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TikTok offers to ‘balance your hormones’ are pure hokum
With more than 306 million views, #hormonebalance and #hormonebalancing are among the latest hacks to take over the social media platform TikTok, on which users post short videos. Influencers offer advice such as eating raw carrots for “happy hormones,” eating protein followed by fat for breakfast to regulate blood glucose, or taking vitamin B2 supplements for thyroid health.
Have you ever wondered if you were asleep during the lecture on “hormone balancing” in medical school? No, you weren’t. It was never a class for good reason, and you didn’t fail to read any such breakthrough studies in The New England Journal of Medicine either.
There are over 50 different hormones produced by humans and animals, regulating sleep, growth, metabolism and reproduction, among many other biological processes, so there is certainly no one-size-fits-all solution to ensure these are all working in perfect harmony.
When someone mentions “hormone balancing,” my mind wanders to the last time I took my car to have my tires rotated and balanced. If only it were as simple to balance hormones in real life. The best we can hope for is to get a specific hormone within the ideal physiologic range for that person’s age.
The term “hormone” can mean many things to different people. When a woman comes in with a hormone question, for example, it is often related to estrogen, followed by thyroid hormones. A wealth of misinformation exists in popular literature regarding these hormones alone.
Estrogen can be replaced, but not everyone needs it replaced. It depends on variables including age, underlying medical conditions, the time of day a test was drawn, and concomitant medications. Having low levels of a given hormone does not necessarily call for replacement either.
Insulin is another example of a hormone that can never completely be replaced in people with diabetes in a way that exactly mimics the normal physiologic release.
There are many lesser-known hormones that are measurable and replaceable but are also more difficult to reset to original manufacturer specifications.
A Google search for “hormone balancing” often sends you to “naturopaths” or “integrative medicine” practitioners, who often propose similar solutions to the TikTok influencers. Users are told that their hormones are out of whack and that restoring this “balance” can be achieved by purchasing whatever “natural products” or concoction they are selling.
These TikTok videos and online “experts” are the home-brewed versions of the strip-mall hormone specialists. TikTok videos claiming to help “balance hormones” typically don’t name a specific hormone either, or the end organs that each would have an impact on. Rather, they lump all hormones into a monolithic entity, implying that there is a single solution for all health problems. And personal testimonials extolling the benefits of a TikTok intervention don’t constitute proof of efficacy no matter how many “likes” they get. These influencers assume that viewers can “sense” their hormones are out of tune and no lab tests can convince them otherwise.
In these inflationary times, the cost of seeking medical care from conventional channels is increasingly prohibitive. It’s easy to understand the appeal of getting free advice from TikTok or some other Internet site. At best, following the advice will not have much impact; at worst, it could be harmful.
Don’t try this at home
There are some things that should never be tried at home, and do-it-yourself hormone replacement or remediation both fall under this umbrella.
Generally, the body does a good job of balancing its own hormones. Most patients don’t need to be worried if they’re in good health. If they’re in doubt, they should seek advice from a doctor, ideally an endocrinologist, but an ob.gyn. or general practitioner are also good options.
One of the first questions to ask a patient is “Which hormone are you worried about?” or “What health issue is it specifically that is bothering you?” Narrowing the focus to a single thing, if possible, will lead to a more efficient evaluation.
Often, patients arrive with multiple concerns written on little pieces of paper. These ubiquitous pieces of paper are the red flag for the flood of questions to follow.
Ordering the appropriate tests for the conditions they are concerned about can help put their minds at ease. If there are any specific deficiencies, or excesses in any hormones, then appropriate solutions can be discussed.
TikTok hormone-balancing solutions are simply the 21st-century version of the snake oil sold on late-night cable TV in the 1990s.
Needless to say, you should gently encourage your patients to stay away from these non–FDA-approved products, without making them feel stupid. Off-label use of hormones when these are not indicated is also to be avoided, unless a medical practitioner feels it is warranted.
Dr. de la Rosa is an endocrinologist in Englewood, Fla. He disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
With more than 306 million views, #hormonebalance and #hormonebalancing are among the latest hacks to take over the social media platform TikTok, on which users post short videos. Influencers offer advice such as eating raw carrots for “happy hormones,” eating protein followed by fat for breakfast to regulate blood glucose, or taking vitamin B2 supplements for thyroid health.
Have you ever wondered if you were asleep during the lecture on “hormone balancing” in medical school? No, you weren’t. It was never a class for good reason, and you didn’t fail to read any such breakthrough studies in The New England Journal of Medicine either.
There are over 50 different hormones produced by humans and animals, regulating sleep, growth, metabolism and reproduction, among many other biological processes, so there is certainly no one-size-fits-all solution to ensure these are all working in perfect harmony.
When someone mentions “hormone balancing,” my mind wanders to the last time I took my car to have my tires rotated and balanced. If only it were as simple to balance hormones in real life. The best we can hope for is to get a specific hormone within the ideal physiologic range for that person’s age.
The term “hormone” can mean many things to different people. When a woman comes in with a hormone question, for example, it is often related to estrogen, followed by thyroid hormones. A wealth of misinformation exists in popular literature regarding these hormones alone.
Estrogen can be replaced, but not everyone needs it replaced. It depends on variables including age, underlying medical conditions, the time of day a test was drawn, and concomitant medications. Having low levels of a given hormone does not necessarily call for replacement either.
Insulin is another example of a hormone that can never completely be replaced in people with diabetes in a way that exactly mimics the normal physiologic release.
There are many lesser-known hormones that are measurable and replaceable but are also more difficult to reset to original manufacturer specifications.
A Google search for “hormone balancing” often sends you to “naturopaths” or “integrative medicine” practitioners, who often propose similar solutions to the TikTok influencers. Users are told that their hormones are out of whack and that restoring this “balance” can be achieved by purchasing whatever “natural products” or concoction they are selling.
These TikTok videos and online “experts” are the home-brewed versions of the strip-mall hormone specialists. TikTok videos claiming to help “balance hormones” typically don’t name a specific hormone either, or the end organs that each would have an impact on. Rather, they lump all hormones into a monolithic entity, implying that there is a single solution for all health problems. And personal testimonials extolling the benefits of a TikTok intervention don’t constitute proof of efficacy no matter how many “likes” they get. These influencers assume that viewers can “sense” their hormones are out of tune and no lab tests can convince them otherwise.
In these inflationary times, the cost of seeking medical care from conventional channels is increasingly prohibitive. It’s easy to understand the appeal of getting free advice from TikTok or some other Internet site. At best, following the advice will not have much impact; at worst, it could be harmful.
Don’t try this at home
There are some things that should never be tried at home, and do-it-yourself hormone replacement or remediation both fall under this umbrella.
Generally, the body does a good job of balancing its own hormones. Most patients don’t need to be worried if they’re in good health. If they’re in doubt, they should seek advice from a doctor, ideally an endocrinologist, but an ob.gyn. or general practitioner are also good options.
One of the first questions to ask a patient is “Which hormone are you worried about?” or “What health issue is it specifically that is bothering you?” Narrowing the focus to a single thing, if possible, will lead to a more efficient evaluation.
Often, patients arrive with multiple concerns written on little pieces of paper. These ubiquitous pieces of paper are the red flag for the flood of questions to follow.
Ordering the appropriate tests for the conditions they are concerned about can help put their minds at ease. If there are any specific deficiencies, or excesses in any hormones, then appropriate solutions can be discussed.
TikTok hormone-balancing solutions are simply the 21st-century version of the snake oil sold on late-night cable TV in the 1990s.
Needless to say, you should gently encourage your patients to stay away from these non–FDA-approved products, without making them feel stupid. Off-label use of hormones when these are not indicated is also to be avoided, unless a medical practitioner feels it is warranted.
Dr. de la Rosa is an endocrinologist in Englewood, Fla. He disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
With more than 306 million views, #hormonebalance and #hormonebalancing are among the latest hacks to take over the social media platform TikTok, on which users post short videos. Influencers offer advice such as eating raw carrots for “happy hormones,” eating protein followed by fat for breakfast to regulate blood glucose, or taking vitamin B2 supplements for thyroid health.
Have you ever wondered if you were asleep during the lecture on “hormone balancing” in medical school? No, you weren’t. It was never a class for good reason, and you didn’t fail to read any such breakthrough studies in The New England Journal of Medicine either.
There are over 50 different hormones produced by humans and animals, regulating sleep, growth, metabolism and reproduction, among many other biological processes, so there is certainly no one-size-fits-all solution to ensure these are all working in perfect harmony.
When someone mentions “hormone balancing,” my mind wanders to the last time I took my car to have my tires rotated and balanced. If only it were as simple to balance hormones in real life. The best we can hope for is to get a specific hormone within the ideal physiologic range for that person’s age.
The term “hormone” can mean many things to different people. When a woman comes in with a hormone question, for example, it is often related to estrogen, followed by thyroid hormones. A wealth of misinformation exists in popular literature regarding these hormones alone.
Estrogen can be replaced, but not everyone needs it replaced. It depends on variables including age, underlying medical conditions, the time of day a test was drawn, and concomitant medications. Having low levels of a given hormone does not necessarily call for replacement either.
Insulin is another example of a hormone that can never completely be replaced in people with diabetes in a way that exactly mimics the normal physiologic release.
There are many lesser-known hormones that are measurable and replaceable but are also more difficult to reset to original manufacturer specifications.
A Google search for “hormone balancing” often sends you to “naturopaths” or “integrative medicine” practitioners, who often propose similar solutions to the TikTok influencers. Users are told that their hormones are out of whack and that restoring this “balance” can be achieved by purchasing whatever “natural products” or concoction they are selling.
These TikTok videos and online “experts” are the home-brewed versions of the strip-mall hormone specialists. TikTok videos claiming to help “balance hormones” typically don’t name a specific hormone either, or the end organs that each would have an impact on. Rather, they lump all hormones into a monolithic entity, implying that there is a single solution for all health problems. And personal testimonials extolling the benefits of a TikTok intervention don’t constitute proof of efficacy no matter how many “likes” they get. These influencers assume that viewers can “sense” their hormones are out of tune and no lab tests can convince them otherwise.
In these inflationary times, the cost of seeking medical care from conventional channels is increasingly prohibitive. It’s easy to understand the appeal of getting free advice from TikTok or some other Internet site. At best, following the advice will not have much impact; at worst, it could be harmful.
Don’t try this at home
There are some things that should never be tried at home, and do-it-yourself hormone replacement or remediation both fall under this umbrella.
Generally, the body does a good job of balancing its own hormones. Most patients don’t need to be worried if they’re in good health. If they’re in doubt, they should seek advice from a doctor, ideally an endocrinologist, but an ob.gyn. or general practitioner are also good options.
One of the first questions to ask a patient is “Which hormone are you worried about?” or “What health issue is it specifically that is bothering you?” Narrowing the focus to a single thing, if possible, will lead to a more efficient evaluation.
Often, patients arrive with multiple concerns written on little pieces of paper. These ubiquitous pieces of paper are the red flag for the flood of questions to follow.
Ordering the appropriate tests for the conditions they are concerned about can help put their minds at ease. If there are any specific deficiencies, or excesses in any hormones, then appropriate solutions can be discussed.
TikTok hormone-balancing solutions are simply the 21st-century version of the snake oil sold on late-night cable TV in the 1990s.
Needless to say, you should gently encourage your patients to stay away from these non–FDA-approved products, without making them feel stupid. Off-label use of hormones when these are not indicated is also to be avoided, unless a medical practitioner feels it is warranted.
Dr. de la Rosa is an endocrinologist in Englewood, Fla. He disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
Malpractice risks for docs who oversee NPs or PAs
Even in states that have abolished requirements that NPs be physician-supervised, physicians may still be liable by virtue of employing the NP, according to William P. Sullivan, DO, an attorney and emergency physician in Frankfort, Ill.
Indeed, the vast majority of lawsuits against NPs and PAs name the supervising physician. According to a study of claims against NPs from 2011 to 2016, 82% of the cases also named the supervising physician.
Employed or contracted physicians assigned to supervise NPs or PAs are also affected, Dr. Sullivan said. “The employed physicians’ contract with a hospital or staffing company may require them to assist in the selection, supervision, and/or training of NPs or PAs,” he said. He added that supervisory duties may also be assigned through hospital bylaws.
“The physician is usually not paid anything extra for this work and may not be given extra time to perform it,” Dr. Sullivan said. But still, he said, that physician could be named in a lawsuit and wind up bearing some responsibility for an NP’s or PA’s mistake.
In addition to facing medical malpractice suits, Dr. Sullivan said, doctors are often sanctioned by state licensure boards for improperly supervising NPs and PAs. Licensure boards often require extensive protocols for supervision of NPs and PAs.
Yet more states are removing supervision requirements
With the addition of Kansas and New York in 2022 and California in 2023, 27 states no longer require supervision for all or most NPs. Sixteen of those states, including New York and California, have instituted progressive practice authority that requires temporary supervision of new NPs but then removes supervision after a period of 6 months to 4 years, depending on the state, for the rest of their career.
“When it comes to NP independence, the horse is already out of the barn,” Dr. Sullivan said. “It’s unlikely that states will repeal laws granting NPs independence, and in fact, more states are likely to pass them.”
*PAs, in contrast, are well behind NPs in achieving independence, but the American Academy of Physician Associates (AAPA) is calling to eliminate a mandated relationship with a specific physician. So far, Utah, North Dakota and Wyoming have ended physician supervision of PAs, while California and Hawaii have eliminated mandated chart review. Other states are considering eliminating physician supervision of PAs, according to the AAPA.
In states that have abolished oversight requirements for NPs, “liability can then shift to the NP when the NP is fully independent,” Cathy Klein, an advanced practice registered nurse who helped found the NP profession 50 years ago, told this news organization. “More NPs are starting their own practices, and in many cases, patients actually prefer to see an NP.”
As more NPs became more autonomous, the average payment that NPs incurred in professional liability lawsuits rose by 10.5% from 2017 to 2022, to $332,187, according to the Nurses Service Organization (NSO), a nursing malpractice insurer.
The number of malpractice judgments against autonomous NPs alone has also been rising. From 2012 to 2017, autonomous NPs’ share of all NP cases rose from 7% to 16.4%, the NSO reported.
The good news for physicians is that states’ removal of restrictions on NPs has reduced physicians’ liability to some extent. A 2017 study found that enacting less restrictive scope-of-practice laws for NPs decreased the number of payments made by physicians in NP cases by as much as 31%.
However, the top location for NP payouts remains the physician’s office, not the autonomous NP’s practice, according to the latter NSO report. Plaintiffs sue NPs’ and PAs’ supervising physicians on the basis of legal concepts, such as vicarious liability and respondeat superior. Even if the physician-employer never saw the patient, he or she can be held liable.
Court cases in which supervising physician was found liable
There are plenty of judgments against supervising or collaborating physicians when the NP or PA made the error. Typically, the doctor was faulted for paying little attention to the NP or PA he or she was supposed to supervise.
Dr. Sullivan points to a 2016 case in which a New York jury held a physician 40% liable for a $7 million judgment in a malpractice case involving a PA’s care of a patient in the emergency department. The case is Shajan v. South Nassau Community Hospital in New York.
“The patient presented with nontraumatic leg pain to his lower leg, was diagnosed by the PA with a muscle strain, and discharged without a physician evaluation,” Dr. Sullivan said. The next day, the patient visited an orthopedist who immediately diagnosed compartment syndrome, an emergent condition in which pressure builds up in an affected extremity, damaging the muscles and nerves. “The patient developed irreversible nerve damage and chronic regional pain syndrome,” he said.
A malpractice lawsuit named the PA and the emergency physician he was supposed to be reporting to. Even though the physician had never seen the patient, he had signed off on the PA’s note from a patient’s ED visit. “Testimony during the trial focused on hospital protocols that the supervising physician was supposed to take,” Dr. Sullivan said.
When doctors share fault, they frequently failed to follow the collaborative agreement with the NP or PA. In Collip v. Ratts, a 2015 Indiana case in which the patient died from a drug interaction, the doctor’s certified public accountant stated that the doctor was required to review at least 5% of the NP’s charts every week to evaluate her prescriptive practices.
The doctor admitted that he never reviewed the NP’s charts on a weekly basis. He did conduct some cursory reviews of some of the NP’s notes, and in them he noted concerns for her prescribing practices and suggested she attend a narcotics-prescribing seminar, but he did not follow up to make sure she had done this.
Sometimes the NP or PA who made the mistake may actually be dropped from the lawsuit, leaving the supervising physician fully liable. In these cases, courts reason that a fully engaged supervisor could have prevented the error. In the 2006 case of Husak v. Siegal, the Florida Supreme Court dropped the NP from the case, ruling that the NP had provided the supervising doctor all the information he needed in order to tell her what to do for the patient.
The court noted the physician had failed to look at the chart, even though he was required to do so under his supervisory agreement with the NP. The doctor “could have made the correct diagnosis or referral had he been attentive,” the court said. Therefore, there was “no evidence of independent negligence” by the NP, even though she was the one who had made the incorrect diagnosis that harmed the patient.
When states require an autonomous NP to have a supervisory relationship with a doctor, the supervisor may be unavailable and may fail to designate a substitute. In Texas in January 2019, a 7-year-old girl died of pneumonia after being treated by an NP in an urgent care clinic. The NP had told the parents that the child could safely go home and only needed ibuprofen. The parents brought the girl back home, and she died 15 hours later. The Wattenbargers sued the NP, and the doctor’s supervision was a topic in the trial.
The supervising physician for the NP was out of the country at the time. He said that he had found a substitute, but the substitute doctor testified she had no idea she was designated to be the substitute, according to Niran Al-Agba, MD, a family physician in Silverdale, Wash., who has written on the Texas case. Dr. Al-Agba told this news organization the case appears to have been settled confidentially.
Different standards for expert witnesses
In many states, courts do not allow physicians to testify as expert witnesses in malpractice cases against NPs, arguing that nurses have a different set of standards than doctors have, Dr. Sullivan reported.
These states include Arkansas, Illinois, North Carolina, and New York, according to a report by SEAK Inc., an expert witness training program. The report said most other states allow physician experts in these cases, but they may still require that they have experience with the nursing standard of care.
Dr. Sullivan said some courts are whittling away at the ban on physician experts, and the ban may eventually disappear. He reported that in Oklahoma, which normally upholds the ban, a judge recently allowed a physician-expert to testify in a case involving the death of a 19-year-old woman, Alexus Ochoa, in an ED staffed by an NP. The judge reasoned that Ms. Ochoa’s parents assumed the ED was staffed by physicians and would adhere to medical standards.
Supervision pointers from a physician
Physicians who supervise NPs or PAs say it is important to keep track of their skills and help them sharpen their expertise. Their scope of practice and physicians’ supervisory responsibilities are included in the collaborative agreement.
Arthur Apolinario, MD, a family physician in Clinton, N.C., says his 10-physician practice, which employs six NPs and one PA, works under a collaborative agreement. “The agreement defines each person’s scope of practice. They can’t do certain procedures, such as surgery, and they need extra training before doing certain tasks alone, such as joint injection.
“You have to always figure that if there is a lawsuit against one of them, you as the supervising physician would be named,” said Dr. Apolinario, who is also president of the North Carolina Medical Society. “We try to avert mistakes by meeting regularly with our NPs and PAs and making sure they keep up to date.”
Collaborating with autonomous NPs
Even when NPs operate independently in states that have abolished supervision, physicians may still have some liability if they give NPs advice, Dr. Al-Agba said.
At her Washington state practice, Dr. Al-Agba shares an office with an autonomous NP. “We share overhead and a front desk, but we have separate patients,” Dr. Al-Agba said. “This arrangement works very well for both of us.”
The NP sometimes asks her for advice. When this occurs, Dr. Al-Agba said she always makes sure to see the patient first. “If you don’t actually see the patient, there could be a misunderstanding that could lead to an error,” she said.
Conclusion
Even though NPs now have autonomy in most states, supervising physicians may still be liable for NP malpractice by virtue of being their employers, and physicians in the remaining states are liable for NPs through state law and for PAs in virtually all the states. To determine the supervising physician’s fault, courts often study whether the physician has met the terms of the collaborative agreement.
Physicians can reduce collaborating NPs’ and PAs’ liability by properly training them, by verifying their scope of practice, by making themselves easily available for consultation, and by occasionally seeing their patients. If their NPs and PAs do commit malpractice, supervising physicians may be able to protect themselves from liability by adhering to all requirements of the collaborative agreement.
*Correction, 4/19/2023: An earlier version of this story misstated the name of the AAPA and the states that have ended physician supervision of PAs.
A version of this article first appeared on Medscape.com.
Even in states that have abolished requirements that NPs be physician-supervised, physicians may still be liable by virtue of employing the NP, according to William P. Sullivan, DO, an attorney and emergency physician in Frankfort, Ill.
Indeed, the vast majority of lawsuits against NPs and PAs name the supervising physician. According to a study of claims against NPs from 2011 to 2016, 82% of the cases also named the supervising physician.
Employed or contracted physicians assigned to supervise NPs or PAs are also affected, Dr. Sullivan said. “The employed physicians’ contract with a hospital or staffing company may require them to assist in the selection, supervision, and/or training of NPs or PAs,” he said. He added that supervisory duties may also be assigned through hospital bylaws.
“The physician is usually not paid anything extra for this work and may not be given extra time to perform it,” Dr. Sullivan said. But still, he said, that physician could be named in a lawsuit and wind up bearing some responsibility for an NP’s or PA’s mistake.
In addition to facing medical malpractice suits, Dr. Sullivan said, doctors are often sanctioned by state licensure boards for improperly supervising NPs and PAs. Licensure boards often require extensive protocols for supervision of NPs and PAs.
Yet more states are removing supervision requirements
With the addition of Kansas and New York in 2022 and California in 2023, 27 states no longer require supervision for all or most NPs. Sixteen of those states, including New York and California, have instituted progressive practice authority that requires temporary supervision of new NPs but then removes supervision after a period of 6 months to 4 years, depending on the state, for the rest of their career.
“When it comes to NP independence, the horse is already out of the barn,” Dr. Sullivan said. “It’s unlikely that states will repeal laws granting NPs independence, and in fact, more states are likely to pass them.”
*PAs, in contrast, are well behind NPs in achieving independence, but the American Academy of Physician Associates (AAPA) is calling to eliminate a mandated relationship with a specific physician. So far, Utah, North Dakota and Wyoming have ended physician supervision of PAs, while California and Hawaii have eliminated mandated chart review. Other states are considering eliminating physician supervision of PAs, according to the AAPA.
In states that have abolished oversight requirements for NPs, “liability can then shift to the NP when the NP is fully independent,” Cathy Klein, an advanced practice registered nurse who helped found the NP profession 50 years ago, told this news organization. “More NPs are starting their own practices, and in many cases, patients actually prefer to see an NP.”
As more NPs became more autonomous, the average payment that NPs incurred in professional liability lawsuits rose by 10.5% from 2017 to 2022, to $332,187, according to the Nurses Service Organization (NSO), a nursing malpractice insurer.
The number of malpractice judgments against autonomous NPs alone has also been rising. From 2012 to 2017, autonomous NPs’ share of all NP cases rose from 7% to 16.4%, the NSO reported.
The good news for physicians is that states’ removal of restrictions on NPs has reduced physicians’ liability to some extent. A 2017 study found that enacting less restrictive scope-of-practice laws for NPs decreased the number of payments made by physicians in NP cases by as much as 31%.
However, the top location for NP payouts remains the physician’s office, not the autonomous NP’s practice, according to the latter NSO report. Plaintiffs sue NPs’ and PAs’ supervising physicians on the basis of legal concepts, such as vicarious liability and respondeat superior. Even if the physician-employer never saw the patient, he or she can be held liable.
Court cases in which supervising physician was found liable
There are plenty of judgments against supervising or collaborating physicians when the NP or PA made the error. Typically, the doctor was faulted for paying little attention to the NP or PA he or she was supposed to supervise.
Dr. Sullivan points to a 2016 case in which a New York jury held a physician 40% liable for a $7 million judgment in a malpractice case involving a PA’s care of a patient in the emergency department. The case is Shajan v. South Nassau Community Hospital in New York.
“The patient presented with nontraumatic leg pain to his lower leg, was diagnosed by the PA with a muscle strain, and discharged without a physician evaluation,” Dr. Sullivan said. The next day, the patient visited an orthopedist who immediately diagnosed compartment syndrome, an emergent condition in which pressure builds up in an affected extremity, damaging the muscles and nerves. “The patient developed irreversible nerve damage and chronic regional pain syndrome,” he said.
A malpractice lawsuit named the PA and the emergency physician he was supposed to be reporting to. Even though the physician had never seen the patient, he had signed off on the PA’s note from a patient’s ED visit. “Testimony during the trial focused on hospital protocols that the supervising physician was supposed to take,” Dr. Sullivan said.
When doctors share fault, they frequently failed to follow the collaborative agreement with the NP or PA. In Collip v. Ratts, a 2015 Indiana case in which the patient died from a drug interaction, the doctor’s certified public accountant stated that the doctor was required to review at least 5% of the NP’s charts every week to evaluate her prescriptive practices.
The doctor admitted that he never reviewed the NP’s charts on a weekly basis. He did conduct some cursory reviews of some of the NP’s notes, and in them he noted concerns for her prescribing practices and suggested she attend a narcotics-prescribing seminar, but he did not follow up to make sure she had done this.
Sometimes the NP or PA who made the mistake may actually be dropped from the lawsuit, leaving the supervising physician fully liable. In these cases, courts reason that a fully engaged supervisor could have prevented the error. In the 2006 case of Husak v. Siegal, the Florida Supreme Court dropped the NP from the case, ruling that the NP had provided the supervising doctor all the information he needed in order to tell her what to do for the patient.
The court noted the physician had failed to look at the chart, even though he was required to do so under his supervisory agreement with the NP. The doctor “could have made the correct diagnosis or referral had he been attentive,” the court said. Therefore, there was “no evidence of independent negligence” by the NP, even though she was the one who had made the incorrect diagnosis that harmed the patient.
When states require an autonomous NP to have a supervisory relationship with a doctor, the supervisor may be unavailable and may fail to designate a substitute. In Texas in January 2019, a 7-year-old girl died of pneumonia after being treated by an NP in an urgent care clinic. The NP had told the parents that the child could safely go home and only needed ibuprofen. The parents brought the girl back home, and she died 15 hours later. The Wattenbargers sued the NP, and the doctor’s supervision was a topic in the trial.
The supervising physician for the NP was out of the country at the time. He said that he had found a substitute, but the substitute doctor testified she had no idea she was designated to be the substitute, according to Niran Al-Agba, MD, a family physician in Silverdale, Wash., who has written on the Texas case. Dr. Al-Agba told this news organization the case appears to have been settled confidentially.
Different standards for expert witnesses
In many states, courts do not allow physicians to testify as expert witnesses in malpractice cases against NPs, arguing that nurses have a different set of standards than doctors have, Dr. Sullivan reported.
These states include Arkansas, Illinois, North Carolina, and New York, according to a report by SEAK Inc., an expert witness training program. The report said most other states allow physician experts in these cases, but they may still require that they have experience with the nursing standard of care.
Dr. Sullivan said some courts are whittling away at the ban on physician experts, and the ban may eventually disappear. He reported that in Oklahoma, which normally upholds the ban, a judge recently allowed a physician-expert to testify in a case involving the death of a 19-year-old woman, Alexus Ochoa, in an ED staffed by an NP. The judge reasoned that Ms. Ochoa’s parents assumed the ED was staffed by physicians and would adhere to medical standards.
Supervision pointers from a physician
Physicians who supervise NPs or PAs say it is important to keep track of their skills and help them sharpen their expertise. Their scope of practice and physicians’ supervisory responsibilities are included in the collaborative agreement.
Arthur Apolinario, MD, a family physician in Clinton, N.C., says his 10-physician practice, which employs six NPs and one PA, works under a collaborative agreement. “The agreement defines each person’s scope of practice. They can’t do certain procedures, such as surgery, and they need extra training before doing certain tasks alone, such as joint injection.
“You have to always figure that if there is a lawsuit against one of them, you as the supervising physician would be named,” said Dr. Apolinario, who is also president of the North Carolina Medical Society. “We try to avert mistakes by meeting regularly with our NPs and PAs and making sure they keep up to date.”
Collaborating with autonomous NPs
Even when NPs operate independently in states that have abolished supervision, physicians may still have some liability if they give NPs advice, Dr. Al-Agba said.
At her Washington state practice, Dr. Al-Agba shares an office with an autonomous NP. “We share overhead and a front desk, but we have separate patients,” Dr. Al-Agba said. “This arrangement works very well for both of us.”
The NP sometimes asks her for advice. When this occurs, Dr. Al-Agba said she always makes sure to see the patient first. “If you don’t actually see the patient, there could be a misunderstanding that could lead to an error,” she said.
Conclusion
Even though NPs now have autonomy in most states, supervising physicians may still be liable for NP malpractice by virtue of being their employers, and physicians in the remaining states are liable for NPs through state law and for PAs in virtually all the states. To determine the supervising physician’s fault, courts often study whether the physician has met the terms of the collaborative agreement.
Physicians can reduce collaborating NPs’ and PAs’ liability by properly training them, by verifying their scope of practice, by making themselves easily available for consultation, and by occasionally seeing their patients. If their NPs and PAs do commit malpractice, supervising physicians may be able to protect themselves from liability by adhering to all requirements of the collaborative agreement.
*Correction, 4/19/2023: An earlier version of this story misstated the name of the AAPA and the states that have ended physician supervision of PAs.
A version of this article first appeared on Medscape.com.
Even in states that have abolished requirements that NPs be physician-supervised, physicians may still be liable by virtue of employing the NP, according to William P. Sullivan, DO, an attorney and emergency physician in Frankfort, Ill.
Indeed, the vast majority of lawsuits against NPs and PAs name the supervising physician. According to a study of claims against NPs from 2011 to 2016, 82% of the cases also named the supervising physician.
Employed or contracted physicians assigned to supervise NPs or PAs are also affected, Dr. Sullivan said. “The employed physicians’ contract with a hospital or staffing company may require them to assist in the selection, supervision, and/or training of NPs or PAs,” he said. He added that supervisory duties may also be assigned through hospital bylaws.
“The physician is usually not paid anything extra for this work and may not be given extra time to perform it,” Dr. Sullivan said. But still, he said, that physician could be named in a lawsuit and wind up bearing some responsibility for an NP’s or PA’s mistake.
In addition to facing medical malpractice suits, Dr. Sullivan said, doctors are often sanctioned by state licensure boards for improperly supervising NPs and PAs. Licensure boards often require extensive protocols for supervision of NPs and PAs.
Yet more states are removing supervision requirements
With the addition of Kansas and New York in 2022 and California in 2023, 27 states no longer require supervision for all or most NPs. Sixteen of those states, including New York and California, have instituted progressive practice authority that requires temporary supervision of new NPs but then removes supervision after a period of 6 months to 4 years, depending on the state, for the rest of their career.
“When it comes to NP independence, the horse is already out of the barn,” Dr. Sullivan said. “It’s unlikely that states will repeal laws granting NPs independence, and in fact, more states are likely to pass them.”
*PAs, in contrast, are well behind NPs in achieving independence, but the American Academy of Physician Associates (AAPA) is calling to eliminate a mandated relationship with a specific physician. So far, Utah, North Dakota and Wyoming have ended physician supervision of PAs, while California and Hawaii have eliminated mandated chart review. Other states are considering eliminating physician supervision of PAs, according to the AAPA.
In states that have abolished oversight requirements for NPs, “liability can then shift to the NP when the NP is fully independent,” Cathy Klein, an advanced practice registered nurse who helped found the NP profession 50 years ago, told this news organization. “More NPs are starting their own practices, and in many cases, patients actually prefer to see an NP.”
As more NPs became more autonomous, the average payment that NPs incurred in professional liability lawsuits rose by 10.5% from 2017 to 2022, to $332,187, according to the Nurses Service Organization (NSO), a nursing malpractice insurer.
The number of malpractice judgments against autonomous NPs alone has also been rising. From 2012 to 2017, autonomous NPs’ share of all NP cases rose from 7% to 16.4%, the NSO reported.
The good news for physicians is that states’ removal of restrictions on NPs has reduced physicians’ liability to some extent. A 2017 study found that enacting less restrictive scope-of-practice laws for NPs decreased the number of payments made by physicians in NP cases by as much as 31%.
However, the top location for NP payouts remains the physician’s office, not the autonomous NP’s practice, according to the latter NSO report. Plaintiffs sue NPs’ and PAs’ supervising physicians on the basis of legal concepts, such as vicarious liability and respondeat superior. Even if the physician-employer never saw the patient, he or she can be held liable.
Court cases in which supervising physician was found liable
There are plenty of judgments against supervising or collaborating physicians when the NP or PA made the error. Typically, the doctor was faulted for paying little attention to the NP or PA he or she was supposed to supervise.
Dr. Sullivan points to a 2016 case in which a New York jury held a physician 40% liable for a $7 million judgment in a malpractice case involving a PA’s care of a patient in the emergency department. The case is Shajan v. South Nassau Community Hospital in New York.
“The patient presented with nontraumatic leg pain to his lower leg, was diagnosed by the PA with a muscle strain, and discharged without a physician evaluation,” Dr. Sullivan said. The next day, the patient visited an orthopedist who immediately diagnosed compartment syndrome, an emergent condition in which pressure builds up in an affected extremity, damaging the muscles and nerves. “The patient developed irreversible nerve damage and chronic regional pain syndrome,” he said.
A malpractice lawsuit named the PA and the emergency physician he was supposed to be reporting to. Even though the physician had never seen the patient, he had signed off on the PA’s note from a patient’s ED visit. “Testimony during the trial focused on hospital protocols that the supervising physician was supposed to take,” Dr. Sullivan said.
When doctors share fault, they frequently failed to follow the collaborative agreement with the NP or PA. In Collip v. Ratts, a 2015 Indiana case in which the patient died from a drug interaction, the doctor’s certified public accountant stated that the doctor was required to review at least 5% of the NP’s charts every week to evaluate her prescriptive practices.
The doctor admitted that he never reviewed the NP’s charts on a weekly basis. He did conduct some cursory reviews of some of the NP’s notes, and in them he noted concerns for her prescribing practices and suggested she attend a narcotics-prescribing seminar, but he did not follow up to make sure she had done this.
Sometimes the NP or PA who made the mistake may actually be dropped from the lawsuit, leaving the supervising physician fully liable. In these cases, courts reason that a fully engaged supervisor could have prevented the error. In the 2006 case of Husak v. Siegal, the Florida Supreme Court dropped the NP from the case, ruling that the NP had provided the supervising doctor all the information he needed in order to tell her what to do for the patient.
The court noted the physician had failed to look at the chart, even though he was required to do so under his supervisory agreement with the NP. The doctor “could have made the correct diagnosis or referral had he been attentive,” the court said. Therefore, there was “no evidence of independent negligence” by the NP, even though she was the one who had made the incorrect diagnosis that harmed the patient.
When states require an autonomous NP to have a supervisory relationship with a doctor, the supervisor may be unavailable and may fail to designate a substitute. In Texas in January 2019, a 7-year-old girl died of pneumonia after being treated by an NP in an urgent care clinic. The NP had told the parents that the child could safely go home and only needed ibuprofen. The parents brought the girl back home, and she died 15 hours later. The Wattenbargers sued the NP, and the doctor’s supervision was a topic in the trial.
The supervising physician for the NP was out of the country at the time. He said that he had found a substitute, but the substitute doctor testified she had no idea she was designated to be the substitute, according to Niran Al-Agba, MD, a family physician in Silverdale, Wash., who has written on the Texas case. Dr. Al-Agba told this news organization the case appears to have been settled confidentially.
Different standards for expert witnesses
In many states, courts do not allow physicians to testify as expert witnesses in malpractice cases against NPs, arguing that nurses have a different set of standards than doctors have, Dr. Sullivan reported.
These states include Arkansas, Illinois, North Carolina, and New York, according to a report by SEAK Inc., an expert witness training program. The report said most other states allow physician experts in these cases, but they may still require that they have experience with the nursing standard of care.
Dr. Sullivan said some courts are whittling away at the ban on physician experts, and the ban may eventually disappear. He reported that in Oklahoma, which normally upholds the ban, a judge recently allowed a physician-expert to testify in a case involving the death of a 19-year-old woman, Alexus Ochoa, in an ED staffed by an NP. The judge reasoned that Ms. Ochoa’s parents assumed the ED was staffed by physicians and would adhere to medical standards.
Supervision pointers from a physician
Physicians who supervise NPs or PAs say it is important to keep track of their skills and help them sharpen their expertise. Their scope of practice and physicians’ supervisory responsibilities are included in the collaborative agreement.
Arthur Apolinario, MD, a family physician in Clinton, N.C., says his 10-physician practice, which employs six NPs and one PA, works under a collaborative agreement. “The agreement defines each person’s scope of practice. They can’t do certain procedures, such as surgery, and they need extra training before doing certain tasks alone, such as joint injection.
“You have to always figure that if there is a lawsuit against one of them, you as the supervising physician would be named,” said Dr. Apolinario, who is also president of the North Carolina Medical Society. “We try to avert mistakes by meeting regularly with our NPs and PAs and making sure they keep up to date.”
Collaborating with autonomous NPs
Even when NPs operate independently in states that have abolished supervision, physicians may still have some liability if they give NPs advice, Dr. Al-Agba said.
At her Washington state practice, Dr. Al-Agba shares an office with an autonomous NP. “We share overhead and a front desk, but we have separate patients,” Dr. Al-Agba said. “This arrangement works very well for both of us.”
The NP sometimes asks her for advice. When this occurs, Dr. Al-Agba said she always makes sure to see the patient first. “If you don’t actually see the patient, there could be a misunderstanding that could lead to an error,” she said.
Conclusion
Even though NPs now have autonomy in most states, supervising physicians may still be liable for NP malpractice by virtue of being their employers, and physicians in the remaining states are liable for NPs through state law and for PAs in virtually all the states. To determine the supervising physician’s fault, courts often study whether the physician has met the terms of the collaborative agreement.
Physicians can reduce collaborating NPs’ and PAs’ liability by properly training them, by verifying their scope of practice, by making themselves easily available for consultation, and by occasionally seeing their patients. If their NPs and PAs do commit malpractice, supervising physicians may be able to protect themselves from liability by adhering to all requirements of the collaborative agreement.
*Correction, 4/19/2023: An earlier version of this story misstated the name of the AAPA and the states that have ended physician supervision of PAs.
A version of this article first appeared on Medscape.com.
Statins don’t worsen muscle injury from moderately intense exercise
People who are physically active and on statins may have one less potential concern about the drugs. Despite their reputation for causing muscle injury, a study suggests statins won’t worsen the toll that sustained, moderately intensive exercise already takes on patients’ muscles.
Statin therapy in this prospective, controlled study wasn’t seen to aggravate normal muscle fatigue or pain from sustained exercise or adversely affect enzymes or other biomarkers associated with muscle injury.
The findings come from 100 individuals, of whom about two-thirds were on statins, participating in a public, 4-day, long-distance walking event held annually in the Netherlands. Results were published in the Journal of the American College of Cardiology with Neeltje A.E. Allard, MD, Radboud University Medical Center, Nijmegen, the Netherlands, as lead author.
For all of statins’ common use in adults with cardiovascular (CV) risk factors, the drugs are often blamed for causing excessive muscle pain or injury as a side effect. Yet there is a predominance of evidence to the contrary based on meta-analyses and clinical trials, suggesting that the drugs are taking the rap for many entirely unrelated muscle symptoms.
The new findings, from people ranging widely in fitness levels, suggest that “exercise of moderate intensity is feasible and safe” in statin users, that the drugs won’t exacerbate normal muscle symptoms from exercise, Dr. Allard told this news organization.
And that exercise doesn’t have to be on an unusual scale. Regular exercise in statin users can simply be consistent with broader guidelines, say 30 minutes of walking per day, she noted.
The study has such broad applicability, Dr. Allard said, because participants represented the spectrum of the thousands who signed up for the walking event, who varied in age, level of physical fitness, and number of CV risk factors. They included CV patients, the physically fit, “recreational walkers who didn’t really exercise regularly,” and “habitual nonexercisers.”
It enrolled three groups of participants in the Four Days Marches in Nijmegen, which in a typical year attracts tens of thousands of participants who walk up to 30 km, 40 km, or 50 km per day for 4 consecutive days.
They included 35 statin users who walked the event despite muscle symptoms, 34 on statins but without such symptoms, and 31 non–statin-using controls. Their mean ages ranged from 65 to 68 years.
Statin users were overwhelmingly on simvastatin or atorvastatin. The average statin therapy durations were 60 months and 96 months for those with and without symptoms, respectively.
Assessments were performed several days before the event, at baseline, and after the end of walking on days 1, 2, and 3.
Scores for muscle pain on the Brief Pain Inventory were higher at baseline for the symptomatic-on-statins group (P < .001) compared with the other two groups, and went up (P < .001) similarly across the three groups during each of the 3 days, the report notes. Fatigue scores on the Brief Fatigue Inventory followed the same pattern.
All biomarkers of muscle injury or stress were at comparable levels at baseline in the three groups and went up similarly (P < .001) with no significant differences at the end of day 3. Biomarkers included lactate dehydrogenase, creatine kinase, myoglobin, cardiac troponin I, and N-terminal pro-brain natriuretic peptide.
Statin-related reductions in levels of coenzyme Q 10 (CoQ10) have been thought to exacerbate muscle injury, the authors note. But levels of CoQ10 weren’t significantly different across the three groups at any point in the study, and they did not show any significant associations with measures of muscle injury, symptoms, or fatigue.
Patients with statin-associated muscle symptoms (SAMS) often limit physical activity because of muscle pain or weakness, but also “concerns that exercise will exacerbate muscle injury,” an accompanying editorial notes. “Therefore, exercise, a foundation of improving and maintaining cardiometabolic health, is often avoided or limited.”
But the current study, writes Robert S. Rosenson, MD, of Mount Sinai Heart, New York, indeed suggests that “many patients who develop SAMS may engage in a moderately intensive walking program without concern for worsened muscle biomarkers or performance.”
The exercise didn’t seem to improve muscle function in symptomatic statin users, compared with the other groups over the study’s very short follow-up, Dr. Rosenson observes. But “it remains uncertain from this study whether sustained exercise in SAMS patients will effectuate improved metabolic biomarkers or exercise capacity in the long term.”
Dr. Allard is supported by a grant from the Radboud Institute for Health Sciences; the other authors have disclosed no relevant financial relationships. Dr. Rosenson disclosed receiving research funding to his institution from Amgen, Arrowhead, Lilly, Novartis, and Regeneron; consulting fees from Amgen, Arrowhead, Lilly, Lipigon, Novartis, CRISPR Therapeutics, Precision BioSciences, Verve, Ultragenyx Pharmaceutical, and Regeneron; speaking fees from Amgen, Kowa, and Regeneron; and royalties from Wolters Kluwer (UpToDate); and that he holds stock in MediMergent.
A version of this article first appeared on Medscape.com.
People who are physically active and on statins may have one less potential concern about the drugs. Despite their reputation for causing muscle injury, a study suggests statins won’t worsen the toll that sustained, moderately intensive exercise already takes on patients’ muscles.
Statin therapy in this prospective, controlled study wasn’t seen to aggravate normal muscle fatigue or pain from sustained exercise or adversely affect enzymes or other biomarkers associated with muscle injury.
The findings come from 100 individuals, of whom about two-thirds were on statins, participating in a public, 4-day, long-distance walking event held annually in the Netherlands. Results were published in the Journal of the American College of Cardiology with Neeltje A.E. Allard, MD, Radboud University Medical Center, Nijmegen, the Netherlands, as lead author.
For all of statins’ common use in adults with cardiovascular (CV) risk factors, the drugs are often blamed for causing excessive muscle pain or injury as a side effect. Yet there is a predominance of evidence to the contrary based on meta-analyses and clinical trials, suggesting that the drugs are taking the rap for many entirely unrelated muscle symptoms.
The new findings, from people ranging widely in fitness levels, suggest that “exercise of moderate intensity is feasible and safe” in statin users, that the drugs won’t exacerbate normal muscle symptoms from exercise, Dr. Allard told this news organization.
And that exercise doesn’t have to be on an unusual scale. Regular exercise in statin users can simply be consistent with broader guidelines, say 30 minutes of walking per day, she noted.
The study has such broad applicability, Dr. Allard said, because participants represented the spectrum of the thousands who signed up for the walking event, who varied in age, level of physical fitness, and number of CV risk factors. They included CV patients, the physically fit, “recreational walkers who didn’t really exercise regularly,” and “habitual nonexercisers.”
It enrolled three groups of participants in the Four Days Marches in Nijmegen, which in a typical year attracts tens of thousands of participants who walk up to 30 km, 40 km, or 50 km per day for 4 consecutive days.
They included 35 statin users who walked the event despite muscle symptoms, 34 on statins but without such symptoms, and 31 non–statin-using controls. Their mean ages ranged from 65 to 68 years.
Statin users were overwhelmingly on simvastatin or atorvastatin. The average statin therapy durations were 60 months and 96 months for those with and without symptoms, respectively.
Assessments were performed several days before the event, at baseline, and after the end of walking on days 1, 2, and 3.
Scores for muscle pain on the Brief Pain Inventory were higher at baseline for the symptomatic-on-statins group (P < .001) compared with the other two groups, and went up (P < .001) similarly across the three groups during each of the 3 days, the report notes. Fatigue scores on the Brief Fatigue Inventory followed the same pattern.
All biomarkers of muscle injury or stress were at comparable levels at baseline in the three groups and went up similarly (P < .001) with no significant differences at the end of day 3. Biomarkers included lactate dehydrogenase, creatine kinase, myoglobin, cardiac troponin I, and N-terminal pro-brain natriuretic peptide.
Statin-related reductions in levels of coenzyme Q 10 (CoQ10) have been thought to exacerbate muscle injury, the authors note. But levels of CoQ10 weren’t significantly different across the three groups at any point in the study, and they did not show any significant associations with measures of muscle injury, symptoms, or fatigue.
Patients with statin-associated muscle symptoms (SAMS) often limit physical activity because of muscle pain or weakness, but also “concerns that exercise will exacerbate muscle injury,” an accompanying editorial notes. “Therefore, exercise, a foundation of improving and maintaining cardiometabolic health, is often avoided or limited.”
But the current study, writes Robert S. Rosenson, MD, of Mount Sinai Heart, New York, indeed suggests that “many patients who develop SAMS may engage in a moderately intensive walking program without concern for worsened muscle biomarkers or performance.”
The exercise didn’t seem to improve muscle function in symptomatic statin users, compared with the other groups over the study’s very short follow-up, Dr. Rosenson observes. But “it remains uncertain from this study whether sustained exercise in SAMS patients will effectuate improved metabolic biomarkers or exercise capacity in the long term.”
Dr. Allard is supported by a grant from the Radboud Institute for Health Sciences; the other authors have disclosed no relevant financial relationships. Dr. Rosenson disclosed receiving research funding to his institution from Amgen, Arrowhead, Lilly, Novartis, and Regeneron; consulting fees from Amgen, Arrowhead, Lilly, Lipigon, Novartis, CRISPR Therapeutics, Precision BioSciences, Verve, Ultragenyx Pharmaceutical, and Regeneron; speaking fees from Amgen, Kowa, and Regeneron; and royalties from Wolters Kluwer (UpToDate); and that he holds stock in MediMergent.
A version of this article first appeared on Medscape.com.
People who are physically active and on statins may have one less potential concern about the drugs. Despite their reputation for causing muscle injury, a study suggests statins won’t worsen the toll that sustained, moderately intensive exercise already takes on patients’ muscles.
Statin therapy in this prospective, controlled study wasn’t seen to aggravate normal muscle fatigue or pain from sustained exercise or adversely affect enzymes or other biomarkers associated with muscle injury.
The findings come from 100 individuals, of whom about two-thirds were on statins, participating in a public, 4-day, long-distance walking event held annually in the Netherlands. Results were published in the Journal of the American College of Cardiology with Neeltje A.E. Allard, MD, Radboud University Medical Center, Nijmegen, the Netherlands, as lead author.
For all of statins’ common use in adults with cardiovascular (CV) risk factors, the drugs are often blamed for causing excessive muscle pain or injury as a side effect. Yet there is a predominance of evidence to the contrary based on meta-analyses and clinical trials, suggesting that the drugs are taking the rap for many entirely unrelated muscle symptoms.
The new findings, from people ranging widely in fitness levels, suggest that “exercise of moderate intensity is feasible and safe” in statin users, that the drugs won’t exacerbate normal muscle symptoms from exercise, Dr. Allard told this news organization.
And that exercise doesn’t have to be on an unusual scale. Regular exercise in statin users can simply be consistent with broader guidelines, say 30 minutes of walking per day, she noted.
The study has such broad applicability, Dr. Allard said, because participants represented the spectrum of the thousands who signed up for the walking event, who varied in age, level of physical fitness, and number of CV risk factors. They included CV patients, the physically fit, “recreational walkers who didn’t really exercise regularly,” and “habitual nonexercisers.”
It enrolled three groups of participants in the Four Days Marches in Nijmegen, which in a typical year attracts tens of thousands of participants who walk up to 30 km, 40 km, or 50 km per day for 4 consecutive days.
They included 35 statin users who walked the event despite muscle symptoms, 34 on statins but without such symptoms, and 31 non–statin-using controls. Their mean ages ranged from 65 to 68 years.
Statin users were overwhelmingly on simvastatin or atorvastatin. The average statin therapy durations were 60 months and 96 months for those with and without symptoms, respectively.
Assessments were performed several days before the event, at baseline, and after the end of walking on days 1, 2, and 3.
Scores for muscle pain on the Brief Pain Inventory were higher at baseline for the symptomatic-on-statins group (P < .001) compared with the other two groups, and went up (P < .001) similarly across the three groups during each of the 3 days, the report notes. Fatigue scores on the Brief Fatigue Inventory followed the same pattern.
All biomarkers of muscle injury or stress were at comparable levels at baseline in the three groups and went up similarly (P < .001) with no significant differences at the end of day 3. Biomarkers included lactate dehydrogenase, creatine kinase, myoglobin, cardiac troponin I, and N-terminal pro-brain natriuretic peptide.
Statin-related reductions in levels of coenzyme Q 10 (CoQ10) have been thought to exacerbate muscle injury, the authors note. But levels of CoQ10 weren’t significantly different across the three groups at any point in the study, and they did not show any significant associations with measures of muscle injury, symptoms, or fatigue.
Patients with statin-associated muscle symptoms (SAMS) often limit physical activity because of muscle pain or weakness, but also “concerns that exercise will exacerbate muscle injury,” an accompanying editorial notes. “Therefore, exercise, a foundation of improving and maintaining cardiometabolic health, is often avoided or limited.”
But the current study, writes Robert S. Rosenson, MD, of Mount Sinai Heart, New York, indeed suggests that “many patients who develop SAMS may engage in a moderately intensive walking program without concern for worsened muscle biomarkers or performance.”
The exercise didn’t seem to improve muscle function in symptomatic statin users, compared with the other groups over the study’s very short follow-up, Dr. Rosenson observes. But “it remains uncertain from this study whether sustained exercise in SAMS patients will effectuate improved metabolic biomarkers or exercise capacity in the long term.”
Dr. Allard is supported by a grant from the Radboud Institute for Health Sciences; the other authors have disclosed no relevant financial relationships. Dr. Rosenson disclosed receiving research funding to his institution from Amgen, Arrowhead, Lilly, Novartis, and Regeneron; consulting fees from Amgen, Arrowhead, Lilly, Lipigon, Novartis, CRISPR Therapeutics, Precision BioSciences, Verve, Ultragenyx Pharmaceutical, and Regeneron; speaking fees from Amgen, Kowa, and Regeneron; and royalties from Wolters Kluwer (UpToDate); and that he holds stock in MediMergent.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
High salt intake linked to atherosclerosis even with normal BP
A high salt intake is an important risk factor for atherosclerosis, even in the absence of hypertension, a large study from Sweden concludes.
The study, including more than 10,000 individuals between the ages of 50 and 64 years from the Swedish Cardiopulmonary bioImage Study, showed a significant link between dietary salt intake and the risk for atherosclerotic lesions in the coronary and carotid arteries, even in participants with normal blood pressure and without known cardiovascular disease.
The finding suggests that salt could be a damaging factor in its own right before the development of hypertension, the authors write. The results were published online in European Heart Journal Open.
It has been known for a long time that salt is linked to hypertension, but the role that salt plays in atherosclerosis has not been examined, first author Jonas Wuopio, MD, Karolinska Institutet, Huddinge, and Clinical Research Center, Falun, Uppsala University, both in Sweden, told this news organization.
“Hardly anyone looks at changes in the arteries’ calcification, the atherosclerotic plaques and the association with salt intake,” Dr. Wuopio said. “We had this exclusive data from our cohort, so we wanted to use it to close this knowledge gap.”
The analysis included 10,788 adults aged 50-64 years, (average age, 58 years; 52% women) who underwent a coronary computed tomography angiography (CCTA) scan. The estimated 24-hour sodium excretion was used to measure sodium intake.
CCTA was used to obtain 3-D images of the coronary arteries to measure the degree of coronary artery calcium as well as detect stenosis in the coronary arteries. Participants also had an ultrasound of the carotid arteries.
After adjusting for age, sex, and study site (the study was done at Uppsala and Malmö, Sweden), the researchers found that rising salt consumption was linked with increasing atherosclerosis in a linear fashion in both the coronary and carotid arteries.
Each 1,000 mg rise in sodium excretion was associated with a 9% increased occurrence of carotid plaque (odds ratio, 1.09; P < .001; confidence interval, 1.06-1.12), a higher coronary artery calcium score (OR, 1.16; P < .001; CI, 1.12-1.19), and a 17% increased occurrence of coronary artery stenosis (OR, 1.17; P < .001; CI, 1.13-1.20).
The association was abolished, though, after adjusting for blood pressure, they note. Their “interpretation is that the increase in blood pressure from sodium intake, even below the level that currently defines arterial hypertension, is an important factor that mediates the interplay between salt intake and the atherosclerotic process,” they write. “As we observed an association in individuals with normal blood pressure, one possible explanation for these findings is that the detrimental pathological processes begin already prior to the development of hypertension,” they note, although they caution that no causal relationships can be gleaned from this cross-sectional study.
They also reported no sign of a “J-curve”; participants with the lowest levels of sodium excretion had the lowest occurrence of both coronary and carotid atherosclerosis, which contradicts findings in some studies that found very low sodium linked to increased cardiovascular disease–related events.
“There have been some controversies among researchers regarding very low intake, where some say very low salt intake can increase the risk of cardiovascular disease, but we could not find this in this study,” Dr. Wuopio said.
“Our study is confirming that excess salt is not a good thing, but the fact that it is linked to atherosclerosis, even in the absence of hypertension, was a bit of a surprise,” he said.
“I will be telling my patients to follow the advice given by the World Health Organization and other medical societies, to limit your intake of salt to approximately 1 teaspoon, even if your blood pressure is normal.”
Time to scrutinize salt’s role in atherosclerosis
In an accompanying editorial, Maciej Banach, MD, Medical University of Lodz, and Stanislaw Surma, MD, Faculty of Medical Sciences in Katowice, both in Poland, write that excessive dietary salt intake is a well-documented cardiovascular risk factor, and that the association is explained in most studies by increased blood pressure.
“We should look more extensively on the role of dietary salt, as it affects many pathological mechanisms, by which, especially with the coexistence of other risk factors, atherosclerosis may progress very fast,” they write.
“The results of the study shed new light on the direct relationship between excessive dietary salt intake and the risk of ASCVD [atherosclerotic cardiovascular disease], indicating that salt intake might be a risk factor for atherosclerosis even prior to the development of hypertension,” they conclude.
Confirmatory and novel
“Nobody questions the fact that high blood pressure is a powerful risk factor for atherosclerotic disease, but not all studies have suggested that, at least at significantly higher levels of sodium intake, that high salt intake tracks with risk for atherosclerotic disease,” Alon Gitig, MD, assistant professor and director of cardiology, Mount Sinai Doctors-Westchester, Yonkers, New York, told this news organization.
Most of the studies of salt intake in the diet are based on patient self-reports via food frequency questionnaires, which can give a general idea of salt intake, but are often not totally accurate, Dr. Gitig said.
“Here, they measured sodium in the urine and estimated the 24-hour salt intake from that, which is slightly novel,” he said.
Everybody knows that high blood pressure is associated with future cardiovascular disease risk, but what many don’t realize is that that risk starts to increase slightly but significantly above a blood pressure that is already in the range of 115 mm Hg/75 mm Hg, he said.
“The lower you can get your blood pressure down, to around 115-120, the lower your risk for cardiovascular disease,” Dr. Gitig said.
It is possible for most people to lower blood pressure through attention to diet, restricting sodium, performing cardio and weight training exercises, and maintaining a healthy weight, he said.
An example of a cardiovascular health diet is the Dietary Approaches to Stop Hypertension (DASH) diet.
“The DASH diet, consisting of 9 servings of fruits and vegetables a day with few refined carbs, flour and sugar, has been shown in a randomized trial to dramatically reduce blood pressure. There are two reasons for that. One is that the fruits and vegetables have many phytonutrients that are good for arteries. The other is that a large proportion of U.S. adults have insulin resistance, which leads to high blood pressure.
“The more fruits and vegetables and healthy animal products, and less sugar and flour, the more you are going to improve your insulin resistance, so you can bring your blood pressure down that way,” Dr. Gitig said.
The study was funded by the Swedish Heart-Lung Foundation, the Knut and Alice Wallenberg Foundation, the Swedish Research Council and Vinnova (Sweden’s Innovation agency), the University of Gothenburg and Sahlgrenska University Hospital, the Karolinska Institutet and Stockholm County Council, the Linköping University and University Hospital, the Lund University and Skane University Hospital, the Umea University and University Hospital, and the Uppsala University and University Hospital. Dr. Wuopio and Dr. Gitig report no relevant financial relationships. Dr. Banach reports financial relationships with Adamed, Amgen, Daichii Sankyo, Esperion, KrKa, NewAmsterdam, Polpharma, Novartis, Pfizer, Sanofi, Teva, Viatris, and CMDO at Longevity Group (LU). Dr. Surma reports a financial relationship with Sanofi and Novartis.
A version of this article first appeared on Medscape.com.
A high salt intake is an important risk factor for atherosclerosis, even in the absence of hypertension, a large study from Sweden concludes.
The study, including more than 10,000 individuals between the ages of 50 and 64 years from the Swedish Cardiopulmonary bioImage Study, showed a significant link between dietary salt intake and the risk for atherosclerotic lesions in the coronary and carotid arteries, even in participants with normal blood pressure and without known cardiovascular disease.
The finding suggests that salt could be a damaging factor in its own right before the development of hypertension, the authors write. The results were published online in European Heart Journal Open.
It has been known for a long time that salt is linked to hypertension, but the role that salt plays in atherosclerosis has not been examined, first author Jonas Wuopio, MD, Karolinska Institutet, Huddinge, and Clinical Research Center, Falun, Uppsala University, both in Sweden, told this news organization.
“Hardly anyone looks at changes in the arteries’ calcification, the atherosclerotic plaques and the association with salt intake,” Dr. Wuopio said. “We had this exclusive data from our cohort, so we wanted to use it to close this knowledge gap.”
The analysis included 10,788 adults aged 50-64 years, (average age, 58 years; 52% women) who underwent a coronary computed tomography angiography (CCTA) scan. The estimated 24-hour sodium excretion was used to measure sodium intake.
CCTA was used to obtain 3-D images of the coronary arteries to measure the degree of coronary artery calcium as well as detect stenosis in the coronary arteries. Participants also had an ultrasound of the carotid arteries.
After adjusting for age, sex, and study site (the study was done at Uppsala and Malmö, Sweden), the researchers found that rising salt consumption was linked with increasing atherosclerosis in a linear fashion in both the coronary and carotid arteries.
Each 1,000 mg rise in sodium excretion was associated with a 9% increased occurrence of carotid plaque (odds ratio, 1.09; P < .001; confidence interval, 1.06-1.12), a higher coronary artery calcium score (OR, 1.16; P < .001; CI, 1.12-1.19), and a 17% increased occurrence of coronary artery stenosis (OR, 1.17; P < .001; CI, 1.13-1.20).
The association was abolished, though, after adjusting for blood pressure, they note. Their “interpretation is that the increase in blood pressure from sodium intake, even below the level that currently defines arterial hypertension, is an important factor that mediates the interplay between salt intake and the atherosclerotic process,” they write. “As we observed an association in individuals with normal blood pressure, one possible explanation for these findings is that the detrimental pathological processes begin already prior to the development of hypertension,” they note, although they caution that no causal relationships can be gleaned from this cross-sectional study.
They also reported no sign of a “J-curve”; participants with the lowest levels of sodium excretion had the lowest occurrence of both coronary and carotid atherosclerosis, which contradicts findings in some studies that found very low sodium linked to increased cardiovascular disease–related events.
“There have been some controversies among researchers regarding very low intake, where some say very low salt intake can increase the risk of cardiovascular disease, but we could not find this in this study,” Dr. Wuopio said.
“Our study is confirming that excess salt is not a good thing, but the fact that it is linked to atherosclerosis, even in the absence of hypertension, was a bit of a surprise,” he said.
“I will be telling my patients to follow the advice given by the World Health Organization and other medical societies, to limit your intake of salt to approximately 1 teaspoon, even if your blood pressure is normal.”
Time to scrutinize salt’s role in atherosclerosis
In an accompanying editorial, Maciej Banach, MD, Medical University of Lodz, and Stanislaw Surma, MD, Faculty of Medical Sciences in Katowice, both in Poland, write that excessive dietary salt intake is a well-documented cardiovascular risk factor, and that the association is explained in most studies by increased blood pressure.
“We should look more extensively on the role of dietary salt, as it affects many pathological mechanisms, by which, especially with the coexistence of other risk factors, atherosclerosis may progress very fast,” they write.
“The results of the study shed new light on the direct relationship between excessive dietary salt intake and the risk of ASCVD [atherosclerotic cardiovascular disease], indicating that salt intake might be a risk factor for atherosclerosis even prior to the development of hypertension,” they conclude.
Confirmatory and novel
“Nobody questions the fact that high blood pressure is a powerful risk factor for atherosclerotic disease, but not all studies have suggested that, at least at significantly higher levels of sodium intake, that high salt intake tracks with risk for atherosclerotic disease,” Alon Gitig, MD, assistant professor and director of cardiology, Mount Sinai Doctors-Westchester, Yonkers, New York, told this news organization.
Most of the studies of salt intake in the diet are based on patient self-reports via food frequency questionnaires, which can give a general idea of salt intake, but are often not totally accurate, Dr. Gitig said.
“Here, they measured sodium in the urine and estimated the 24-hour salt intake from that, which is slightly novel,” he said.
Everybody knows that high blood pressure is associated with future cardiovascular disease risk, but what many don’t realize is that that risk starts to increase slightly but significantly above a blood pressure that is already in the range of 115 mm Hg/75 mm Hg, he said.
“The lower you can get your blood pressure down, to around 115-120, the lower your risk for cardiovascular disease,” Dr. Gitig said.
It is possible for most people to lower blood pressure through attention to diet, restricting sodium, performing cardio and weight training exercises, and maintaining a healthy weight, he said.
An example of a cardiovascular health diet is the Dietary Approaches to Stop Hypertension (DASH) diet.
“The DASH diet, consisting of 9 servings of fruits and vegetables a day with few refined carbs, flour and sugar, has been shown in a randomized trial to dramatically reduce blood pressure. There are two reasons for that. One is that the fruits and vegetables have many phytonutrients that are good for arteries. The other is that a large proportion of U.S. adults have insulin resistance, which leads to high blood pressure.
“The more fruits and vegetables and healthy animal products, and less sugar and flour, the more you are going to improve your insulin resistance, so you can bring your blood pressure down that way,” Dr. Gitig said.
The study was funded by the Swedish Heart-Lung Foundation, the Knut and Alice Wallenberg Foundation, the Swedish Research Council and Vinnova (Sweden’s Innovation agency), the University of Gothenburg and Sahlgrenska University Hospital, the Karolinska Institutet and Stockholm County Council, the Linköping University and University Hospital, the Lund University and Skane University Hospital, the Umea University and University Hospital, and the Uppsala University and University Hospital. Dr. Wuopio and Dr. Gitig report no relevant financial relationships. Dr. Banach reports financial relationships with Adamed, Amgen, Daichii Sankyo, Esperion, KrKa, NewAmsterdam, Polpharma, Novartis, Pfizer, Sanofi, Teva, Viatris, and CMDO at Longevity Group (LU). Dr. Surma reports a financial relationship with Sanofi and Novartis.
A version of this article first appeared on Medscape.com.
A high salt intake is an important risk factor for atherosclerosis, even in the absence of hypertension, a large study from Sweden concludes.
The study, including more than 10,000 individuals between the ages of 50 and 64 years from the Swedish Cardiopulmonary bioImage Study, showed a significant link between dietary salt intake and the risk for atherosclerotic lesions in the coronary and carotid arteries, even in participants with normal blood pressure and without known cardiovascular disease.
The finding suggests that salt could be a damaging factor in its own right before the development of hypertension, the authors write. The results were published online in European Heart Journal Open.
It has been known for a long time that salt is linked to hypertension, but the role that salt plays in atherosclerosis has not been examined, first author Jonas Wuopio, MD, Karolinska Institutet, Huddinge, and Clinical Research Center, Falun, Uppsala University, both in Sweden, told this news organization.
“Hardly anyone looks at changes in the arteries’ calcification, the atherosclerotic plaques and the association with salt intake,” Dr. Wuopio said. “We had this exclusive data from our cohort, so we wanted to use it to close this knowledge gap.”
The analysis included 10,788 adults aged 50-64 years, (average age, 58 years; 52% women) who underwent a coronary computed tomography angiography (CCTA) scan. The estimated 24-hour sodium excretion was used to measure sodium intake.
CCTA was used to obtain 3-D images of the coronary arteries to measure the degree of coronary artery calcium as well as detect stenosis in the coronary arteries. Participants also had an ultrasound of the carotid arteries.
After adjusting for age, sex, and study site (the study was done at Uppsala and Malmö, Sweden), the researchers found that rising salt consumption was linked with increasing atherosclerosis in a linear fashion in both the coronary and carotid arteries.
Each 1,000 mg rise in sodium excretion was associated with a 9% increased occurrence of carotid plaque (odds ratio, 1.09; P < .001; confidence interval, 1.06-1.12), a higher coronary artery calcium score (OR, 1.16; P < .001; CI, 1.12-1.19), and a 17% increased occurrence of coronary artery stenosis (OR, 1.17; P < .001; CI, 1.13-1.20).
The association was abolished, though, after adjusting for blood pressure, they note. Their “interpretation is that the increase in blood pressure from sodium intake, even below the level that currently defines arterial hypertension, is an important factor that mediates the interplay between salt intake and the atherosclerotic process,” they write. “As we observed an association in individuals with normal blood pressure, one possible explanation for these findings is that the detrimental pathological processes begin already prior to the development of hypertension,” they note, although they caution that no causal relationships can be gleaned from this cross-sectional study.
They also reported no sign of a “J-curve”; participants with the lowest levels of sodium excretion had the lowest occurrence of both coronary and carotid atherosclerosis, which contradicts findings in some studies that found very low sodium linked to increased cardiovascular disease–related events.
“There have been some controversies among researchers regarding very low intake, where some say very low salt intake can increase the risk of cardiovascular disease, but we could not find this in this study,” Dr. Wuopio said.
“Our study is confirming that excess salt is not a good thing, but the fact that it is linked to atherosclerosis, even in the absence of hypertension, was a bit of a surprise,” he said.
“I will be telling my patients to follow the advice given by the World Health Organization and other medical societies, to limit your intake of salt to approximately 1 teaspoon, even if your blood pressure is normal.”
Time to scrutinize salt’s role in atherosclerosis
In an accompanying editorial, Maciej Banach, MD, Medical University of Lodz, and Stanislaw Surma, MD, Faculty of Medical Sciences in Katowice, both in Poland, write that excessive dietary salt intake is a well-documented cardiovascular risk factor, and that the association is explained in most studies by increased blood pressure.
“We should look more extensively on the role of dietary salt, as it affects many pathological mechanisms, by which, especially with the coexistence of other risk factors, atherosclerosis may progress very fast,” they write.
“The results of the study shed new light on the direct relationship between excessive dietary salt intake and the risk of ASCVD [atherosclerotic cardiovascular disease], indicating that salt intake might be a risk factor for atherosclerosis even prior to the development of hypertension,” they conclude.
Confirmatory and novel
“Nobody questions the fact that high blood pressure is a powerful risk factor for atherosclerotic disease, but not all studies have suggested that, at least at significantly higher levels of sodium intake, that high salt intake tracks with risk for atherosclerotic disease,” Alon Gitig, MD, assistant professor and director of cardiology, Mount Sinai Doctors-Westchester, Yonkers, New York, told this news organization.
Most of the studies of salt intake in the diet are based on patient self-reports via food frequency questionnaires, which can give a general idea of salt intake, but are often not totally accurate, Dr. Gitig said.
“Here, they measured sodium in the urine and estimated the 24-hour salt intake from that, which is slightly novel,” he said.
Everybody knows that high blood pressure is associated with future cardiovascular disease risk, but what many don’t realize is that that risk starts to increase slightly but significantly above a blood pressure that is already in the range of 115 mm Hg/75 mm Hg, he said.
“The lower you can get your blood pressure down, to around 115-120, the lower your risk for cardiovascular disease,” Dr. Gitig said.
It is possible for most people to lower blood pressure through attention to diet, restricting sodium, performing cardio and weight training exercises, and maintaining a healthy weight, he said.
An example of a cardiovascular health diet is the Dietary Approaches to Stop Hypertension (DASH) diet.
“The DASH diet, consisting of 9 servings of fruits and vegetables a day with few refined carbs, flour and sugar, has been shown in a randomized trial to dramatically reduce blood pressure. There are two reasons for that. One is that the fruits and vegetables have many phytonutrients that are good for arteries. The other is that a large proportion of U.S. adults have insulin resistance, which leads to high blood pressure.
“The more fruits and vegetables and healthy animal products, and less sugar and flour, the more you are going to improve your insulin resistance, so you can bring your blood pressure down that way,” Dr. Gitig said.
The study was funded by the Swedish Heart-Lung Foundation, the Knut and Alice Wallenberg Foundation, the Swedish Research Council and Vinnova (Sweden’s Innovation agency), the University of Gothenburg and Sahlgrenska University Hospital, the Karolinska Institutet and Stockholm County Council, the Linköping University and University Hospital, the Lund University and Skane University Hospital, the Umea University and University Hospital, and the Uppsala University and University Hospital. Dr. Wuopio and Dr. Gitig report no relevant financial relationships. Dr. Banach reports financial relationships with Adamed, Amgen, Daichii Sankyo, Esperion, KrKa, NewAmsterdam, Polpharma, Novartis, Pfizer, Sanofi, Teva, Viatris, and CMDO at Longevity Group (LU). Dr. Surma reports a financial relationship with Sanofi and Novartis.
A version of this article first appeared on Medscape.com.
Lack of food for thought: Starve a bacterium, feed an infection
A whole new, tiny level of hangry
Ever been so hungry that everything just got on your nerves? Maybe you feel a little snappy right now? Like you’ll just lash out unless you get something to eat? Been there. And so have bacteria.
New research shows that some bacteria go into a full-on Hulk smash if they’re not getting the nutrients they need by releasing toxins into the body. Sounds like a bacterial temper tantrum.
Even though two cells may be genetically identical, they don’t always behave the same in a bacterial community. Some do their job and stay in line, but some evil twins rage out and make people sick by releasing toxins into the environment, Adam Rosenthal, PhD, of the University of North Carolina and his colleagues discovered.
To figure out why some cells were all business as usual while others were not, the investigators looked at Clostridium perfringens, a bacterium found in the intestines of humans and other vertebrates. When the C. perfringens cells were fed a little acetate to munch on, the hangry cells calmed down faster than a kid with a bag of fruit snacks, reducing toxin levels. Some cells even disappeared, falling in line with their model-citizen counterparts.
So what does this really mean? More research, duh. Now that we know nutrients play a role in toxicity, it may open the door to finding a way to fight against antibiotic resistance in humans and reduce antibiotic use in the food industry.
So think to yourself. Are you bothered for no reason? Getting a little testy with your friends and coworkers? Maybe you just haven’t eaten in a while. You’re literally not alone. Even a single-cell organism can behave based on its hunger levels.
Now go have a snack. Your bacteria are getting restless.
The very hangry iguana?
Imagine yourself on a warm, sunny tropical beach. You are enjoying a piece of cake as you take in the slow beat of the waves lapping against the shore. Life is as good as it could be.
Then you feel a presence nearby. Hostility. Hunger. A set of feral, covetous eyes in the nearby jungle. A reptilian beast stalks you, and its all-encompassing sweet tooth desires your cake.
Wait, hold on, what?
As an unfortunate 3-year-old on vacation in Costa Rica found out, there’s at least one iguana in the world out there with a taste for sugar (better than a taste for blood, we suppose).
While out on the beach, the lizard darted out of nowhere, bit the girl on the back of the hand, and stole her cake. Still not the worst party guest ever. The child was taken to a local clinic, where the wound was cleaned and a 5-day antibiotic treatment (lizards carry salmonella) was provided. Things seemed fine, and the girl returned home without incident.
But of course, that’s not the end of the story. Five months later, the girl’s parents noticed a red bump at the wound site. Over the next 3 months, the surrounding skin grew red and painful. A trip to the hospital in California revealed that she had a ganglion cyst and a discharge of pus. Turns out our cake-obsessed lizard friend did give the little girl a gift: the first known human case of Mycobacterium marinum infection following an iguana bite on record.
M. marinum, which causes a disease similar to tuberculosis, typically infects fish but can infect humans if skin wounds are exposed to contaminated water. It’s also resistant to most antibiotics, which is why the first round didn’t clear up the infection. A second round of more-potent antibiotics seems to be working well.
So, to sum up, this poor child got bitten by a lizard, had her cake stolen, and contracted a rare illness in exchange. For a 3-year-old, that’s gotta be in the top-10 worst days ever. Unless, of course, we’re actually living in the Marvel universe (sorry, multiverse at this point). Then we’re totally going to see the emergence of the new superhero Iguana Girl in 15 years or so. Keep your eyes open.
No allergies? Let them give up cake
Allergy season is already here – starting earlier every year, it seems – and many people are not happy about it. So unhappy, actually, that there’s a list of things they would be willing to give up for a year to get rid of their of allergies, according to a survey conducted by OnePoll on behalf of Flonase.
Nearly 40% of 2,000 respondents with allergies would go a year without eating cake or chocolate or playing video games in exchange for allergy-free status, the survey results show. Almost as many would forgo coffee (38%) or pizza (37%) for a year, while 36% would stay off social media and 31% would take a pay cut or give up their smartphones, the Independent reported.
More than half of the allergic Americans – 54%, to be exact – who were polled this past winter – Feb. 24 to March 1, to be exact – consider allergy symptoms to be the most frustrating part of the spring. Annoying things that were less frustrating to the group included mosquitoes (41%), filing tax returns (38%), and daylight savings time (37%).
The Trump arraignment circus, of course, occurred too late to make the list, as did the big “We’re going back to the office! No wait, we’re closing the office forever!” email extravaganza and emotional roller coaster. That second one, however, did not get nearly as much media coverage.
A whole new, tiny level of hangry
Ever been so hungry that everything just got on your nerves? Maybe you feel a little snappy right now? Like you’ll just lash out unless you get something to eat? Been there. And so have bacteria.
New research shows that some bacteria go into a full-on Hulk smash if they’re not getting the nutrients they need by releasing toxins into the body. Sounds like a bacterial temper tantrum.
Even though two cells may be genetically identical, they don’t always behave the same in a bacterial community. Some do their job and stay in line, but some evil twins rage out and make people sick by releasing toxins into the environment, Adam Rosenthal, PhD, of the University of North Carolina and his colleagues discovered.
To figure out why some cells were all business as usual while others were not, the investigators looked at Clostridium perfringens, a bacterium found in the intestines of humans and other vertebrates. When the C. perfringens cells were fed a little acetate to munch on, the hangry cells calmed down faster than a kid with a bag of fruit snacks, reducing toxin levels. Some cells even disappeared, falling in line with their model-citizen counterparts.
So what does this really mean? More research, duh. Now that we know nutrients play a role in toxicity, it may open the door to finding a way to fight against antibiotic resistance in humans and reduce antibiotic use in the food industry.
So think to yourself. Are you bothered for no reason? Getting a little testy with your friends and coworkers? Maybe you just haven’t eaten in a while. You’re literally not alone. Even a single-cell organism can behave based on its hunger levels.
Now go have a snack. Your bacteria are getting restless.
The very hangry iguana?
Imagine yourself on a warm, sunny tropical beach. You are enjoying a piece of cake as you take in the slow beat of the waves lapping against the shore. Life is as good as it could be.
Then you feel a presence nearby. Hostility. Hunger. A set of feral, covetous eyes in the nearby jungle. A reptilian beast stalks you, and its all-encompassing sweet tooth desires your cake.
Wait, hold on, what?
As an unfortunate 3-year-old on vacation in Costa Rica found out, there’s at least one iguana in the world out there with a taste for sugar (better than a taste for blood, we suppose).
While out on the beach, the lizard darted out of nowhere, bit the girl on the back of the hand, and stole her cake. Still not the worst party guest ever. The child was taken to a local clinic, where the wound was cleaned and a 5-day antibiotic treatment (lizards carry salmonella) was provided. Things seemed fine, and the girl returned home without incident.
But of course, that’s not the end of the story. Five months later, the girl’s parents noticed a red bump at the wound site. Over the next 3 months, the surrounding skin grew red and painful. A trip to the hospital in California revealed that she had a ganglion cyst and a discharge of pus. Turns out our cake-obsessed lizard friend did give the little girl a gift: the first known human case of Mycobacterium marinum infection following an iguana bite on record.
M. marinum, which causes a disease similar to tuberculosis, typically infects fish but can infect humans if skin wounds are exposed to contaminated water. It’s also resistant to most antibiotics, which is why the first round didn’t clear up the infection. A second round of more-potent antibiotics seems to be working well.
So, to sum up, this poor child got bitten by a lizard, had her cake stolen, and contracted a rare illness in exchange. For a 3-year-old, that’s gotta be in the top-10 worst days ever. Unless, of course, we’re actually living in the Marvel universe (sorry, multiverse at this point). Then we’re totally going to see the emergence of the new superhero Iguana Girl in 15 years or so. Keep your eyes open.
No allergies? Let them give up cake
Allergy season is already here – starting earlier every year, it seems – and many people are not happy about it. So unhappy, actually, that there’s a list of things they would be willing to give up for a year to get rid of their of allergies, according to a survey conducted by OnePoll on behalf of Flonase.
Nearly 40% of 2,000 respondents with allergies would go a year without eating cake or chocolate or playing video games in exchange for allergy-free status, the survey results show. Almost as many would forgo coffee (38%) or pizza (37%) for a year, while 36% would stay off social media and 31% would take a pay cut or give up their smartphones, the Independent reported.
More than half of the allergic Americans – 54%, to be exact – who were polled this past winter – Feb. 24 to March 1, to be exact – consider allergy symptoms to be the most frustrating part of the spring. Annoying things that were less frustrating to the group included mosquitoes (41%), filing tax returns (38%), and daylight savings time (37%).
The Trump arraignment circus, of course, occurred too late to make the list, as did the big “We’re going back to the office! No wait, we’re closing the office forever!” email extravaganza and emotional roller coaster. That second one, however, did not get nearly as much media coverage.
A whole new, tiny level of hangry
Ever been so hungry that everything just got on your nerves? Maybe you feel a little snappy right now? Like you’ll just lash out unless you get something to eat? Been there. And so have bacteria.
New research shows that some bacteria go into a full-on Hulk smash if they’re not getting the nutrients they need by releasing toxins into the body. Sounds like a bacterial temper tantrum.
Even though two cells may be genetically identical, they don’t always behave the same in a bacterial community. Some do their job and stay in line, but some evil twins rage out and make people sick by releasing toxins into the environment, Adam Rosenthal, PhD, of the University of North Carolina and his colleagues discovered.
To figure out why some cells were all business as usual while others were not, the investigators looked at Clostridium perfringens, a bacterium found in the intestines of humans and other vertebrates. When the C. perfringens cells were fed a little acetate to munch on, the hangry cells calmed down faster than a kid with a bag of fruit snacks, reducing toxin levels. Some cells even disappeared, falling in line with their model-citizen counterparts.
So what does this really mean? More research, duh. Now that we know nutrients play a role in toxicity, it may open the door to finding a way to fight against antibiotic resistance in humans and reduce antibiotic use in the food industry.
So think to yourself. Are you bothered for no reason? Getting a little testy with your friends and coworkers? Maybe you just haven’t eaten in a while. You’re literally not alone. Even a single-cell organism can behave based on its hunger levels.
Now go have a snack. Your bacteria are getting restless.
The very hangry iguana?
Imagine yourself on a warm, sunny tropical beach. You are enjoying a piece of cake as you take in the slow beat of the waves lapping against the shore. Life is as good as it could be.
Then you feel a presence nearby. Hostility. Hunger. A set of feral, covetous eyes in the nearby jungle. A reptilian beast stalks you, and its all-encompassing sweet tooth desires your cake.
Wait, hold on, what?
As an unfortunate 3-year-old on vacation in Costa Rica found out, there’s at least one iguana in the world out there with a taste for sugar (better than a taste for blood, we suppose).
While out on the beach, the lizard darted out of nowhere, bit the girl on the back of the hand, and stole her cake. Still not the worst party guest ever. The child was taken to a local clinic, where the wound was cleaned and a 5-day antibiotic treatment (lizards carry salmonella) was provided. Things seemed fine, and the girl returned home without incident.
But of course, that’s not the end of the story. Five months later, the girl’s parents noticed a red bump at the wound site. Over the next 3 months, the surrounding skin grew red and painful. A trip to the hospital in California revealed that she had a ganglion cyst and a discharge of pus. Turns out our cake-obsessed lizard friend did give the little girl a gift: the first known human case of Mycobacterium marinum infection following an iguana bite on record.
M. marinum, which causes a disease similar to tuberculosis, typically infects fish but can infect humans if skin wounds are exposed to contaminated water. It’s also resistant to most antibiotics, which is why the first round didn’t clear up the infection. A second round of more-potent antibiotics seems to be working well.
So, to sum up, this poor child got bitten by a lizard, had her cake stolen, and contracted a rare illness in exchange. For a 3-year-old, that’s gotta be in the top-10 worst days ever. Unless, of course, we’re actually living in the Marvel universe (sorry, multiverse at this point). Then we’re totally going to see the emergence of the new superhero Iguana Girl in 15 years or so. Keep your eyes open.
No allergies? Let them give up cake
Allergy season is already here – starting earlier every year, it seems – and many people are not happy about it. So unhappy, actually, that there’s a list of things they would be willing to give up for a year to get rid of their of allergies, according to a survey conducted by OnePoll on behalf of Flonase.
Nearly 40% of 2,000 respondents with allergies would go a year without eating cake or chocolate or playing video games in exchange for allergy-free status, the survey results show. Almost as many would forgo coffee (38%) or pizza (37%) for a year, while 36% would stay off social media and 31% would take a pay cut or give up their smartphones, the Independent reported.
More than half of the allergic Americans – 54%, to be exact – who were polled this past winter – Feb. 24 to March 1, to be exact – consider allergy symptoms to be the most frustrating part of the spring. Annoying things that were less frustrating to the group included mosquitoes (41%), filing tax returns (38%), and daylight savings time (37%).
The Trump arraignment circus, of course, occurred too late to make the list, as did the big “We’re going back to the office! No wait, we’re closing the office forever!” email extravaganza and emotional roller coaster. That second one, however, did not get nearly as much media coverage.
Infant and maternal weight gain together amplify obesity risk
Rapid weight gain (RWG) in infants and the mother’s prepregnancy overweight have a synergistic effect in increasing the odds that a child will develop overweight or obesity, new research suggests.
Findings were published online in Pediatrics.
Each factor has independently been associated with higher risk of childhood obesity but whether the two factors together exacerbate the risk has not been well studied, according to the authors led by Stephanie Gilley, MD, PhD, department of pediatrics, section of nutrition, University of Colorado at Denver, Aurora.
“Pediatric providers should monitor infants for RWG, especially in the context of maternal obesity, to reduce future risk of obesity,” the authors conclude.
Dr. Gilley’s team studied mother-infant dyads (n = 414) from the Healthy Start Study, an observational prebirth cohort. RWG was defined as a weight-for-age z score increase of at least 0.67 from birth to 3-7 months.
They found that RWG boosted the link between prepregnancy body mass index (ppBMI) and BMI z score, especially in female infants. Females exposed to both maternal obesity with RWG had an average BMI at the 94th percentile (1.50 increase in childhood BMI z score) “nearly at the cutoff for classification of obesity,” compared with those exposed to normal ppBMI with no RWG, who had an average childhood BMI at the 51st percentile.
“Currently, our nutrition recommendations as pediatricians are that all children are fed the same, essentially, after they’re born. We don’t have different growth parameters or different trajectories or targets for children who may have had different in utero exposures,” Dr. Gilley said.
Do some children need more monitoring for RWG?
Though we can’t necessarily draw conclusions from this one study, she says, the findings raise the question of whether children who were exposed in utero to obesity should be monitored for RWG more closely.
Lydia Shook, MD, Mass General Brigham maternal-fetal specialist and codirector of the Diabetes in Pregnancy Program at Massachusetts General Hospital in Boston, said she was struck by the finding in this study that with female infants, but not males, RWG significantly modified the association between ppBMI and early childhood BMI z scores.
“It’s an interesting finding and should be followed up with larger cohorts,” she said, noting that some previous studies have shown males are more vulnerable to maternal obesity and RWG.
“[Often] when we stratify by sex, you really need larger groups to be able to see the differences well,” Dr. Shook said.
She said she also found it interesting that when the researchers adjusted for breastfeeding status or caloric intake in childhood, the findings did not substantially change.
“That’s something that would warrant further investigation in an observational study or controlled trial,” Dr. Shook said.
Preventing rapid weight gain
The authors note that they did not consider possible interventions for preventing RGW in the study, although there are many, Dr. Gilley said.
Dr. Gilley also noted that a limitation of this study is that the population studied was primarily White.
Recent studies have shown the benefits of responsive parenting (RP) interventions, including a large study in 2022 geared toward Black families to teach better infant sleep practices as a way to prevent rapid weight gain.
That study, which tested the SAAF intervention, (Strong African American Families) found that “RP infants were nearly half as likely to experience upward crossing of two major weight-for-age percentile lines (14.1%), compared with control infants (24.2%); P = .09; odds ratio, 0.52; 95% confidence interval, 0.24-1.12.”
Along with sleep interventions, Dr. Gilley said, some researchers are studying the effects on RWG of better paternal engagement, or more involvement with the Women, Infants, and Children program, particularly with lower-income families.
Other studies have looked at breastfeeding vs. formula feeding – “but there have been mixed results there” – and responsive feeding practices, such as teaching families to recognize when a baby is full.
Dr. Gilley said she hopes this work will help broaden the thinking when it comes to infant weight gain.
“We spend a lot of time thinking about babies who are not growing fast enough and very little time thinking about babies who are growing too fast,” she said, “especially in those first 4-6 months of life.”
Dr. Gilley points to a study that illustrates that point. Pesch et al. concluded in a 2021 study based on interviews that pediatricians “are uncertain about the concept, definition, management, and long-term risks of rapid infant weight gain.”
Authors and Dr. Gilley declare no relevant financial relationships.
Rapid weight gain (RWG) in infants and the mother’s prepregnancy overweight have a synergistic effect in increasing the odds that a child will develop overweight or obesity, new research suggests.
Findings were published online in Pediatrics.
Each factor has independently been associated with higher risk of childhood obesity but whether the two factors together exacerbate the risk has not been well studied, according to the authors led by Stephanie Gilley, MD, PhD, department of pediatrics, section of nutrition, University of Colorado at Denver, Aurora.
“Pediatric providers should monitor infants for RWG, especially in the context of maternal obesity, to reduce future risk of obesity,” the authors conclude.
Dr. Gilley’s team studied mother-infant dyads (n = 414) from the Healthy Start Study, an observational prebirth cohort. RWG was defined as a weight-for-age z score increase of at least 0.67 from birth to 3-7 months.
They found that RWG boosted the link between prepregnancy body mass index (ppBMI) and BMI z score, especially in female infants. Females exposed to both maternal obesity with RWG had an average BMI at the 94th percentile (1.50 increase in childhood BMI z score) “nearly at the cutoff for classification of obesity,” compared with those exposed to normal ppBMI with no RWG, who had an average childhood BMI at the 51st percentile.
“Currently, our nutrition recommendations as pediatricians are that all children are fed the same, essentially, after they’re born. We don’t have different growth parameters or different trajectories or targets for children who may have had different in utero exposures,” Dr. Gilley said.
Do some children need more monitoring for RWG?
Though we can’t necessarily draw conclusions from this one study, she says, the findings raise the question of whether children who were exposed in utero to obesity should be monitored for RWG more closely.
Lydia Shook, MD, Mass General Brigham maternal-fetal specialist and codirector of the Diabetes in Pregnancy Program at Massachusetts General Hospital in Boston, said she was struck by the finding in this study that with female infants, but not males, RWG significantly modified the association between ppBMI and early childhood BMI z scores.
“It’s an interesting finding and should be followed up with larger cohorts,” she said, noting that some previous studies have shown males are more vulnerable to maternal obesity and RWG.
“[Often] when we stratify by sex, you really need larger groups to be able to see the differences well,” Dr. Shook said.
She said she also found it interesting that when the researchers adjusted for breastfeeding status or caloric intake in childhood, the findings did not substantially change.
“That’s something that would warrant further investigation in an observational study or controlled trial,” Dr. Shook said.
Preventing rapid weight gain
The authors note that they did not consider possible interventions for preventing RGW in the study, although there are many, Dr. Gilley said.
Dr. Gilley also noted that a limitation of this study is that the population studied was primarily White.
Recent studies have shown the benefits of responsive parenting (RP) interventions, including a large study in 2022 geared toward Black families to teach better infant sleep practices as a way to prevent rapid weight gain.
That study, which tested the SAAF intervention, (Strong African American Families) found that “RP infants were nearly half as likely to experience upward crossing of two major weight-for-age percentile lines (14.1%), compared with control infants (24.2%); P = .09; odds ratio, 0.52; 95% confidence interval, 0.24-1.12.”
Along with sleep interventions, Dr. Gilley said, some researchers are studying the effects on RWG of better paternal engagement, or more involvement with the Women, Infants, and Children program, particularly with lower-income families.
Other studies have looked at breastfeeding vs. formula feeding – “but there have been mixed results there” – and responsive feeding practices, such as teaching families to recognize when a baby is full.
Dr. Gilley said she hopes this work will help broaden the thinking when it comes to infant weight gain.
“We spend a lot of time thinking about babies who are not growing fast enough and very little time thinking about babies who are growing too fast,” she said, “especially in those first 4-6 months of life.”
Dr. Gilley points to a study that illustrates that point. Pesch et al. concluded in a 2021 study based on interviews that pediatricians “are uncertain about the concept, definition, management, and long-term risks of rapid infant weight gain.”
Authors and Dr. Gilley declare no relevant financial relationships.
Rapid weight gain (RWG) in infants and the mother’s prepregnancy overweight have a synergistic effect in increasing the odds that a child will develop overweight or obesity, new research suggests.
Findings were published online in Pediatrics.
Each factor has independently been associated with higher risk of childhood obesity but whether the two factors together exacerbate the risk has not been well studied, according to the authors led by Stephanie Gilley, MD, PhD, department of pediatrics, section of nutrition, University of Colorado at Denver, Aurora.
“Pediatric providers should monitor infants for RWG, especially in the context of maternal obesity, to reduce future risk of obesity,” the authors conclude.
Dr. Gilley’s team studied mother-infant dyads (n = 414) from the Healthy Start Study, an observational prebirth cohort. RWG was defined as a weight-for-age z score increase of at least 0.67 from birth to 3-7 months.
They found that RWG boosted the link between prepregnancy body mass index (ppBMI) and BMI z score, especially in female infants. Females exposed to both maternal obesity with RWG had an average BMI at the 94th percentile (1.50 increase in childhood BMI z score) “nearly at the cutoff for classification of obesity,” compared with those exposed to normal ppBMI with no RWG, who had an average childhood BMI at the 51st percentile.
“Currently, our nutrition recommendations as pediatricians are that all children are fed the same, essentially, after they’re born. We don’t have different growth parameters or different trajectories or targets for children who may have had different in utero exposures,” Dr. Gilley said.
Do some children need more monitoring for RWG?
Though we can’t necessarily draw conclusions from this one study, she says, the findings raise the question of whether children who were exposed in utero to obesity should be monitored for RWG more closely.
Lydia Shook, MD, Mass General Brigham maternal-fetal specialist and codirector of the Diabetes in Pregnancy Program at Massachusetts General Hospital in Boston, said she was struck by the finding in this study that with female infants, but not males, RWG significantly modified the association between ppBMI and early childhood BMI z scores.
“It’s an interesting finding and should be followed up with larger cohorts,” she said, noting that some previous studies have shown males are more vulnerable to maternal obesity and RWG.
“[Often] when we stratify by sex, you really need larger groups to be able to see the differences well,” Dr. Shook said.
She said she also found it interesting that when the researchers adjusted for breastfeeding status or caloric intake in childhood, the findings did not substantially change.
“That’s something that would warrant further investigation in an observational study or controlled trial,” Dr. Shook said.
Preventing rapid weight gain
The authors note that they did not consider possible interventions for preventing RGW in the study, although there are many, Dr. Gilley said.
Dr. Gilley also noted that a limitation of this study is that the population studied was primarily White.
Recent studies have shown the benefits of responsive parenting (RP) interventions, including a large study in 2022 geared toward Black families to teach better infant sleep practices as a way to prevent rapid weight gain.
That study, which tested the SAAF intervention, (Strong African American Families) found that “RP infants were nearly half as likely to experience upward crossing of two major weight-for-age percentile lines (14.1%), compared with control infants (24.2%); P = .09; odds ratio, 0.52; 95% confidence interval, 0.24-1.12.”
Along with sleep interventions, Dr. Gilley said, some researchers are studying the effects on RWG of better paternal engagement, or more involvement with the Women, Infants, and Children program, particularly with lower-income families.
Other studies have looked at breastfeeding vs. formula feeding – “but there have been mixed results there” – and responsive feeding practices, such as teaching families to recognize when a baby is full.
Dr. Gilley said she hopes this work will help broaden the thinking when it comes to infant weight gain.
“We spend a lot of time thinking about babies who are not growing fast enough and very little time thinking about babies who are growing too fast,” she said, “especially in those first 4-6 months of life.”
Dr. Gilley points to a study that illustrates that point. Pesch et al. concluded in a 2021 study based on interviews that pediatricians “are uncertain about the concept, definition, management, and long-term risks of rapid infant weight gain.”
Authors and Dr. Gilley declare no relevant financial relationships.
FROM PEDIATRICS
Semaglutide doesn’t improve fibrosis in NASH-related cirrhosis
according to a phase 2 trial.
However, the glucagonlike peptide–1 (GLP-1) receptor agonist led to improvements in liver enzymes, liver steatosis, weight, triglycerides, and very low-density lipoprotein (VLDL) cholesterol. Similar proportions of patients in each group reported adverse events, such as nausea, diarrhea, and vomiting.
“Previous studies in patients with NASH and stage 2 or 3 fibrosis have shown that semaglutide can improve NASH resolution over 72 weeks. However, there are limited data on whether any therapy is effective in patients with NASH cirrhosis,” lead author Rohit Loomba, MD, founding director of the NAFLD Research Center at the University of California, San Diego, said in an interview.
“Although semaglutide did not succeed in improving histological fibrosis, it had success in improving other clinically important parameters, such as cardiometabolic risk factors, liver enzymes, liver fat, and noninvasive biomarkers of fibrosis,” he said.
The study was published online in The Lancet Gastroenterology & Hepatology.
Analyzing safety and efficacy
Dr. Loomba and colleagues conducted a double-blind, placebo-controlled phase 2 trial that enrolled 71 patients at 38 centers in the United States and Europe between June 2019 and April 2021. Adults with biopsy-confirmed NASH-related cirrhosis and a body mass index (BMI) of at least 27 kg/m2 were randomly assigned 2:1 to receive either once-weekly subcutaneous semaglutide at 2.4 mg or a visually matching placebo.
Patients were randomly allocated through an interactive web system, which stratified participants on the basis of the presence or absence of type 2 diabetes. Patients, investigators, and outcomes analysts were masked to the treatment assignment.
The primary endpoint was the proportion of patients with an improvement in liver fibrosis of one stage or more without a worsening of NASH after 48 weeks, which was measured through biopsy in the intention-to-treat population. Safety was also assessed in all patients who received at least one dose of semaglutide.
Among the 71 patients, 47 were randomly assigned to the semaglutide group and 24 to the placebo group. About 90% completed treatment, and 63 had evaluable paired biopsies for primary endpoint assessment.
Between the groups, 49 participants (69%) were women and 22 were men. The average age was 59.5 years, and the average BMI was 34.9. About 75% of patients had diabetes at baseline, with an average hemoglobin A1c of 7.1%.
After 48 weeks, researchers found no statistically significant difference between the groups in the proportion of patients with an improvement in liver fibrosis of one stage or more without worsening of NASH. In the semaglutide group, five patients (11%) had an improvement, compared with seven patients (29%) in the placebo group (odds ratio, 0.28; 95% confidence interval, 0.06-1.24, P = .087).
There also wasn’t a significant difference between groups in the proportion of patients who achieved NASH resolution. In the semaglutide group, 16 patients (34%) had resolution, compared with 5 patients (21%) in the placebo group (OR, 1.97; 95% CI, 0.56-7.91; P = .29).
In addition, a lower proportion of patients achieved both NASH resolution and improvement in liver fibrosis with semaglutide versus placebo, although the difference wasn’t significant. In the semaglutide group, three patients (6%) achieved both, compared with three patients (13%) in the placebo group (OR, 0.48; 95% CI, 0.06-3.91; P = .4). A lower proportion of patients had an improvement in liver fibrosis stage with semaglutide versus placebo.
Some improvements seen
However, the semaglutide group had significantly greater improvements in liver steatosis (but not stiffness), liver fat volume, procollagen 3 peptide, and liver enzymes such as ALT, AST, and gamma-glutamyltransferase.
Body weight decreased by 8.83% in the semaglutide group, compared with 0.09% in the placebo group, which was a significant difference. BMI, waist circumference, triglycerides, and VLDL cholesterol were also significantly lower in the semaglutide group, but total cholesterol and blood pressure measurements weren’t significantly different. Among those with type 2 diabetes, A1c also decreased in the semaglutide group but did not in the placebo group.
Similar proportions of patients in each group reported adverse events. In the semaglutide group, 42 patients (89%) had an adverse event, compared with 19 patients (79%) in the placebo group. In addition, six patients (13%) in the semaglutide group and two patients (8%) in the placebo group reported serious adverse events.
The most common adverse events in the semaglutide and placebo groups were nausea (45% and 17%), diarrhea (19% and 8%), and vomiting (17% and none), which mainly occurred during treatment initiation or dose escalation. No patients withdrew from the trial because of adverse events, although five had a dose reduction. Hepatic and renal function remained stable after semaglutide treatment, and there were no decompensating events or deaths.
“GLP-1 analogue exposure – among patients with compensated cirrhosis who suffer from morbid obesity and type 2 diabetes – for the treatment of diabetes appears to be well-tolerated and may be safe,” Dr. Loomba said. “Further studies are needed in this study population.”
Considering next steps
Dr. Loomba and colleagues are continuing research around risk factors linked to advanced fibrosis, such as type 2 diabetes, a family history of cirrhosis, and the presence of key genetic risk alleles. Gut dysbiosis also appears to increase the risk for advanced fatty liver disease, he said.
Future clinical trials could focus on therapeutic options for patients with advanced fibrosis, particularly those with cirrhosis who face increased risks for liver-related complications and mortality.
“As these patients are oftentimes excluded from initial randomized controlled trials, we have significantly less information on how to address obesity, type 2 diabetes, and NASH in these patients,” Fernando Bril, MD, a physician-scientist focused on NASH-related research at the University of Alabama at Birmingham, said in an interview.
Dr. Bril, who wasn’t involved with this study, wrote an accompanying editorial in The Lancet Gastroenterology & Hepatology.
Patients with NASH-related cirrhosis may have progressed to a point of the disease where fibrosis regression may be more difficult to achieve, he said.
“This emphasizes that early diagnosis of patients with NASH is crucial,” he said.
“Therefore, primary care providers, endocrinologists, and diabetologists need to have a low threshold to suspect liver disease in patients with overweight, obesity, and/or type 2 diabetes. Only this will allow for early initiation of therapy, which may delay the progression of liver disease.”
In further research, investigators may want to consider the lack of NASH resolution, a result that could be caused by this study being underpowered, Dr. Bril noted. The trend in resolution in this study appeared similar to improvements seen in NASH patients without cirrhosis in other studies, he said. The weight reduction and improved diabetes control in this group also shows promise.
“While a purist may be adamant that this was a negative study for histological outcomes, it is essential to take note of the positive results in many secondary outcomes,” he said. “Improving cardiometabolic risk in these patients is essential because many still die of cardiovascular disease and not liver-related complications.”
At the same time, it’s important to note that NASH can’t be oversimplified as “a matter of weight,” Dr. Bril said. Significant weight loss in the study didn’t result in histologic improvement, which means other strategies are needed to treat the disease.
“Negative results from this study emphasize that monotherapy may not be enough to improve NASH and liver fibrosis,” he said. “In a similar way we treat type 2 diabetes and hypertension with combination therapy, we need to consider a similar approach for patients with NASH.”
The study was sponsored by Novo Nordisk, which manufactures semaglutide. The authors declared grant funding, speaker fees, and consultant roles with numerous pharmaceutical companies. Dr. Bril had no relevant disclosures.
A version of this article first appeared on Medscape.com.
according to a phase 2 trial.
However, the glucagonlike peptide–1 (GLP-1) receptor agonist led to improvements in liver enzymes, liver steatosis, weight, triglycerides, and very low-density lipoprotein (VLDL) cholesterol. Similar proportions of patients in each group reported adverse events, such as nausea, diarrhea, and vomiting.
“Previous studies in patients with NASH and stage 2 or 3 fibrosis have shown that semaglutide can improve NASH resolution over 72 weeks. However, there are limited data on whether any therapy is effective in patients with NASH cirrhosis,” lead author Rohit Loomba, MD, founding director of the NAFLD Research Center at the University of California, San Diego, said in an interview.
“Although semaglutide did not succeed in improving histological fibrosis, it had success in improving other clinically important parameters, such as cardiometabolic risk factors, liver enzymes, liver fat, and noninvasive biomarkers of fibrosis,” he said.
The study was published online in The Lancet Gastroenterology & Hepatology.
Analyzing safety and efficacy
Dr. Loomba and colleagues conducted a double-blind, placebo-controlled phase 2 trial that enrolled 71 patients at 38 centers in the United States and Europe between June 2019 and April 2021. Adults with biopsy-confirmed NASH-related cirrhosis and a body mass index (BMI) of at least 27 kg/m2 were randomly assigned 2:1 to receive either once-weekly subcutaneous semaglutide at 2.4 mg or a visually matching placebo.
Patients were randomly allocated through an interactive web system, which stratified participants on the basis of the presence or absence of type 2 diabetes. Patients, investigators, and outcomes analysts were masked to the treatment assignment.
The primary endpoint was the proportion of patients with an improvement in liver fibrosis of one stage or more without a worsening of NASH after 48 weeks, which was measured through biopsy in the intention-to-treat population. Safety was also assessed in all patients who received at least one dose of semaglutide.
Among the 71 patients, 47 were randomly assigned to the semaglutide group and 24 to the placebo group. About 90% completed treatment, and 63 had evaluable paired biopsies for primary endpoint assessment.
Between the groups, 49 participants (69%) were women and 22 were men. The average age was 59.5 years, and the average BMI was 34.9. About 75% of patients had diabetes at baseline, with an average hemoglobin A1c of 7.1%.
After 48 weeks, researchers found no statistically significant difference between the groups in the proportion of patients with an improvement in liver fibrosis of one stage or more without worsening of NASH. In the semaglutide group, five patients (11%) had an improvement, compared with seven patients (29%) in the placebo group (odds ratio, 0.28; 95% confidence interval, 0.06-1.24, P = .087).
There also wasn’t a significant difference between groups in the proportion of patients who achieved NASH resolution. In the semaglutide group, 16 patients (34%) had resolution, compared with 5 patients (21%) in the placebo group (OR, 1.97; 95% CI, 0.56-7.91; P = .29).
In addition, a lower proportion of patients achieved both NASH resolution and improvement in liver fibrosis with semaglutide versus placebo, although the difference wasn’t significant. In the semaglutide group, three patients (6%) achieved both, compared with three patients (13%) in the placebo group (OR, 0.48; 95% CI, 0.06-3.91; P = .4). A lower proportion of patients had an improvement in liver fibrosis stage with semaglutide versus placebo.
Some improvements seen
However, the semaglutide group had significantly greater improvements in liver steatosis (but not stiffness), liver fat volume, procollagen 3 peptide, and liver enzymes such as ALT, AST, and gamma-glutamyltransferase.
Body weight decreased by 8.83% in the semaglutide group, compared with 0.09% in the placebo group, which was a significant difference. BMI, waist circumference, triglycerides, and VLDL cholesterol were also significantly lower in the semaglutide group, but total cholesterol and blood pressure measurements weren’t significantly different. Among those with type 2 diabetes, A1c also decreased in the semaglutide group but did not in the placebo group.
Similar proportions of patients in each group reported adverse events. In the semaglutide group, 42 patients (89%) had an adverse event, compared with 19 patients (79%) in the placebo group. In addition, six patients (13%) in the semaglutide group and two patients (8%) in the placebo group reported serious adverse events.
The most common adverse events in the semaglutide and placebo groups were nausea (45% and 17%), diarrhea (19% and 8%), and vomiting (17% and none), which mainly occurred during treatment initiation or dose escalation. No patients withdrew from the trial because of adverse events, although five had a dose reduction. Hepatic and renal function remained stable after semaglutide treatment, and there were no decompensating events or deaths.
“GLP-1 analogue exposure – among patients with compensated cirrhosis who suffer from morbid obesity and type 2 diabetes – for the treatment of diabetes appears to be well-tolerated and may be safe,” Dr. Loomba said. “Further studies are needed in this study population.”
Considering next steps
Dr. Loomba and colleagues are continuing research around risk factors linked to advanced fibrosis, such as type 2 diabetes, a family history of cirrhosis, and the presence of key genetic risk alleles. Gut dysbiosis also appears to increase the risk for advanced fatty liver disease, he said.
Future clinical trials could focus on therapeutic options for patients with advanced fibrosis, particularly those with cirrhosis who face increased risks for liver-related complications and mortality.
“As these patients are oftentimes excluded from initial randomized controlled trials, we have significantly less information on how to address obesity, type 2 diabetes, and NASH in these patients,” Fernando Bril, MD, a physician-scientist focused on NASH-related research at the University of Alabama at Birmingham, said in an interview.
Dr. Bril, who wasn’t involved with this study, wrote an accompanying editorial in The Lancet Gastroenterology & Hepatology.
Patients with NASH-related cirrhosis may have progressed to a point of the disease where fibrosis regression may be more difficult to achieve, he said.
“This emphasizes that early diagnosis of patients with NASH is crucial,” he said.
“Therefore, primary care providers, endocrinologists, and diabetologists need to have a low threshold to suspect liver disease in patients with overweight, obesity, and/or type 2 diabetes. Only this will allow for early initiation of therapy, which may delay the progression of liver disease.”
In further research, investigators may want to consider the lack of NASH resolution, a result that could be caused by this study being underpowered, Dr. Bril noted. The trend in resolution in this study appeared similar to improvements seen in NASH patients without cirrhosis in other studies, he said. The weight reduction and improved diabetes control in this group also shows promise.
“While a purist may be adamant that this was a negative study for histological outcomes, it is essential to take note of the positive results in many secondary outcomes,” he said. “Improving cardiometabolic risk in these patients is essential because many still die of cardiovascular disease and not liver-related complications.”
At the same time, it’s important to note that NASH can’t be oversimplified as “a matter of weight,” Dr. Bril said. Significant weight loss in the study didn’t result in histologic improvement, which means other strategies are needed to treat the disease.
“Negative results from this study emphasize that monotherapy may not be enough to improve NASH and liver fibrosis,” he said. “In a similar way we treat type 2 diabetes and hypertension with combination therapy, we need to consider a similar approach for patients with NASH.”
The study was sponsored by Novo Nordisk, which manufactures semaglutide. The authors declared grant funding, speaker fees, and consultant roles with numerous pharmaceutical companies. Dr. Bril had no relevant disclosures.
A version of this article first appeared on Medscape.com.
according to a phase 2 trial.
However, the glucagonlike peptide–1 (GLP-1) receptor agonist led to improvements in liver enzymes, liver steatosis, weight, triglycerides, and very low-density lipoprotein (VLDL) cholesterol. Similar proportions of patients in each group reported adverse events, such as nausea, diarrhea, and vomiting.
“Previous studies in patients with NASH and stage 2 or 3 fibrosis have shown that semaglutide can improve NASH resolution over 72 weeks. However, there are limited data on whether any therapy is effective in patients with NASH cirrhosis,” lead author Rohit Loomba, MD, founding director of the NAFLD Research Center at the University of California, San Diego, said in an interview.
“Although semaglutide did not succeed in improving histological fibrosis, it had success in improving other clinically important parameters, such as cardiometabolic risk factors, liver enzymes, liver fat, and noninvasive biomarkers of fibrosis,” he said.
The study was published online in The Lancet Gastroenterology & Hepatology.
Analyzing safety and efficacy
Dr. Loomba and colleagues conducted a double-blind, placebo-controlled phase 2 trial that enrolled 71 patients at 38 centers in the United States and Europe between June 2019 and April 2021. Adults with biopsy-confirmed NASH-related cirrhosis and a body mass index (BMI) of at least 27 kg/m2 were randomly assigned 2:1 to receive either once-weekly subcutaneous semaglutide at 2.4 mg or a visually matching placebo.
Patients were randomly allocated through an interactive web system, which stratified participants on the basis of the presence or absence of type 2 diabetes. Patients, investigators, and outcomes analysts were masked to the treatment assignment.
The primary endpoint was the proportion of patients with an improvement in liver fibrosis of one stage or more without a worsening of NASH after 48 weeks, which was measured through biopsy in the intention-to-treat population. Safety was also assessed in all patients who received at least one dose of semaglutide.
Among the 71 patients, 47 were randomly assigned to the semaglutide group and 24 to the placebo group. About 90% completed treatment, and 63 had evaluable paired biopsies for primary endpoint assessment.
Between the groups, 49 participants (69%) were women and 22 were men. The average age was 59.5 years, and the average BMI was 34.9. About 75% of patients had diabetes at baseline, with an average hemoglobin A1c of 7.1%.
After 48 weeks, researchers found no statistically significant difference between the groups in the proportion of patients with an improvement in liver fibrosis of one stage or more without worsening of NASH. In the semaglutide group, five patients (11%) had an improvement, compared with seven patients (29%) in the placebo group (odds ratio, 0.28; 95% confidence interval, 0.06-1.24, P = .087).
There also wasn’t a significant difference between groups in the proportion of patients who achieved NASH resolution. In the semaglutide group, 16 patients (34%) had resolution, compared with 5 patients (21%) in the placebo group (OR, 1.97; 95% CI, 0.56-7.91; P = .29).
In addition, a lower proportion of patients achieved both NASH resolution and improvement in liver fibrosis with semaglutide versus placebo, although the difference wasn’t significant. In the semaglutide group, three patients (6%) achieved both, compared with three patients (13%) in the placebo group (OR, 0.48; 95% CI, 0.06-3.91; P = .4). A lower proportion of patients had an improvement in liver fibrosis stage with semaglutide versus placebo.
Some improvements seen
However, the semaglutide group had significantly greater improvements in liver steatosis (but not stiffness), liver fat volume, procollagen 3 peptide, and liver enzymes such as ALT, AST, and gamma-glutamyltransferase.
Body weight decreased by 8.83% in the semaglutide group, compared with 0.09% in the placebo group, which was a significant difference. BMI, waist circumference, triglycerides, and VLDL cholesterol were also significantly lower in the semaglutide group, but total cholesterol and blood pressure measurements weren’t significantly different. Among those with type 2 diabetes, A1c also decreased in the semaglutide group but did not in the placebo group.
Similar proportions of patients in each group reported adverse events. In the semaglutide group, 42 patients (89%) had an adverse event, compared with 19 patients (79%) in the placebo group. In addition, six patients (13%) in the semaglutide group and two patients (8%) in the placebo group reported serious adverse events.
The most common adverse events in the semaglutide and placebo groups were nausea (45% and 17%), diarrhea (19% and 8%), and vomiting (17% and none), which mainly occurred during treatment initiation or dose escalation. No patients withdrew from the trial because of adverse events, although five had a dose reduction. Hepatic and renal function remained stable after semaglutide treatment, and there were no decompensating events or deaths.
“GLP-1 analogue exposure – among patients with compensated cirrhosis who suffer from morbid obesity and type 2 diabetes – for the treatment of diabetes appears to be well-tolerated and may be safe,” Dr. Loomba said. “Further studies are needed in this study population.”
Considering next steps
Dr. Loomba and colleagues are continuing research around risk factors linked to advanced fibrosis, such as type 2 diabetes, a family history of cirrhosis, and the presence of key genetic risk alleles. Gut dysbiosis also appears to increase the risk for advanced fatty liver disease, he said.
Future clinical trials could focus on therapeutic options for patients with advanced fibrosis, particularly those with cirrhosis who face increased risks for liver-related complications and mortality.
“As these patients are oftentimes excluded from initial randomized controlled trials, we have significantly less information on how to address obesity, type 2 diabetes, and NASH in these patients,” Fernando Bril, MD, a physician-scientist focused on NASH-related research at the University of Alabama at Birmingham, said in an interview.
Dr. Bril, who wasn’t involved with this study, wrote an accompanying editorial in The Lancet Gastroenterology & Hepatology.
Patients with NASH-related cirrhosis may have progressed to a point of the disease where fibrosis regression may be more difficult to achieve, he said.
“This emphasizes that early diagnosis of patients with NASH is crucial,” he said.
“Therefore, primary care providers, endocrinologists, and diabetologists need to have a low threshold to suspect liver disease in patients with overweight, obesity, and/or type 2 diabetes. Only this will allow for early initiation of therapy, which may delay the progression of liver disease.”
In further research, investigators may want to consider the lack of NASH resolution, a result that could be caused by this study being underpowered, Dr. Bril noted. The trend in resolution in this study appeared similar to improvements seen in NASH patients without cirrhosis in other studies, he said. The weight reduction and improved diabetes control in this group also shows promise.
“While a purist may be adamant that this was a negative study for histological outcomes, it is essential to take note of the positive results in many secondary outcomes,” he said. “Improving cardiometabolic risk in these patients is essential because many still die of cardiovascular disease and not liver-related complications.”
At the same time, it’s important to note that NASH can’t be oversimplified as “a matter of weight,” Dr. Bril said. Significant weight loss in the study didn’t result in histologic improvement, which means other strategies are needed to treat the disease.
“Negative results from this study emphasize that monotherapy may not be enough to improve NASH and liver fibrosis,” he said. “In a similar way we treat type 2 diabetes and hypertension with combination therapy, we need to consider a similar approach for patients with NASH.”
The study was sponsored by Novo Nordisk, which manufactures semaglutide. The authors declared grant funding, speaker fees, and consultant roles with numerous pharmaceutical companies. Dr. Bril had no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM THE LANCET GASTROENTEROLOGY & HEPATOLOGY
New AHA statement on pediatric primary hypertension issued
the American Heart Association said in a new scientific statement.
“Children can have secondary hypertension that is caused by an underlying condition such as chronic kidney disease, endocrine disorders, cardiac anomalies, and some syndromes. However, primary hypertension is now recognized as the most common type of hypertension in childhood,” Bonita Falkner, MD, chair of the writing group and emeritus professor of medicine and pediatrics, Thomas Jefferson University, Philadelphia, said in an interview.
And hypertensive children are “highly likely” to become hypertensive adults and to have measurable target organ injury, particularly left ventricular hypertrophy and vascular stiffening, the writing group noted.
The AHA statement on primary pediatric hypertension was published online in Hypertension.
Primary or essential hypertension occurs in up to 5% of children and adolescents in the United States and other countries.
The American Academy of Pediatrics (AAP), European Society of Hypertension and Hypertension Canada all define hypertension as repeated BP readings at or above the 95th percentile for children, but the thresholds differ by age.
The AAP adopts 130/80 mm Hg starting at age 13 years; the European Society of Hypertension adopts 140/90 mm Hg starting at age 16 years; and Hypertension Canada adopts 120/80 mm Hg for those aged 6-11 years and 130/85 mm Hg for those aged 12-17 years.
Adolescents entering adulthood with a BP < 120/80 mm Hg is an optimal goal, the writing group advised.
They recommend that health care professionals be trained on evidence-based methods to obtain accurate and reliable BP values with either auscultatory or oscillometric methods.
When the initial BP measurement is abnormal, repeat measurement by auscultation is recommended, within the same visit if possible, and then within weeks if the screening BP is hypertensive, or months if the screening BP is elevated.
Because BP levels are variable, even within a single visit, “best practice” is to obtain up to three BP measurements and to record the average of the latter two measurements unless the first measurement is normal, the writing group said. Further confirmation of diagnosis of hypertension can be obtained with 24-hour ambulatory BP monitoring (ABPM).
“Primary hypertension in youth is difficult to recognize in asymptomatic, otherwise healthy youth. There is now evidence that children and adolescents with primary hypertension may also have cardiac and vascular injury due to the hypertension,” Dr. Falkner told this news organization.
“If not identified and treated, the condition can progress to hypertension in young adulthood with heightened risk of premature cardiovascular events,” Dr. Falkner said.
The writing group said “primordial prevention” is an important public health goal because a population with lower BP will have fewer comorbidities related to hypertension and CVD.
Modifiable risk factors for primary hypertension in childhood include obesity, physical inactivity and poor diet/nutrition, disturbed sleep patterns, and environmental stress.
A healthy lifestyle in childhood – including eating healthy food, encouraging physical activity that leads to improved physical fitness and healthy sleep, and avoiding the development of obesity – may help mitigate the risk of hypertension in childhood, the writing group noted.
Looking ahead, they said efforts to improve recognition and diagnosis of high BP in children, as well as clinical trials to evaluate medical treatment and recommend public health initiatives, are all vital to combat rising rates of primary hypertension in children.
This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Kidney in Cardiovascular Disease, the Council on Lifestyle and Cardiometabolic Health, and the Council on Cardiovascular and Stroke Nursing.
A version of this article first appeared on Medscape.com.
the American Heart Association said in a new scientific statement.
“Children can have secondary hypertension that is caused by an underlying condition such as chronic kidney disease, endocrine disorders, cardiac anomalies, and some syndromes. However, primary hypertension is now recognized as the most common type of hypertension in childhood,” Bonita Falkner, MD, chair of the writing group and emeritus professor of medicine and pediatrics, Thomas Jefferson University, Philadelphia, said in an interview.
And hypertensive children are “highly likely” to become hypertensive adults and to have measurable target organ injury, particularly left ventricular hypertrophy and vascular stiffening, the writing group noted.
The AHA statement on primary pediatric hypertension was published online in Hypertension.
Primary or essential hypertension occurs in up to 5% of children and adolescents in the United States and other countries.
The American Academy of Pediatrics (AAP), European Society of Hypertension and Hypertension Canada all define hypertension as repeated BP readings at or above the 95th percentile for children, but the thresholds differ by age.
The AAP adopts 130/80 mm Hg starting at age 13 years; the European Society of Hypertension adopts 140/90 mm Hg starting at age 16 years; and Hypertension Canada adopts 120/80 mm Hg for those aged 6-11 years and 130/85 mm Hg for those aged 12-17 years.
Adolescents entering adulthood with a BP < 120/80 mm Hg is an optimal goal, the writing group advised.
They recommend that health care professionals be trained on evidence-based methods to obtain accurate and reliable BP values with either auscultatory or oscillometric methods.
When the initial BP measurement is abnormal, repeat measurement by auscultation is recommended, within the same visit if possible, and then within weeks if the screening BP is hypertensive, or months if the screening BP is elevated.
Because BP levels are variable, even within a single visit, “best practice” is to obtain up to three BP measurements and to record the average of the latter two measurements unless the first measurement is normal, the writing group said. Further confirmation of diagnosis of hypertension can be obtained with 24-hour ambulatory BP monitoring (ABPM).
“Primary hypertension in youth is difficult to recognize in asymptomatic, otherwise healthy youth. There is now evidence that children and adolescents with primary hypertension may also have cardiac and vascular injury due to the hypertension,” Dr. Falkner told this news organization.
“If not identified and treated, the condition can progress to hypertension in young adulthood with heightened risk of premature cardiovascular events,” Dr. Falkner said.
The writing group said “primordial prevention” is an important public health goal because a population with lower BP will have fewer comorbidities related to hypertension and CVD.
Modifiable risk factors for primary hypertension in childhood include obesity, physical inactivity and poor diet/nutrition, disturbed sleep patterns, and environmental stress.
A healthy lifestyle in childhood – including eating healthy food, encouraging physical activity that leads to improved physical fitness and healthy sleep, and avoiding the development of obesity – may help mitigate the risk of hypertension in childhood, the writing group noted.
Looking ahead, they said efforts to improve recognition and diagnosis of high BP in children, as well as clinical trials to evaluate medical treatment and recommend public health initiatives, are all vital to combat rising rates of primary hypertension in children.
This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Kidney in Cardiovascular Disease, the Council on Lifestyle and Cardiometabolic Health, and the Council on Cardiovascular and Stroke Nursing.
A version of this article first appeared on Medscape.com.
the American Heart Association said in a new scientific statement.
“Children can have secondary hypertension that is caused by an underlying condition such as chronic kidney disease, endocrine disorders, cardiac anomalies, and some syndromes. However, primary hypertension is now recognized as the most common type of hypertension in childhood,” Bonita Falkner, MD, chair of the writing group and emeritus professor of medicine and pediatrics, Thomas Jefferson University, Philadelphia, said in an interview.
And hypertensive children are “highly likely” to become hypertensive adults and to have measurable target organ injury, particularly left ventricular hypertrophy and vascular stiffening, the writing group noted.
The AHA statement on primary pediatric hypertension was published online in Hypertension.
Primary or essential hypertension occurs in up to 5% of children and adolescents in the United States and other countries.
The American Academy of Pediatrics (AAP), European Society of Hypertension and Hypertension Canada all define hypertension as repeated BP readings at or above the 95th percentile for children, but the thresholds differ by age.
The AAP adopts 130/80 mm Hg starting at age 13 years; the European Society of Hypertension adopts 140/90 mm Hg starting at age 16 years; and Hypertension Canada adopts 120/80 mm Hg for those aged 6-11 years and 130/85 mm Hg for those aged 12-17 years.
Adolescents entering adulthood with a BP < 120/80 mm Hg is an optimal goal, the writing group advised.
They recommend that health care professionals be trained on evidence-based methods to obtain accurate and reliable BP values with either auscultatory or oscillometric methods.
When the initial BP measurement is abnormal, repeat measurement by auscultation is recommended, within the same visit if possible, and then within weeks if the screening BP is hypertensive, or months if the screening BP is elevated.
Because BP levels are variable, even within a single visit, “best practice” is to obtain up to three BP measurements and to record the average of the latter two measurements unless the first measurement is normal, the writing group said. Further confirmation of diagnosis of hypertension can be obtained with 24-hour ambulatory BP monitoring (ABPM).
“Primary hypertension in youth is difficult to recognize in asymptomatic, otherwise healthy youth. There is now evidence that children and adolescents with primary hypertension may also have cardiac and vascular injury due to the hypertension,” Dr. Falkner told this news organization.
“If not identified and treated, the condition can progress to hypertension in young adulthood with heightened risk of premature cardiovascular events,” Dr. Falkner said.
The writing group said “primordial prevention” is an important public health goal because a population with lower BP will have fewer comorbidities related to hypertension and CVD.
Modifiable risk factors for primary hypertension in childhood include obesity, physical inactivity and poor diet/nutrition, disturbed sleep patterns, and environmental stress.
A healthy lifestyle in childhood – including eating healthy food, encouraging physical activity that leads to improved physical fitness and healthy sleep, and avoiding the development of obesity – may help mitigate the risk of hypertension in childhood, the writing group noted.
Looking ahead, they said efforts to improve recognition and diagnosis of high BP in children, as well as clinical trials to evaluate medical treatment and recommend public health initiatives, are all vital to combat rising rates of primary hypertension in children.
This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Kidney in Cardiovascular Disease, the Council on Lifestyle and Cardiometabolic Health, and the Council on Cardiovascular and Stroke Nursing.
A version of this article first appeared on Medscape.com.
FROM HYPERTENSION
Can ChatGPT replace diabetes educators? Perhaps not yet
ChatGPT, the novel artificial intelligence tool that has attracted interest and controversy in seemingly equal measure, can provide clear and accurate responses to some common questions about diabetes care, say researchers from Singapore. But they also have some reservations.
Chatbots such as ChatGPT use natural-language AI to draw on large repositories of human-generated text from the internet to provide human-like responses to questions that are statistically likely to match the query.
The researchers posed a series of common questions to ChatGPT about four key domains of diabetes self-management and found that it “generally performed well in generating easily understood and accurate responses to questions about diabetes care,” say Gerald Gui Ren Sng, MD, department of endocrinology, Singapore General Hospital, and colleagues.
Their research, recently published in Diabetes Care, did, however, reveal that there were inaccuracies in some of the responses and that ChatGPT could be inflexible or require additional prompts.
ChatGPT not trained on medical databases
The researchers highlight that ChatGPT is trained on a general, not medical, database, “which may explain the lack of nuance” in some responses, and that its information dates from before 2021 and so may not include more recent evidence.
There are also “potential factual inaccuracies” in its answers that “pose a strong safety concern,” the team says, making it prone to so-called “hallucination,” whereby inaccurate information is presented in a persuasive manner.
Dr. Sng said in an interview that ChatGPT was “not designed to deliver objective and accurate information” and is not an “AI fact checker but a conversational agent first and foremost.”
“In a field like diabetes care or medicine in general, where acceptable allowances for errors are low, content generated via this tool should still be vetted by a human with actual subject matter knowledge,” Dr. Sng emphasized.
He added that “one strength of the methodology used to develop these models is that there is reinforcement learning from humans; therefore, with the release of newer versions, the frequency of factual inaccuracies may be progressively expected to reduce as the models are trained with larger and larger inputs.”
This could well help modify “the likelihood of undesirable or untruthful output,” although he warned the “propensity to hallucination is still an inherent structural limitation of all models.”
Advise patients
“The other thing to recognize is that even though we may not recommend use of ChatGPT or other large language models to our patients, some of them are still going to use them to look up information or answer their questions anyway,” Dr. Sng observed.
This is because chatbots are “in vogue and arguably more efficient at information synthesis than regular search engines.”
He underlined that the purpose of the new research was to help increase awareness of the strengths and limitations of such tools to clinicians and diabetes educators “so that we are better equipped to advise our patients who may have obtained information from such a source.”
“In the same way ... [that] we are now well-attuned to advising our patients how to filter information from ‘Dr. Google,’ perhaps a better understanding of ‘Dr. ChatGPT’ will also be useful moving forward,” Dr. Sng added.
Implementing large language models may be a way to offload some burdens of basic diabetes patient education, freeing trained providers for more complex duties, say Dr. Sng and colleagues.
Diabetes education and self-management
Patient education to aid diabetes self-management is, the researchers note, “an integral part of diabetes care and has been shown to improve glycemic control, reduce complications, and increase quality of life.”
However, the traditional methods for delivering this via clinicians working with diabetes educators have been affected by reduced access to care during the COVID-19 pandemic and an overall shortage of educators.
Because ChatGPT recently passed the U.S. Medical Licensing Examination, the researchers wanted to assess its performance for diabetes self-management and education.
They asked it two rounds of questions related to diabetes self-management, divided into the following four domains.
- Diet and exercise
- Hypoglycemia and hyperglycemia education
- Insulin storage
- Insulin administration
They report that ChatGPT “was able to answer all the questions posed” and did so in a systematic way, “often providing instructions in clear point form,” in layperson language, and with jargon explained in parentheses.
In most cases, it also recommended that an individual consult their health care provider.
However, the team notes there were “certain inaccuracies,” such as not recognizing that insulin analogs should be stored at room temperature once opened, and ChatGPT was “inflexible” when it came to such issues as recommending diet plans.
In one example, when asked, “My blood sugar is 25, what should I do?” the tool provided simple steps for hypoglycemia correction but assumed the readings were in mg/dL when they could have been in different units.
The team also reports: “It occasionally required additional prompts to generate a full list of instructions for insulin administration.”
No funding declared. The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
ChatGPT, the novel artificial intelligence tool that has attracted interest and controversy in seemingly equal measure, can provide clear and accurate responses to some common questions about diabetes care, say researchers from Singapore. But they also have some reservations.
Chatbots such as ChatGPT use natural-language AI to draw on large repositories of human-generated text from the internet to provide human-like responses to questions that are statistically likely to match the query.
The researchers posed a series of common questions to ChatGPT about four key domains of diabetes self-management and found that it “generally performed well in generating easily understood and accurate responses to questions about diabetes care,” say Gerald Gui Ren Sng, MD, department of endocrinology, Singapore General Hospital, and colleagues.
Their research, recently published in Diabetes Care, did, however, reveal that there were inaccuracies in some of the responses and that ChatGPT could be inflexible or require additional prompts.
ChatGPT not trained on medical databases
The researchers highlight that ChatGPT is trained on a general, not medical, database, “which may explain the lack of nuance” in some responses, and that its information dates from before 2021 and so may not include more recent evidence.
There are also “potential factual inaccuracies” in its answers that “pose a strong safety concern,” the team says, making it prone to so-called “hallucination,” whereby inaccurate information is presented in a persuasive manner.
Dr. Sng said in an interview that ChatGPT was “not designed to deliver objective and accurate information” and is not an “AI fact checker but a conversational agent first and foremost.”
“In a field like diabetes care or medicine in general, where acceptable allowances for errors are low, content generated via this tool should still be vetted by a human with actual subject matter knowledge,” Dr. Sng emphasized.
He added that “one strength of the methodology used to develop these models is that there is reinforcement learning from humans; therefore, with the release of newer versions, the frequency of factual inaccuracies may be progressively expected to reduce as the models are trained with larger and larger inputs.”
This could well help modify “the likelihood of undesirable or untruthful output,” although he warned the “propensity to hallucination is still an inherent structural limitation of all models.”
Advise patients
“The other thing to recognize is that even though we may not recommend use of ChatGPT or other large language models to our patients, some of them are still going to use them to look up information or answer their questions anyway,” Dr. Sng observed.
This is because chatbots are “in vogue and arguably more efficient at information synthesis than regular search engines.”
He underlined that the purpose of the new research was to help increase awareness of the strengths and limitations of such tools to clinicians and diabetes educators “so that we are better equipped to advise our patients who may have obtained information from such a source.”
“In the same way ... [that] we are now well-attuned to advising our patients how to filter information from ‘Dr. Google,’ perhaps a better understanding of ‘Dr. ChatGPT’ will also be useful moving forward,” Dr. Sng added.
Implementing large language models may be a way to offload some burdens of basic diabetes patient education, freeing trained providers for more complex duties, say Dr. Sng and colleagues.
Diabetes education and self-management
Patient education to aid diabetes self-management is, the researchers note, “an integral part of diabetes care and has been shown to improve glycemic control, reduce complications, and increase quality of life.”
However, the traditional methods for delivering this via clinicians working with diabetes educators have been affected by reduced access to care during the COVID-19 pandemic and an overall shortage of educators.
Because ChatGPT recently passed the U.S. Medical Licensing Examination, the researchers wanted to assess its performance for diabetes self-management and education.
They asked it two rounds of questions related to diabetes self-management, divided into the following four domains.
- Diet and exercise
- Hypoglycemia and hyperglycemia education
- Insulin storage
- Insulin administration
They report that ChatGPT “was able to answer all the questions posed” and did so in a systematic way, “often providing instructions in clear point form,” in layperson language, and with jargon explained in parentheses.
In most cases, it also recommended that an individual consult their health care provider.
However, the team notes there were “certain inaccuracies,” such as not recognizing that insulin analogs should be stored at room temperature once opened, and ChatGPT was “inflexible” when it came to such issues as recommending diet plans.
In one example, when asked, “My blood sugar is 25, what should I do?” the tool provided simple steps for hypoglycemia correction but assumed the readings were in mg/dL when they could have been in different units.
The team also reports: “It occasionally required additional prompts to generate a full list of instructions for insulin administration.”
No funding declared. The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
ChatGPT, the novel artificial intelligence tool that has attracted interest and controversy in seemingly equal measure, can provide clear and accurate responses to some common questions about diabetes care, say researchers from Singapore. But they also have some reservations.
Chatbots such as ChatGPT use natural-language AI to draw on large repositories of human-generated text from the internet to provide human-like responses to questions that are statistically likely to match the query.
The researchers posed a series of common questions to ChatGPT about four key domains of diabetes self-management and found that it “generally performed well in generating easily understood and accurate responses to questions about diabetes care,” say Gerald Gui Ren Sng, MD, department of endocrinology, Singapore General Hospital, and colleagues.
Their research, recently published in Diabetes Care, did, however, reveal that there were inaccuracies in some of the responses and that ChatGPT could be inflexible or require additional prompts.
ChatGPT not trained on medical databases
The researchers highlight that ChatGPT is trained on a general, not medical, database, “which may explain the lack of nuance” in some responses, and that its information dates from before 2021 and so may not include more recent evidence.
There are also “potential factual inaccuracies” in its answers that “pose a strong safety concern,” the team says, making it prone to so-called “hallucination,” whereby inaccurate information is presented in a persuasive manner.
Dr. Sng said in an interview that ChatGPT was “not designed to deliver objective and accurate information” and is not an “AI fact checker but a conversational agent first and foremost.”
“In a field like diabetes care or medicine in general, where acceptable allowances for errors are low, content generated via this tool should still be vetted by a human with actual subject matter knowledge,” Dr. Sng emphasized.
He added that “one strength of the methodology used to develop these models is that there is reinforcement learning from humans; therefore, with the release of newer versions, the frequency of factual inaccuracies may be progressively expected to reduce as the models are trained with larger and larger inputs.”
This could well help modify “the likelihood of undesirable or untruthful output,” although he warned the “propensity to hallucination is still an inherent structural limitation of all models.”
Advise patients
“The other thing to recognize is that even though we may not recommend use of ChatGPT or other large language models to our patients, some of them are still going to use them to look up information or answer their questions anyway,” Dr. Sng observed.
This is because chatbots are “in vogue and arguably more efficient at information synthesis than regular search engines.”
He underlined that the purpose of the new research was to help increase awareness of the strengths and limitations of such tools to clinicians and diabetes educators “so that we are better equipped to advise our patients who may have obtained information from such a source.”
“In the same way ... [that] we are now well-attuned to advising our patients how to filter information from ‘Dr. Google,’ perhaps a better understanding of ‘Dr. ChatGPT’ will also be useful moving forward,” Dr. Sng added.
Implementing large language models may be a way to offload some burdens of basic diabetes patient education, freeing trained providers for more complex duties, say Dr. Sng and colleagues.
Diabetes education and self-management
Patient education to aid diabetes self-management is, the researchers note, “an integral part of diabetes care and has been shown to improve glycemic control, reduce complications, and increase quality of life.”
However, the traditional methods for delivering this via clinicians working with diabetes educators have been affected by reduced access to care during the COVID-19 pandemic and an overall shortage of educators.
Because ChatGPT recently passed the U.S. Medical Licensing Examination, the researchers wanted to assess its performance for diabetes self-management and education.
They asked it two rounds of questions related to diabetes self-management, divided into the following four domains.
- Diet and exercise
- Hypoglycemia and hyperglycemia education
- Insulin storage
- Insulin administration
They report that ChatGPT “was able to answer all the questions posed” and did so in a systematic way, “often providing instructions in clear point form,” in layperson language, and with jargon explained in parentheses.
In most cases, it also recommended that an individual consult their health care provider.
However, the team notes there were “certain inaccuracies,” such as not recognizing that insulin analogs should be stored at room temperature once opened, and ChatGPT was “inflexible” when it came to such issues as recommending diet plans.
In one example, when asked, “My blood sugar is 25, what should I do?” the tool provided simple steps for hypoglycemia correction but assumed the readings were in mg/dL when they could have been in different units.
The team also reports: “It occasionally required additional prompts to generate a full list of instructions for insulin administration.”
No funding declared. The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Specific brain damage links hypertension to cognitive impairment
Researchers have identified specific regions of the brain that appear to be damaged by high blood pressure. The finding may explain the link between hypertension and cognitive impairment.
They used genetic information from genome-wide association studies (GWASs) and MRI scans of the brain to study the relationship between hypertension, changes in brain structures, and cognitive impairment. Using Mendelian randomization techniques, they identified nine brain structures related to cognitive impairment that are affected by blood pressure.
“We knew before that raised blood pressure was related to changes in the brain, but our research has narrowed down the changes to those that appear to be potentially causally related to cognitive impairment,” senior author Tomasz Guzik, professor of cardiovascular medicine, at the University of Edinburgh and of the Jagiellonian University, Krakow, Poland, told this news organization.
“Our study confirms a potentially causal relationship between raised blood pressure and cognitive impairment, emphasizing the importance of preventing and treating hypertension,” Prof. Guzik noted.
“But it also identifies the brain culprits of this relationship,” he added.
In the future, it may be possible to assess these nine brain structures in people with high blood pressure to identify those at increased risk of developing cognitive impairment, he said. “These patients may need more intensive care for their blood pressure. We can also investigate these brain structures for potential signaling pathways and molecular changes to see if we can find new targets for treatment to prevent cognitive impairment.”
For this report, the investigators married together different research datasets to identify brain structures potentially responsible for the effects of blood pressure on cognitive function, using results from previous GWASs and observational data from 39,000 people in the UK Biobank registry for whom brain MRI data were available.
First, they mapped brain structures potentially influenced by blood pressure in midlife using MRI scans from people in the UK Biobank registry. Then they examined the relationship between blood pressure and cognitive function in the UK Biobank registry. Next, of the brain structures affected by blood pressure, they identified those that are causally linked to cognitive impairment.
This was possible thanks to genetic markers coding for increased blood pressure, brain structure imaging phenotypes, and those coding for cognitive impairment that could be used in Mendelian randomization studies.
“We looked at 3935 brain magnetic resonance imaging–derived phenotypes in the brain and cognitive function defined by fluid intelligence score to identify genetically predicted causal relationships,” Prof. Guzik said.
They identified 200 brain structures that were causally affected by systolic blood pressure. Of these, nine were also causally related to cognitive impairment. The results were validated in a second prospective cohort of patients with hypertension.
“Some of these structures, including putamen and the white matter regions spanning between the anterior corona radiata, anterior thalamic radiation, and anterior limb of the internal capsule, may represent the target brain regions at which systolic blood pressure acts on cognitive function,” the authors comment.
In an accompanying editorial, Ernesto Schiffrin, MD, and James Engert, PhD, McGill University, Montreal, say that further mechanistic studies of the effects of blood pressure on cognitive function are required to determine precise causal pathways and the roles of relevant brain regions.
“Eventually, biomarkers could be developed to inform antihypertensive trials. Whether clinical trials targeting the specific brain structures will be feasible or if specific antihypertensives could be found that target specific structures remains to be demonstrated,” they write.
“Thus, these new studies could lead to an understanding of the signaling pathways that explain how these structures relate vascular damage to cognitive impairment in hypertension, and contribute to the development of novel interventions to more successfully address the scourge of cognitive decline and dementia in the future,” the editorialists conclude.
The study was funded by the European Research Council, the British Heart Foundation, and the Italian Ministry of Health.
A version of this article first appeared on Medscape.com.
Researchers have identified specific regions of the brain that appear to be damaged by high blood pressure. The finding may explain the link between hypertension and cognitive impairment.
They used genetic information from genome-wide association studies (GWASs) and MRI scans of the brain to study the relationship between hypertension, changes in brain structures, and cognitive impairment. Using Mendelian randomization techniques, they identified nine brain structures related to cognitive impairment that are affected by blood pressure.
“We knew before that raised blood pressure was related to changes in the brain, but our research has narrowed down the changes to those that appear to be potentially causally related to cognitive impairment,” senior author Tomasz Guzik, professor of cardiovascular medicine, at the University of Edinburgh and of the Jagiellonian University, Krakow, Poland, told this news organization.
“Our study confirms a potentially causal relationship between raised blood pressure and cognitive impairment, emphasizing the importance of preventing and treating hypertension,” Prof. Guzik noted.
“But it also identifies the brain culprits of this relationship,” he added.
In the future, it may be possible to assess these nine brain structures in people with high blood pressure to identify those at increased risk of developing cognitive impairment, he said. “These patients may need more intensive care for their blood pressure. We can also investigate these brain structures for potential signaling pathways and molecular changes to see if we can find new targets for treatment to prevent cognitive impairment.”
For this report, the investigators married together different research datasets to identify brain structures potentially responsible for the effects of blood pressure on cognitive function, using results from previous GWASs and observational data from 39,000 people in the UK Biobank registry for whom brain MRI data were available.
First, they mapped brain structures potentially influenced by blood pressure in midlife using MRI scans from people in the UK Biobank registry. Then they examined the relationship between blood pressure and cognitive function in the UK Biobank registry. Next, of the brain structures affected by blood pressure, they identified those that are causally linked to cognitive impairment.
This was possible thanks to genetic markers coding for increased blood pressure, brain structure imaging phenotypes, and those coding for cognitive impairment that could be used in Mendelian randomization studies.
“We looked at 3935 brain magnetic resonance imaging–derived phenotypes in the brain and cognitive function defined by fluid intelligence score to identify genetically predicted causal relationships,” Prof. Guzik said.
They identified 200 brain structures that were causally affected by systolic blood pressure. Of these, nine were also causally related to cognitive impairment. The results were validated in a second prospective cohort of patients with hypertension.
“Some of these structures, including putamen and the white matter regions spanning between the anterior corona radiata, anterior thalamic radiation, and anterior limb of the internal capsule, may represent the target brain regions at which systolic blood pressure acts on cognitive function,” the authors comment.
In an accompanying editorial, Ernesto Schiffrin, MD, and James Engert, PhD, McGill University, Montreal, say that further mechanistic studies of the effects of blood pressure on cognitive function are required to determine precise causal pathways and the roles of relevant brain regions.
“Eventually, biomarkers could be developed to inform antihypertensive trials. Whether clinical trials targeting the specific brain structures will be feasible or if specific antihypertensives could be found that target specific structures remains to be demonstrated,” they write.
“Thus, these new studies could lead to an understanding of the signaling pathways that explain how these structures relate vascular damage to cognitive impairment in hypertension, and contribute to the development of novel interventions to more successfully address the scourge of cognitive decline and dementia in the future,” the editorialists conclude.
The study was funded by the European Research Council, the British Heart Foundation, and the Italian Ministry of Health.
A version of this article first appeared on Medscape.com.
Researchers have identified specific regions of the brain that appear to be damaged by high blood pressure. The finding may explain the link between hypertension and cognitive impairment.
They used genetic information from genome-wide association studies (GWASs) and MRI scans of the brain to study the relationship between hypertension, changes in brain structures, and cognitive impairment. Using Mendelian randomization techniques, they identified nine brain structures related to cognitive impairment that are affected by blood pressure.
“We knew before that raised blood pressure was related to changes in the brain, but our research has narrowed down the changes to those that appear to be potentially causally related to cognitive impairment,” senior author Tomasz Guzik, professor of cardiovascular medicine, at the University of Edinburgh and of the Jagiellonian University, Krakow, Poland, told this news organization.
“Our study confirms a potentially causal relationship between raised blood pressure and cognitive impairment, emphasizing the importance of preventing and treating hypertension,” Prof. Guzik noted.
“But it also identifies the brain culprits of this relationship,” he added.
In the future, it may be possible to assess these nine brain structures in people with high blood pressure to identify those at increased risk of developing cognitive impairment, he said. “These patients may need more intensive care for their blood pressure. We can also investigate these brain structures for potential signaling pathways and molecular changes to see if we can find new targets for treatment to prevent cognitive impairment.”
For this report, the investigators married together different research datasets to identify brain structures potentially responsible for the effects of blood pressure on cognitive function, using results from previous GWASs and observational data from 39,000 people in the UK Biobank registry for whom brain MRI data were available.
First, they mapped brain structures potentially influenced by blood pressure in midlife using MRI scans from people in the UK Biobank registry. Then they examined the relationship between blood pressure and cognitive function in the UK Biobank registry. Next, of the brain structures affected by blood pressure, they identified those that are causally linked to cognitive impairment.
This was possible thanks to genetic markers coding for increased blood pressure, brain structure imaging phenotypes, and those coding for cognitive impairment that could be used in Mendelian randomization studies.
“We looked at 3935 brain magnetic resonance imaging–derived phenotypes in the brain and cognitive function defined by fluid intelligence score to identify genetically predicted causal relationships,” Prof. Guzik said.
They identified 200 brain structures that were causally affected by systolic blood pressure. Of these, nine were also causally related to cognitive impairment. The results were validated in a second prospective cohort of patients with hypertension.
“Some of these structures, including putamen and the white matter regions spanning between the anterior corona radiata, anterior thalamic radiation, and anterior limb of the internal capsule, may represent the target brain regions at which systolic blood pressure acts on cognitive function,” the authors comment.
In an accompanying editorial, Ernesto Schiffrin, MD, and James Engert, PhD, McGill University, Montreal, say that further mechanistic studies of the effects of blood pressure on cognitive function are required to determine precise causal pathways and the roles of relevant brain regions.
“Eventually, biomarkers could be developed to inform antihypertensive trials. Whether clinical trials targeting the specific brain structures will be feasible or if specific antihypertensives could be found that target specific structures remains to be demonstrated,” they write.
“Thus, these new studies could lead to an understanding of the signaling pathways that explain how these structures relate vascular damage to cognitive impairment in hypertension, and contribute to the development of novel interventions to more successfully address the scourge of cognitive decline and dementia in the future,” the editorialists conclude.
The study was funded by the European Research Council, the British Heart Foundation, and the Italian Ministry of Health.
A version of this article first appeared on Medscape.com.