events, hospitalizations, suicide, and symptom scores, as well as sociodemographic variables.
An interim analysis of the first 125 patients recruited to the study showed that the most common CYP2D6 phenotype was normal metabolizers (NM), at 60.5%, followed by intermediate metabolizers (IM), at 28.2%, ultrarapid metabolizers (UR), at 8.9%, and poor metabolizers (PM), at 2.4%.
For CYP2C19, the most common phenotype was NM (49%), followed by IM (29.0%), UR (25.0%), and PM (4.0%). While there were differences in the overall European averages, they were not significant.
To highlight the potential impact that pharmacogenetic testing could have had on patient care and outcome, Dr. Squassina highlighted two cases.
The first concerned a patient with a CYP2D6 IM and CYP2C19 UR phenotype, who did not respond to escitalopram. The FDA drug label indicates this phenotype is actionable and recommends an alternative drug.
The patient was subsequently switched to venlafaxine. The FDA drug label on venlafaxine notes that patients with this phenotype are likely to have a suboptimal response to this drug, and again, this patient did not respond to treatment.
Another patient with a CYP2D6 NM and CYP2C19 IM phenotype was also prescribed escitalopram. The FDA label on this drug notes that patients with this phenotype can try venlafaxine but may not respond. Indeed, this patient did not respond and was switched to venlafaxine and started responding.
“The psychiatrists [in these cases] may made have made different [drug] choices if they had known the genotypes in advance,” Dr. Squassina said.
Cost effective?
To determine the cost-effectiveness of screening for CYP2D6 and CYP2C19 phenotypes in patients with MDD, the researchers used real-world data to develop a Markov model with a hypothetical cohort of 2000 MDD patients, half of whom underwent pharmacogenetic testing, to determine the potential impact on outcomes over an 18-week period.
The model included the cost of medications and hospitalization, psychiatric counseling, loss of productivity, and the estimated probability of response and adverse events, adjusted for the patient’s likelihood of having a particular metabolizing phenotype.
Results showed that, for CYP2C19, compared to no testing, pharmacogenetic testing would be cost-effective at an incremental cost-effective ratio (ICER) of €60,000 ($64,000 USD) per quality-adjusted life-year (QALY).
This, Squassina said, is “below the willingness to pay threshold” for health authorities in developed countries.
For CYP2D6, pharmacogenetic testing would become cost-effective at an ICER of approximately €47,000 ($40,000 USD) per QALY.
The team plans to complete recruitment and perform a “detailed evaluation of all the variables, especially those relating to the medication history and changes in dosage, and adverse drug reactions.” The researchers would also like to study genetic phenotypes for other metabolizing enzymes and repeat the pharmacoeconomic analysis with the complete dataset.
A glimpse into the future
Approached for comment, Alessandro Serretti, MD, PhD, department of biomedical and neuromotor sciences, University of Bologna (Italy), who was not involved in the study, said the findings show there is a “small but evident benefit” from CYP profiling, “which makes sense.”
He added that in the Netherlands and other European countries, efforts are already underway to record the CYP status of patients at a national level. “Sooner or later, all Western countries will implement it as a routine,” he said in an interview.
He explained that, when such testing is widely available, electronic health record data will allow physicians to immediately select the optimal antidepressant for an individual patient. This will end the current trial-and-error process that leads to delayed treatment and will help avoid serious consequences, such as suicide.
While reducing a single patient’s treatment by a few weeks with the most appropriate antidepressant choice does not make a large difference in the cost per episode, at a population level, it has the potential to make a significant difference.
Dr. Serretti does not envisage genotyping all 333 million Europeans for the CYP phenotype at this point but imagines that in the future, individuals will undergo whole-genome sequencing to determine risks for cancer, dementia, and heart disease, at which point they will also undergo CYP functional allele profiling, and all these data will be recorded on individuals’ EHR.
“So, every doctor, a psychiatrist or cardiologist, can see everything, whenever they need it,” he said.
The study was funded by Fondazione di Sardegna and Regione Autonoma della Sardegna. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
CYP2D6 and CYP2C19, from the cytochrome P450 family, are involved in the metabolism and elimination of various molecules, including medications. Variants in the genes encoding these enzymes affect the speed at which drugs are metabolized, altering their pharmacokinetic profiles.
The researchers studied 125 patients with MDD and used CYP2D6 and CYP2C19 genotyping to determine the presence of actionable phenotypes in line with Food and Drug Administration labeling.
They found that, in many cases, pharmacogenetic testing could have predicted poor response to the initial treatment selection and could have helped guide subsequent choices to improve outcomes.
In addition, a pharmacoeconomic evaluation that combined direct and indirect costs resulting from MDD with the prevalence of CYP2D6 and CYP2C19 phenotypes showed that testing for functional variants in both genes would be cost effective at a national level.
Had psychiatrists who treated patients in the study known about their metabolizing profiles, it “might have contributed to switches in medication” and could have reduced “delays in response,” said lead researcher Alessio Squassina, PhD, associate professor of pharmacology at the University of Cagliari (Italy).
The findings were presented at the European Psychiatric Association 2022 Congress.
Highly variable response rates
Dr. Squassina noted that the response to antidepressants is a “highly variable trait,” and while it is known that genetics play a role, their contribution is “still not completely understood.”
He explained that the use of pharmacogenetics, which leverages genetic information to guide treatment decision-making, has increased significantly.
While regulatory bodies, including the FDA, have been “very active” in defining strict criteria for interpreting the information from pharmacogenetic tests, there remains some “discrepancy” in their clinical utility.
Dr. Squassina said the FDA provides guidance on use of genetic testing on the labels of 34 psychiatric medications. Of these, 79% relate to CYP2D6, 12% relate to CYP2C19, and 9% relate to other genes.
These labels provide guidance on when genetic testing is recommended or required, as well as potentially clinically actionable gene-drug associations in patients with certain functional alleles.
However, Dr. Squassina noted that the distribution of such alleles is not the same across Europe, so it’s possible that a psychiatrist in Italy may be less likely to treat a patient with a phenotype affecting response to treatment or risk of adverse events than one in Norway or Sweden.
For the study, the investigators examined the frequency of CYP2D6 and CYP2C19 phenotypes in psychiatric patients in Sardinia and their relationship with pharmacologic treatment and cost-effectiveness.
They set out to recruit 200 patients with MDD who had a documented 5-year medical and treatment history, including alterations in treatment, adverse events, hospitalizations, suicide, and symptom scores, as well as sociodemographic variables.
An interim analysis of the first 125 patients recruited to the study showed that the most common CYP2D6 phenotype was normal metabolizers (NM), at 60.5%, followed by intermediate metabolizers (IM), at 28.2%, ultrarapid metabolizers (UR), at 8.9%, and poor metabolizers (PM), at 2.4%.
For CYP2C19, the most common phenotype was NM (49%), followed by IM (29.0%), UR (25.0%), and PM (4.0%). While there were differences in the overall European averages, they were not significant.
To highlight the potential impact that pharmacogenetic testing could have had on patient care and outcome, Dr. Squassina highlighted two cases.
The first concerned a patient with a CYP2D6 IM and CYP2C19 UR phenotype, who did not respond to escitalopram. The FDA drug label indicates this phenotype is actionable and recommends an alternative drug.
The patient was subsequently switched to venlafaxine. The FDA drug label on venlafaxine notes that patients with this phenotype are likely to have a suboptimal response to this drug, and again, this patient did not respond to treatment.
Another patient with a CYP2D6 NM and CYP2C19 IM phenotype was also prescribed escitalopram. The FDA label on this drug notes that patients with this phenotype can try venlafaxine but may not respond. Indeed, this patient did not respond and was switched to venlafaxine and started responding.
“The psychiatrists [in these cases] may made have made different [drug] choices if they had known the genotypes in advance,” Dr. Squassina said.
Cost effective?
To determine the cost-effectiveness of screening for CYP2D6 and CYP2C19 phenotypes in patients with MDD, the researchers used real-world data to develop a Markov model with a hypothetical cohort of 2000 MDD patients, half of whom underwent pharmacogenetic testing, to determine the potential impact on outcomes over an 18-week period.
The model included the cost of medications and hospitalization, psychiatric counseling, loss of productivity, and the estimated probability of response and adverse events, adjusted for the patient’s likelihood of having a particular metabolizing phenotype.
Results showed that, for CYP2C19, compared to no testing, pharmacogenetic testing would be cost-effective at an incremental cost-effective ratio (ICER) of €60,000 ($64,000 USD) per quality-adjusted life-year (QALY).
This, Squassina said, is “below the willingness to pay threshold” for health authorities in developed countries.
For CYP2D6, pharmacogenetic testing would become cost-effective at an ICER of approximately €47,000 ($40,000 USD) per QALY.
The team plans to complete recruitment and perform a “detailed evaluation of all the variables, especially those relating to the medication history and changes in dosage, and adverse drug reactions.” The researchers would also like to study genetic phenotypes for other metabolizing enzymes and repeat the pharmacoeconomic analysis with the complete dataset.
A glimpse into the future
Approached for comment, Alessandro Serretti, MD, PhD, department of biomedical and neuromotor sciences, University of Bologna (Italy), who was not involved in the study, said the findings show there is a “small but evident benefit” from CYP profiling, “which makes sense.”
He added that in the Netherlands and other European countries, efforts are already underway to record the CYP status of patients at a national level. “Sooner or later, all Western countries will implement it as a routine,” he said in an interview.
He explained that, when such testing is widely available, electronic health record data will allow physicians to immediately select the optimal antidepressant for an individual patient. This will end the current trial-and-error process that leads to delayed treatment and will help avoid serious consequences, such as suicide.
While reducing a single patient’s treatment by a few weeks with the most appropriate antidepressant choice does not make a large difference in the cost per episode, at a population level, it has the potential to make a significant difference.
Dr. Serretti does not envisage genotyping all 333 million Europeans for the CYP phenotype at this point but imagines that in the future, individuals will undergo whole-genome sequencing to determine risks for cancer, dementia, and heart disease, at which point they will also undergo CYP functional allele profiling, and all these data will be recorded on individuals’ EHR.
“So, every doctor, a psychiatrist or cardiologist, can see everything, whenever they need it,” he said.
The study was funded by Fondazione di Sardegna and Regione Autonoma della Sardegna. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
CYP2D6 and CYP2C19, from the cytochrome P450 family, are involved in the metabolism and elimination of various molecules, including medications. Variants in the genes encoding these enzymes affect the speed at which drugs are metabolized, altering their pharmacokinetic profiles.
The researchers studied 125 patients with MDD and used CYP2D6 and CYP2C19 genotyping to determine the presence of actionable phenotypes in line with Food and Drug Administration labeling.
They found that, in many cases, pharmacogenetic testing could have predicted poor response to the initial treatment selection and could have helped guide subsequent choices to improve outcomes.
In addition, a pharmacoeconomic evaluation that combined direct and indirect costs resulting from MDD with the prevalence of CYP2D6 and CYP2C19 phenotypes showed that testing for functional variants in both genes would be cost effective at a national level.
Had psychiatrists who treated patients in the study known about their metabolizing profiles, it “might have contributed to switches in medication” and could have reduced “delays in response,” said lead researcher Alessio Squassina, PhD, associate professor of pharmacology at the University of Cagliari (Italy).
The findings were presented at the European Psychiatric Association 2022 Congress.
Highly variable response rates
Dr. Squassina noted that the response to antidepressants is a “highly variable trait,” and while it is known that genetics play a role, their contribution is “still not completely understood.”
He explained that the use of pharmacogenetics, which leverages genetic information to guide treatment decision-making, has increased significantly.
While regulatory bodies, including the FDA, have been “very active” in defining strict criteria for interpreting the information from pharmacogenetic tests, there remains some “discrepancy” in their clinical utility.
Dr. Squassina said the FDA provides guidance on use of genetic testing on the labels of 34 psychiatric medications. Of these, 79% relate to CYP2D6, 12% relate to CYP2C19, and 9% relate to other genes.
These labels provide guidance on when genetic testing is recommended or required, as well as potentially clinically actionable gene-drug associations in patients with certain functional alleles.
However, Dr. Squassina noted that the distribution of such alleles is not the same across Europe, so it’s possible that a psychiatrist in Italy may be less likely to treat a patient with a phenotype affecting response to treatment or risk of adverse events than one in Norway or Sweden.
For the study, the investigators examined the frequency of CYP2D6 and CYP2C19 phenotypes in psychiatric patients in Sardinia and their relationship with pharmacologic treatment and cost-effectiveness.
They set out to recruit 200 patients with MDD who had a documented 5-year medical and treatment history, including alterations in treatment, adverse events, hospitalizations, suicide, and symptom scores, as well as sociodemographic variables.
An interim analysis of the first 125 patients recruited to the study showed that the most common CYP2D6 phenotype was normal metabolizers (NM), at 60.5%, followed by intermediate metabolizers (IM), at 28.2%, ultrarapid metabolizers (UR), at 8.9%, and poor metabolizers (PM), at 2.4%.
For CYP2C19, the most common phenotype was NM (49%), followed by IM (29.0%), UR (25.0%), and PM (4.0%). While there were differences in the overall European averages, they were not significant.
To highlight the potential impact that pharmacogenetic testing could have had on patient care and outcome, Dr. Squassina highlighted two cases.
The first concerned a patient with a CYP2D6 IM and CYP2C19 UR phenotype, who did not respond to escitalopram. The FDA drug label indicates this phenotype is actionable and recommends an alternative drug.
The patient was subsequently switched to venlafaxine. The FDA drug label on venlafaxine notes that patients with this phenotype are likely to have a suboptimal response to this drug, and again, this patient did not respond to treatment.
Another patient with a CYP2D6 NM and CYP2C19 IM phenotype was also prescribed escitalopram. The FDA label on this drug notes that patients with this phenotype can try venlafaxine but may not respond. Indeed, this patient did not respond and was switched to venlafaxine and started responding.
“The psychiatrists [in these cases] may made have made different [drug] choices if they had known the genotypes in advance,” Dr. Squassina said.
Cost effective?
To determine the cost-effectiveness of screening for CYP2D6 and CYP2C19 phenotypes in patients with MDD, the researchers used real-world data to develop a Markov model with a hypothetical cohort of 2000 MDD patients, half of whom underwent pharmacogenetic testing, to determine the potential impact on outcomes over an 18-week period.
The model included the cost of medications and hospitalization, psychiatric counseling, loss of productivity, and the estimated probability of response and adverse events, adjusted for the patient’s likelihood of having a particular metabolizing phenotype.
Results showed that, for CYP2C19, compared to no testing, pharmacogenetic testing would be cost-effective at an incremental cost-effective ratio (ICER) of €60,000 ($64,000 USD) per quality-adjusted life-year (QALY).
This, Squassina said, is “below the willingness to pay threshold” for health authorities in developed countries.
For CYP2D6, pharmacogenetic testing would become cost-effective at an ICER of approximately €47,000 ($40,000 USD) per QALY.
The team plans to complete recruitment and perform a “detailed evaluation of all the variables, especially those relating to the medication history and changes in dosage, and adverse drug reactions.” The researchers would also like to study genetic phenotypes for other metabolizing enzymes and repeat the pharmacoeconomic analysis with the complete dataset.
A glimpse into the future
Approached for comment, Alessandro Serretti, MD, PhD, department of biomedical and neuromotor sciences, University of Bologna (Italy), who was not involved in the study, said the findings show there is a “small but evident benefit” from CYP profiling, “which makes sense.”
He added that in the Netherlands and other European countries, efforts are already underway to record the CYP status of patients at a national level. “Sooner or later, all Western countries will implement it as a routine,” he said in an interview.
He explained that, when such testing is widely available, electronic health record data will allow physicians to immediately select the optimal antidepressant for an individual patient. This will end the current trial-and-error process that leads to delayed treatment and will help avoid serious consequences, such as suicide.
While reducing a single patient’s treatment by a few weeks with the most appropriate antidepressant choice does not make a large difference in the cost per episode, at a population level, it has the potential to make a significant difference.
Dr. Serretti does not envisage genotyping all 333 million Europeans for the CYP phenotype at this point but imagines that in the future, individuals will undergo whole-genome sequencing to determine risks for cancer, dementia, and heart disease, at which point they will also undergo CYP functional allele profiling, and all these data will be recorded on individuals’ EHR.
“So, every doctor, a psychiatrist or cardiologist, can see everything, whenever they need it,” he said.
The study was funded by Fondazione di Sardegna and Regione Autonoma della Sardegna. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM EPA 2022
Insurer told to pay $5.2 million to woman who caught STD in a car
A Missouri lawsuit adds a new twist to the kind of “bodily harm” in a car that’s covered by insurance.
On June 7,
The woman, identified in court documents as M.O., said she contracted human papillomavirus from her boyfriend. She said he knew he had the disease but didn’t tell her.
An arbitrator found in May 2021 that the in-car sex had “directly caused, or directly contributed to cause” the STD transmission. The man was found liable. The woman was awarded $5.2 million to be paid by GEICO, which insured the man’s vehicle.
GEICO filed for the award to be overturned, alleging it had been denied due process and that the arbitration deal was unenforceable.
Court documents show that GEICO claimed the man’s policy covered only injuries that came “out of the ownership, maintenance or use of the ... auto” and that the woman’s “injuries arose from an intervening cause – namely, her failure to prevent transmission of STDs by having unprotected sex.”
The state appellate panel ruled that the lower court made no mistake in the case and upheld the decision.
The Kansas City Star reported that one of the judges concurred but said GEICO was offered “no meaningful opportunity to participate” in the lawsuit and existing law “relegat(es) the insurer to the status of a bystander.”
“This case presents novel and potentially important issues about whether an insurance carrier can be held liable under such policies for the consequences of two adults voluntarily having unprotected sex in the insured’s automobile,” noted U.S. Magistrate Judge Angel D. Mitchell in court documents. “Interpretation of these policies could have far-reaching implications for other policies with similar terms.”
A version of this article first appeared on WebMD.com.
A Missouri lawsuit adds a new twist to the kind of “bodily harm” in a car that’s covered by insurance.
On June 7,
The woman, identified in court documents as M.O., said she contracted human papillomavirus from her boyfriend. She said he knew he had the disease but didn’t tell her.
An arbitrator found in May 2021 that the in-car sex had “directly caused, or directly contributed to cause” the STD transmission. The man was found liable. The woman was awarded $5.2 million to be paid by GEICO, which insured the man’s vehicle.
GEICO filed for the award to be overturned, alleging it had been denied due process and that the arbitration deal was unenforceable.
Court documents show that GEICO claimed the man’s policy covered only injuries that came “out of the ownership, maintenance or use of the ... auto” and that the woman’s “injuries arose from an intervening cause – namely, her failure to prevent transmission of STDs by having unprotected sex.”
The state appellate panel ruled that the lower court made no mistake in the case and upheld the decision.
The Kansas City Star reported that one of the judges concurred but said GEICO was offered “no meaningful opportunity to participate” in the lawsuit and existing law “relegat(es) the insurer to the status of a bystander.”
“This case presents novel and potentially important issues about whether an insurance carrier can be held liable under such policies for the consequences of two adults voluntarily having unprotected sex in the insured’s automobile,” noted U.S. Magistrate Judge Angel D. Mitchell in court documents. “Interpretation of these policies could have far-reaching implications for other policies with similar terms.”
A version of this article first appeared on WebMD.com.
A Missouri lawsuit adds a new twist to the kind of “bodily harm” in a car that’s covered by insurance.
On June 7,
The woman, identified in court documents as M.O., said she contracted human papillomavirus from her boyfriend. She said he knew he had the disease but didn’t tell her.
An arbitrator found in May 2021 that the in-car sex had “directly caused, or directly contributed to cause” the STD transmission. The man was found liable. The woman was awarded $5.2 million to be paid by GEICO, which insured the man’s vehicle.
GEICO filed for the award to be overturned, alleging it had been denied due process and that the arbitration deal was unenforceable.
Court documents show that GEICO claimed the man’s policy covered only injuries that came “out of the ownership, maintenance or use of the ... auto” and that the woman’s “injuries arose from an intervening cause – namely, her failure to prevent transmission of STDs by having unprotected sex.”
The state appellate panel ruled that the lower court made no mistake in the case and upheld the decision.
The Kansas City Star reported that one of the judges concurred but said GEICO was offered “no meaningful opportunity to participate” in the lawsuit and existing law “relegat(es) the insurer to the status of a bystander.”
“This case presents novel and potentially important issues about whether an insurance carrier can be held liable under such policies for the consequences of two adults voluntarily having unprotected sex in the insured’s automobile,” noted U.S. Magistrate Judge Angel D. Mitchell in court documents. “Interpretation of these policies could have far-reaching implications for other policies with similar terms.”
A version of this article first appeared on WebMD.com.
ADA updates on finerenone, SGLT2 inhibitors, and race-based eGFR
As it gears up for the first in-person scientific sessions for 3 years, the American Diabetes Association has issued an addendum to its most recent annual clinical practice recommendations published in December 2021, the 2022 Standards of Medical Care in Diabetes, based on recent trial evidence and consensus.
The update informs clinicians about:
- The effect of the nonsteroidal mineralocorticoid antagonist (Kerendia) on cardiovascular outcomes in patients with type 2 diabetes and chronic kidney disease.
- The effect of a sodium-glucose cotransporter 2 (SGLT2) inhibitor on heart failure and renal outcomes in patients with type 2 diabetes.
The National Kidney Foundation and the American Society of Nephrology Task Force recommendation to remove race in the formula for calculating estimated glomerular filtration rate (eGFR).
“This is the fifth year that we are able to update the Standards of Care after it has been published through our Living Standards of Care updates, making it possible to give diabetes care providers the most important information and the latest evidence relevant to their practice,” Robert A. Gabbay, MD, PhD, ADA chief scientific and medical officer, said in a press release from the organization.
The addendum, entitled, “Living Standards of Care,” updates Section 10, “Cardiovascular Disease and Risk Management,” and Section 11, “Chronic Kidney Disease and Risk Management” of the 2022 Standards of Medical Care in Diabetes.
The amendments were approved by the ADA Professional Practice Committee, which is responsible for developing the Standards of Care. The American College of Cardiology reviewed and endorsed the section on CVD and risk management.
The Living Standards Update was published online in Diabetes Care.
CVD and risk management
In the Addendum to Section 10, “Cardiovascular Disease and Risk Management,” the committee writes:
- “For patients with type 2 diabetes and chronic kidney disease treated with maximum tolerated doses of ACE inhibitors or angiotensin receptor blockers, addition of finerenone should be considered to improve cardiovascular outcomes and reduce the risk of chronic kidney disease progression. A”
- “Patients with type 2 diabetes and chronic kidney disease should be considered for treatment with finerenone to reduce cardiovascular outcomes and the risk of chronic kidney disease progression.”
- “In patients with type 2 diabetes and established heart failure with either preserved or reduced ejection fraction, an SGLT2 inhibitor [with proven benefit in this patient population] is recommended to reduce risk of worsening heart failure, hospitalizations for heart failure, and cardiovascular death. ”
In the section “Statin Treatment,” the addendum no longer states that “a prospective trial of a newer fibrate ... is ongoing,” because that trial investigating pemafibrate (Kowa), a novel selective peroxisome proliferator-activated receptor alpha modulator (or fibrate), has been discontinued.
Chronic kidney disease and risk management
In the Addendum to Section 11, “Chronic Kidney Disease and Risk Management,” the committee writes:
- “Traditionally, eGFR is calculated from serum creatinine using a validated formula. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation is preferred. ... Historically, a correction factor for muscle mass was included in a modified equation for African Americans; however, due to various issues with inequities, it was decided to the equation such that it applies to all. Hence, a committee was convened, resulting in the recommendation for immediate implementation of the CKD-EPI creatinine equation refit without the race variable in all laboratories in the U.S.” (This is based on an National Kidney Foundation and American Society of Nephrology Task Force recommendation.)
- “Additionally, increased use of cystatin C, especially to confirm estimated GFR in adults who are at risk for or have chronic kidney disease, because combining filtration markers (creatinine and cystatin C) is more accurate and would support better clinical decisions than either marker alone.”
Evidence from clinical trials
The update is based on findings from the following clinical trials:
- Efficacy and Safety of Finerenone in Subjects With Type 2 Diabetes Mellitus and Diabetic Kidney Disease (FIDELIO-DKD)
- Efficacy and Safety of Finerenone in Subjects With Type 2 Diabetes Mellitus and the Clinical Diagnosis of Diabetic Kidney Disease (FIGARO-DKD)
- FIDELITY, a prespecified pooled analysis of FIDELIO-DKD and FIGARO-DKD
- Empagliflozin Outcome Trial in Patients With Chronic Heart Failure With Preserved Ejection Fraction (EMPEROR-Preserved)
- Effects of Dapagliflozin on Biomarkers, Symptoms and Functional Status in Patients with PRESERVED Ejection Fraction Heart Failure (PRESERVED-HF)
- Pemafibrate to Reduce Cardiovascular Outcomes by Reducing Triglycerides in Patients with Diabetes (PROMINENT).
A version of this article first appeared on Medscape.com.
As it gears up for the first in-person scientific sessions for 3 years, the American Diabetes Association has issued an addendum to its most recent annual clinical practice recommendations published in December 2021, the 2022 Standards of Medical Care in Diabetes, based on recent trial evidence and consensus.
The update informs clinicians about:
- The effect of the nonsteroidal mineralocorticoid antagonist (Kerendia) on cardiovascular outcomes in patients with type 2 diabetes and chronic kidney disease.
- The effect of a sodium-glucose cotransporter 2 (SGLT2) inhibitor on heart failure and renal outcomes in patients with type 2 diabetes.
The National Kidney Foundation and the American Society of Nephrology Task Force recommendation to remove race in the formula for calculating estimated glomerular filtration rate (eGFR).
“This is the fifth year that we are able to update the Standards of Care after it has been published through our Living Standards of Care updates, making it possible to give diabetes care providers the most important information and the latest evidence relevant to their practice,” Robert A. Gabbay, MD, PhD, ADA chief scientific and medical officer, said in a press release from the organization.
The addendum, entitled, “Living Standards of Care,” updates Section 10, “Cardiovascular Disease and Risk Management,” and Section 11, “Chronic Kidney Disease and Risk Management” of the 2022 Standards of Medical Care in Diabetes.
The amendments were approved by the ADA Professional Practice Committee, which is responsible for developing the Standards of Care. The American College of Cardiology reviewed and endorsed the section on CVD and risk management.
The Living Standards Update was published online in Diabetes Care.
CVD and risk management
In the Addendum to Section 10, “Cardiovascular Disease and Risk Management,” the committee writes:
- “For patients with type 2 diabetes and chronic kidney disease treated with maximum tolerated doses of ACE inhibitors or angiotensin receptor blockers, addition of finerenone should be considered to improve cardiovascular outcomes and reduce the risk of chronic kidney disease progression. A”
- “Patients with type 2 diabetes and chronic kidney disease should be considered for treatment with finerenone to reduce cardiovascular outcomes and the risk of chronic kidney disease progression.”
- “In patients with type 2 diabetes and established heart failure with either preserved or reduced ejection fraction, an SGLT2 inhibitor [with proven benefit in this patient population] is recommended to reduce risk of worsening heart failure, hospitalizations for heart failure, and cardiovascular death. ”
In the section “Statin Treatment,” the addendum no longer states that “a prospective trial of a newer fibrate ... is ongoing,” because that trial investigating pemafibrate (Kowa), a novel selective peroxisome proliferator-activated receptor alpha modulator (or fibrate), has been discontinued.
Chronic kidney disease and risk management
In the Addendum to Section 11, “Chronic Kidney Disease and Risk Management,” the committee writes:
- “Traditionally, eGFR is calculated from serum creatinine using a validated formula. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation is preferred. ... Historically, a correction factor for muscle mass was included in a modified equation for African Americans; however, due to various issues with inequities, it was decided to the equation such that it applies to all. Hence, a committee was convened, resulting in the recommendation for immediate implementation of the CKD-EPI creatinine equation refit without the race variable in all laboratories in the U.S.” (This is based on an National Kidney Foundation and American Society of Nephrology Task Force recommendation.)
- “Additionally, increased use of cystatin C, especially to confirm estimated GFR in adults who are at risk for or have chronic kidney disease, because combining filtration markers (creatinine and cystatin C) is more accurate and would support better clinical decisions than either marker alone.”
Evidence from clinical trials
The update is based on findings from the following clinical trials:
- Efficacy and Safety of Finerenone in Subjects With Type 2 Diabetes Mellitus and Diabetic Kidney Disease (FIDELIO-DKD)
- Efficacy and Safety of Finerenone in Subjects With Type 2 Diabetes Mellitus and the Clinical Diagnosis of Diabetic Kidney Disease (FIGARO-DKD)
- FIDELITY, a prespecified pooled analysis of FIDELIO-DKD and FIGARO-DKD
- Empagliflozin Outcome Trial in Patients With Chronic Heart Failure With Preserved Ejection Fraction (EMPEROR-Preserved)
- Effects of Dapagliflozin on Biomarkers, Symptoms and Functional Status in Patients with PRESERVED Ejection Fraction Heart Failure (PRESERVED-HF)
- Pemafibrate to Reduce Cardiovascular Outcomes by Reducing Triglycerides in Patients with Diabetes (PROMINENT).
A version of this article first appeared on Medscape.com.
As it gears up for the first in-person scientific sessions for 3 years, the American Diabetes Association has issued an addendum to its most recent annual clinical practice recommendations published in December 2021, the 2022 Standards of Medical Care in Diabetes, based on recent trial evidence and consensus.
The update informs clinicians about:
- The effect of the nonsteroidal mineralocorticoid antagonist (Kerendia) on cardiovascular outcomes in patients with type 2 diabetes and chronic kidney disease.
- The effect of a sodium-glucose cotransporter 2 (SGLT2) inhibitor on heart failure and renal outcomes in patients with type 2 diabetes.
The National Kidney Foundation and the American Society of Nephrology Task Force recommendation to remove race in the formula for calculating estimated glomerular filtration rate (eGFR).
“This is the fifth year that we are able to update the Standards of Care after it has been published through our Living Standards of Care updates, making it possible to give diabetes care providers the most important information and the latest evidence relevant to their practice,” Robert A. Gabbay, MD, PhD, ADA chief scientific and medical officer, said in a press release from the organization.
The addendum, entitled, “Living Standards of Care,” updates Section 10, “Cardiovascular Disease and Risk Management,” and Section 11, “Chronic Kidney Disease and Risk Management” of the 2022 Standards of Medical Care in Diabetes.
The amendments were approved by the ADA Professional Practice Committee, which is responsible for developing the Standards of Care. The American College of Cardiology reviewed and endorsed the section on CVD and risk management.
The Living Standards Update was published online in Diabetes Care.
CVD and risk management
In the Addendum to Section 10, “Cardiovascular Disease and Risk Management,” the committee writes:
- “For patients with type 2 diabetes and chronic kidney disease treated with maximum tolerated doses of ACE inhibitors or angiotensin receptor blockers, addition of finerenone should be considered to improve cardiovascular outcomes and reduce the risk of chronic kidney disease progression. A”
- “Patients with type 2 diabetes and chronic kidney disease should be considered for treatment with finerenone to reduce cardiovascular outcomes and the risk of chronic kidney disease progression.”
- “In patients with type 2 diabetes and established heart failure with either preserved or reduced ejection fraction, an SGLT2 inhibitor [with proven benefit in this patient population] is recommended to reduce risk of worsening heart failure, hospitalizations for heart failure, and cardiovascular death. ”
In the section “Statin Treatment,” the addendum no longer states that “a prospective trial of a newer fibrate ... is ongoing,” because that trial investigating pemafibrate (Kowa), a novel selective peroxisome proliferator-activated receptor alpha modulator (or fibrate), has been discontinued.
Chronic kidney disease and risk management
In the Addendum to Section 11, “Chronic Kidney Disease and Risk Management,” the committee writes:
- “Traditionally, eGFR is calculated from serum creatinine using a validated formula. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation is preferred. ... Historically, a correction factor for muscle mass was included in a modified equation for African Americans; however, due to various issues with inequities, it was decided to the equation such that it applies to all. Hence, a committee was convened, resulting in the recommendation for immediate implementation of the CKD-EPI creatinine equation refit without the race variable in all laboratories in the U.S.” (This is based on an National Kidney Foundation and American Society of Nephrology Task Force recommendation.)
- “Additionally, increased use of cystatin C, especially to confirm estimated GFR in adults who are at risk for or have chronic kidney disease, because combining filtration markers (creatinine and cystatin C) is more accurate and would support better clinical decisions than either marker alone.”
Evidence from clinical trials
The update is based on findings from the following clinical trials:
- Efficacy and Safety of Finerenone in Subjects With Type 2 Diabetes Mellitus and Diabetic Kidney Disease (FIDELIO-DKD)
- Efficacy and Safety of Finerenone in Subjects With Type 2 Diabetes Mellitus and the Clinical Diagnosis of Diabetic Kidney Disease (FIGARO-DKD)
- FIDELITY, a prespecified pooled analysis of FIDELIO-DKD and FIGARO-DKD
- Empagliflozin Outcome Trial in Patients With Chronic Heart Failure With Preserved Ejection Fraction (EMPEROR-Preserved)
- Effects of Dapagliflozin on Biomarkers, Symptoms and Functional Status in Patients with PRESERVED Ejection Fraction Heart Failure (PRESERVED-HF)
- Pemafibrate to Reduce Cardiovascular Outcomes by Reducing Triglycerides in Patients with Diabetes (PROMINENT).
A version of this article first appeared on Medscape.com.
FROM DIABETES CARE
FDA warning released for Volara respiratory system
The Food and Drug Administration published a warning from the medical device company Baxter International, citing problems with their device used for at-home respiratory therapy. The release cautions Volara system users that using certain therapies from the device may cause a change in lung pressure and a decrease in oxygen level. This cautionary warning was issued following a single reported case of oxygen loss while using the device.
The Volara system is meant to help patients with persistent pulmonary problems who are transitioning from the hospital to the outpatient setting. It can connect to three pieces commonly used in treating the respiratory conditions – a tracheostomy tube, a mask, and an in-line ventilator. The device offers three therapies – one to expand lungs (OLE), one to shake mucus from the lungs (CHFO), and a nebulizer to deliver medication.
This particular warning is relevant only to patients who use the system with an in-line ventilator or to patients who use OLE and CHFO therapies. The concern is that a rapid change in lung pressure (barotrauma), could damage the tissue by overextending the surface of the organ. Additionally, as noted in the reported case, Volara users may be at risk for a decrease in the level of oxygen while using the device (oxygen desaturation).
If patients have been directed to use Volara by a physician, the FDA recommends they continue to use it as prescribed. But they should look out for signs of respiratory distress. These include changes in alertness, the appearance of a blue tint around the mouth, increased breathing rate, and wheezing. If a patient or caregiver sees these signs, the patient should stop using Volara immediately and should seek help if their symptoms don’t improve.
In response to these precautions, Baxter says it will update the instructions for the use of its device and will add additional warnings. The company says it will dispatch a trainer to patients’ homes to help them understand the newest guidelines.
Both the FDA and Baxter urge patients who have experienced any problems with the device to report it to the hotlines listed at the bottom of their release.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration published a warning from the medical device company Baxter International, citing problems with their device used for at-home respiratory therapy. The release cautions Volara system users that using certain therapies from the device may cause a change in lung pressure and a decrease in oxygen level. This cautionary warning was issued following a single reported case of oxygen loss while using the device.
The Volara system is meant to help patients with persistent pulmonary problems who are transitioning from the hospital to the outpatient setting. It can connect to three pieces commonly used in treating the respiratory conditions – a tracheostomy tube, a mask, and an in-line ventilator. The device offers three therapies – one to expand lungs (OLE), one to shake mucus from the lungs (CHFO), and a nebulizer to deliver medication.
This particular warning is relevant only to patients who use the system with an in-line ventilator or to patients who use OLE and CHFO therapies. The concern is that a rapid change in lung pressure (barotrauma), could damage the tissue by overextending the surface of the organ. Additionally, as noted in the reported case, Volara users may be at risk for a decrease in the level of oxygen while using the device (oxygen desaturation).
If patients have been directed to use Volara by a physician, the FDA recommends they continue to use it as prescribed. But they should look out for signs of respiratory distress. These include changes in alertness, the appearance of a blue tint around the mouth, increased breathing rate, and wheezing. If a patient or caregiver sees these signs, the patient should stop using Volara immediately and should seek help if their symptoms don’t improve.
In response to these precautions, Baxter says it will update the instructions for the use of its device and will add additional warnings. The company says it will dispatch a trainer to patients’ homes to help them understand the newest guidelines.
Both the FDA and Baxter urge patients who have experienced any problems with the device to report it to the hotlines listed at the bottom of their release.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration published a warning from the medical device company Baxter International, citing problems with their device used for at-home respiratory therapy. The release cautions Volara system users that using certain therapies from the device may cause a change in lung pressure and a decrease in oxygen level. This cautionary warning was issued following a single reported case of oxygen loss while using the device.
The Volara system is meant to help patients with persistent pulmonary problems who are transitioning from the hospital to the outpatient setting. It can connect to three pieces commonly used in treating the respiratory conditions – a tracheostomy tube, a mask, and an in-line ventilator. The device offers three therapies – one to expand lungs (OLE), one to shake mucus from the lungs (CHFO), and a nebulizer to deliver medication.
This particular warning is relevant only to patients who use the system with an in-line ventilator or to patients who use OLE and CHFO therapies. The concern is that a rapid change in lung pressure (barotrauma), could damage the tissue by overextending the surface of the organ. Additionally, as noted in the reported case, Volara users may be at risk for a decrease in the level of oxygen while using the device (oxygen desaturation).
If patients have been directed to use Volara by a physician, the FDA recommends they continue to use it as prescribed. But they should look out for signs of respiratory distress. These include changes in alertness, the appearance of a blue tint around the mouth, increased breathing rate, and wheezing. If a patient or caregiver sees these signs, the patient should stop using Volara immediately and should seek help if their symptoms don’t improve.
In response to these precautions, Baxter says it will update the instructions for the use of its device and will add additional warnings. The company says it will dispatch a trainer to patients’ homes to help them understand the newest guidelines.
Both the FDA and Baxter urge patients who have experienced any problems with the device to report it to the hotlines listed at the bottom of their release.
A version of this article first appeared on Medscape.com.