MDedge Endocrinology

LAS VEGAS – While frontline health care workers may have been disproportionately impacted by the COVID-19 pandemic, the entire workforce has experienced some level of anxiety, stress, loss, grief, and trauma, according to Jon A. Levenson, MD.

“There are those who will need mental health treatment, so creating an easy way to reach out for help and facilitate linkage with care is critically important,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “The vast majority of our workforce will thrive with proper support. But what can each of us do to take care of ourselves?”

Step one is to recognize common stress reactions as well as signs of distress. He offered the oxygen mask metaphor, the idea that before we can take care of and support anyone else, we must first take care of ourselves. “When people are stressed, they don’t always think about the oxygen mask metaphor,” Dr. Levenson said. Step two is to practice and model self-care by adopting principles often discussed in acceptance and commitment therapy: to focus on what you can control, not on what you can’t control.

“We can’t control the amount of toilet paper at the grocery store, how long the pandemic will last, or how others have reacted,” Dr. Levenson said. “We also can’t control other people’s motives, predict what will happen, or the actions of others, including whether they will follow social distancing guidelines or not.”

How about what we can control? One is a positive attitude, “which can sustain people during times of intense stress,” he said. “Other things that we can do include turn off the news and find fun and enriching activities to do at home, whether it be playing a game with family or reaching out to friends through an iPad or a smartphone. You can also follow [Centers for Disease Control and Prevention] recommendations, control your own social distancing, and limit social media activity, which can be stressful. We can also control our kindness and grace.” He added that resilience does not mean “snapping back” to how you were before the pandemic, but rather “learning to integrate the adverse experiences into who you are and growing with them, which is sometimes known as posttraumatic growth.”

Dr. Levenson encouraged health care workers to use their coping resources, connect to others, and cultivate their values and purpose in life as they navigate these challenging times. “You also want to promote realistic optimism; find a way to stay positive,” he said. “We emphasize to our staff that while you won’t forget this time, focus on what you can control – your positive relationships – and remind yourself of your values and sources of gratitude. Figure out, and reflect on, what you care about, and then care about it. Remind yourself in a deliberate, purposeful way what anchors you to your job, which in the health care setting tends to be a desire to care for others, to assist those in need, and to work in teams. We also encourage staff to refrain from judgment. Guilt is a normal and near-universal response to this stressor, but there are many ways to contribute without a judgmental or guilty tone.”

Other tips for self-support are to remind yourself that it is not selfish to take breaks. “The needs of your patients are not more important than your own needs,” Dr. Levenson said. “Working nonstop can put you at higher risk for stress, exhaustion, and illness. You may need to give yourself more time to step back and recover from workplace challenges or extended coverage for peers; this is important. We remind our staff that your work may feel more emotionally draining than usual because everything is more intense overall during the COVID-19 pandemic. This reminder helps staff normalize what they already may be experiencing, and in turn, to further support each other.”

Soothing activities to relieve stress include meditation, prayer, deep and slow breathing, relaxation exercises, yoga, mindfulness, stretching, staying hydrated, eating healthfully, exercise, and getting sufficient sleep. Other stress management tips include avoiding excessive alcohol intake, reaching out to others, asking for assistance, and delegating when possible. “We want to promote psychological flexibility: the ability to stay in contact with the present moment,” he said. “We encourage our peers to be aware of unpleasant thoughts and feelings, and to try to redirect negative thought patterns to a proactive problem-solving approach; this includes choosing one’s behaviors based on the situation and personal values.”

Dr. Levenson reported having no disclosures related to his presentation.

LAS VEGAS – While frontline health care workers may have been disproportionately impacted by the COVID-19 pandemic, the entire workforce has experienced some level of anxiety, stress, loss, grief, and trauma, according to Jon A. Levenson, MD.

“There are those who will need mental health treatment, so creating an easy way to reach out for help and facilitate linkage with care is critically important,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “The vast majority of our workforce will thrive with proper support. But what can each of us do to take care of ourselves?”

Step one is to recognize common stress reactions as well as signs of distress. He offered the oxygen mask metaphor, the idea that before we can take care of and support anyone else, we must first take care of ourselves. “When people are stressed, they don’t always think about the oxygen mask metaphor,” Dr. Levenson said. Step two is to practice and model self-care by adopting principles often discussed in acceptance and commitment therapy: to focus on what you can control, not on what you can’t control.

“We can’t control the amount of toilet paper at the grocery store, how long the pandemic will last, or how others have reacted,” Dr. Levenson said. “We also can’t control other people’s motives, predict what will happen, or the actions of others, including whether they will follow social distancing guidelines or not.”

How about what we can control? One is a positive attitude, “which can sustain people during times of intense stress,” he said. “Other things that we can do include turn off the news and find fun and enriching activities to do at home, whether it be playing a game with family or reaching out to friends through an iPad or a smartphone. You can also follow [Centers for Disease Control and Prevention] recommendations, control your own social distancing, and limit social media activity, which can be stressful. We can also control our kindness and grace.” He added that resilience does not mean “snapping back” to how you were before the pandemic, but rather “learning to integrate the adverse experiences into who you are and growing with them, which is sometimes known as posttraumatic growth.”

Dr. Levenson encouraged health care workers to use their coping resources, connect to others, and cultivate their values and purpose in life as they navigate these challenging times. “You also want to promote realistic optimism; find a way to stay positive,” he said. “We emphasize to our staff that while you won’t forget this time, focus on what you can control – your positive relationships – and remind yourself of your values and sources of gratitude. Figure out, and reflect on, what you care about, and then care about it. Remind yourself in a deliberate, purposeful way what anchors you to your job, which in the health care setting tends to be a desire to care for others, to assist those in need, and to work in teams. We also encourage staff to refrain from judgment. Guilt is a normal and near-universal response to this stressor, but there are many ways to contribute without a judgmental or guilty tone.”

Other tips for self-support are to remind yourself that it is not selfish to take breaks. “The needs of your patients are not more important than your own needs,” Dr. Levenson said. “Working nonstop can put you at higher risk for stress, exhaustion, and illness. You may need to give yourself more time to step back and recover from workplace challenges or extended coverage for peers; this is important. We remind our staff that your work may feel more emotionally draining than usual because everything is more intense overall during the COVID-19 pandemic. This reminder helps staff normalize what they already may be experiencing, and in turn, to further support each other.”

Soothing activities to relieve stress include meditation, prayer, deep and slow breathing, relaxation exercises, yoga, mindfulness, stretching, staying hydrated, eating healthfully, exercise, and getting sufficient sleep. Other stress management tips include avoiding excessive alcohol intake, reaching out to others, asking for assistance, and delegating when possible. “We want to promote psychological flexibility: the ability to stay in contact with the present moment,” he said. “We encourage our peers to be aware of unpleasant thoughts and feelings, and to try to redirect negative thought patterns to a proactive problem-solving approach; this includes choosing one’s behaviors based on the situation and personal values.”

Dr. Levenson reported having no disclosures related to his presentation.

LAS VEGAS – While frontline health care workers may have been disproportionately impacted by the COVID-19 pandemic, the entire workforce has experienced some level of anxiety, stress, loss, grief, and trauma, according to Jon A. Levenson, MD.

“There are those who will need mental health treatment, so creating an easy way to reach out for help and facilitate linkage with care is critically important,” Dr. Levenson, associate professor of psychiatry at Columbia University Irving Medical Center, New York, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “The vast majority of our workforce will thrive with proper support. But what can each of us do to take care of ourselves?”

Step one is to recognize common stress reactions as well as signs of distress. He offered the oxygen mask metaphor, the idea that before we can take care of and support anyone else, we must first take care of ourselves. “When people are stressed, they don’t always think about the oxygen mask metaphor,” Dr. Levenson said. Step two is to practice and model self-care by adopting principles often discussed in acceptance and commitment therapy: to focus on what you can control, not on what you can’t control.

“We can’t control the amount of toilet paper at the grocery store, how long the pandemic will last, or how others have reacted,” Dr. Levenson said. “We also can’t control other people’s motives, predict what will happen, or the actions of others, including whether they will follow social distancing guidelines or not.”

How about what we can control? One is a positive attitude, “which can sustain people during times of intense stress,” he said. “Other things that we can do include turn off the news and find fun and enriching activities to do at home, whether it be playing a game with family or reaching out to friends through an iPad or a smartphone. You can also follow [Centers for Disease Control and Prevention] recommendations, control your own social distancing, and limit social media activity, which can be stressful. We can also control our kindness and grace.” He added that resilience does not mean “snapping back” to how you were before the pandemic, but rather “learning to integrate the adverse experiences into who you are and growing with them, which is sometimes known as posttraumatic growth.”

Dr. Levenson encouraged health care workers to use their coping resources, connect to others, and cultivate their values and purpose in life as they navigate these challenging times. “You also want to promote realistic optimism; find a way to stay positive,” he said. “We emphasize to our staff that while you won’t forget this time, focus on what you can control – your positive relationships – and remind yourself of your values and sources of gratitude. Figure out, and reflect on, what you care about, and then care about it. Remind yourself in a deliberate, purposeful way what anchors you to your job, which in the health care setting tends to be a desire to care for others, to assist those in need, and to work in teams. We also encourage staff to refrain from judgment. Guilt is a normal and near-universal response to this stressor, but there are many ways to contribute without a judgmental or guilty tone.”

Other tips for self-support are to remind yourself that it is not selfish to take breaks. “The needs of your patients are not more important than your own needs,” Dr. Levenson said. “Working nonstop can put you at higher risk for stress, exhaustion, and illness. You may need to give yourself more time to step back and recover from workplace challenges or extended coverage for peers; this is important. We remind our staff that your work may feel more emotionally draining than usual because everything is more intense overall during the COVID-19 pandemic. This reminder helps staff normalize what they already may be experiencing, and in turn, to further support each other.”

Soothing activities to relieve stress include meditation, prayer, deep and slow breathing, relaxation exercises, yoga, mindfulness, stretching, staying hydrated, eating healthfully, exercise, and getting sufficient sleep. Other stress management tips include avoiding excessive alcohol intake, reaching out to others, asking for assistance, and delegating when possible. “We want to promote psychological flexibility: the ability to stay in contact with the present moment,” he said. “We encourage our peers to be aware of unpleasant thoughts and feelings, and to try to redirect negative thought patterns to a proactive problem-solving approach; this includes choosing one’s behaviors based on the situation and personal values.”

Dr. Levenson reported having no disclosures related to his presentation.

Chocolate: Now part of a well-balanced diet

Asking if someone loves chocolate is like asking if they love breathing. It’s really not a question that needs to be asked. The thing with chocolate, however, is that most people who love chocolate actually love sugar, since your typical milk chocolate contains only about 30% cacao. The rest, of course, is sugar.

Now, dark chocolate is actually kind of good for you since it contains beneficial flavonoids and less sugar. But that healthiness comes at a cost: Dark chocolate is quite bitter, and gets more so as the cacao content rises, to the point where 100% cacao chocolate is very nearly inedible. That’s the chocolate conundrum, the healthier it is, the worse it tastes. But what if there’s another way? What if you can have tasty chocolate that’s good for you?

Sascha Luehr/Pixabay

That’s the question a group of researchers from Penn State University dared to ask. The secret, they discovered, is to subject the cacao beans to extra-intense roasting. We’re not sure how screaming insults at a bunch of beans will help, but if science says so ... YOU USELESS LUMP OF BARELY EDIBLE FOOD! HOW DARE YOU EXIST!

Oh, not that kind of roasting. Oops.

For their study, the researchers made 27 unsweetened chocolates, prepared using various cacao bean roasting times and temperatures, and served them to volunteers. Those volunteers reported that chocolates made with cacao beans roasted more intensely (such as 20 minutes at 340° F, 80 min at 275° F, and 54 min at 304° F) were far more acceptable than were chocolates prepared with raw or lightly roasted cacao beans.

The implications of healthy yet tasty chocolate are obvious: Master the chocolate and you’ll make millions. Imagine a future where parents say to their kids: “Don’t forget to eat your chocolate.” So, we’re off to do some cooking. Don’t want Hershey to make all the money off of this revelation.
 

The villain hiding in dairy for some MS patients

For some of us, lactose can be a real heartbreaker when it comes to dairy consumption, but for people with multiple sclerosis (MS) there’s another villain they may also have to face that can make their symptoms worse.

fcafotodigital/Getty Images

Physicians at the Institute of Anatomy at University Hospital Bonn (Germany) were getting so many complaints from patients with MS about how much worse they felt about after having cheese, yogurt, and milk that they decided to get to the bottom of it. The culprit, it seems, is casein, a protein specifically found in cow’s milk.

The researchers injected mice with various proteins found in cow’s milk and found perforated myelin sheaths in those given casein. In MS, the patient’s own immune system destroys that sheath, which leads to paresthesia, vision problems, and movement disorders.

“The body’s defenses actually attack the casein, but in the process they also destroy proteins involved in the formation of myelin, “ said Rittika Chunder, a postdoctoral fellow at the University of Bonn. How? Apparently it’s all a big misunderstanding.

While looking at molecules needed for myelin production, the researchers came across MAG, which is very similar to casein, which is a problem when patients with MS are allergic to casein. After they have dairy products, the B-cell squad gets called in to clean up the evil twin, casein, but can’t differentiate it from the good twin, MAG, so it all gets a wash and the myelin sheath suffers.

Since this happens only to patients with MS who have a casein allergy, the researchers advise them to stay away from milk, yogurt, or cottage cheese while they work on a self-test to check if patients carry the antibodies.

A small price to pay, perhaps, to stop a villainous evil twin.
 

You would even say it glows

If you’re anything like us – and we think you are since you’re reading this – you’ve been asking yourself: Are there any common medications in my house that will make good radiation sensors?

Vnukko/Pixabay

Not that anyone needs to worry about excess radiation or anything. Far from it. We were just wondering.

It just so happens that Anna Mrozik and Paweł Bilski, both of the Institute of Nuclear Physics Polish Academy of Sciences (IFJ PAN) in Kraków, Poland, were wondering the same thing: “During an uncontrolled release of radiation, it is highly unlikely that members of the public will be equipped with personal radiation dose monitors.”

People would need to use something they had lying around the house. A smartphone would work, the investigators explained in a statement from the IFJ PAN, but the process of converting one to radiation-sensor duty, which involves dismantling it and breaking the display glass, “is laborious and time-consuming [and] the destruction of a valuable and useful device does not seem to be the optimal solution.”

Naturally, they turned to drugs. The key, in this case, is optically stimulated luminescence. They needed to find materials that would glow with greater intensity as the radiation dose increased. Turns out that ibuprofen- and paracetamol-based painkillers fit the bill quite nicely, although aspirin also works.

It’s not known exactly which substance is causing the luminescence, but rest assured, the “physicists from the IFJ PAN intend to identify it.”
 

This is why you don’t interrupt someone using headphones

There’s nothing like taking a nice relaxing walk with your headphones. Whether you’re listening to a podcast or a song or talking on the phone, it’s an escape from reality that makes you feel like you’re completely in tune with what you’re listening to.

Weedezign/Thinkstock

According to a new study, headphones, as opposed to speakers, make people feel more connected to what they are listening to. Data collected from more than 4,000 people showed that listening with headphones makes more of an impact than listening to speakers.

“Headphones produce a phenomenon called in-head localization, which makes the speaker sound as if they’re inside your head,” study coauthor On Amir of the University of California, San Diego, said in a statement. Because of this, people feel like the speakers are close to them and there’s more of a sense of empathy for the speakers and the listener is more likely to be swayed toward the ideas of the speaker.

These findings could lead to more efficient training programs, online work, and advertising, the investigators suggested.

We now finally understand why people get so mad when they have to take out their headphones to answer or talk to us. We ruined a satisfying moment going on in their brains.

Chocolate: Now part of a well-balanced diet

Asking if someone loves chocolate is like asking if they love breathing. It’s really not a question that needs to be asked. The thing with chocolate, however, is that most people who love chocolate actually love sugar, since your typical milk chocolate contains only about 30% cacao. The rest, of course, is sugar.

Now, dark chocolate is actually kind of good for you since it contains beneficial flavonoids and less sugar. But that healthiness comes at a cost: Dark chocolate is quite bitter, and gets more so as the cacao content rises, to the point where 100% cacao chocolate is very nearly inedible. That’s the chocolate conundrum, the healthier it is, the worse it tastes. But what if there’s another way? What if you can have tasty chocolate that’s good for you?

Sascha Luehr/Pixabay

That’s the question a group of researchers from Penn State University dared to ask. The secret, they discovered, is to subject the cacao beans to extra-intense roasting. We’re not sure how screaming insults at a bunch of beans will help, but if science says so ... YOU USELESS LUMP OF BARELY EDIBLE FOOD! HOW DARE YOU EXIST!

Oh, not that kind of roasting. Oops.

For their study, the researchers made 27 unsweetened chocolates, prepared using various cacao bean roasting times and temperatures, and served them to volunteers. Those volunteers reported that chocolates made with cacao beans roasted more intensely (such as 20 minutes at 340° F, 80 min at 275° F, and 54 min at 304° F) were far more acceptable than were chocolates prepared with raw or lightly roasted cacao beans.

The implications of healthy yet tasty chocolate are obvious: Master the chocolate and you’ll make millions. Imagine a future where parents say to their kids: “Don’t forget to eat your chocolate.” So, we’re off to do some cooking. Don’t want Hershey to make all the money off of this revelation.
 

The villain hiding in dairy for some MS patients

For some of us, lactose can be a real heartbreaker when it comes to dairy consumption, but for people with multiple sclerosis (MS) there’s another villain they may also have to face that can make their symptoms worse.

fcafotodigital/Getty Images

Physicians at the Institute of Anatomy at University Hospital Bonn (Germany) were getting so many complaints from patients with MS about how much worse they felt about after having cheese, yogurt, and milk that they decided to get to the bottom of it. The culprit, it seems, is casein, a protein specifically found in cow’s milk.

The researchers injected mice with various proteins found in cow’s milk and found perforated myelin sheaths in those given casein. In MS, the patient’s own immune system destroys that sheath, which leads to paresthesia, vision problems, and movement disorders.

“The body’s defenses actually attack the casein, but in the process they also destroy proteins involved in the formation of myelin, “ said Rittika Chunder, a postdoctoral fellow at the University of Bonn. How? Apparently it’s all a big misunderstanding.

While looking at molecules needed for myelin production, the researchers came across MAG, which is very similar to casein, which is a problem when patients with MS are allergic to casein. After they have dairy products, the B-cell squad gets called in to clean up the evil twin, casein, but can’t differentiate it from the good twin, MAG, so it all gets a wash and the myelin sheath suffers.

Since this happens only to patients with MS who have a casein allergy, the researchers advise them to stay away from milk, yogurt, or cottage cheese while they work on a self-test to check if patients carry the antibodies.

A small price to pay, perhaps, to stop a villainous evil twin.
 

You would even say it glows

If you’re anything like us – and we think you are since you’re reading this – you’ve been asking yourself: Are there any common medications in my house that will make good radiation sensors?

Vnukko/Pixabay

Not that anyone needs to worry about excess radiation or anything. Far from it. We were just wondering.

It just so happens that Anna Mrozik and Paweł Bilski, both of the Institute of Nuclear Physics Polish Academy of Sciences (IFJ PAN) in Kraków, Poland, were wondering the same thing: “During an uncontrolled release of radiation, it is highly unlikely that members of the public will be equipped with personal radiation dose monitors.”

People would need to use something they had lying around the house. A smartphone would work, the investigators explained in a statement from the IFJ PAN, but the process of converting one to radiation-sensor duty, which involves dismantling it and breaking the display glass, “is laborious and time-consuming [and] the destruction of a valuable and useful device does not seem to be the optimal solution.”

Naturally, they turned to drugs. The key, in this case, is optically stimulated luminescence. They needed to find materials that would glow with greater intensity as the radiation dose increased. Turns out that ibuprofen- and paracetamol-based painkillers fit the bill quite nicely, although aspirin also works.

It’s not known exactly which substance is causing the luminescence, but rest assured, the “physicists from the IFJ PAN intend to identify it.”
 

This is why you don’t interrupt someone using headphones

There’s nothing like taking a nice relaxing walk with your headphones. Whether you’re listening to a podcast or a song or talking on the phone, it’s an escape from reality that makes you feel like you’re completely in tune with what you’re listening to.

Weedezign/Thinkstock

According to a new study, headphones, as opposed to speakers, make people feel more connected to what they are listening to. Data collected from more than 4,000 people showed that listening with headphones makes more of an impact than listening to speakers.

“Headphones produce a phenomenon called in-head localization, which makes the speaker sound as if they’re inside your head,” study coauthor On Amir of the University of California, San Diego, said in a statement. Because of this, people feel like the speakers are close to them and there’s more of a sense of empathy for the speakers and the listener is more likely to be swayed toward the ideas of the speaker.

These findings could lead to more efficient training programs, online work, and advertising, the investigators suggested.

We now finally understand why people get so mad when they have to take out their headphones to answer or talk to us. We ruined a satisfying moment going on in their brains.

Chocolate: Now part of a well-balanced diet

Asking if someone loves chocolate is like asking if they love breathing. It’s really not a question that needs to be asked. The thing with chocolate, however, is that most people who love chocolate actually love sugar, since your typical milk chocolate contains only about 30% cacao. The rest, of course, is sugar.

Now, dark chocolate is actually kind of good for you since it contains beneficial flavonoids and less sugar. But that healthiness comes at a cost: Dark chocolate is quite bitter, and gets more so as the cacao content rises, to the point where 100% cacao chocolate is very nearly inedible. That’s the chocolate conundrum, the healthier it is, the worse it tastes. But what if there’s another way? What if you can have tasty chocolate that’s good for you?

Sascha Luehr/Pixabay

That’s the question a group of researchers from Penn State University dared to ask. The secret, they discovered, is to subject the cacao beans to extra-intense roasting. We’re not sure how screaming insults at a bunch of beans will help, but if science says so ... YOU USELESS LUMP OF BARELY EDIBLE FOOD! HOW DARE YOU EXIST!

Oh, not that kind of roasting. Oops.

For their study, the researchers made 27 unsweetened chocolates, prepared using various cacao bean roasting times and temperatures, and served them to volunteers. Those volunteers reported that chocolates made with cacao beans roasted more intensely (such as 20 minutes at 340° F, 80 min at 275° F, and 54 min at 304° F) were far more acceptable than were chocolates prepared with raw or lightly roasted cacao beans.

The implications of healthy yet tasty chocolate are obvious: Master the chocolate and you’ll make millions. Imagine a future where parents say to their kids: “Don’t forget to eat your chocolate.” So, we’re off to do some cooking. Don’t want Hershey to make all the money off of this revelation.
 

The villain hiding in dairy for some MS patients

For some of us, lactose can be a real heartbreaker when it comes to dairy consumption, but for people with multiple sclerosis (MS) there’s another villain they may also have to face that can make their symptoms worse.

fcafotodigital/Getty Images

Physicians at the Institute of Anatomy at University Hospital Bonn (Germany) were getting so many complaints from patients with MS about how much worse they felt about after having cheese, yogurt, and milk that they decided to get to the bottom of it. The culprit, it seems, is casein, a protein specifically found in cow’s milk.

The researchers injected mice with various proteins found in cow’s milk and found perforated myelin sheaths in those given casein. In MS, the patient’s own immune system destroys that sheath, which leads to paresthesia, vision problems, and movement disorders.

“The body’s defenses actually attack the casein, but in the process they also destroy proteins involved in the formation of myelin, “ said Rittika Chunder, a postdoctoral fellow at the University of Bonn. How? Apparently it’s all a big misunderstanding.

While looking at molecules needed for myelin production, the researchers came across MAG, which is very similar to casein, which is a problem when patients with MS are allergic to casein. After they have dairy products, the B-cell squad gets called in to clean up the evil twin, casein, but can’t differentiate it from the good twin, MAG, so it all gets a wash and the myelin sheath suffers.

Since this happens only to patients with MS who have a casein allergy, the researchers advise them to stay away from milk, yogurt, or cottage cheese while they work on a self-test to check if patients carry the antibodies.

A small price to pay, perhaps, to stop a villainous evil twin.
 

You would even say it glows

If you’re anything like us – and we think you are since you’re reading this – you’ve been asking yourself: Are there any common medications in my house that will make good radiation sensors?

Vnukko/Pixabay

Not that anyone needs to worry about excess radiation or anything. Far from it. We were just wondering.

It just so happens that Anna Mrozik and Paweł Bilski, both of the Institute of Nuclear Physics Polish Academy of Sciences (IFJ PAN) in Kraków, Poland, were wondering the same thing: “During an uncontrolled release of radiation, it is highly unlikely that members of the public will be equipped with personal radiation dose monitors.”

People would need to use something they had lying around the house. A smartphone would work, the investigators explained in a statement from the IFJ PAN, but the process of converting one to radiation-sensor duty, which involves dismantling it and breaking the display glass, “is laborious and time-consuming [and] the destruction of a valuable and useful device does not seem to be the optimal solution.”

Naturally, they turned to drugs. The key, in this case, is optically stimulated luminescence. They needed to find materials that would glow with greater intensity as the radiation dose increased. Turns out that ibuprofen- and paracetamol-based painkillers fit the bill quite nicely, although aspirin also works.

It’s not known exactly which substance is causing the luminescence, but rest assured, the “physicists from the IFJ PAN intend to identify it.”
 

This is why you don’t interrupt someone using headphones

There’s nothing like taking a nice relaxing walk with your headphones. Whether you’re listening to a podcast or a song or talking on the phone, it’s an escape from reality that makes you feel like you’re completely in tune with what you’re listening to.

Weedezign/Thinkstock

According to a new study, headphones, as opposed to speakers, make people feel more connected to what they are listening to. Data collected from more than 4,000 people showed that listening with headphones makes more of an impact than listening to speakers.

“Headphones produce a phenomenon called in-head localization, which makes the speaker sound as if they’re inside your head,” study coauthor On Amir of the University of California, San Diego, said in a statement. Because of this, people feel like the speakers are close to them and there’s more of a sense of empathy for the speakers and the listener is more likely to be swayed toward the ideas of the speaker.

These findings could lead to more efficient training programs, online work, and advertising, the investigators suggested.

We now finally understand why people get so mad when they have to take out their headphones to answer or talk to us. We ruined a satisfying moment going on in their brains.

Strong new evidence on the need to use an appropriately sized cuff in blood pressure measurement has come from the cross-sectional randomized trial Cuff(SZ).

The study found that in people in whom a small adult cuff was appropriate, systolic BP readings were on average 3.6 mm Hg lower when a regular adult size cuff was used.

However, systolic readings were on average 4.8 mm Hg higher when a regular cuff was used in people who required a large adult cuff and 19.5 mm Hg higher in those needing an extra-large cuff based on their mid-arm circumference.

The diastolic readings followed a similar pattern (-1.3 mm Hg, 1.8 mm Hg, and 7.4 mm Hg, respectively).

“We found that using the regular adult cuff in all individuals had striking differences in blood pressure,” lead author Tammy M. Brady, MD, PhD, Johns Hopkins University School of Medicine, Baltimore, told this news organization. “And that has a lot of clinical implications.”

A version of this article first appeared on Medscape.com.

Strong new evidence on the need to use an appropriately sized cuff in blood pressure measurement has come from the cross-sectional randomized trial Cuff(SZ).

The study found that in people in whom a small adult cuff was appropriate, systolic BP readings were on average 3.6 mm Hg lower when a regular adult size cuff was used.

However, systolic readings were on average 4.8 mm Hg higher when a regular cuff was used in people who required a large adult cuff and 19.5 mm Hg higher in those needing an extra-large cuff based on their mid-arm circumference.

The diastolic readings followed a similar pattern (-1.3 mm Hg, 1.8 mm Hg, and 7.4 mm Hg, respectively).

“We found that using the regular adult cuff in all individuals had striking differences in blood pressure,” lead author Tammy M. Brady, MD, PhD, Johns Hopkins University School of Medicine, Baltimore, told this news organization. “And that has a lot of clinical implications.”

A version of this article first appeared on Medscape.com.

Strong new evidence on the need to use an appropriately sized cuff in blood pressure measurement has come from the cross-sectional randomized trial Cuff(SZ).

The study found that in people in whom a small adult cuff was appropriate, systolic BP readings were on average 3.6 mm Hg lower when a regular adult size cuff was used.

However, systolic readings were on average 4.8 mm Hg higher when a regular cuff was used in people who required a large adult cuff and 19.5 mm Hg higher in those needing an extra-large cuff based on their mid-arm circumference.

The diastolic readings followed a similar pattern (-1.3 mm Hg, 1.8 mm Hg, and 7.4 mm Hg, respectively).

“We found that using the regular adult cuff in all individuals had striking differences in blood pressure,” lead author Tammy M. Brady, MD, PhD, Johns Hopkins University School of Medicine, Baltimore, told this news organization. “And that has a lot of clinical implications.”

A version of this article first appeared on Medscape.com.

Elective surgical procedures should be delayed at least 7 weeks after COVID-19 infection in unvaccinated patients, according to a new joint statement issued by the American Society of Anesthesiologists and the Anesthesia Patient Safety Foundation (APSF).

For patients fully vaccinated against COVID-19 with breakthrough infections, there is no consensus on how vaccination affects the time between COVID-19 infection and elective surgery. Clinicians should use their clinical judgment to schedule procedures, said Randall M. Clark, MD, president of the American Society of Anesthesiologists (ASA). “We need all physicians, anesthesiologists, surgeons, and others to base their decision to go ahead with elective surgery on the patient’s symptoms, their need for the procedure, and whether delays could cause other problems with their health,” he said in an interview.

Prior to these updated recommendations, which were published Feb. 22, the ASA and the APSF recommended a 4-week gap between COVID-19 diagnosis and elective surgery for asymptomatic or mild cases, regardless of a patient’s vaccination status.

Extending the wait time from 4 to 7 weeks was based on a multination study conducted in October 2020 following more than 140,000 surgical patients. Patients with previous COVID-19 infection had an increased risk for complications and death in elective surgery for up to 6 weeks following their diagnosis, compared with patients without COVID-19. Additional research in the United States found that patients with a preoperative COVID diagnosis were at higher risk for postoperative complications of respiratory failure for up to 4 weeks after diagnosis and postoperative pneumonia complications for up to 8 weeks after diagnosis.

Because these studies were conducted in unvaccinated populations or those with low vaccination rates, and preliminary data suggest vaccinated patients with breakthrough infections may have a lower risk for complications and death postinfection, “we felt that it was prudent to just make recommendations specific to unvaccinated patients,” Dr. Clark added.

Although this guidance is “very helpful” in that it summarizes the currently available research to give evidence-based recommendations, the 7-week wait time is a “very conservative estimate,” Brent Matthews, MD, surgeon-in-chief of the surgery care division of Atrium Health, Charlotte, N.C., told this news organization. At Atrium Health, surgery is scheduled at least 21 days after a patient’s COVID-19 diagnosis, regardless of their vaccination status, Dr. Matthews said.

The studies currently available were conducted earlier in the pandemic, when a different variant was prevalent, Dr. Matthews explained. The Omicron variant is currently the most prevalent COVID-19 variant and is less virulent than earlier strains of the virus. The joint statement does note that there is currently “no robust data” on patients infected with the Delta or Omicron variants of COVID-19, and that “the Omicron variant causes less severe disease and is more likely to reside in the oro- and nasopharynx without infiltration and damage to the lungs.”

Still, the new recommendations are a reminder to re-evaluate the potential complications from surgery for previously infected patients and to consider what comorbidities might make them more vulnerable, Dr. Matthews said. “The real power of the joint statement is to get people to ensure that they make an assessment of every patient that comes in front of them who has had a recent positive COVID test.”

A version of this article first appeared on Medscape.com.

Elective surgical procedures should be delayed at least 7 weeks after COVID-19 infection in unvaccinated patients, according to a new joint statement issued by the American Society of Anesthesiologists and the Anesthesia Patient Safety Foundation (APSF).

For patients fully vaccinated against COVID-19 with breakthrough infections, there is no consensus on how vaccination affects the time between COVID-19 infection and elective surgery. Clinicians should use their clinical judgment to schedule procedures, said Randall M. Clark, MD, president of the American Society of Anesthesiologists (ASA). “We need all physicians, anesthesiologists, surgeons, and others to base their decision to go ahead with elective surgery on the patient’s symptoms, their need for the procedure, and whether delays could cause other problems with their health,” he said in an interview.

Prior to these updated recommendations, which were published Feb. 22, the ASA and the APSF recommended a 4-week gap between COVID-19 diagnosis and elective surgery for asymptomatic or mild cases, regardless of a patient’s vaccination status.

Extending the wait time from 4 to 7 weeks was based on a multination study conducted in October 2020 following more than 140,000 surgical patients. Patients with previous COVID-19 infection had an increased risk for complications and death in elective surgery for up to 6 weeks following their diagnosis, compared with patients without COVID-19. Additional research in the United States found that patients with a preoperative COVID diagnosis were at higher risk for postoperative complications of respiratory failure for up to 4 weeks after diagnosis and postoperative pneumonia complications for up to 8 weeks after diagnosis.

Because these studies were conducted in unvaccinated populations or those with low vaccination rates, and preliminary data suggest vaccinated patients with breakthrough infections may have a lower risk for complications and death postinfection, “we felt that it was prudent to just make recommendations specific to unvaccinated patients,” Dr. Clark added.

Although this guidance is “very helpful” in that it summarizes the currently available research to give evidence-based recommendations, the 7-week wait time is a “very conservative estimate,” Brent Matthews, MD, surgeon-in-chief of the surgery care division of Atrium Health, Charlotte, N.C., told this news organization. At Atrium Health, surgery is scheduled at least 21 days after a patient’s COVID-19 diagnosis, regardless of their vaccination status, Dr. Matthews said.

The studies currently available were conducted earlier in the pandemic, when a different variant was prevalent, Dr. Matthews explained. The Omicron variant is currently the most prevalent COVID-19 variant and is less virulent than earlier strains of the virus. The joint statement does note that there is currently “no robust data” on patients infected with the Delta or Omicron variants of COVID-19, and that “the Omicron variant causes less severe disease and is more likely to reside in the oro- and nasopharynx without infiltration and damage to the lungs.”

Still, the new recommendations are a reminder to re-evaluate the potential complications from surgery for previously infected patients and to consider what comorbidities might make them more vulnerable, Dr. Matthews said. “The real power of the joint statement is to get people to ensure that they make an assessment of every patient that comes in front of them who has had a recent positive COVID test.”

A version of this article first appeared on Medscape.com.

Elective surgical procedures should be delayed at least 7 weeks after COVID-19 infection in unvaccinated patients, according to a new joint statement issued by the American Society of Anesthesiologists and the Anesthesia Patient Safety Foundation (APSF).

For patients fully vaccinated against COVID-19 with breakthrough infections, there is no consensus on how vaccination affects the time between COVID-19 infection and elective surgery. Clinicians should use their clinical judgment to schedule procedures, said Randall M. Clark, MD, president of the American Society of Anesthesiologists (ASA). “We need all physicians, anesthesiologists, surgeons, and others to base their decision to go ahead with elective surgery on the patient’s symptoms, their need for the procedure, and whether delays could cause other problems with their health,” he said in an interview.

Prior to these updated recommendations, which were published Feb. 22, the ASA and the APSF recommended a 4-week gap between COVID-19 diagnosis and elective surgery for asymptomatic or mild cases, regardless of a patient’s vaccination status.

Extending the wait time from 4 to 7 weeks was based on a multination study conducted in October 2020 following more than 140,000 surgical patients. Patients with previous COVID-19 infection had an increased risk for complications and death in elective surgery for up to 6 weeks following their diagnosis, compared with patients without COVID-19. Additional research in the United States found that patients with a preoperative COVID diagnosis were at higher risk for postoperative complications of respiratory failure for up to 4 weeks after diagnosis and postoperative pneumonia complications for up to 8 weeks after diagnosis.

Because these studies were conducted in unvaccinated populations or those with low vaccination rates, and preliminary data suggest vaccinated patients with breakthrough infections may have a lower risk for complications and death postinfection, “we felt that it was prudent to just make recommendations specific to unvaccinated patients,” Dr. Clark added.

Although this guidance is “very helpful” in that it summarizes the currently available research to give evidence-based recommendations, the 7-week wait time is a “very conservative estimate,” Brent Matthews, MD, surgeon-in-chief of the surgery care division of Atrium Health, Charlotte, N.C., told this news organization. At Atrium Health, surgery is scheduled at least 21 days after a patient’s COVID-19 diagnosis, regardless of their vaccination status, Dr. Matthews said.

The studies currently available were conducted earlier in the pandemic, when a different variant was prevalent, Dr. Matthews explained. The Omicron variant is currently the most prevalent COVID-19 variant and is less virulent than earlier strains of the virus. The joint statement does note that there is currently “no robust data” on patients infected with the Delta or Omicron variants of COVID-19, and that “the Omicron variant causes less severe disease and is more likely to reside in the oro- and nasopharynx without infiltration and damage to the lungs.”

Still, the new recommendations are a reminder to re-evaluate the potential complications from surgery for previously infected patients and to consider what comorbidities might make them more vulnerable, Dr. Matthews said. “The real power of the joint statement is to get people to ensure that they make an assessment of every patient that comes in front of them who has had a recent positive COVID test.”

A version of this article first appeared on Medscape.com.

A look back at a pair of large cohort studies suggests a telling relation between two distinct predictors of atherosclerotic cardiovascular disease (ASCVD) risk and may offer guidance on how to interpret them together.

Elevated levels of lipoprotein(a), or Lp(a), and high coronary artery calcium (CAC) scores were both predictive of ASCVD risk over 10 years, but independent of each other and a host of more traditional cardiovascular risk factors, for example, in the analysis of data from the MESA (Multi-Ethnic Study of Atherosclerosis) and DHS (Dallas Heart Study) longitudinal cohorts.

Notably, the risk when both Lp(a) and CAC scores were high far exceeded that associated with either marker alone. But when CAC scores were less than 100 Agatston units, predicted ASCVD risk wasn’t influenced by levels of Lp(a). Indeed, a CAC score of 0 predicted the lowest levels of ASCVD risk, even with elevated Lp(a).

That is, the findings suggest, the addition of Lp(a) makes a difference to the risk assessment only when CAC scores are high, at least 100 units, and elevated Lp(a) doesn’t mean increased ASCVD risk in the absence of coronary calcium.

“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score,” concluded a report on the analysis, published in the Journal of the American College of Cardiology, with lead author Anurag Mehta, MD, Emory University, Atlanta.

There are no formal recommendations on how to interpret Lp(a) and CAC scores together, but the current findings “provide impetus for measuring Lp(a) in more individuals as part of the shared decision-making process,” the authors contended.

“Really, the calcium score carries the majority of the information in terms of risk, except in the highest CAC score group. That is, if you have a high Lp(a) and a high burden of calcium, your risk is significantly higher than if you just have the high calcium score and the normal Lp(a),” senior author Parag H. Joshi, MD, MHS, said in an interview.

“We thought we would see that the group with higher Lp(a) would have more events over 10 years, even among those who didn’t have coronary calcium,” said Dr. Joshi, of the University of Texas Southwestern Medical Center, Dallas. “But we really don’t see that, at least in a statistically significant way.”

A CAC score of 0 would at least support a more conservative approach in a patient with elevated Lp(a) “who is hesitant to be on a statin or to be more aggressive managing their risk,” Dr. Joshi said.

“This study should be very reassuring for a patient like that,” Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital, Boston, said in an interview.

“If you have a high Lp(a) and you’re concerned, I think this study really supports the role of calcium scoring for further risk assessment,” said Dr. Blankstein, who is not associated with the new report. “We often check Lp(a) in individuals who perhaps have a family history or who come to see us in a preventive cardiology clinic. If it is high and there is concern, a calcium score can be very helpful. If it’s zero, that really means a very low risk of events. And if it’s elevated, I think we’re going to be more concerned about that patient.”

The current analysis suggests “that, when a patient without clinical cardiovascular disease is identified with either CAC ≥100 or Lp(a) >50 mg/dL, the next step in the risk evaluation should be to measure either Lp(a) or CAC, respectively – if not already performed – to identify the patients at highest risk,” Sotirios Tsimikas, MD, director of vascular medicine at University of California, San Diego, wrote in an accompanying editorial.

“Both Lp(a) and CAC should be more broadly applied in clinical care settings in patients without prior ASCVD to identify those that most likely will benefit from more aggressive therapy and, in the future, from Lp(a)-lowering therapies,” he wrote.

The analyses were conducted separately on data from 4,512 initially asymptomatic patients in MESA and 2,078 from the DHS cohort, who were followed for ASCVD events an average of 13 years and 11 years, respectively. Such events included coronary heart disease–related death, nonfatal MI, and fatal or nonfatal stroke.

In the MESA cohort – 52% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese – elevated Lp(a) (quintile 5 vs. quintiles 1-4) and CAC scores of 1-99 and above 100 (both compared with 0) were each independently associated with increased risk for ASCVD events. The hazard ratio was 1.29 (P = .02) for elevated Lp(a), 1.68 (P < .01) for a CAC score of 1-99, and 2.66 (P < .01) for a CAC score of at least 100.

The corresponding HRs in the DHS cohort were 1.54 (P = .07) for Lp(a), 3.32 (P < .01) for a CAC score of 1-99, and 5.21 (P < .01) for a CAC score of at least 100.

Of note, the authors wrote, ASCVD risk among MESA participants with a CAC score of 0 was not significantly different in those with normal and elevated Lp(a).

A version of this article first appeared on Medscape.com.

A look back at a pair of large cohort studies suggests a telling relation between two distinct predictors of atherosclerotic cardiovascular disease (ASCVD) risk and may offer guidance on how to interpret them together.

Elevated levels of lipoprotein(a), or Lp(a), and high coronary artery calcium (CAC) scores were both predictive of ASCVD risk over 10 years, but independent of each other and a host of more traditional cardiovascular risk factors, for example, in the analysis of data from the MESA (Multi-Ethnic Study of Atherosclerosis) and DHS (Dallas Heart Study) longitudinal cohorts.

Notably, the risk when both Lp(a) and CAC scores were high far exceeded that associated with either marker alone. But when CAC scores were less than 100 Agatston units, predicted ASCVD risk wasn’t influenced by levels of Lp(a). Indeed, a CAC score of 0 predicted the lowest levels of ASCVD risk, even with elevated Lp(a).

That is, the findings suggest, the addition of Lp(a) makes a difference to the risk assessment only when CAC scores are high, at least 100 units, and elevated Lp(a) doesn’t mean increased ASCVD risk in the absence of coronary calcium.

“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score,” concluded a report on the analysis, published in the Journal of the American College of Cardiology, with lead author Anurag Mehta, MD, Emory University, Atlanta.

There are no formal recommendations on how to interpret Lp(a) and CAC scores together, but the current findings “provide impetus for measuring Lp(a) in more individuals as part of the shared decision-making process,” the authors contended.

“Really, the calcium score carries the majority of the information in terms of risk, except in the highest CAC score group. That is, if you have a high Lp(a) and a high burden of calcium, your risk is significantly higher than if you just have the high calcium score and the normal Lp(a),” senior author Parag H. Joshi, MD, MHS, said in an interview.

“We thought we would see that the group with higher Lp(a) would have more events over 10 years, even among those who didn’t have coronary calcium,” said Dr. Joshi, of the University of Texas Southwestern Medical Center, Dallas. “But we really don’t see that, at least in a statistically significant way.”

A CAC score of 0 would at least support a more conservative approach in a patient with elevated Lp(a) “who is hesitant to be on a statin or to be more aggressive managing their risk,” Dr. Joshi said.

“This study should be very reassuring for a patient like that,” Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital, Boston, said in an interview.

“If you have a high Lp(a) and you’re concerned, I think this study really supports the role of calcium scoring for further risk assessment,” said Dr. Blankstein, who is not associated with the new report. “We often check Lp(a) in individuals who perhaps have a family history or who come to see us in a preventive cardiology clinic. If it is high and there is concern, a calcium score can be very helpful. If it’s zero, that really means a very low risk of events. And if it’s elevated, I think we’re going to be more concerned about that patient.”

The current analysis suggests “that, when a patient without clinical cardiovascular disease is identified with either CAC ≥100 or Lp(a) >50 mg/dL, the next step in the risk evaluation should be to measure either Lp(a) or CAC, respectively – if not already performed – to identify the patients at highest risk,” Sotirios Tsimikas, MD, director of vascular medicine at University of California, San Diego, wrote in an accompanying editorial.

“Both Lp(a) and CAC should be more broadly applied in clinical care settings in patients without prior ASCVD to identify those that most likely will benefit from more aggressive therapy and, in the future, from Lp(a)-lowering therapies,” he wrote.

The analyses were conducted separately on data from 4,512 initially asymptomatic patients in MESA and 2,078 from the DHS cohort, who were followed for ASCVD events an average of 13 years and 11 years, respectively. Such events included coronary heart disease–related death, nonfatal MI, and fatal or nonfatal stroke.

In the MESA cohort – 52% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese – elevated Lp(a) (quintile 5 vs. quintiles 1-4) and CAC scores of 1-99 and above 100 (both compared with 0) were each independently associated with increased risk for ASCVD events. The hazard ratio was 1.29 (P = .02) for elevated Lp(a), 1.68 (P < .01) for a CAC score of 1-99, and 2.66 (P < .01) for a CAC score of at least 100.

The corresponding HRs in the DHS cohort were 1.54 (P = .07) for Lp(a), 3.32 (P < .01) for a CAC score of 1-99, and 5.21 (P < .01) for a CAC score of at least 100.

Of note, the authors wrote, ASCVD risk among MESA participants with a CAC score of 0 was not significantly different in those with normal and elevated Lp(a).

A version of this article first appeared on Medscape.com.

A look back at a pair of large cohort studies suggests a telling relation between two distinct predictors of atherosclerotic cardiovascular disease (ASCVD) risk and may offer guidance on how to interpret them together.

Elevated levels of lipoprotein(a), or Lp(a), and high coronary artery calcium (CAC) scores were both predictive of ASCVD risk over 10 years, but independent of each other and a host of more traditional cardiovascular risk factors, for example, in the analysis of data from the MESA (Multi-Ethnic Study of Atherosclerosis) and DHS (Dallas Heart Study) longitudinal cohorts.

Notably, the risk when both Lp(a) and CAC scores were high far exceeded that associated with either marker alone. But when CAC scores were less than 100 Agatston units, predicted ASCVD risk wasn’t influenced by levels of Lp(a). Indeed, a CAC score of 0 predicted the lowest levels of ASCVD risk, even with elevated Lp(a).

That is, the findings suggest, the addition of Lp(a) makes a difference to the risk assessment only when CAC scores are high, at least 100 units, and elevated Lp(a) doesn’t mean increased ASCVD risk in the absence of coronary calcium.

“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score,” concluded a report on the analysis, published in the Journal of the American College of Cardiology, with lead author Anurag Mehta, MD, Emory University, Atlanta.

There are no formal recommendations on how to interpret Lp(a) and CAC scores together, but the current findings “provide impetus for measuring Lp(a) in more individuals as part of the shared decision-making process,” the authors contended.

“Really, the calcium score carries the majority of the information in terms of risk, except in the highest CAC score group. That is, if you have a high Lp(a) and a high burden of calcium, your risk is significantly higher than if you just have the high calcium score and the normal Lp(a),” senior author Parag H. Joshi, MD, MHS, said in an interview.

“We thought we would see that the group with higher Lp(a) would have more events over 10 years, even among those who didn’t have coronary calcium,” said Dr. Joshi, of the University of Texas Southwestern Medical Center, Dallas. “But we really don’t see that, at least in a statistically significant way.”

A CAC score of 0 would at least support a more conservative approach in a patient with elevated Lp(a) “who is hesitant to be on a statin or to be more aggressive managing their risk,” Dr. Joshi said.

“This study should be very reassuring for a patient like that,” Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital, Boston, said in an interview.

“If you have a high Lp(a) and you’re concerned, I think this study really supports the role of calcium scoring for further risk assessment,” said Dr. Blankstein, who is not associated with the new report. “We often check Lp(a) in individuals who perhaps have a family history or who come to see us in a preventive cardiology clinic. If it is high and there is concern, a calcium score can be very helpful. If it’s zero, that really means a very low risk of events. And if it’s elevated, I think we’re going to be more concerned about that patient.”

The current analysis suggests “that, when a patient without clinical cardiovascular disease is identified with either CAC ≥100 or Lp(a) >50 mg/dL, the next step in the risk evaluation should be to measure either Lp(a) or CAC, respectively – if not already performed – to identify the patients at highest risk,” Sotirios Tsimikas, MD, director of vascular medicine at University of California, San Diego, wrote in an accompanying editorial.

“Both Lp(a) and CAC should be more broadly applied in clinical care settings in patients without prior ASCVD to identify those that most likely will benefit from more aggressive therapy and, in the future, from Lp(a)-lowering therapies,” he wrote.

The analyses were conducted separately on data from 4,512 initially asymptomatic patients in MESA and 2,078 from the DHS cohort, who were followed for ASCVD events an average of 13 years and 11 years, respectively. Such events included coronary heart disease–related death, nonfatal MI, and fatal or nonfatal stroke.

In the MESA cohort – 52% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese – elevated Lp(a) (quintile 5 vs. quintiles 1-4) and CAC scores of 1-99 and above 100 (both compared with 0) were each independently associated with increased risk for ASCVD events. The hazard ratio was 1.29 (P = .02) for elevated Lp(a), 1.68 (P < .01) for a CAC score of 1-99, and 2.66 (P < .01) for a CAC score of at least 100.

The corresponding HRs in the DHS cohort were 1.54 (P = .07) for Lp(a), 3.32 (P < .01) for a CAC score of 1-99, and 5.21 (P < .01) for a CAC score of at least 100.

Of note, the authors wrote, ASCVD risk among MESA participants with a CAC score of 0 was not significantly different in those with normal and elevated Lp(a).

A version of this article first appeared on Medscape.com.

Exposure to phthalates through maternal blood and cord blood affected outcomes including head circumference and anogenital index for male and female infants, according to data from 65 mother-infant pairs.

Phthalates are recognized endocrine disruptors that have been associated with adverse birth outcomes, but the specific relationship between maternal phthalate exposure and birth outcomes has not been well studied, wrote Hsiao-Lin Hwa, MD, of National Taiwan University, Taipei, and colleagues.

Previous research suggests that trace exposure to hazardous chemicals during the fetal period “may cause fetal metabolic dysfunction and adversely change the morphology of body systems,” they said. In 2011, “the Taiwan Food and Drug Administration found that di‐2‐ethylhexyl phthalate (DEHP) and DiNP [di‐isononyl phthalate] had been illegally added as emulsifiers to replace palm oil in beverages and food,” they added. The researchers sought to examine the association between infant birth outcomes and phthalate exposure levels in the Taiwanese population after 2011. In a study published in Environmental Toxicology and Chemistry, the researchers recruited 65 pregnant women in Taiwan between 2016 and 2017. Birth length, birth weight, head circumference, anogenital distance (AGD), anoscrotal distance (ASD), and anofourchette distance (AFD) were measured for each newborn at the time of delivery. The average age of the women was 33.6 years, and the rate of low birth weight was 13.7%. The mean measures of birth length, birth weight, head circumference, and chest circumference were 47.6 cm, 3022 g, 32.9 cm, and 30.8 mm, respectively. The mean AFD and ASD were 14.2 mm and 22.3 mm, respectively.

The researchers tested for 12 phthalates in maternal blood and cord blood samples. Of these, the six most frequently detected phthalate metabolites were mono‐ethyl phthalate (MEP), mono‐isobutyl phthalate (MiBP), mono‐n‐butyl phthalate (MnBP), mono‐(2‐ethyl‐5‐oxohexyl)‐phthalate (MEOHP), mono‐(2‐ethyl‐5‐hydroxyhexyl) phthalate (MEHHP), and mono‐n‐octyl phthalate (MOP); these six were present in 80%–100% of the maternal blood samples.

Overall, the mean levels of MEP, MiBP, MnBP, and MEHP were relatively higher in both maternal and infant blood than other phthalates, the researchers noted. The mean concentrations of metabolites in maternal blood and infant cord blood were 0.03-2.27 ng/mL and 0.01-3.74 ng/mL, respectively.

Among male infants, levels of MMP, MiBP, and MEHP in maternal blood were inversely related to anogenital index (AGI), with P values for regression coefficients ranging from .011 to .033. In addition, the total concentration of MEHP, MEOHP, and MEHHP (designated as Σdi‐2‐ethylhexyl phthalate, ΣDEHP) was inversely related to AGI in males.

Among female infants, however, phthalates in cord blood, rather than maternal blood, were positively related to AGI, including MMP, MibP, MnBP, and MOP, with P values for regression coefficients ranging from .001 to .034.

Cord blood levels of MnBP, MEOHP, MEHP, and ΣDEHP were inversely associated with gestational age-adjusted head circumference in all infants, with beta coefficients of –0.15, –0.12, –0.01, and –0.01, respectively (P < .05 for all).

“The detection rates of MEHHP, MEOHP, and MEHP in the cord blood were lower than those in the maternal blood, particularly those of MEHHP and MEOHP, which were approximately 25% lower,” which may be caused by slow placental transfer, the researchers wrote in their discussion section. “The high detection rate of phthalate metabolites indicated that our subjects may continue to be exposed to these phthalates even after the 2011 Taiwan DEHP incident,” they noted.

The study findings were limited by several factors including the possibility for contamination of samples and other environmental confounders, the researchers noted. However, the results support the role of phthalates as endocrine disruptors, and the distinction in effects between males and females “may suggest that phthalate monoesters are potentially estrogenic and antiandrogenic chemicals,” they added.

“Further investigations involving multiple phthalate analyses during pregnancy and measurements throughout childhood are necessary to confirm our findings,” they concluded.
 

Direct clinical implications remain uncertain

“Phthalates are a group of chemicals that are used to make plastic more durable; they are found in multiple everyday materials, food products, and common household products,” Marissa Platner, MD, of Emory University, Atlanta, said in an interview. “It is known that we are exposed to phthalates on a routine basis but the long-term effects of this exposure are unclear,” she said.

The current study findings “were not entirely surprising given data from prior animal studies because they do imply that there is some placental transfer of the phthalate metabolites that can cause adverse effects on the developing fetus,” said Dr. Platner. “However, they also demonstrate that the placenta acts as a filter for certain larger molecules to protect the fetus,” she said.

“This study was based on a small sample size, therefore the clinical implications are not clear,” Dr. Platner noted. “However it may be worthwhile after further research to encourage our pregnant patients to try to decrease their exposure to phthalates,” she said.

Dr. Platner identified two areas for additional research to explore the role of phthalate exposure.

“The first would be to assess the level of maternal phthalate exposure throughout the pregnancy instead of just at one point in time, and the second would be to assess how the reproductive system differences at birth translate to long-term outcomes in children, such as early puberty in females or decreased fertility in males,” she said.  

The study was funded by the Ministry of Science and Technology of Taiwan and the Far Eastern Memorial Hospital‐National Taiwan University Hospital. The researchers and Dr. Platner had no financial conflicts to disclose.

Exposure to phthalates through maternal blood and cord blood affected outcomes including head circumference and anogenital index for male and female infants, according to data from 65 mother-infant pairs.

Phthalates are recognized endocrine disruptors that have been associated with adverse birth outcomes, but the specific relationship between maternal phthalate exposure and birth outcomes has not been well studied, wrote Hsiao-Lin Hwa, MD, of National Taiwan University, Taipei, and colleagues.

Previous research suggests that trace exposure to hazardous chemicals during the fetal period “may cause fetal metabolic dysfunction and adversely change the morphology of body systems,” they said. In 2011, “the Taiwan Food and Drug Administration found that di‐2‐ethylhexyl phthalate (DEHP) and DiNP [di‐isononyl phthalate] had been illegally added as emulsifiers to replace palm oil in beverages and food,” they added. The researchers sought to examine the association between infant birth outcomes and phthalate exposure levels in the Taiwanese population after 2011. In a study published in Environmental Toxicology and Chemistry, the researchers recruited 65 pregnant women in Taiwan between 2016 and 2017. Birth length, birth weight, head circumference, anogenital distance (AGD), anoscrotal distance (ASD), and anofourchette distance (AFD) were measured for each newborn at the time of delivery. The average age of the women was 33.6 years, and the rate of low birth weight was 13.7%. The mean measures of birth length, birth weight, head circumference, and chest circumference were 47.6 cm, 3022 g, 32.9 cm, and 30.8 mm, respectively. The mean AFD and ASD were 14.2 mm and 22.3 mm, respectively.

The researchers tested for 12 phthalates in maternal blood and cord blood samples. Of these, the six most frequently detected phthalate metabolites were mono‐ethyl phthalate (MEP), mono‐isobutyl phthalate (MiBP), mono‐n‐butyl phthalate (MnBP), mono‐(2‐ethyl‐5‐oxohexyl)‐phthalate (MEOHP), mono‐(2‐ethyl‐5‐hydroxyhexyl) phthalate (MEHHP), and mono‐n‐octyl phthalate (MOP); these six were present in 80%–100% of the maternal blood samples.

Overall, the mean levels of MEP, MiBP, MnBP, and MEHP were relatively higher in both maternal and infant blood than other phthalates, the researchers noted. The mean concentrations of metabolites in maternal blood and infant cord blood were 0.03-2.27 ng/mL and 0.01-3.74 ng/mL, respectively.

Among male infants, levels of MMP, MiBP, and MEHP in maternal blood were inversely related to anogenital index (AGI), with P values for regression coefficients ranging from .011 to .033. In addition, the total concentration of MEHP, MEOHP, and MEHHP (designated as Σdi‐2‐ethylhexyl phthalate, ΣDEHP) was inversely related to AGI in males.

Among female infants, however, phthalates in cord blood, rather than maternal blood, were positively related to AGI, including MMP, MibP, MnBP, and MOP, with P values for regression coefficients ranging from .001 to .034.

Cord blood levels of MnBP, MEOHP, MEHP, and ΣDEHP were inversely associated with gestational age-adjusted head circumference in all infants, with beta coefficients of –0.15, –0.12, –0.01, and –0.01, respectively (P < .05 for all).

“The detection rates of MEHHP, MEOHP, and MEHP in the cord blood were lower than those in the maternal blood, particularly those of MEHHP and MEOHP, which were approximately 25% lower,” which may be caused by slow placental transfer, the researchers wrote in their discussion section. “The high detection rate of phthalate metabolites indicated that our subjects may continue to be exposed to these phthalates even after the 2011 Taiwan DEHP incident,” they noted.

The study findings were limited by several factors including the possibility for contamination of samples and other environmental confounders, the researchers noted. However, the results support the role of phthalates as endocrine disruptors, and the distinction in effects between males and females “may suggest that phthalate monoesters are potentially estrogenic and antiandrogenic chemicals,” they added.

“Further investigations involving multiple phthalate analyses during pregnancy and measurements throughout childhood are necessary to confirm our findings,” they concluded.
 

Direct clinical implications remain uncertain

“Phthalates are a group of chemicals that are used to make plastic more durable; they are found in multiple everyday materials, food products, and common household products,” Marissa Platner, MD, of Emory University, Atlanta, said in an interview. “It is known that we are exposed to phthalates on a routine basis but the long-term effects of this exposure are unclear,” she said.

The current study findings “were not entirely surprising given data from prior animal studies because they do imply that there is some placental transfer of the phthalate metabolites that can cause adverse effects on the developing fetus,” said Dr. Platner. “However, they also demonstrate that the placenta acts as a filter for certain larger molecules to protect the fetus,” she said.

“This study was based on a small sample size, therefore the clinical implications are not clear,” Dr. Platner noted. “However it may be worthwhile after further research to encourage our pregnant patients to try to decrease their exposure to phthalates,” she said.

Dr. Platner identified two areas for additional research to explore the role of phthalate exposure.

“The first would be to assess the level of maternal phthalate exposure throughout the pregnancy instead of just at one point in time, and the second would be to assess how the reproductive system differences at birth translate to long-term outcomes in children, such as early puberty in females or decreased fertility in males,” she said.  

The study was funded by the Ministry of Science and Technology of Taiwan and the Far Eastern Memorial Hospital‐National Taiwan University Hospital. The researchers and Dr. Platner had no financial conflicts to disclose.

Exposure to phthalates through maternal blood and cord blood affected outcomes including head circumference and anogenital index for male and female infants, according to data from 65 mother-infant pairs.

Phthalates are recognized endocrine disruptors that have been associated with adverse birth outcomes, but the specific relationship between maternal phthalate exposure and birth outcomes has not been well studied, wrote Hsiao-Lin Hwa, MD, of National Taiwan University, Taipei, and colleagues.

Previous research suggests that trace exposure to hazardous chemicals during the fetal period “may cause fetal metabolic dysfunction and adversely change the morphology of body systems,” they said. In 2011, “the Taiwan Food and Drug Administration found that di‐2‐ethylhexyl phthalate (DEHP) and DiNP [di‐isononyl phthalate] had been illegally added as emulsifiers to replace palm oil in beverages and food,” they added. The researchers sought to examine the association between infant birth outcomes and phthalate exposure levels in the Taiwanese population after 2011. In a study published in Environmental Toxicology and Chemistry, the researchers recruited 65 pregnant women in Taiwan between 2016 and 2017. Birth length, birth weight, head circumference, anogenital distance (AGD), anoscrotal distance (ASD), and anofourchette distance (AFD) were measured for each newborn at the time of delivery. The average age of the women was 33.6 years, and the rate of low birth weight was 13.7%. The mean measures of birth length, birth weight, head circumference, and chest circumference were 47.6 cm, 3022 g, 32.9 cm, and 30.8 mm, respectively. The mean AFD and ASD were 14.2 mm and 22.3 mm, respectively.

The researchers tested for 12 phthalates in maternal blood and cord blood samples. Of these, the six most frequently detected phthalate metabolites were mono‐ethyl phthalate (MEP), mono‐isobutyl phthalate (MiBP), mono‐n‐butyl phthalate (MnBP), mono‐(2‐ethyl‐5‐oxohexyl)‐phthalate (MEOHP), mono‐(2‐ethyl‐5‐hydroxyhexyl) phthalate (MEHHP), and mono‐n‐octyl phthalate (MOP); these six were present in 80%–100% of the maternal blood samples.

Overall, the mean levels of MEP, MiBP, MnBP, and MEHP were relatively higher in both maternal and infant blood than other phthalates, the researchers noted. The mean concentrations of metabolites in maternal blood and infant cord blood were 0.03-2.27 ng/mL and 0.01-3.74 ng/mL, respectively.

Among male infants, levels of MMP, MiBP, and MEHP in maternal blood were inversely related to anogenital index (AGI), with P values for regression coefficients ranging from .011 to .033. In addition, the total concentration of MEHP, MEOHP, and MEHHP (designated as Σdi‐2‐ethylhexyl phthalate, ΣDEHP) was inversely related to AGI in males.

Among female infants, however, phthalates in cord blood, rather than maternal blood, were positively related to AGI, including MMP, MibP, MnBP, and MOP, with P values for regression coefficients ranging from .001 to .034.

Cord blood levels of MnBP, MEOHP, MEHP, and ΣDEHP were inversely associated with gestational age-adjusted head circumference in all infants, with beta coefficients of –0.15, –0.12, –0.01, and –0.01, respectively (P < .05 for all).

“The detection rates of MEHHP, MEOHP, and MEHP in the cord blood were lower than those in the maternal blood, particularly those of MEHHP and MEOHP, which were approximately 25% lower,” which may be caused by slow placental transfer, the researchers wrote in their discussion section. “The high detection rate of phthalate metabolites indicated that our subjects may continue to be exposed to these phthalates even after the 2011 Taiwan DEHP incident,” they noted.

The study findings were limited by several factors including the possibility for contamination of samples and other environmental confounders, the researchers noted. However, the results support the role of phthalates as endocrine disruptors, and the distinction in effects between males and females “may suggest that phthalate monoesters are potentially estrogenic and antiandrogenic chemicals,” they added.

“Further investigations involving multiple phthalate analyses during pregnancy and measurements throughout childhood are necessary to confirm our findings,” they concluded.
 

Direct clinical implications remain uncertain

“Phthalates are a group of chemicals that are used to make plastic more durable; they are found in multiple everyday materials, food products, and common household products,” Marissa Platner, MD, of Emory University, Atlanta, said in an interview. “It is known that we are exposed to phthalates on a routine basis but the long-term effects of this exposure are unclear,” she said.

The current study findings “were not entirely surprising given data from prior animal studies because they do imply that there is some placental transfer of the phthalate metabolites that can cause adverse effects on the developing fetus,” said Dr. Platner. “However, they also demonstrate that the placenta acts as a filter for certain larger molecules to protect the fetus,” she said.

“This study was based on a small sample size, therefore the clinical implications are not clear,” Dr. Platner noted. “However it may be worthwhile after further research to encourage our pregnant patients to try to decrease their exposure to phthalates,” she said.

Dr. Platner identified two areas for additional research to explore the role of phthalate exposure.

“The first would be to assess the level of maternal phthalate exposure throughout the pregnancy instead of just at one point in time, and the second would be to assess how the reproductive system differences at birth translate to long-term outcomes in children, such as early puberty in females or decreased fertility in males,” she said.  

The study was funded by the Ministry of Science and Technology of Taiwan and the Far Eastern Memorial Hospital‐National Taiwan University Hospital. The researchers and Dr. Platner had no financial conflicts to disclose.

When we refer to “regular table salt,” it is most commonly in the form of sodium chloride, which is also a major constituent of packaged and ultraprocessed foods.

The best approach to finding the “healthiest salt” – which really means the lowest in sodium – is to look for the amount on the label. “Sodium-free” usually indicates less than 5 mg of sodium per serving, and “low-sodium” usually means 140 mg or less per serving. In contrast, regular table salt can contain as much as 560 mg of sodium in one serving.

Other en vogue salts, such as pink Himalayan salt, sea salt, and kosher salt, are high in sodium content – like regular table salt – but because of their larger crystal size, less sodium is delivered per serving.

Georges Lievre / Fotolia.com

FDA issues guidance on reducing salt

Currently, the U.S. sodium dietary guidelines for persons older than 14 stipulate 2,300 mg/d, which is equivalent to 1 teaspoon a day. However it is estimated that the average person in the United States consumes more than this – around 3,400 mg of sodium daily.

In October 2021, the U.S. Food and Drug Administration published guidance on voluntary sodium limitations in commercially processed, packaged, and prepared food. The FDA’s short-term approach is to slowly reduce exposure to sodium in processed and restaurant food by 2025, on the basis that people will eventually get used to less salt, as has happened in the United Kingdom and other countries.

Such strategies to reduce salt intake are now being used in national programs in several countries. Many of these successful initiatives include active engagement with the food industry to reduce the amount of sodium added to processed food, as well as public awareness campaigns to alert consumers to the dangers of eating too much salt. This includes increasing potassium in manufactured foods, primarily to target hypertension and heart disease, as described by Clare Farrand, MSc, BSc, and colleagues, in the Journal of Clinical Hypertension. The authors also make several recommendations regarding salt reduction policies:

• Food manufacturers should gradually reduce sodium in food to the lowest possible levels and explore the use of potassium-based sodium replacers to reduce sodium levels even further.
• Governments should continue to monitor sodium and potassium levels in processed foods.
• Further consideration may need to be given to how best to label salt substitutes (namely potassium) in processed foods to ensure that people who may be adversely affected are aware.
• Governments should systematically monitor potassium intake at the population level, including for specific susceptible groups.
• Governments should continue to systematically monitor sodium (salt) intake and iodine intake at the population level to adjust salt iodization over time as necessary, depending on observed salt intake in specific targeted groups, to ensure that they have sufficient but not excessive iodine intakes as salt intakes are reduced.
• Governments should consider opportunities for promoting and subsidizing salt substitutes, particularly in countries where salt added during cooking or at the table is the major source of salt in the diet.

The new FDA document includes 163 subcategories of foods in its voluntary salt reduction strategy.
 

Salt substitutes, high blood pressure, and mortality

Lowering sodium intake is almost certainly beneficial for persons with high blood pressure. In 2020, a review in Hypertension highlighted the benefit of salt substitutes in reducing hypertension, reporting that they lower systolic blood pressure by 5.58 mm Hg and diastolic blood pressure by 2.88 mm Hg.

And changes to dietary sodium intake can potentially reduce or obviate the need for medications for essential hypertension in some individuals. Although there are only a few studies on this topic, a study by Bruce Neal, MB, ChB, PhD, and colleagues, revealed a reduction in stroke, cardiovascular events, and deaths with the use of potassium-based salt substitutes.
 

Salt substitutes and sodium and potassium handling in the kidneys

Many studies have shown that potassium-rich salt substitutes are safe in individuals with normal kidney function, but are they safe and beneficial for people with chronic kidney disease (CKD)?

For anyone who is on a renal diet, potassium and sodium intake goals are limited according to their absolute level of kidney function.

There have been case reports of life-threatening blood potassium levels (hyperkalemia) due to potassium-rich salt substitutes in people with CKD, but no larger published studies on this topic can be found.

A diet modeling study by Rebecca Morrison and colleagues evaluated varying degrees of potassium-enriched salt substituted bread products and their impact on dietary intake in persons with CKD. They used dietary data from the National Nutrition and Physical Activity Survey 2011-2012 in Australia for 12,152 participants, 154 of whom had CKD. Replacing the sodium in bread with varying amounts of potassium chloride (20%, 30%, and 40%) would result in one-third of people with CKD exceeding the safe limits for dietary potassium consumption (31.8%, 32.6%, and 33%, respectively), they found.

“Potassium chloride substitution in staple foods such as bread and bread products have serious and potentially fatal consequences for people who need to restrict dietary potassium. Improved food labelling is required for consumers to avoid excessive consumption,” Ms. Morrison and colleagues concluded. They added that more studies are needed to further understand the risks of potassium dietary intake and hyperkalemia in CKD from potassium-based salt substitutes.

The American Heart Association recommends no more than 1,500 mg of sodium intake daily for persons with CKD, diabetes, or high blood pressure; those older than 51; and African American persons of any age.

The recommended daily intake of potassium in persons with CKD can range from 2,000 mg to 4,000 mg, depending on the individual and their degree of CKD. The potassium content in some salt substitutes varies from 440 mg to 2,800 mg per teaspoon.

The best recommendation for individuals with CKD and a goal to reduce their sodium intake is to use herbs and lower-sodium seasonings as a substitute, but these should always be reviewed with their physician and renal nutritionist.

Dr. Brookins is a board-certified nephrologist and internist practicing in Georgia. She is the founder and owner of Remote Renal Care, a telehealth kidney practice. She reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

When we refer to “regular table salt,” it is most commonly in the form of sodium chloride, which is also a major constituent of packaged and ultraprocessed foods.

The best approach to finding the “healthiest salt” – which really means the lowest in sodium – is to look for the amount on the label. “Sodium-free” usually indicates less than 5 mg of sodium per serving, and “low-sodium” usually means 140 mg or less per serving. In contrast, regular table salt can contain as much as 560 mg of sodium in one serving.

Other en vogue salts, such as pink Himalayan salt, sea salt, and kosher salt, are high in sodium content – like regular table salt – but because of their larger crystal size, less sodium is delivered per serving.

Georges Lievre / Fotolia.com

FDA issues guidance on reducing salt

Currently, the U.S. sodium dietary guidelines for persons older than 14 stipulate 2,300 mg/d, which is equivalent to 1 teaspoon a day. However it is estimated that the average person in the United States consumes more than this – around 3,400 mg of sodium daily.

In October 2021, the U.S. Food and Drug Administration published guidance on voluntary sodium limitations in commercially processed, packaged, and prepared food. The FDA’s short-term approach is to slowly reduce exposure to sodium in processed and restaurant food by 2025, on the basis that people will eventually get used to less salt, as has happened in the United Kingdom and other countries.

Such strategies to reduce salt intake are now being used in national programs in several countries. Many of these successful initiatives include active engagement with the food industry to reduce the amount of sodium added to processed food, as well as public awareness campaigns to alert consumers to the dangers of eating too much salt. This includes increasing potassium in manufactured foods, primarily to target hypertension and heart disease, as described by Clare Farrand, MSc, BSc, and colleagues, in the Journal of Clinical Hypertension. The authors also make several recommendations regarding salt reduction policies:

• Food manufacturers should gradually reduce sodium in food to the lowest possible levels and explore the use of potassium-based sodium replacers to reduce sodium levels even further.
• Governments should continue to monitor sodium and potassium levels in processed foods.
• Further consideration may need to be given to how best to label salt substitutes (namely potassium) in processed foods to ensure that people who may be adversely affected are aware.
• Governments should systematically monitor potassium intake at the population level, including for specific susceptible groups.
• Governments should continue to systematically monitor sodium (salt) intake and iodine intake at the population level to adjust salt iodization over time as necessary, depending on observed salt intake in specific targeted groups, to ensure that they have sufficient but not excessive iodine intakes as salt intakes are reduced.
• Governments should consider opportunities for promoting and subsidizing salt substitutes, particularly in countries where salt added during cooking or at the table is the major source of salt in the diet.

The new FDA document includes 163 subcategories of foods in its voluntary salt reduction strategy.
 

Salt substitutes, high blood pressure, and mortality

Lowering sodium intake is almost certainly beneficial for persons with high blood pressure. In 2020, a review in Hypertension highlighted the benefit of salt substitutes in reducing hypertension, reporting that they lower systolic blood pressure by 5.58 mm Hg and diastolic blood pressure by 2.88 mm Hg.

And changes to dietary sodium intake can potentially reduce or obviate the need for medications for essential hypertension in some individuals. Although there are only a few studies on this topic, a study by Bruce Neal, MB, ChB, PhD, and colleagues, revealed a reduction in stroke, cardiovascular events, and deaths with the use of potassium-based salt substitutes.
 

Salt substitutes and sodium and potassium handling in the kidneys

Many studies have shown that potassium-rich salt substitutes are safe in individuals with normal kidney function, but are they safe and beneficial for people with chronic kidney disease (CKD)?

For anyone who is on a renal diet, potassium and sodium intake goals are limited according to their absolute level of kidney function.

There have been case reports of life-threatening blood potassium levels (hyperkalemia) due to potassium-rich salt substitutes in people with CKD, but no larger published studies on this topic can be found.

A diet modeling study by Rebecca Morrison and colleagues evaluated varying degrees of potassium-enriched salt substituted bread products and their impact on dietary intake in persons with CKD. They used dietary data from the National Nutrition and Physical Activity Survey 2011-2012 in Australia for 12,152 participants, 154 of whom had CKD. Replacing the sodium in bread with varying amounts of potassium chloride (20%, 30%, and 40%) would result in one-third of people with CKD exceeding the safe limits for dietary potassium consumption (31.8%, 32.6%, and 33%, respectively), they found.

“Potassium chloride substitution in staple foods such as bread and bread products have serious and potentially fatal consequences for people who need to restrict dietary potassium. Improved food labelling is required for consumers to avoid excessive consumption,” Ms. Morrison and colleagues concluded. They added that more studies are needed to further understand the risks of potassium dietary intake and hyperkalemia in CKD from potassium-based salt substitutes.

The American Heart Association recommends no more than 1,500 mg of sodium intake daily for persons with CKD, diabetes, or high blood pressure; those older than 51; and African American persons of any age.

The recommended daily intake of potassium in persons with CKD can range from 2,000 mg to 4,000 mg, depending on the individual and their degree of CKD. The potassium content in some salt substitutes varies from 440 mg to 2,800 mg per teaspoon.

The best recommendation for individuals with CKD and a goal to reduce their sodium intake is to use herbs and lower-sodium seasonings as a substitute, but these should always be reviewed with their physician and renal nutritionist.

Dr. Brookins is a board-certified nephrologist and internist practicing in Georgia. She is the founder and owner of Remote Renal Care, a telehealth kidney practice. She reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

When we refer to “regular table salt,” it is most commonly in the form of sodium chloride, which is also a major constituent of packaged and ultraprocessed foods.

The best approach to finding the “healthiest salt” – which really means the lowest in sodium – is to look for the amount on the label. “Sodium-free” usually indicates less than 5 mg of sodium per serving, and “low-sodium” usually means 140 mg or less per serving. In contrast, regular table salt can contain as much as 560 mg of sodium in one serving.

Other en vogue salts, such as pink Himalayan salt, sea salt, and kosher salt, are high in sodium content – like regular table salt – but because of their larger crystal size, less sodium is delivered per serving.

Georges Lievre / Fotolia.com

FDA issues guidance on reducing salt

Currently, the U.S. sodium dietary guidelines for persons older than 14 stipulate 2,300 mg/d, which is equivalent to 1 teaspoon a day. However it is estimated that the average person in the United States consumes more than this – around 3,400 mg of sodium daily.

In October 2021, the U.S. Food and Drug Administration published guidance on voluntary sodium limitations in commercially processed, packaged, and prepared food. The FDA’s short-term approach is to slowly reduce exposure to sodium in processed and restaurant food by 2025, on the basis that people will eventually get used to less salt, as has happened in the United Kingdom and other countries.

Such strategies to reduce salt intake are now being used in national programs in several countries. Many of these successful initiatives include active engagement with the food industry to reduce the amount of sodium added to processed food, as well as public awareness campaigns to alert consumers to the dangers of eating too much salt. This includes increasing potassium in manufactured foods, primarily to target hypertension and heart disease, as described by Clare Farrand, MSc, BSc, and colleagues, in the Journal of Clinical Hypertension. The authors also make several recommendations regarding salt reduction policies:

• Food manufacturers should gradually reduce sodium in food to the lowest possible levels and explore the use of potassium-based sodium replacers to reduce sodium levels even further.
• Governments should continue to monitor sodium and potassium levels in processed foods.
• Further consideration may need to be given to how best to label salt substitutes (namely potassium) in processed foods to ensure that people who may be adversely affected are aware.
• Governments should systematically monitor potassium intake at the population level, including for specific susceptible groups.
• Governments should continue to systematically monitor sodium (salt) intake and iodine intake at the population level to adjust salt iodization over time as necessary, depending on observed salt intake in specific targeted groups, to ensure that they have sufficient but not excessive iodine intakes as salt intakes are reduced.
• Governments should consider opportunities for promoting and subsidizing salt substitutes, particularly in countries where salt added during cooking or at the table is the major source of salt in the diet.

The new FDA document includes 163 subcategories of foods in its voluntary salt reduction strategy.
 

Salt substitutes, high blood pressure, and mortality

Lowering sodium intake is almost certainly beneficial for persons with high blood pressure. In 2020, a review in Hypertension highlighted the benefit of salt substitutes in reducing hypertension, reporting that they lower systolic blood pressure by 5.58 mm Hg and diastolic blood pressure by 2.88 mm Hg.

And changes to dietary sodium intake can potentially reduce or obviate the need for medications for essential hypertension in some individuals. Although there are only a few studies on this topic, a study by Bruce Neal, MB, ChB, PhD, and colleagues, revealed a reduction in stroke, cardiovascular events, and deaths with the use of potassium-based salt substitutes.
 

Salt substitutes and sodium and potassium handling in the kidneys

Many studies have shown that potassium-rich salt substitutes are safe in individuals with normal kidney function, but are they safe and beneficial for people with chronic kidney disease (CKD)?

For anyone who is on a renal diet, potassium and sodium intake goals are limited according to their absolute level of kidney function.

There have been case reports of life-threatening blood potassium levels (hyperkalemia) due to potassium-rich salt substitutes in people with CKD, but no larger published studies on this topic can be found.

A diet modeling study by Rebecca Morrison and colleagues evaluated varying degrees of potassium-enriched salt substituted bread products and their impact on dietary intake in persons with CKD. They used dietary data from the National Nutrition and Physical Activity Survey 2011-2012 in Australia for 12,152 participants, 154 of whom had CKD. Replacing the sodium in bread with varying amounts of potassium chloride (20%, 30%, and 40%) would result in one-third of people with CKD exceeding the safe limits for dietary potassium consumption (31.8%, 32.6%, and 33%, respectively), they found.

“Potassium chloride substitution in staple foods such as bread and bread products have serious and potentially fatal consequences for people who need to restrict dietary potassium. Improved food labelling is required for consumers to avoid excessive consumption,” Ms. Morrison and colleagues concluded. They added that more studies are needed to further understand the risks of potassium dietary intake and hyperkalemia in CKD from potassium-based salt substitutes.

The American Heart Association recommends no more than 1,500 mg of sodium intake daily for persons with CKD, diabetes, or high blood pressure; those older than 51; and African American persons of any age.

The recommended daily intake of potassium in persons with CKD can range from 2,000 mg to 4,000 mg, depending on the individual and their degree of CKD. The potassium content in some salt substitutes varies from 440 mg to 2,800 mg per teaspoon.

The best recommendation for individuals with CKD and a goal to reduce their sodium intake is to use herbs and lower-sodium seasonings as a substitute, but these should always be reviewed with their physician and renal nutritionist.

Dr. Brookins is a board-certified nephrologist and internist practicing in Georgia. She is the founder and owner of Remote Renal Care, a telehealth kidney practice. She reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

Workers who had the highest exposure to hydrocarbons during the Deepwater Horizon oil spill disaster had a higher risk of having a hypertension diagnosis in the years following the event, a new study suggests.

Results showed that the highest exposure to total petroleum hydrocarbons during the cleanup operation was associated with a 31% higher risk of new hypertension 1-3 years later.

“What is remarkable is that we still found an increased risk of hypertension a couple of years after the cleanup had been completed. This suggests working in this environment even for a short period could have long-term health consequences,” lead author Richard Kwok, PhD, told this news organization.

The study was published online in JAMA Network Open.

For the study, Dr. Kwok, a scientist at the U.S. National Institute of Environmental Health Sciences, and colleagues estimated the levels of exposure to toxic hydrocarbons in 6,846 adults who had worked on the oil spill cleanup after the Deepwater Horizon disaster in 2010, during which 200 million gallons of oil spilled into the Gulf of Mexico. They then investigated whether there was an association with the development of hypertension 1-3 years later.

“Clean-up efforts started almost immediately and lasted over a year,” Dr. Kwok noted. “In the first few months, oil flowed freely into the Gulf of Mexico which released high levels of volatile organic compounds into the air that the workers could have been exposed to. The exposures change over time because the oil becomes weathered and starts to decompose and harden. This is associated with a lower level of volatile organic compounds but can still cause damage.”

Workers involved in the cleanup may have been there for just a few days or could have spent many months at the site and would have had different exposures depending on what types of jobs they were doing, Dr. Kwok reported.

“The highest levels of exposure to total hydrocarbons would have been to those involved in the early months of the oil spill response and cleanup when the oil was flowing freely, and those who were skimming oil off the water, burning oil, handling dispersants, or involved in the decontamination of the vessels. Others who were involved in the cleanup on land or support functions would have had lower exposures,” he said.

Each worker was interviewed and asked about their activities during the cleanup operation, the location of work, and period of work. Their level of exposure to total petroleum hydrocarbons (THCs) was estimated based on their self-reported activities, and when and where they worked.

Two measures of estimated cumulative THC were calculated: cumulative maximum daily exposure, which summed the maximum daily THC exposure level, and cumulative mean exposure, which summed the mean daily exposure levels. These THC values were categorized into quintiles based on the exposure distribution among workers.

Systolic and diastolic blood pressure measurements were collected for the workers during home exams from 2011 to 2013 using automated oscillometric monitors. Newly detected hypertension was defined as either antihypertensive medication use or elevated blood pressure since the spill.

Results showed a clear dose relationship between the level of THC exposure and the development of hypertension at follow-up.

A version of this article first appeared on Medscape.com.

Workers who had the highest exposure to hydrocarbons during the Deepwater Horizon oil spill disaster had a higher risk of having a hypertension diagnosis in the years following the event, a new study suggests.

Results showed that the highest exposure to total petroleum hydrocarbons during the cleanup operation was associated with a 31% higher risk of new hypertension 1-3 years later.

“What is remarkable is that we still found an increased risk of hypertension a couple of years after the cleanup had been completed. This suggests working in this environment even for a short period could have long-term health consequences,” lead author Richard Kwok, PhD, told this news organization.

The study was published online in JAMA Network Open.

For the study, Dr. Kwok, a scientist at the U.S. National Institute of Environmental Health Sciences, and colleagues estimated the levels of exposure to toxic hydrocarbons in 6,846 adults who had worked on the oil spill cleanup after the Deepwater Horizon disaster in 2010, during which 200 million gallons of oil spilled into the Gulf of Mexico. They then investigated whether there was an association with the development of hypertension 1-3 years later.

“Clean-up efforts started almost immediately and lasted over a year,” Dr. Kwok noted. “In the first few months, oil flowed freely into the Gulf of Mexico which released high levels of volatile organic compounds into the air that the workers could have been exposed to. The exposures change over time because the oil becomes weathered and starts to decompose and harden. This is associated with a lower level of volatile organic compounds but can still cause damage.”

Workers involved in the cleanup may have been there for just a few days or could have spent many months at the site and would have had different exposures depending on what types of jobs they were doing, Dr. Kwok reported.

“The highest levels of exposure to total hydrocarbons would have been to those involved in the early months of the oil spill response and cleanup when the oil was flowing freely, and those who were skimming oil off the water, burning oil, handling dispersants, or involved in the decontamination of the vessels. Others who were involved in the cleanup on land or support functions would have had lower exposures,” he said.

Each worker was interviewed and asked about their activities during the cleanup operation, the location of work, and period of work. Their level of exposure to total petroleum hydrocarbons (THCs) was estimated based on their self-reported activities, and when and where they worked.

Two measures of estimated cumulative THC were calculated: cumulative maximum daily exposure, which summed the maximum daily THC exposure level, and cumulative mean exposure, which summed the mean daily exposure levels. These THC values were categorized into quintiles based on the exposure distribution among workers.

Systolic and diastolic blood pressure measurements were collected for the workers during home exams from 2011 to 2013 using automated oscillometric monitors. Newly detected hypertension was defined as either antihypertensive medication use or elevated blood pressure since the spill.

Results showed a clear dose relationship between the level of THC exposure and the development of hypertension at follow-up.

A version of this article first appeared on Medscape.com.

Workers who had the highest exposure to hydrocarbons during the Deepwater Horizon oil spill disaster had a higher risk of having a hypertension diagnosis in the years following the event, a new study suggests.

Results showed that the highest exposure to total petroleum hydrocarbons during the cleanup operation was associated with a 31% higher risk of new hypertension 1-3 years later.

“What is remarkable is that we still found an increased risk of hypertension a couple of years after the cleanup had been completed. This suggests working in this environment even for a short period could have long-term health consequences,” lead author Richard Kwok, PhD, told this news organization.

The study was published online in JAMA Network Open.

For the study, Dr. Kwok, a scientist at the U.S. National Institute of Environmental Health Sciences, and colleagues estimated the levels of exposure to toxic hydrocarbons in 6,846 adults who had worked on the oil spill cleanup after the Deepwater Horizon disaster in 2010, during which 200 million gallons of oil spilled into the Gulf of Mexico. They then investigated whether there was an association with the development of hypertension 1-3 years later.

“Clean-up efforts started almost immediately and lasted over a year,” Dr. Kwok noted. “In the first few months, oil flowed freely into the Gulf of Mexico which released high levels of volatile organic compounds into the air that the workers could have been exposed to. The exposures change over time because the oil becomes weathered and starts to decompose and harden. This is associated with a lower level of volatile organic compounds but can still cause damage.”

Workers involved in the cleanup may have been there for just a few days or could have spent many months at the site and would have had different exposures depending on what types of jobs they were doing, Dr. Kwok reported.

“The highest levels of exposure to total hydrocarbons would have been to those involved in the early months of the oil spill response and cleanup when the oil was flowing freely, and those who were skimming oil off the water, burning oil, handling dispersants, or involved in the decontamination of the vessels. Others who were involved in the cleanup on land or support functions would have had lower exposures,” he said.

Each worker was interviewed and asked about their activities during the cleanup operation, the location of work, and period of work. Their level of exposure to total petroleum hydrocarbons (THCs) was estimated based on their self-reported activities, and when and where they worked.

Two measures of estimated cumulative THC were calculated: cumulative maximum daily exposure, which summed the maximum daily THC exposure level, and cumulative mean exposure, which summed the mean daily exposure levels. These THC values were categorized into quintiles based on the exposure distribution among workers.

Systolic and diastolic blood pressure measurements were collected for the workers during home exams from 2011 to 2013 using automated oscillometric monitors. Newly detected hypertension was defined as either antihypertensive medication use or elevated blood pressure since the spill.

Results showed a clear dose relationship between the level of THC exposure and the development of hypertension at follow-up.

A version of this article first appeared on Medscape.com.

Circulating antiphospholipid autoantibodies may contribute to endothelial cell activation and dysfunction in severe COVID-19, researchers report.

In 2020, the same researchers reported results from a preclinical study demonstrating that autoantibodies from patients with active COVID-19 caused clotting in mice.

The new study, published in Arthritis and Rheumatology, found higher-than-expected levels of antiphospholipid autoantibodies in the blood samples of 244 patients hospitalized with COVID-19.

“While endothelial dysfunction has been implicated in the widespread thromboinflammatory complications of COVID-19, the upstream mediators of endotheliopathy remain for the most part cryptic,” write Hui Shi, MD, PhD, and coauthors from the University of Michigan, Ann Arbor, and the National Heart, Lung, and Blood Institute.

When asked for comment on the study, Eline T. Luning Prak, MD, PhD, professor of pathology and laboratory medicine at the Hospital of the University of Pennsylvania in Philadelphia, said, “The autopsy cases for COVID-19 strongly point to thromboembolic complications in many individuals who succumbed to sequelae of the infection.

“Importantly, however, many factors can contribute to this pathology, including the inflammatory milieu, monocyte activation, neutrophil extracellular traps, immune complexes, complement, as well as effects on endothelial cells,” explained Dr. Luning Prak, who was not involved in the study.

“The findings in this paper nicely complement another study by Schmaier et al. that came out recently in JCI Insight that also suggests that endothelial cells can be activated by antibodies, she said.
 

‘Even stronger connection between autoantibody formation and clotting in COVID-19’

Dr. Shi and her team cultured human endothelial cells in serum or plasma from 244 patients hospitalized with COVID-19 and plasma from 100 patients with non-COVID sepsis. Using in-cell enzyme-linked immunosorbent assay, they measured levels of key cell adhesion molecules.

After analysis, the researchers found that serum from COVID-19 patients activated cultured endothelial cells to express surface adhesion molecules essential to inflammation and thrombosis, particularly E-selectin, ICAM-1, and VCAM-1.

“The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID-19 serum to activate endothelium,” they explain.

Further analyses revealed that, for a subset of serum samples from patients with severe infection, this activation could be mitigated by depleting total immunoglobulin G.

In addition, supplementation of control serum with patient IgG was adequate to trigger endothelial activation.

On the basis of these results, the researchers hypothesize that antiphospholipid autoantibodies may characterize antibody profiles in severe COVID-19 that activate the endothelium and transition the usually quiescent blood-vessel wall interface toward inflammation and coagulation.

“[These findings] provide an even stronger connection between autoantibody formation and clotting in COVID-19,” Dr. Shi said in an accompanying press release.

Clinical implications

From a clinical perspective, Dr. Shi and her team question whether patients with severe COVID-19 should be tested for antiphospholipid antibodies to assess their risk of thrombosis and progression to respiratory failure.

Moreover, they question whether patients with high antiphospholipid antibody titers might benefit from therapies used in conventional cases of severe antiphospholipid syndrome, such as plasmapheresis, anticoagulation therapy, and complement inhibition, Dr. Shi added.

The researchers hope to answer these and other remaining questions in future studies. “Eventually, we may be able to repurpose treatments used in traditional cases of antiphospholipid syndrome for COVID-19.

“As we await definitive solutions to the pandemic, these findings add important context to the complex interplay between SARS-CoV-2 infection, the human immune system, and vascular immunobiology,” she concluded.

The study was supported by grants from the Rheumatology Research Foundation, the Michigan Medicine Frankel Cardiovascular Center, and the A. Alfred Taubman Medical Research Institute. One author is an inventor on an unrelated pending patent to the University of Michigan. The other authors and Dr. Luning Prak have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Circulating antiphospholipid autoantibodies may contribute to endothelial cell activation and dysfunction in severe COVID-19, researchers report.

In 2020, the same researchers reported results from a preclinical study demonstrating that autoantibodies from patients with active COVID-19 caused clotting in mice.

The new study, published in Arthritis and Rheumatology, found higher-than-expected levels of antiphospholipid autoantibodies in the blood samples of 244 patients hospitalized with COVID-19.

“While endothelial dysfunction has been implicated in the widespread thromboinflammatory complications of COVID-19, the upstream mediators of endotheliopathy remain for the most part cryptic,” write Hui Shi, MD, PhD, and coauthors from the University of Michigan, Ann Arbor, and the National Heart, Lung, and Blood Institute.

When asked for comment on the study, Eline T. Luning Prak, MD, PhD, professor of pathology and laboratory medicine at the Hospital of the University of Pennsylvania in Philadelphia, said, “The autopsy cases for COVID-19 strongly point to thromboembolic complications in many individuals who succumbed to sequelae of the infection.

“Importantly, however, many factors can contribute to this pathology, including the inflammatory milieu, monocyte activation, neutrophil extracellular traps, immune complexes, complement, as well as effects on endothelial cells,” explained Dr. Luning Prak, who was not involved in the study.

“The findings in this paper nicely complement another study by Schmaier et al. that came out recently in JCI Insight that also suggests that endothelial cells can be activated by antibodies, she said.
 

‘Even stronger connection between autoantibody formation and clotting in COVID-19’

Dr. Shi and her team cultured human endothelial cells in serum or plasma from 244 patients hospitalized with COVID-19 and plasma from 100 patients with non-COVID sepsis. Using in-cell enzyme-linked immunosorbent assay, they measured levels of key cell adhesion molecules.

After analysis, the researchers found that serum from COVID-19 patients activated cultured endothelial cells to express surface adhesion molecules essential to inflammation and thrombosis, particularly E-selectin, ICAM-1, and VCAM-1.

“The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID-19 serum to activate endothelium,” they explain.

Further analyses revealed that, for a subset of serum samples from patients with severe infection, this activation could be mitigated by depleting total immunoglobulin G.

In addition, supplementation of control serum with patient IgG was adequate to trigger endothelial activation.

On the basis of these results, the researchers hypothesize that antiphospholipid autoantibodies may characterize antibody profiles in severe COVID-19 that activate the endothelium and transition the usually quiescent blood-vessel wall interface toward inflammation and coagulation.

“[These findings] provide an even stronger connection between autoantibody formation and clotting in COVID-19,” Dr. Shi said in an accompanying press release.

Clinical implications

From a clinical perspective, Dr. Shi and her team question whether patients with severe COVID-19 should be tested for antiphospholipid antibodies to assess their risk of thrombosis and progression to respiratory failure.

Moreover, they question whether patients with high antiphospholipid antibody titers might benefit from therapies used in conventional cases of severe antiphospholipid syndrome, such as plasmapheresis, anticoagulation therapy, and complement inhibition, Dr. Shi added.

The researchers hope to answer these and other remaining questions in future studies. “Eventually, we may be able to repurpose treatments used in traditional cases of antiphospholipid syndrome for COVID-19.

“As we await definitive solutions to the pandemic, these findings add important context to the complex interplay between SARS-CoV-2 infection, the human immune system, and vascular immunobiology,” she concluded.

The study was supported by grants from the Rheumatology Research Foundation, the Michigan Medicine Frankel Cardiovascular Center, and the A. Alfred Taubman Medical Research Institute. One author is an inventor on an unrelated pending patent to the University of Michigan. The other authors and Dr. Luning Prak have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Circulating antiphospholipid autoantibodies may contribute to endothelial cell activation and dysfunction in severe COVID-19, researchers report.

In 2020, the same researchers reported results from a preclinical study demonstrating that autoantibodies from patients with active COVID-19 caused clotting in mice.

The new study, published in Arthritis and Rheumatology, found higher-than-expected levels of antiphospholipid autoantibodies in the blood samples of 244 patients hospitalized with COVID-19.

“While endothelial dysfunction has been implicated in the widespread thromboinflammatory complications of COVID-19, the upstream mediators of endotheliopathy remain for the most part cryptic,” write Hui Shi, MD, PhD, and coauthors from the University of Michigan, Ann Arbor, and the National Heart, Lung, and Blood Institute.

When asked for comment on the study, Eline T. Luning Prak, MD, PhD, professor of pathology and laboratory medicine at the Hospital of the University of Pennsylvania in Philadelphia, said, “The autopsy cases for COVID-19 strongly point to thromboembolic complications in many individuals who succumbed to sequelae of the infection.

“Importantly, however, many factors can contribute to this pathology, including the inflammatory milieu, monocyte activation, neutrophil extracellular traps, immune complexes, complement, as well as effects on endothelial cells,” explained Dr. Luning Prak, who was not involved in the study.

“The findings in this paper nicely complement another study by Schmaier et al. that came out recently in JCI Insight that also suggests that endothelial cells can be activated by antibodies, she said.
 

‘Even stronger connection between autoantibody formation and clotting in COVID-19’

Dr. Shi and her team cultured human endothelial cells in serum or plasma from 244 patients hospitalized with COVID-19 and plasma from 100 patients with non-COVID sepsis. Using in-cell enzyme-linked immunosorbent assay, they measured levels of key cell adhesion molecules.

After analysis, the researchers found that serum from COVID-19 patients activated cultured endothelial cells to express surface adhesion molecules essential to inflammation and thrombosis, particularly E-selectin, ICAM-1, and VCAM-1.

“The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID-19 serum to activate endothelium,” they explain.

Further analyses revealed that, for a subset of serum samples from patients with severe infection, this activation could be mitigated by depleting total immunoglobulin G.

In addition, supplementation of control serum with patient IgG was adequate to trigger endothelial activation.

On the basis of these results, the researchers hypothesize that antiphospholipid autoantibodies may characterize antibody profiles in severe COVID-19 that activate the endothelium and transition the usually quiescent blood-vessel wall interface toward inflammation and coagulation.

“[These findings] provide an even stronger connection between autoantibody formation and clotting in COVID-19,” Dr. Shi said in an accompanying press release.

Clinical implications

From a clinical perspective, Dr. Shi and her team question whether patients with severe COVID-19 should be tested for antiphospholipid antibodies to assess their risk of thrombosis and progression to respiratory failure.

Moreover, they question whether patients with high antiphospholipid antibody titers might benefit from therapies used in conventional cases of severe antiphospholipid syndrome, such as plasmapheresis, anticoagulation therapy, and complement inhibition, Dr. Shi added.

The researchers hope to answer these and other remaining questions in future studies. “Eventually, we may be able to repurpose treatments used in traditional cases of antiphospholipid syndrome for COVID-19.

“As we await definitive solutions to the pandemic, these findings add important context to the complex interplay between SARS-CoV-2 infection, the human immune system, and vascular immunobiology,” she concluded.

The study was supported by grants from the Rheumatology Research Foundation, the Michigan Medicine Frankel Cardiovascular Center, and the A. Alfred Taubman Medical Research Institute. One author is an inventor on an unrelated pending patent to the University of Michigan. The other authors and Dr. Luning Prak have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Universal screening for presymptomatic type 1 diabetes among schoolchildren would cost approximately 22 euros (about $25) per child screened, and about 7,000 euros (about $7,900) per child diagnosed, a new analysis of data from a German program finds.

The data come from the Fr1da study, in which a blood test for type 1 diabetes–associated islet autoantibodies is offered to all children aged 21 months to 6 years old in Bavaria.

Families of those who test positive are offered participation in a program of diabetes education, metabolic staging, psychological evaluation for stress, and prospective follow-up.

The researchers explain that, worldwide, 4 in 1,000 people under the age of 20 years have type 1 diabetes. It is the most common metabolic disease in children and adolescents. Only about 1 in 10 of those affected has a close relative with the disease. This means that type 1 diabetes can affect any child.

However, in many cases, the disease does not become known until a severe to life-threatening metabolic derailment known as diabetic ketoacidosis (DKA) occurs. This often leads to intensive medical treatment, a longer hospitalization, and poorer blood glucose control, which can result in an increased risk of secondary diseases and very high costs for the health care system.

“We want to protect as many children as possible from serious metabolic derailments. This is only possible with type 1 diabetes screenings. Therefore, we strongly support to include early detection tests in standard medical care,” Peter Achenbach, DrMed, senior author of the study, said in a statement from his institution, Helmholtz Zentrum München in Neuherberg, Germany.

The new findings were published in Diabetes Care by Florian M. Karl, also of Helmholtz Zentrum München, and colleagues.

In 2020, the Fr1da investigators reported that, of 90,632 children who participated from February 2015 to May 2019, 0.31% (280) were diagnosed with presymptomatic type 1 diabetes through the presence of two or more islet autoantibodies.

This news organization asked Brett McQueen, PhD, who led a similar study examining cost and cost-effectiveness in the Autoimmunity Screening for Kids (ASK) program, in which Denver-area children aged 2-17 years are offered autoantibody screening for both type 1 diabetes and celiac disease, for comment.

“If we have a chance to change a child’s life from when they’re 2 or 3 years old and there’s even a small chance that this thing potentially improves health outcomes for a decent price, what are we waiting for?” said Dr. McQueen, who is assistant professor in the department of clinical pharmacy at the University of Colorado, Aurora.
 

Is DKA prevention enough to justify universal screening?

Although identifying type 1 diabetes before symptoms arise could help avoid DKA, currently no therapeutic interventions are available to prevent or delay the trajectory from presymptomatic to clinical type 1 diabetes.

A possible future intervention – the anti-CD3 monoclonal antibody teplizumab (Tzield, Provention Bio) – had a setback in July 2021 when the Food and Drug Administration declined to approve it for the delay of type 1 diabetes in at-risk individuals.

However, on Feb. 22 Provention Bio announced that it has resubmitted the Biologics License Application for teplizumab for the delay of clinical type 1 diabetes in at-risk individuals. The FDA now has 30 days to review the resubmission, determine whether it is complete and acceptable for review, and provide a review goal date, according to a company statement.

But even without the ability to forestall the development of type 1 diabetes, screening proponents point to the potential benefit from educating families about early signs of diabetes onset and thereby preventing progression to DKA and both its short-term and possible long-term sequelae.

Prevention of DKA at diagnosis has been linked to improved long-term glycemic control and other potential health benefits.

And the frequency of DKA at the onset of type 1 diabetes has increased in recent years, to more than 20% in Germany and over 45% in the United States.

But, prior data have suggested that universal screening for presymptomatic type 1 diabetes is unlikely to be cost effective if only the health and economic benefits of prevention of DKA at type 1 diabetes onset is considered, unless the screening costs are exceedingly low.
 

What will it take to implement universal screening?

“What this paper does is contribute really to our understanding of more around resource utilization,” noted Dr. McQueen. “As they correctly identify, it’s really hard to compare country prices. It’s easier to compare utilization.”

In Dr. McQueen’s ASK program, the cost per child screened and per case detected in that program were similar to those found in the German study, even though the cost of the antibody testing itself was considerably lower in Germany than in the United States.

Fr1da included more components of screening and monitoring than did ASK, Dr. McQueen told this news organization.

The conclusions of the ASK study were that “presymptomatic type 1 diabetes screening may be cost effective in areas with a high prevalence of DKA and an infrastructure facilitating screening and monitoring if the benefits of avoiding DKA events and improved [hemoglobin] A1c persist over long-run time horizons.”

Nonetheless, Dr. McQueen thinks it’s unlikely that universal screening will be recommended by professional societies or covered by payers in the United States until a pharmacologic intervention to forestall disease progression is available.“Teplizumab approval could move this along. ... We’re just trying to take one factor, the economics of it, to create the most efficient scenario so that if it were to be adopted we would catch the most cases, prevent the most complications, benefit children the most in terms of their lifetime health outcomes – all at the minimum cost possible.”
 

‘A benchmark for the expected implementation cost of screening’

Mr. Karl and colleagues simulated the cost of implementation of this screening as standard care in Germany – assuming the same 0.31% prevalence found in Fr1da – the average cost per child was estimated at 21.73 euros, including 9.34 euros for laboratory costs, 12.25 euros for pediatrician costs, and 0.14 euros for local diabetes clinics to perform metabolic staging and education for children diagnosed with presymptomatic type 1 diabetes.

The model included 50% of the costs incurred in Fr1da for obtaining informed consent. Negative autoantibody results from the initial screening were not communicated to families, and all children with presymptomatic type 1 diabetes received staging and education. The estimated average cost per diagnosed child was 7,035 euros.

“Although our analyses are subject to some level of uncertainty, they provide a benchmark for the expected implementation cost of screening,” said coauthor Michael Laxy, MSc, PhD, also at Helmholtz Zentrum München.

“Next, we aim to evaluate the long-term ratio of screening costs, potential cost savings through the prevention of metabolic derailment and its consequences, and potentially increased quality of life with a type 1 diabetes screening compared to the costs and quality of life without a screening.”

Dr. McQueen is working along similar lines in Colorado, attempting to create a model that incorporates all the different possibilities including DKA monitoring, teplizumab availability, screening children at different ages, and the effect of including blood glucose monitoring in children identified with presymptomatic type 1 diabetes.

“There are so many different potential answers and avenues and no one has really put it all together,” he observed.

But he believes that economics shouldn’t be the only factor used in deciding whether to institute widespread screening.

This study was supported by grants from the German Federal Ministry of Education and Research to the German Center for Diabetes Research (DZD). The Fr1da study was supported by grants from the LifeScience-Stiftung, JDRF International, the Bavarian State Ministry of Health and Care, the Leona M. and Harry B. Helmsley Charitable Trust, Deutsche Diabetes-Stiftung, Landesverband Bayern der Betriebskrankenkassen, B. Braun-Stiftung, Deutsche Diabetes Hilfe, and the German Federal Ministry of Education and Research to the DZD. The authors disclosed no relevant financial relationships. The ASK study was funded by JDRF International, the Leona M. and Harry B. Helmsley Charitable Trust, and Janssen Research and Development. Dr. McQueen has received institutional funding for value assessment applications from the Institute for Clinical and Economic Review, the PhRMA Foundation, and PhRMA.

A version of this article first appeared on Medscape.com.

Universal screening for presymptomatic type 1 diabetes among schoolchildren would cost approximately 22 euros (about $25) per child screened, and about 7,000 euros (about $7,900) per child diagnosed, a new analysis of data from a German program finds.

The data come from the Fr1da study, in which a blood test for type 1 diabetes–associated islet autoantibodies is offered to all children aged 21 months to 6 years old in Bavaria.

Families of those who test positive are offered participation in a program of diabetes education, metabolic staging, psychological evaluation for stress, and prospective follow-up.

The researchers explain that, worldwide, 4 in 1,000 people under the age of 20 years have type 1 diabetes. It is the most common metabolic disease in children and adolescents. Only about 1 in 10 of those affected has a close relative with the disease. This means that type 1 diabetes can affect any child.

However, in many cases, the disease does not become known until a severe to life-threatening metabolic derailment known as diabetic ketoacidosis (DKA) occurs. This often leads to intensive medical treatment, a longer hospitalization, and poorer blood glucose control, which can result in an increased risk of secondary diseases and very high costs for the health care system.

“We want to protect as many children as possible from serious metabolic derailments. This is only possible with type 1 diabetes screenings. Therefore, we strongly support to include early detection tests in standard medical care,” Peter Achenbach, DrMed, senior author of the study, said in a statement from his institution, Helmholtz Zentrum München in Neuherberg, Germany.

The new findings were published in Diabetes Care by Florian M. Karl, also of Helmholtz Zentrum München, and colleagues.

In 2020, the Fr1da investigators reported that, of 90,632 children who participated from February 2015 to May 2019, 0.31% (280) were diagnosed with presymptomatic type 1 diabetes through the presence of two or more islet autoantibodies.

This news organization asked Brett McQueen, PhD, who led a similar study examining cost and cost-effectiveness in the Autoimmunity Screening for Kids (ASK) program, in which Denver-area children aged 2-17 years are offered autoantibody screening for both type 1 diabetes and celiac disease, for comment.

“If we have a chance to change a child’s life from when they’re 2 or 3 years old and there’s even a small chance that this thing potentially improves health outcomes for a decent price, what are we waiting for?” said Dr. McQueen, who is assistant professor in the department of clinical pharmacy at the University of Colorado, Aurora.
 

Is DKA prevention enough to justify universal screening?

Although identifying type 1 diabetes before symptoms arise could help avoid DKA, currently no therapeutic interventions are available to prevent or delay the trajectory from presymptomatic to clinical type 1 diabetes.

A possible future intervention – the anti-CD3 monoclonal antibody teplizumab (Tzield, Provention Bio) – had a setback in July 2021 when the Food and Drug Administration declined to approve it for the delay of type 1 diabetes in at-risk individuals.

However, on Feb. 22 Provention Bio announced that it has resubmitted the Biologics License Application for teplizumab for the delay of clinical type 1 diabetes in at-risk individuals. The FDA now has 30 days to review the resubmission, determine whether it is complete and acceptable for review, and provide a review goal date, according to a company statement.

But even without the ability to forestall the development of type 1 diabetes, screening proponents point to the potential benefit from educating families about early signs of diabetes onset and thereby preventing progression to DKA and both its short-term and possible long-term sequelae.

Prevention of DKA at diagnosis has been linked to improved long-term glycemic control and other potential health benefits.

And the frequency of DKA at the onset of type 1 diabetes has increased in recent years, to more than 20% in Germany and over 45% in the United States.

But, prior data have suggested that universal screening for presymptomatic type 1 diabetes is unlikely to be cost effective if only the health and economic benefits of prevention of DKA at type 1 diabetes onset is considered, unless the screening costs are exceedingly low.
 

What will it take to implement universal screening?

“What this paper does is contribute really to our understanding of more around resource utilization,” noted Dr. McQueen. “As they correctly identify, it’s really hard to compare country prices. It’s easier to compare utilization.”

In Dr. McQueen’s ASK program, the cost per child screened and per case detected in that program were similar to those found in the German study, even though the cost of the antibody testing itself was considerably lower in Germany than in the United States.

Fr1da included more components of screening and monitoring than did ASK, Dr. McQueen told this news organization.

The conclusions of the ASK study were that “presymptomatic type 1 diabetes screening may be cost effective in areas with a high prevalence of DKA and an infrastructure facilitating screening and monitoring if the benefits of avoiding DKA events and improved [hemoglobin] A1c persist over long-run time horizons.”

Nonetheless, Dr. McQueen thinks it’s unlikely that universal screening will be recommended by professional societies or covered by payers in the United States until a pharmacologic intervention to forestall disease progression is available.“Teplizumab approval could move this along. ... We’re just trying to take one factor, the economics of it, to create the most efficient scenario so that if it were to be adopted we would catch the most cases, prevent the most complications, benefit children the most in terms of their lifetime health outcomes – all at the minimum cost possible.”
 

‘A benchmark for the expected implementation cost of screening’

Mr. Karl and colleagues simulated the cost of implementation of this screening as standard care in Germany – assuming the same 0.31% prevalence found in Fr1da – the average cost per child was estimated at 21.73 euros, including 9.34 euros for laboratory costs, 12.25 euros for pediatrician costs, and 0.14 euros for local diabetes clinics to perform metabolic staging and education for children diagnosed with presymptomatic type 1 diabetes.

The model included 50% of the costs incurred in Fr1da for obtaining informed consent. Negative autoantibody results from the initial screening were not communicated to families, and all children with presymptomatic type 1 diabetes received staging and education. The estimated average cost per diagnosed child was 7,035 euros.

“Although our analyses are subject to some level of uncertainty, they provide a benchmark for the expected implementation cost of screening,” said coauthor Michael Laxy, MSc, PhD, also at Helmholtz Zentrum München.

“Next, we aim to evaluate the long-term ratio of screening costs, potential cost savings through the prevention of metabolic derailment and its consequences, and potentially increased quality of life with a type 1 diabetes screening compared to the costs and quality of life without a screening.”

Dr. McQueen is working along similar lines in Colorado, attempting to create a model that incorporates all the different possibilities including DKA monitoring, teplizumab availability, screening children at different ages, and the effect of including blood glucose monitoring in children identified with presymptomatic type 1 diabetes.

“There are so many different potential answers and avenues and no one has really put it all together,” he observed.

But he believes that economics shouldn’t be the only factor used in deciding whether to institute widespread screening.

This study was supported by grants from the German Federal Ministry of Education and Research to the German Center for Diabetes Research (DZD). The Fr1da study was supported by grants from the LifeScience-Stiftung, JDRF International, the Bavarian State Ministry of Health and Care, the Leona M. and Harry B. Helmsley Charitable Trust, Deutsche Diabetes-Stiftung, Landesverband Bayern der Betriebskrankenkassen, B. Braun-Stiftung, Deutsche Diabetes Hilfe, and the German Federal Ministry of Education and Research to the DZD. The authors disclosed no relevant financial relationships. The ASK study was funded by JDRF International, the Leona M. and Harry B. Helmsley Charitable Trust, and Janssen Research and Development. Dr. McQueen has received institutional funding for value assessment applications from the Institute for Clinical and Economic Review, the PhRMA Foundation, and PhRMA.

A version of this article first appeared on Medscape.com.

Universal screening for presymptomatic type 1 diabetes among schoolchildren would cost approximately 22 euros (about $25) per child screened, and about 7,000 euros (about $7,900) per child diagnosed, a new analysis of data from a German program finds.

The data come from the Fr1da study, in which a blood test for type 1 diabetes–associated islet autoantibodies is offered to all children aged 21 months to 6 years old in Bavaria.

Families of those who test positive are offered participation in a program of diabetes education, metabolic staging, psychological evaluation for stress, and prospective follow-up.

The researchers explain that, worldwide, 4 in 1,000 people under the age of 20 years have type 1 diabetes. It is the most common metabolic disease in children and adolescents. Only about 1 in 10 of those affected has a close relative with the disease. This means that type 1 diabetes can affect any child.

However, in many cases, the disease does not become known until a severe to life-threatening metabolic derailment known as diabetic ketoacidosis (DKA) occurs. This often leads to intensive medical treatment, a longer hospitalization, and poorer blood glucose control, which can result in an increased risk of secondary diseases and very high costs for the health care system.

“We want to protect as many children as possible from serious metabolic derailments. This is only possible with type 1 diabetes screenings. Therefore, we strongly support to include early detection tests in standard medical care,” Peter Achenbach, DrMed, senior author of the study, said in a statement from his institution, Helmholtz Zentrum München in Neuherberg, Germany.

The new findings were published in Diabetes Care by Florian M. Karl, also of Helmholtz Zentrum München, and colleagues.

In 2020, the Fr1da investigators reported that, of 90,632 children who participated from February 2015 to May 2019, 0.31% (280) were diagnosed with presymptomatic type 1 diabetes through the presence of two or more islet autoantibodies.

This news organization asked Brett McQueen, PhD, who led a similar study examining cost and cost-effectiveness in the Autoimmunity Screening for Kids (ASK) program, in which Denver-area children aged 2-17 years are offered autoantibody screening for both type 1 diabetes and celiac disease, for comment.

“If we have a chance to change a child’s life from when they’re 2 or 3 years old and there’s even a small chance that this thing potentially improves health outcomes for a decent price, what are we waiting for?” said Dr. McQueen, who is assistant professor in the department of clinical pharmacy at the University of Colorado, Aurora.
 

Is DKA prevention enough to justify universal screening?

Although identifying type 1 diabetes before symptoms arise could help avoid DKA, currently no therapeutic interventions are available to prevent or delay the trajectory from presymptomatic to clinical type 1 diabetes.

A possible future intervention – the anti-CD3 monoclonal antibody teplizumab (Tzield, Provention Bio) – had a setback in July 2021 when the Food and Drug Administration declined to approve it for the delay of type 1 diabetes in at-risk individuals.

However, on Feb. 22 Provention Bio announced that it has resubmitted the Biologics License Application for teplizumab for the delay of clinical type 1 diabetes in at-risk individuals. The FDA now has 30 days to review the resubmission, determine whether it is complete and acceptable for review, and provide a review goal date, according to a company statement.

But even without the ability to forestall the development of type 1 diabetes, screening proponents point to the potential benefit from educating families about early signs of diabetes onset and thereby preventing progression to DKA and both its short-term and possible long-term sequelae.

Prevention of DKA at diagnosis has been linked to improved long-term glycemic control and other potential health benefits.

And the frequency of DKA at the onset of type 1 diabetes has increased in recent years, to more than 20% in Germany and over 45% in the United States.

But, prior data have suggested that universal screening for presymptomatic type 1 diabetes is unlikely to be cost effective if only the health and economic benefits of prevention of DKA at type 1 diabetes onset is considered, unless the screening costs are exceedingly low.
 

What will it take to implement universal screening?

“What this paper does is contribute really to our understanding of more around resource utilization,” noted Dr. McQueen. “As they correctly identify, it’s really hard to compare country prices. It’s easier to compare utilization.”

In Dr. McQueen’s ASK program, the cost per child screened and per case detected in that program were similar to those found in the German study, even though the cost of the antibody testing itself was considerably lower in Germany than in the United States.

Fr1da included more components of screening and monitoring than did ASK, Dr. McQueen told this news organization.

The conclusions of the ASK study were that “presymptomatic type 1 diabetes screening may be cost effective in areas with a high prevalence of DKA and an infrastructure facilitating screening and monitoring if the benefits of avoiding DKA events and improved [hemoglobin] A1c persist over long-run time horizons.”

Nonetheless, Dr. McQueen thinks it’s unlikely that universal screening will be recommended by professional societies or covered by payers in the United States until a pharmacologic intervention to forestall disease progression is available.“Teplizumab approval could move this along. ... We’re just trying to take one factor, the economics of it, to create the most efficient scenario so that if it were to be adopted we would catch the most cases, prevent the most complications, benefit children the most in terms of their lifetime health outcomes – all at the minimum cost possible.”
 

‘A benchmark for the expected implementation cost of screening’

Mr. Karl and colleagues simulated the cost of implementation of this screening as standard care in Germany – assuming the same 0.31% prevalence found in Fr1da – the average cost per child was estimated at 21.73 euros, including 9.34 euros for laboratory costs, 12.25 euros for pediatrician costs, and 0.14 euros for local diabetes clinics to perform metabolic staging and education for children diagnosed with presymptomatic type 1 diabetes.

The model included 50% of the costs incurred in Fr1da for obtaining informed consent. Negative autoantibody results from the initial screening were not communicated to families, and all children with presymptomatic type 1 diabetes received staging and education. The estimated average cost per diagnosed child was 7,035 euros.

“Although our analyses are subject to some level of uncertainty, they provide a benchmark for the expected implementation cost of screening,” said coauthor Michael Laxy, MSc, PhD, also at Helmholtz Zentrum München.

“Next, we aim to evaluate the long-term ratio of screening costs, potential cost savings through the prevention of metabolic derailment and its consequences, and potentially increased quality of life with a type 1 diabetes screening compared to the costs and quality of life without a screening.”

Dr. McQueen is working along similar lines in Colorado, attempting to create a model that incorporates all the different possibilities including DKA monitoring, teplizumab availability, screening children at different ages, and the effect of including blood glucose monitoring in children identified with presymptomatic type 1 diabetes.

“There are so many different potential answers and avenues and no one has really put it all together,” he observed.

But he believes that economics shouldn’t be the only factor used in deciding whether to institute widespread screening.

This study was supported by grants from the German Federal Ministry of Education and Research to the German Center for Diabetes Research (DZD). The Fr1da study was supported by grants from the LifeScience-Stiftung, JDRF International, the Bavarian State Ministry of Health and Care, the Leona M. and Harry B. Helmsley Charitable Trust, Deutsche Diabetes-Stiftung, Landesverband Bayern der Betriebskrankenkassen, B. Braun-Stiftung, Deutsche Diabetes Hilfe, and the German Federal Ministry of Education and Research to the DZD. The authors disclosed no relevant financial relationships. The ASK study was funded by JDRF International, the Leona M. and Harry B. Helmsley Charitable Trust, and Janssen Research and Development. Dr. McQueen has received institutional funding for value assessment applications from the Institute for Clinical and Economic Review, the PhRMA Foundation, and PhRMA.

A version of this article first appeared on Medscape.com.